C. Tubercle Bacilli in Meningeal Fluid 
Descriptive Text, Page xviii. 
B. Tubercle Bacilli in Sputum 
A. Tubercle Bacilli in Sputum Handbook of Tuberculosis 
for 
Medical Students and Practitioners 
of Medicine 
by 
JOHN RITTER, PhG., M.D. 
W I 
Assistant Professor in Medicine (Department of Tuberculosis) Rush 
Medical College, Medical Department of the University of 
Chicago, Instructor in Physical Diagnosis, 
Clinical Instructor and Lecturer 
on Tuberculosis, etc. 
Member National Tuberculosis Association, Mississippi Valley Tuber- 
culosis Conference, Chicago Tuberculosis Institute and 
President Chicago Tuberculosis Society, 
Past President Robert Koch 
Society, etc. 
One Colored Plate (frontispiece) Showing Stained Specimens 
with Tubercle Bacilli Under the Microscope, and Sixty- 
One Illustrations Throughout the Text 
CHICAGO, 1923 Copyrighted 1923 
by 
John Ritter. 
CRAFTSMEN PRINTERS 
701-703 So. La Salle St. 
Chicago This Volume 
is affectionately inscribed to the earnest medical 
student in quest of accurate knowledge concern- 
ing the many intricate problems in tuberculosis, 
and to the busy practitioner who wishes to re- 
fresh his memory about the various tuberculous 
disorders which may confront him in his usual 
daily labor, it is respectfully dedicated by the 
AUTHOR. INTRODUCTION 
The compilation of this volume is based upon lectures, reci- 
tations, quizzes and clinical demonstrations given for many 
years at Rush Medical College to students of medicine and to 
medical practitioners who were especially interested in the 
problem of tuberculosis. In addition, abstracts which have been 
prepared from papers on tuberculosis topics which were read 
before the National Tuberculosis Association and from addresses 
delivered before various tuberculosis and health conferences 
furnish a part of this volume. Further, in the second part of the 
book—the section on Clinical Tuberculosis—appear many lec- 
tures and papers on Tuberculosis and its Complications delivered 
or read before my classes by well-known specialists in their re- 
spective branches, to whom due credit is given and mention 
made. These lectures and papers have been either abstracted or 
appear in their entirety in that section. 
A perusal of this volume will convince the reader that in many 
respects it differs very much from the general text or hand books 
of tuberculosis. Having taught for years the principles under- 
lying physical diagnosis, I have learned one thing, namely, that 
these principles as they are imparted to students are not always 
well understood and not only that, often times, even after years 
of practice, these principles of physical diagnosis are still some- 
what hazy and vague. 
The principles of physical examination like anything else in 
medicine which is to lead to success, can only be acquired by 
constant and diligent observation, repetition and study, and this 
requires time. For a number of years I have taught that a mas- 
tering of the principles of physical diagnosis requires the care- 
ful examination of hundreds of chests or perhaps a thousand, but 
I have long since modified this teaching and I now say that when 
you have made many thousand careful chest examinations, you 
may, perhaps, have acquired a fairly good knowledge of these 
physical findings, provided you have thoroughly understood and 
were able to interpret correctly the signs observed and the 
sounds heard. 
As a thorough knowledge of physical diagnosis is most essen- 
tial to an understanding and a proper interpretation of the sounds 
V VI 
INTRODUCTION 
produced within the chest cavity (and this applies particularly to 
pulmonary tuberculosis), it occurred to me that a constant re- 
minder of the findings in the normal chest is absolutely necessary, 
and so I have drawn parallel lines between which I constantly 
endeavor at all times to draw a comparison—the normal with the 
pathological. It has been my privilege to observe that by such 
a method the student is better prepared to master and to under- 
stand the different chest findings, that is, by comparing the 
abnormal with the normal, right on the spot, rather than to refer 
only occasionally to normal findings; this plan is followed 
throughout the entire section on clinical tuberculosis. 
The study of tuberculosis and of the tuberculosis problem in 
general as the physician encounters it in his daily work may be 
viewed from a threefold angle, namely, the social, the economic 
and the medical aspect. Both the social and the economic aspect 
belong more appropriately to the domain of the social worker, 
the philanthropist, the charity organizations and to the various 
antituberculosis organizations and movements. Although the 
physician must be vitally interested in the whole problem of 
tuberculosis, in the social as well as in the economic aspects, his 
chief interest, usefulness and influence lie in combating the dis- 
order from the medical standpoint. 
As this manual is mainly of interest to students in medicine 
and to physicians, I will not consider the problem other than 
from a medical standpoint, leaving the social and economic 
aspects to their proper domain. The medical aspect of this im- 
portant and interesting problem in tuberculosis may for conveni- 
ence of study be presented in three distinct and separate parts, 
namely, part one, which considers all those questions purely of 
an academic nature, part two, the elucidation of clinical tuber- 
culosis, which forms by far the greater division; and part three, 
which views the subject from the standpoint of laboratory 
diagnosis. COLLABORATORS AND CONTRIBUTORS 
In the compiling of a supposedly standard, up-to-date hand book 
of tuberculosis, one especially intended for medical students, I have 
aimed to include, as nearly as possible, all the various phases of the 
disorder as they manifest themselves in disturbances in the organs 
and tissues of the human body; so, in the second part, the section on 
clinical tuberculosis, I have availed myself in many instances of the 
services of such of my colleagues who are specialists in the various 
branches of Medicine and who have made an intensive study of the 
problems of tuberculosis as they relate to these various branches. 
Many of the following chapters are based either upon the lectures 
delivered or the clinical instruction given before my classes during 
the various summer quarters at Rush Medical College. Some ap- 
pear almost in entirety, some have been abstracted, and additions 
and notations made so as to appear in harmony with the up-to-date 
teachings concerning tuberculosis of the different organs of the 
human body. 
The credit for this labor and the compiling of these chapters is due 
to my associates and colleagues as follows: 
Chapter 16. “Roentgenology in Pulmonary Tuberculosis.” Dr. Cassie 
Bell Rose, Roentgenologist to the Presbyterian Hospital and Instructor 
in Surgery (Radiology) Rush Medical College. 
Chapter 20. “The Surgical Treatment of Pulmonary Tuberculosis.” That 
part of this chapter which describes the technic for the treatment of pul- 
monary tuberculosis by means of artificial pneumothorax is based upon 
a lecture delivered and the clinical demonstration for the induction of 
lung compression given by Dr. Everett Morris, formerly Medical Super- 
intendent of the Oak Forest, Illinois, Tuberculosis Sanatorium. 
Chapter 22. “Physiotherapy—Occupational, Vocational.” Dr. Clarence L. 
Wheaton, Instructor in Medicine. 
Chapter 23. “Tuberculosis in Children.” That part of the physical exam- 
ination, “Radiography, or the Roentgenology of Tuberculosis in Chil- 
dren,” should also be accredited to the labors of Dr. Cassie Bell Rose, and 
the treatment of Tuberculous Adenitis be accredited to Dr. A. R. Metz, 
Surgeon and Roentgenologist at the Washington Boulevard Hospital. 
Chapter 26. “Tuberculosis and Pregnancy.” Dr. C. Henry Davis, Mil- 
waukee, Wisconsin. Formerly Assistant Professor of Obstetrics and 
Gynecology at Rush. 
Chapter 28. “Tuberculous Laryngitis.” Dr. Elmer L. Kenyon, Assistant 
Professor of Laryngology and Otology. 
VII VIII 
COLLABORATORS AND CONTRIBUTORS 
Chapter 30. “Tuberculosis of Bones and Joints.” Dr. Edwin W. Ryerson, 
Associate Professor of Surgery (Orthopedic). 
Chapter 31. “Tuberculosis of the Genito-Urinary Organs.” Dr. Herman 
L. Kretschmer, Assistant Professor of Surgery (Genito-Urinary). 
Chapter 32. “Tuberculosis of the Skin.” Dr. Edward A. Oliver, Assistant 
Professor of Skin and Venereal Diseases. 
Chapter 33. “Tuberculosis of the Eye.” Dr. William G. Reeder, Assistant 
Professor of Ophthalmology. 
Chapter 37. In the third part of this book—“The Blood in Tubercu- 
losis.” “Complement-fixation in Tuberculosis”—Dr. H. J. Corper. for- 
merly in charge of the Pathological Laboratory of the Municipal Tuber- 
culosis Sanatorium of this city, has kindly contributed this part of the 
chapter which is given somewhat in detail. 
Others, who in no less degree have contributed to the success of this 
volume, should here be mentioned—The late Dr. Willard W. Dicker, who 
for many years was associated with me in tuberculosis work at the Muni- 
cipal Tuberculosis Dispensary at Rush Medical College. To Drs, Fuller 
B. Bailey and Rollin H. Moser, internes at the Washington Boulevard 
Hospital, for their kind contributions to that part of the volume cover- 
ing the field of physical exploration of the chest, to Dr. Harry Gauss, 
Denver, Colorado, who so kindly suggested some of the necessary correc- 
tions, additions and notations to Chapter 37—“The Blood in Tubercu- 
losis.” To the Librarian, Miss Catherine A. McAuliff, and Assistant Lib- 
rarian, Miss Anna P. McAuliff of the Rush Medical College Library for 
their kind assistance in looking up the literature on various tuberculosis 
topics, and to Miss Eleanor P. Fox for the arranging and executing of 
the necessary stenographic manuscripts, notes, etc. 
I am most grateful and under lasting obligation to all for the generous 
collegiate spirit shown, for the noble contribution of both time and labor, 
which alone was the incentive which enabled me to present to the student 
body a concise and clear survey of this most intricate, interesting, and 
engaging problem—“The Study of Tuberculosis.” TABLE OF CONTENTS 
PART ONE 
CHAPTER 1 
Page 
The Purely Academic Questions in the Study of Tuberculosis . 1 
A Breif History of Tuberculosis Beginning With Remote Time and 
Leading up to the Present 3 
Hippocrates; Aristotle; Celsus; Pliny; Galen; Areteus; Avicenna; 
Paracelsus; Sylvius; Fracastori; Fabricius; Forester; Richard Mor- 
ton ; Morgagni; Rush; Matthew Baillie; Mangetus; Bayle; Laen- 
nec; Broussais; Lebert; Virchow; Buhl; Cruveilhier; Kortum; 
Klenke; Villemin; Chaveaux; Weigert; Edwin Klebs; Rokitansky; 
Koster; Schueppel; Friedlander; Lannelongue; Robert Koch; 
Cornet; v. Behring; Calmette; v. Pirquet; Mantoux; Marcus Pater- 
son; Nathan Raw; Edward S. Trudeau; Theobold Smith. 
CHAPTER 2 
The Etiology of Tuberculosis. The Tubercle Bacillus. Its Growth, 
Development and Peculiar Characteristics 9 
The tubercle bacillus; Types and varieties; Other known varieties; 
Description and characteristics; Morphology; Pleomorphism; Tinc- 
torial characteristics; Cultural characteristics; Pathogenic character- 
istics ; Infecting characteristics; Chemical composition; Special 
adaptation characteristics; Much’s granules. 
CHAPTER 3 
The Portals of Entry or Atria of Infection. How and in What 
Way the Germs Gain Entrance Into the Human Body . . 16 
Porta Infectionis: (1) The aerogenous route; (2) The enterogenous 
route; (3) The cutaneous or dermal route; (4) The genitogenetic 
route, congenital or inherited, placental transmission; (5) The 
cryptogenetic route; Animal experimentation. 
CHAPTER 4 
Description and Explanation of the Various Theories Advanced 
About Heredity, Disposition, Predisposition and Diathesis in 
Tuberculosis 24 
The tuberculous tendency; The idiopathic disposition; The toxipathic 
disposition; The toxipathic factors; The hereditary factors; Other 
noticeable tendencies or dispositions. 
CHAPTER 5 
A Logical Conception of Our Present Day Knowledge Concerning 
Infection and Contagion in Tuberculosis 29 
Infection and contagion; Definition of terms; Communicable disease; 
Infrequently from adult to adult; Infection in infancy; In the mar- 
ried; Husband from wife or wife from husband; Conjugal tuberculosis 
infrequent; Implantation not sufficient. 
IX TABLE OF CONTENTS 
X 
CHAPTER 6 
The Primary Focus or Foci of Infection Most Frequent in the Lungs 
and the Subsequent Effect on the Pulmonary Tissue . . 35 
Historical data; Parrot’s law; The primary foci; Kiiss; Albrecht; 
Ghon; Peribronchial lymph nodes; The bronchial tree; The muscle 
fibres; The bronchial lymphatics; The epithelial lining; The nucleus 
of a cell; The non-nucleated cells; The lymph flow; Retrogressive 
changes; Reactivation; Special predilection; Recapitulation. 
CHAPTER 7 
The Course of Tuberculous Disease in the Different Ages—from 
Infancy to Old Age 50 
General consideration; Intra-uterine infection; Extra-uterine infec- 
tion; Massive infection; Mild infection; Primary tuberculous disease; 
Secondary tuberculous disease; Tertiary tuberculous disease; The 
tuberculosis mortality; In infancy avoid infection, in youth disease; 
Resume. 
CHAPTER 8 
Histology and Pathology of the Tubercle 56 
Structure and formation of the tubercle; Genesis of the tubercle; 
Epithelioid cells; Cell proliferation; Inflammations, necrosis, fibrosis; 
Giant cells; Encapsulation, caseation, softening; Location of the 
tubercle; Ultimate fate. 
CHAPTER 9 
The Mechanism of Immunity or the Immunizing Activities . . 61 
General Consideration; Immunity; Virulence; Resistance; Acquired 
or inherited; Congenital immunity; The tuberculous immunity; The 
acquired tuberculous immunity; Reinfection; Primitive races; Im- 
munity only in the tuberculous organism; Bacteria and body cells in 
constant warfare; Various methods of tuberculous immunization; 
Resistance in animals; The local suppurative process; Hypersensitive- 
ness; Sensitization. 
PART TWO 
CLINICAL TUBERCULOSIS 
CHAPTER 10 
Clinical Tuberculosis 69 
Pulmonary Tuberculosis, Phthisis Pulmonum, Phthisis Pulmon- 
alis, Phthisis, Consumption, Tuberculosis, etc. Schematic 
Classification 71 
Terms, generic, specific; A progressive disease; Variable duration; 
Incipiens, Confirmata, Desperata; National Tuberculosis Association 
schema for the classification of patient on examination; Incipient, 
first stage; Moderately advanced, second stage; Far advanced, third 
stage; Acute tertiary tuberculosis; Generalized; Turban-Gerhardt 
schema; Supplemental report; Lesions; Symptoms; The author’s 
classification; Pottenger’s schema; The term incipient in use. 
CHAPTER 11 
The Symptomatology of Tuberculous Disease 79 
Symptoms of latency; Symptoms of activity; Prodromal symptoms, 
the symptoms of latency; Subjective and objective symptoms, the 
symptoms of activity, cough, expectoration, pain, gastric distress, 
dyspnoea, hemorrhage, night sweats, temperature, pulse, mental symp- 
toms, loss in weight, menstruation, hoarseness, blood pressure, etc. TABLE OF CONTENTS 
XI 
CHAPTER 12 
Clinical Forms of Pulmonary Tuberculosis, Clinical Varieties . 88 
Grouping and Classification; Typical and atypical forms; Clinical 
nomenclature; Typical types of tuberculosis; The exudative, caseous 
form; Characteristic signs and symptoms; Differentiation, from 
broncho-pneumonia, from lobar or croupous pneumonia; The pro- 
liferative, nodular form; Characteristic signs and symptoms; The 
cirrhotic, fibroid form; Characteristic signs and symptoms; Differ- 
entiation of the three forms; Atypical or aberrant forms; Miliary 
tuberculosis; Diagnosis; Symptoms; Other atypical forms of tuber- 
culosis. 
The Diagnosis of Pulmonary Tuberculosis 100 
Introduction into the methods of physical examination of the chest; 
History taking in tuberculosis; Family history; Personal history; 
Present history. 
CHAPTER 13 
Inspection of the Chest 105 
How to examine the chest; Position of patient; The normal chest on 
inspection; The landmarks; Symmetrical or asymmetrical; Anterior, 
posterior and lateral; The abnormal chest; Prima vista diagnosis; 
The stigmata of tuberculosis; Chest deformities; The stenotic chest; 
The infantile chest; The phthisical chest; Other suspicious signs 
pointing to tuberculous disease; Chest measurements; Kyphosis, 
scoliosis, kypo-scoloisis, lordosis; Habitus asthenicus; Litten’s phe- 
nomenon; Integument atrophy; The phthisical facies, etc. 
CHAPTER 14 
Palpation of the Chest 119 
Definition; Methods of palpation; Palpation of the normal chest; 
Palpation of the abnormal chest; Muscle spasm; Tender points; 
Algoscopy. 
CHAPTER 15 
Percussion of the Chest . 125 
Topography of the thoracic organs; Anterior, posterior, lateral sur- 
face; The borders of the lungs; Methods of percussion; Percussion 
of the normal chest; How to percuss correctly; Percussion of the 
abnormal chest; Kroenig’s method; Goldscheider’s method; Aberra- 
tions; Sources of error, percussion sounds which may be mistaken 
for tuberculous infiltration; Palpatory percussion; The (tubercu- 
lously) infiltrated lung (schematically). 
CHAPTER 16 
Auscultation of the Chest. (Including the Mechanism of Breathing) 148 
General consideration; Methods of Auscultation; Auscultation of the 
normal thoracic sounds, the normal breath sounds; Abnormal auscul- 
tory murmurs in pulmonary tuberculosis; Auscultory catarrhal signs, 
dry and moist rales, adventitious sounds, abnormal chest sounds; 
Normal vocal sounds; Voice resonance; Abnormal vocal sounds; 
Whispering bronchophony in pulmonary tuberculosis; How and when 
to ausculatate; Errors in the auscultory sounds; The mechanism of 
breathing; Explanatory notes to figure 22. XII 
TABLE OF CONTENTS 
CHAPTER 17 
Roentgenology. The Relation of the X-Ray to the Diagnosis of 
Pulmonary Tuberculosis 164 
Historical data; General consideration; The normal chest plate; 
Markings, shadows and findings; Normal findings; The diagnostic 
quality of plate or screen; Contour and subcutaneous structure; The 
bony structures; The diaphragm; The mediastinum; The hilus shad- 
ows; The lung markings; Variations from the normal; Interpretation 
of pathological chest findings; Screen examinations, fluoroscopy; 
Advancing tuberculosis; Active tuberculosis; Differential diagnosis; 
Pneumonia; Broncho-pneumonia; Influenzal pneumonia; Miliary tu- 
berculosis ; Carcinoma, metastatic; Sarcoma ; Pulmonary hemorrhage; 
Fibroid phthisis; Cavitation; Hydrothorax; Pleural thickening; 
Densities, localized, generalized; Pneumothorax; Hydro-pneumo- 
thorax. 
CHAPTER 18 
Mensuration, Succussion, Vital Capacity, etc 194 
Mensuration, measurements of the Chest; Succussion; Succussion 
murmurs, splashing sounds; Vital capacity; Spirometry; Estimation 
of the vital capacity. 
CHAPTER 19 
The Care of the Tuberculous. 199 
The treatment of pulmonary tuberculosis. General Therapy: Ambula- 
tory; Home; Sanatorium; Dietetic-Hygienic; Medical; Tuberculin, 
etc. Health and disease; Sources of infection; The general care of 
the Tuberculous; The ambulatory cases; The bedfast or home cases; 
The sanatorium cases; A threefold problem; General therapy in tuber- 
culosis; The six necessary factors; (1) Contentment, or ease of 
mind; (2) Wholesome fresh air; (3) Rest and exercise; (4) (a) 
Dietetic-Hygienic; (b) Zomotherapy; (c) Lactotherapy; (5) Time; 
(6) Obedience; Symptomatic treatment; Fever; Pulse; Cough; 
Night sweats; Dyspnoea; Sleeplessness; Gastro-intestinal disturb- 
ances ; Diarrhoea, etc. 
CHAPTER 20 
The Care of the Tuberculous (Continued) 228 
The surgical treatment of pulmonary tuberculosis; Artificial pneumo- 
thorax or compression of the lung; Historical notes; Resume from 
Historical data; Observation on compression of the lungs; Cases 
suitable for lung compression; Indications and contraindications; To 
summarize; Apparatus and technic; Complications incident to the 
production of artificial pneumothorax; Immediate and Ultimate re- 
sults ; Thoracotomy; Pneumonotomy; Pneumonectomy; Pneumolysis; 
Phrenicotomy; Thoracoplasty; Chondrotomy. 
CHAPTER 21 
Some Associated Therapeutic Measures in Pulmonary Tuberculosis. 250 
Chemotherapy in pulmonary tuberculosis; Chemicals and chemical 
bases; Water soluble dyes; Organic acids; Tincture of iodine; 
Heliotherapy; Sunbaths; Historical note; Heliotherapy in tubercu- 
losis ; Effect of Heliotherapy on the human body; The effect of insola- 
tion on individual organs and tissues of the body; Heart, blood pres- 
sure, kidneys, mind, metabolism, etc.; Posological consideration; 
Technic and clinical results; Results in Europe; Results in our coun- 
try; Hydrotherapy in pulmonary tuberculosis; The cold bath; The 
warm bath; Pulmonary gymnastics; Use and abuse; Indications and 
contraindications; How to practice pulmonary gymnastics. TABLE OF CONTENTS 
XIII 
CHAPTER 22 
Physiotherapy in Pulmonary Tuberculosis 273 
Vocational and occupational therapy, rehabilitation, reconstruction. 
Historical data; General consideration; Rational physiotherapy; Re- 
habilitation of the handicapped, the tuberculous soldier; Reconstruc- 
tion of the tuberculous in civil life; Graduated labor, rest and exer- 
cise; Paterson’s method for applying “Rest and Exercise” treatment. 
CHAPTER 23 
Tuberculosis in Children. Tuberculosis of the Tracheo-bronchial 
Lymph Nodes 284 
(a) The primary stage of tuberculous disease in children; Primary 
tuberculosis; Clinical manifestations as seen in infant life; Bronchial 
gland tuberculosis; Tuberculosis of the tracheo-bronchial lymph 
nodes; Glandulae tracheo-bronchialis; Signs and symptoms of gland 
tuberculosis; Physical examination and diagnosis; Inspection; Pal- 
pation; Percussion; Auscultation; Roentgenology; Tuberculin; (b) 
The secondary stage of tuberculous disease in children; Secondary 
tuberculosis; The secondary form of the disease; Metastatic form; 
Acute miliary tuberculosis in children; Meningeal tuberculosis in 
children; (c) The tertiary stage of tuberculosis in children; The 
tertiary or pulmonary form of the disease. Therapy; (a) The treat- 
ment of tuberculosis of the tracheo-bronchial lymph nodes. (1) Pro- 
phylaxis; (2) Symptomatic treatment; (3) Specific therapy; (b) The 
treatment and care of the metastatic form of tuberculosis in children; 
■(c) The treatment and care of the tertiary form of tuberculosis in 
children, the pulmonary; The groups of glands; (a) cervical, (b) 
tracheo-bronch'al and (c) other lymph nodes; Palpable glands in 
children; The treatment of tuberculous adenitis; Constitutional con- 
dition; Local treatment; The primary point of invasion; The fre- 
quency of tuberculosis in children. 
CHAPTER 24 
Tuberculin, a Probuct of Bacillary Growth and of Metabolism . . 307 
Descriptive note; What led to the discovery of tuberculin? The tuber- 
culin reaction; Explanation of the tuberculin reaction; (1) Koch’s 
view or explanation; (2) The Wolff-Eisner theory; (3) Ponndorf’s 
law; Various kinds of tuberculins; (1) old tuberculin O. T.; (2) 
Deny’s boullion filtrate B. F.; (3) Tuberculin, B. O. T.; (4) New tu- 
berculin T. R.; (5) Bacillen emulsion, B. E.; (6) Polyvalent teubercu- 
Iin; (7) Tuberculin, Beraneck, T. B. K.; (8) Spengler’s I. K.; (9) 
Albumose, free tuberculin, T. A. F.; (10) Endotoxin, tuberculinum 
purum ; (11) Partial antigens; (12) Friedmann’s vaccine; (13) Serum 
therapy, Maragliano, Marmoreck; The use of tuberculin; therapeutic 
indications; (1) In localized colonies; (2) In generalized tuberculosis; 
When, how and how long should tuberculin be administered? The 
methods of administration; Begin with most minute doses; Various 
other therapeutic methods for the tuberculin administration; Contra- 
indications in the use of tuberculin; Tuberculin for diagnostic 
purposes; The various tuberculin tests; (1) The ophthalmic or con- 
junctival; (2) The Moro or percutaneous; (3) The v. Pirquet or cu- 
taneous; (4) The Mantoux or intradermal; The negative tuberculin 
reaction; The positive tuberculin reaction; The nature of resistance 
to tuberculosis; Tuberculin dilutions; The Beraneck scale; The stand- 
ard tuberculin dosage; The standard scale; Table of standard dilu- 
tions. See page 542, TABLE OF CONTENTS 
XIV 
CHAPTER 25 
Tuberculosis and Pleurisy, Idiopathic Pleurisy, Tuberculous Pleu- 
risy 335 
General consideration: The frequency of tuberculous pleurisy, Symp- 
toms; The course of the disease; Physical examination; (a) By in- 
spection; (b) By palpation; (c) By percussion; (d) By auscultation; 
Diagnosis; Differential diagnosis; Differentiation between lobar pneu- 
monia and pleurisy; Exploratory puncture and paracentesis; Where 
to puncture; Prognosis; Medical treatment; Surgical treatment of 
pleurisy; Empyema, rib resection, etc.; Autoserotherapy; Diaphrag- 
matic pleurisy; Sacculated pleurisy; Summary and conclusions. 
CHAPTER 26 
Tuberculosis and Pregnancy 347 
General consideration: (1) Amenorrhoea and sterility in tuberculous 
women (2) Incidence of tuberculosis among pregnant women; (3) 
Effect of tuberculosis on pregnancy; (4) Effect of pregnancy on 
tuberculosis; (5) Effects of maternal tuberculosis on the fetus; 
(6) Nursing and tuberculosis; (7) Birth control among the tubercu- 
lous; (8) Prophylaxis of tuberculosis in pregnancy; (9) Treatment 
of tuberculosis with pregnancy; (10) Treatment of pregnancy with 
tuberculosis; Therapeutic abortion. 
CHAPTER 27 
Tuberculosis and Pulmonary Hemorrhage 367 
Hemorrhage in tuberculosis; Symptoms of pulmonary hemorrhage; 
General consideration; The treatment of pulmonary hemorrhage; By 
mechanical methods; By medicinal means; Prophylaxis; Practical 
rules for controlling pulmonary hemorrhage. 
CHAPTER 28 
Tuberculous Laryngitis 369 
Tuberculosis of the larynx, laryngeal phthisis; General consideration; 
Etiology; Primary tuberculosis of the larynx; Course of the Disease; 
Physical manifestations; The earliest manifestations; Forms of laryn- 
geal disease; (1) Infiltration; (2) Tumor formation; (3) Ulceration; 
(4) The miliary form; Pathology; Symptoms; Diagnosis; Differen- 
tial diagnosis; (a) Tuberculous laryngitis; (b) Chronic simple laryn- 
gitis; (c) Syphilitic laryngitis; (d) Carcinoma of the larynx; 
(e) Lupus of the larynx; Prognosis; Treatment; (1) Prophylactic; 
(2) General local measures; Nerve blocking. 
CHAPTER 29 
Tuberculous Peritonitis 388 
Tuberculosis of the peritoneum; Tuberculosis of the abdomen; Tabes 
mesenterica; Primary and secondary; General consideration; Etiol- 
ogy; Clinical forms; Symptoms of tuberculous peritonitis; Diagnosis; 
Differential diagnosis; Prognosis; Therapy; Surgical treatment; 
Medical treatment. 
CHAPTER 30 
Tuberculosis of Bones and Joints . ... . . . . 396 
General consideration; Symptomatology and diagnosis of bone and 
joint tuberculosis; Symptoms of reflex pain; Differential diagnosis; 
Complications; Treatment of bone and joint tuberculosis; (a) Con- 
servative treatment; The treatment of spinal tuberculosis; The treat- 
ment of hip and knee joint tuberculosis; (b) Operative treatment; 
Tuberculosis of the spine in adults; Tuberculin. TABLE OF CONTENTS 
XV 
CHAPTER 31 
Tuberculosis of the Genito-Urinary Organs 410 
General consideration; fA) Tuberculosis of the urinary tract; (1) Tu- 
berculosis of the kidney; Frequency; Age; Sex; Side involved; Pre- 
disposing factors; fa) Tramatism; (b) Stone; (c) Pyelitis; Patho- 
genesis; fl) Hematogenous; (2) Lymphogenous; f3) Urogenous; 
Symptoms; fa) Kidney; Tenderness to pressure; fb) Colic; (c) Blad- 
der symptoms: Frequency of urination; fd) Pain; fe) Pyuria; 
ff) Hematuria; Pathology; General symptoms; Diagnosis; fa) Gen- 
eral; fb) Urinalysis; fc) Tubercle bacilli in the urine; fd) Animal 
inoculation; Diagnostic use of tuberculin ; Special methods of diag- 
nosis; fl) Cystoscopy and uretral catherization; (2) Roentgen ray; 
f3) Functional kidney tests; f4) Chromoscopy; Differential diagnosis: 
fl) Lesions of the kidney other than tuberculosis; f2) Lesions of 
other abdominal viscera; fl) Gallstones; (2) Appendicitis; f3) Pel- 
vic disease in women; The course of renal tuberculosis; Prognosis; 
Causes of death; Treatment; Tuberculin: Surgical treatment; Results 
of operation; After treatment. fB) Genital tuberculosis: Patho- 
genesis ; Pathology; Symptoms: Diagnosis; Differential diagnosis; 
Prognosis; Treatment; Tuberculin; Surgical treatment; Conserva- 
tive; Radical. 
CHAPTER 32 
Tuberculosis of the Skin 429 
General consideration: Etiology; Types and varieties; Pathology; 
Diagnosis and description of the lesions; fl) Lupus vulgaris; Differ- 
entiation; fa) Nodtilar svphilide; fb) Blastomycosis; fc) Lupus 
erthyematosus; fd) Sacroid of boeck; f2) Tuberculosis verrucosa 
cutis; f3) Scrofuloderma; f4) Tuberculosis cutis orificialis; The 
tuberculides; fl) Lichen scrofulosorum; Acne variolaformis; 
f2) Folliclis; f3) Acnitis; (4) Acne scrofulosorum: f5) Acne 
cachecticorum: f6) Erythema induratum; f7) Sarcoid of boeck; 
f8)Lupus erythematosus; The treatment of cutaneous tuberculosis; 
General and local treatment; Erythema nodosum and tuberculosis; 
Etiology and semeiologv. 
CHAPTER 33 
Tuberculosis of the Eye and the Mucous Surfaces .... 441 
fA) Tuberculosis of the Eye; General consideration; Predisposing 
factors; Symptoms: Tuberculosis of the evelids: The conjunctiva, 
nhlyctenular keratitis; The cornea; The sclera; The tunica vascu- 
losa; fa) The ciliarv body and the iris; fb) The choroid: fc) The 
retina: fd) The optic nerve; fe) The orbit; Diagnosis; Treatment; 
fB) Tuberculosis of the mucous surfaces; fa) Primary; fb) Secon- 
dary; Treatment. 
CHAPTER 34 
Tuberculosis and the Cardio-Vascular System 450 
fl) Tuberculosis and the heart; (2) Tuberculosis and the pulmonary 
circulation; (3) Tuberculosis and tachycardia; f4) Tuberculosis and 
hypotension; (5) Blood pressure observations in tuberculosis; Sum- 
marizing. 
CHAPTER 35 
Tuberculosis Following Trauma and Shock 463 
The relation of trauma and shock to pulmonary tuberculosis: (1) 
Causes and definition of shock; (2) Signs and symptoms; (3) The 
influence of trauma and shock upon the tuberculous process; fa) Class 
in which traumatism itself is the causative factor; (b) Class in which 
shock appears as the main cause; Case histories; Summarizing. PART THREE 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
CHAPTER 36 
The Sputum in Tuberculosis 475 
General consideration; The non-tuberculous sputum; The sputum in 
pulmonary tuberculosis; How and when to collect the sputum; Exam- 
ination of the sputum; (1) Microscopical; (a) The tubercle bacillus 
in the sputum; An improved staining technic; Much’s granular stain; 
Ritter’s scale; Gaffky’s scale; Solutions used for staining and de- 
staining; (b) The small lymphocytes in tuberculous sputum; (2) 
The chemical examination of the sputum; The great importance of 
properly collecting the sputum for chemical examinations; Direc- 
tions for making the albumin test; (3) Combined microscopical and 
chemical examination of the sputum. 
CHAPTER 37 
The Blood in Tuberculosis . 489 
General consideration; Hematology; The hemoglobin; The erythro- 
cytes ; The leucocytes; The blood as a whole in pulmonary tubercu- 
losis ; Arneth’s blood picture of the polymorphonuclear leucocytes in 
tuberculosis; The tubercle bacillus in the blood stream; The technic 
for preparing blood for microscopic examination; (a) The apparatus; 
(b) The technic; Serological and immunological considerations of the 
blood; Complement fixation in tuberculosis; General considerations; 
Historical data in complement fixation; Antigens; The Wassermann 
reaction; The complement fixation test in tuberculosis; Technic of 
the complement fixation test for tuberculosis. 
CHAPTER 38 
The Urine, Milk, Feces, Bile, Pleural Exudates, Spinal and Peri- 
toneal Fluids, etc., in Tuberculosis 507 
Bacilli (a) In the urine; (b) In mother’s milk; (c) In the feces; 
(d) In bile; (e) In exudates and fluids; The urochromogen test; 
Lime salts elimination; Cytodiagnosis; Inoscopy; Examination of the 
urine in tuberculosis; (1) The characteristics of normal urine; 
(2) Characteristics of the urine in pulmonary tuberculosis; (a) Meth- 
ods for demonstration of tubercle bacilli in the urine; Acid fast bacilli 
in the urine; (b) The demonstration of tubercle bacilli in mother's 
milk; (c) The tubercle bacilli in the feces; Animal experimentation; 
fd) Tubercle bacilli in the bile and gall bladder; Maxson’s technic; 
(e) Tubercle bacilli in exudates and other body fluids; The uro- 
chrome or coloring matter of the urine in tuberculosis; Lime elimina- 
tion in tuberculosis; Demineralization, decalcification; Cytodiagnosis 
in tuberculosis; Inoscopy. 
XVI MISCELLANEOUS 
CHAPTER 39 
Calories or Food Values 523 
The food values of proteids, fats and carbo-hydrates; Vitamines; 
Approximate table in calories; Health crusade bulletin table; Calories 
per ounce. 
CHAPTER 40 
Definition of Words, Terms and Phrases Used in Conversation and 
in the Literature on Tuberculosis 529 
Tuberculosis, tuberculous and tubercular; Tuberculously infected and 
tuberculously diseased; The open and the closed cases of pulmonary 
tuberculosis; Phthis and tuberculosis; Sanitarium and sanatorium; 
Ambulant, ambulatory; Hilum, hila, hilus; Allergy and anergy or 
anaphylaxis and ananaphylaxis; Tuberculin; (a) The positive and 
negative reaction; (b) The positive and negative phase. Manifest 
tuberculosis; Latent tuberculosis; Clinical tuberculosis; The tubercu- 
lous lesion; Immunity and virulence; Infection and contagion; Sub- 
jective and objective symptoms; Terms used in definition of “Incipient 
Tuberculosis”; (1) Slight constitutional disturbance; (2) Slight ele- 
vation of temperature; (3) Slight acceleration of pulse; (4) Absence 
of tubercle bacilli; (5) Infiltration; (6) Apex; (7) A small part of 
one lobe; Terms used in definition of “moderately advanced tubercu- 
losis”; (1) Marked impairment of function, local or constitutional; 
(2) Moderate extent of localized consolidation; (3) Evidence of 
destruction of tissue; (4) Disseminated fibroid deposits; (5) Serious 
complications; Terms used in definition of “Far Advanced Tubercu- 
losis”; (1) Marked consolidation, tubular breathing, etc.; Classifica- 
tion of terms used upon the discharge of patients; (a) Apparently 
cured; (b) Arrested; (c) Apparently arrested; (d) Quiescent; 
(e) Improved; (f) Unimproved; (g) Died; Terms used in definition 
of “Apparently Cured”; (1) Constitutional symptoms; (2) Physical 
signs of healed lesions; Terms used in definition of “Improved”; 
Terms used in definition of “Unimproved”; Terms used in definition 
of “Cured”; Terms used in definition of “Onset”; Definition of terms, 
“Temperature on admission”; Definition of “General condition on 
admission and on discharge”; Definition of term “Temperature on 
discharge”; Definition of term “Digestion on admission and on 
discharge.” 
INDEX OF SUBJECTS 
Table of Normal Standard Weights of Males Stripped and Without 
Shoes 541 
Table of Standard Tuberculin Dilutions and Their Equivalents . 542 
Index, Names of Authors and Contributors 545 
Bibliographic Index, The Literature Consulted 545 
Index (General) 559 
XVII LIST OF ILLUSTRATIONS 
Fig. Page 
FRONTISPIECE 
(A) Tubercle Bacilli in Sputum. The usual sputum picture so com- 
monly seen under the miscroscope with tubercle bacilli (some pre- 
cipitated stain), and a preponderance of small lymphocytes. See 
page 483. 
(B) Tubercle Bacilli in Sputum. From a case of miliary tuberculosis. 
The general appearance of sputum after intense and prolonged iodine 
medication. Male patient age 40, received continuously and for many 
months very large doses of tincture of iodine. (Author’s observa- 
tion. Note the clear, sharp outline of each lymphocyte, the irregu- 
lar or beaded appearance of the tubercle bacilli.) 
(C) Tubercle Bacilli in Meningeal Fluid. Miliary tuberculosis, post- 
mortem findings (smear) ; Patient, a tuberculous soldier died at 
Camp Pike, Arkansas, in 1919, age 30. (From smear prepared by 
Dr. Ernest D. Nora, Bacteriologist, Prof. Bevan’s Research Labora- 
tory, Presbyterian Hospital, Chicago.) 
1. The lung (schematic) showing a single primary focus, A. Ghon. The 
primary lung focus of Tuberculosis in Children. 1912. . . .36 
2. Lateral view of the bovine lung. From Sissons J. A. M. A., p. 1513. 
1918 .38 
3. The lung (schematic) showing the contents of a gland emptying into 
a bronchus. A. Ghon. The primary lung focus of Tuberculosis in 
Children. 1912 39 
4. A primary lobule of the lung (schematic). Prof. W. Snow Miller, 
University of Wisconsin 41 
5. The lung (schematic) showing a single primary focus and a single 
regional gland secondarily involved. A. Ghon. The primary lung 
focus of Tuberculosis in Children. 1912 45 
6. The lungs in situ in the bovine. Showing point of tuberculous elec- 
tion. From Sissons, J. A. M. A., p. 1512. 1918 47 
7. Tuberculosis Giant cell. From Koch’s original paper, 1882. (Bulle- 
tin, Chicago Tuberculosis Institute, 1916.) 57 
8. The relative death rate from Tuberculosis among Indians, Colored 
and Whites. From U. S. Public Health and Marine Hospital Serv- 
ice. 1908. 64 
9. The natural or normal landmarks on the anterior chest. Original. 107 
10. The natural or normal landmarks on the posterior chest. Original. 108 
11. Integument atrophy. Original 118 
12. The topography of the anterior chest. Original. . . . . 126 
13. The topography of the posterior chest. Original 127 
14. Viscera of the thoracic cavity in situ, right side, (TO- Original. . 129 
15. Viscera of the thoracic cavity in situ, left side, (L). Original. . 130 
16. The normal lung borders of the anterior chest. Original. . . 138 
17. The normal lung borders of the posterior chest. Original. . . 139 
18. Isthmus percussion in health according to Kroenig. Anterior and pos- 
terior view 140 
19. Posterior view of the thorax showing tuberculous involvement of the 
upper lobes (schematic). Original. ..;.... 146 
20. Anterior view of the chest showing tuberculous involvement of both 
apices (schematic). Original 147 
21. Adventitious sounds or murmurs. Original. 154 
22. The cycle of breathing. Normal breathing rhythm. Original. . 163 
XVIII LIST OF ILLUSTRATIONS 
XIX 
Fig. Page 
23. The normal chest plate. Original 166 
24. Early tuberculosis. First stage. Original 173 
25. Advancing tuberculosis. Original 176 
26. Active tuberculosis. Far advanced, third stage. Original. . . 177 
27. Pneumonia. Original .. .178 
28. Influenzal pneumonia. Post-Influenzal changes. Original. . . 179 
29. Miliary tuberculosis. Original. . 180 
30. Metastatic carcinoma, Nodular type. Original. ..... 181 
31. Metastatic sarcoma. Original. 182 
32. Pulmonary hemorrhage Original 183 
33. Fibroid phthisis. Original 184 
34. Hvdrothorax. Original 186 
35. Metastatic carcinoma, Infiltrative type. Original 189 
36. Pneumothorax. Original. 191 
37. Hydro-Pneumothorax. Original 192 
38. The death rate from Tuberculosis in the U. S. (Comparative, 1908). 
U. S. Public Health and Marine Hospital Service 208 
39. (A) The Floyd-Robinson Apparatus for compression of the lung. 
(B) Floyd-Robinson Needle. V. Mueller & Co., Chicago, 111. . 239 
40. Insolation (Schematic Diagram). From Reprint, N. Y. Medical 
Journal, 105, 11, 1917. Clarence L. Hyde and Horace La Grasso. 264 
41. The Lung (schematic) showing early cavity formation in child of 
three years. A. Ghon. The primary lung focus of tuberculosis 
in children. 1912. 285 
42. The Lung (schematic) showing early miliary disease with cavitation. 
A. Ghon. The primary lung focus of tuberculosis in children. 1912. 294 
43. Illustrating the degree of Tuberculin tolerance. Original. . . 321 
44. Tuberculin dilutions. Standard scale. Original 331 
45. The normal larynx (viewed from above) 370 
46. Sagittal section of the Upper air passages (normal). From wax 
model, E. L. Kenyon Collection. 371 
47. Interior Surface of left side of larynx (normal). From wax model, 
E. L. Kenyon Collection 372 
48. Tuberculous Laryngitis. Swelling of the Arytenoid. From E. 
Fletcher Ingals’ Collection ... 376 
49. Tuberculous Laryngitis, Granulation Tumor of the left cord. From 
E. Fletcher Ingals’ Collection 376 
50. Tuberculous Laryngitis, superficial ulceration. From E. Fletcher In- 
gals’ Collection 377 
51. Tuberculosis of the Knee Joint. Antero-posterior view. Original. . 397 
52. Tuberculosis of the Knee Joint (Lateral view, Figure 51). Original. 398 
53. Tuberculosis of the Kidney, early lesions. Original. .... 413 
54. Tuberculosis of the Kidney, Advanced. Original 415 
55. Lupus Vulgaris. Original. (Courtesy of Dr. J. F. Waugh.) . . 430 
56. Lupus Vulgaris. Original 432 
57. Tuberculosis Verrucosa Cutis. (Face.) Original 433 
58. Tuberculosis Verrucosa Cutis. (Hand.) Original 435 
59. Section of the eye (schematic). After Leber 442 
60. Zeissler Tube. From Munch. Med. Wochenschrift. 1913. . . 496 
61. Road to Health for the Tuberculous 543 PART ONE 
THE PURELY ACADEMIC QUESTIONS IN THE 
STUDY OF TUBERCULOSIS 
In order to be able to understand the various tuberculosis 
problems arising, we must at the very beginning of this study, 
at the very threshold, have a clear conception of how these micro- 
organisms first became implanted in the human body and later 
produced active disorder. Being a germ disease, we ask 
intuitively whence come these germs, how do they gain access 
into our bodies, and how do they produce or bring about dis- 
turbances? This brings us to an intensive and interesting study 
of various questions, most of which have only a more or less 
academic importance. These questions will be taken up sepa- 
rately in orderly sequence, divided into nine chapters. CHAPTER 1 
THE HISTORY OF TUBERCULOSIS 
Tuberculosis, the most widely disseminated and most chronic 
of all diseases, was well known to the ancients and, although no 
special mention is made in the writings of the Egyptians, Baby- 
lonians, Chinese, Jews, etc., all primitive races were undoubt- 
edly acquainted with this disease (13), (30). 
Hippocrates, B. C. 464-376, the father of Medicine, has handed 
down to us a good description of pulmonary as well as laryngeal 
tuberculosis. His classic description of the clinical nature of 
tuberculosis had not been reached for more than fifteen hundred 
years (A. C.) He speaks of fever, hemorrhage, cough, pain in 
chest and pleurisy, of clubbing of the fingers, recognized the 
chronicity of the disease, considered tuberculosis contagious, 
gives most ingenious directions for the arrest of the disease, to 
remain much out of doors, to drink freely of milk, to avoid in- 
toxicants, venereal and other excesses and advised a change of 
climate. Aristotle, B. C. 384-322, mentions that the Greeks con- 
sidered tuberculosis very contagious. Celsus B. C. 30-A. C. 50, 
although not a physician, recognized the ulcerative processes of 
both the larynx and trachea; and Pliny, A. C. 79, recommends a 
sojourn in the pine forests. Galenus or Galen, A. C. 131-201, 
recognized ulcerative tuberculosis of the larynx and its connec- 
tion with the lungs. He opined that the ulceration was primary 
and that the irritating secretions from the ulcer infected the 
lungs. He recommends the free use of milk and a residence in 
the mountains. Areteus1 (A. C. 200) classic description gives us 
the first clear picture of phthisis. He recognized the difference 
between tuberculosis and emphyaema, recommended a sea voy- 
age and country air for the cure of the disease; and Avicenna, 
_ JIt may be of interest to note in studying the history of tuberculosis that in remote 
times, in antiquity, the observers were chiefly concerned with the symptomatology of 
tuberculosis, that later in the writings of Sylvius, Fracastori and others of their time, we 
observe the first clear conception of the tubercle as the fundamental anatomical lesion of 
the disease. During the 17th and 18th century, the anatomists concerned themselves 
with the anatomy and the pathology, and during the 19th century, the beginning of the 
experimental epoch, which led to the discovery of the bacillus as the etiological factor of 
the •disease, the true fundamental conception of tuberculosis in all its protean forms, the 
exact nature of the disease was established. ~ « "' , - - .—*3." ’■> 
3 4 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
A. C. 1000, an Arabian physician, mentions that phthisis is pro- 
duced by ulceration in the respiratory apparatus, small ulcers 
healing large ones remaining incurable. 
From Galen’s time until the 16th century, with the exception 
of Avicenna, no mention is made of tuberculosis as a disease 
entity, and in that century the first attempt was made at an 
anatomical and physiological orientation. 
Paracelsus, 1493-1541, wrote a comprehensive treatise on acute 
and chronic diseases consisting of eight books in which he speaks 
at length on tuberculosis; Sylvius, 1478-1555, (Latinized from 
Jacques du Bois) a French anatomist, first recognized the 
tubercles which he considered to be glands analogous to scrofula 
and upon which depended the scrofulous inheritance. He be- 
lieved in the contagiousness of the disease and associated 
scrofula with tuberculosis, and recognized the existence of 
lymph nodes in connection with suppuration of the lungs. 
Fracastori, 1483-1553, a native of Verona, attributed the origin 
of tuberculosis to extremely minute germs or seeds, anticipating 
our present germ theory of disease. He maintained the trans- 
missibility of the disease from the breath of the tuberculous. 
Fabricius, 1537-1619, a pupil of Fallopius whom he succeeded 
as Anatomist at the University of Padua and who was a teacher 
of Harvey, the supposed discoverer of the circulation of the 
blood, records a number of dissections, both pulmonary and 
mesenteric and published a monograph on the anatomy and 
physiology of the larynx. Forester in his published book at 
Rouen 1653, described a variety of cases of tuberculosis as 
observed by him. 
Richard Morton’s book entitled “Phthisiologia” 1689 says: 
Yea, when I consider with myself how often in one year there 
is cause enough ministered for producing these swellings even 
to those that are wont to observe the strictest rules of living, I 
can not sufficiently admire that any one at least after he came to 
the flower of his youth can die without a touch of consumption.” 
He believed in the heredity and contagion of the disease. 
Morgagni, 1688-1771, doubts the identity of tubercles and 
glands as had been taught, and he would not dissect the body of 
the phthisical. We notice, here for the first time a fear ex- 
pressed as to tuberculosis. It is worthy of note that in 1782, 
just 100 years before the discovery of the tubercule bacillus, a 
dogma was issued at Naples, of the infallible contagiousness of THE HISTORY OF TUBERCULOSIS 
5 
tuberculosis and that all bedding, clothing and wearing apparel 
belonging to the deceased tuberculous must be destroyed or 
burned. 
Benjamin Rush, 1783, in his “Thoughts upon the cause and 
cure of Pulmonary Tuberculosis” firmly believed it contagious 
and Matthew Baillie, 1793, in his book on morbid anatomy shows 
more exact observation, describes the tubercules as firm white 
bodies dispersed throughout the lungs and which are appar- 
ently found in the cellular structure. 
Mangetus, 1790, recording his observations states that in a 
post mortem, he found little bodies which he compared in size 
and appearance to that of millet seeds. He found these little 
bodies in the lungs, liver, spleen and other organs and regarded 
them as phthisical. He believed that they arose from lymph 
nodes. 
Bayle, 1774-1816, teacher of the great Laennec, was the first to 
attempt a classification of pulmonary tuberculosis on a strictly 
anatomical basis, a correct teaching, a lesion of the lung causing 
destruction of tissue. He recognized the disease as occurring in 
different organs and not limited to the lungs, and concluded that 
it was not an inflammatory process, but a generalized disease, a 
diathesis. He classified tuberculosis into six varieties and cor- 
rectly described miliary tuberculosis. 
Laennec, 1781-1826, the father of modern auscultation, taught 
the unity of phthisis in all of its various forms. He recognized 
scrofula as tuberculosis of the lymph nodes, recognized its 
specific character, a pathological entity, which is characterized 
by the tubercle as an accidental product foreign to the normal 
healthy tissue. He recognized a favorable soil and a healthy 
seed. He also recognized the tubercle as undergoing change, 
softening, caseation and finally breaking down from the center 
and discharging pus. He distinguished gangrene from carci- 
noma and established the true theory of unity. He taught that 
all tuberculosis depends upon the tubercle, that phthisis and 
tuberculosis are identical, that tuberculosis is an accidental 
product in the lung, a neoplasm and considered scrofula gland 
tuberculous. 
Broussais, 1772-1838, and his school opposed the teaching of 
Laennac, believing in the doctrine of chronic inflammation of the 
lungs, and considered this to be of two kinds, namely, that of 
the blood vessels and that of the lymph channels. The latter is 6 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
tuberculization and is preceded by the first as pneumonia and 
pleurisy. With the iitiproved microscope at that time he was 
able to recognize irregular nuclei containing cells which he con- 
sidered pathognomonic of tuberculosis. Lebert, 1844, came next. 
He recognized a tuberculous corpuscle with degenerated nuclei 
and epithelial cells. In 1847 Virchow advanced the dualistic 
theory. All products of the tubercle are inflammatory and bear 
directly no relation to the tuberculous process. He recognized 
only the miliary tubercle. Lymph glands are secondary to an 
inflammatory area; if glands are enlarged and not inflammatory, 
it is called scrofula. He recognized the tubercle as a neoplasm, 
a cellular but not a vascular structure, and that the tubercle may 
caseate, undergo calcification or fatty degeneration, and is then 
absorbed and the process healed. The expression prevailed that 
the greatest misfortune that can befall a phthisical patient is 
when he becomes tuberculous. The tubercle was a non-specific 
process, a lymphoma. 
Buhl, 1857, states: “Acute miliary tuberculosis depends upon 
preexisting caseating products which may enter the blood and 
produce miliary tuberculosis in other organs.” * - 
Cruveilhier in 1862 produced artificial tubercles in the lungs, 
liver, mesentary, etc., by injecting mercury intratracheally and 
intravascularly, and concluded that tubercles are not specific 
products, endeavoring to discredit the labors of Virchow. Up to 
this time the transmissibility of tuberculosis from the dead was 
firmly believed. Morgagni as well as Valsalva would not dissect 
a tuberculous subject and Laennec, who died from tuberculosis 
(after returning from Paris he lived for ten years—during all 
this time fighting the disease) maintained to the last that he was 
infected at the dissecting table. Morton, 1834, a student of 
Laennec, in a treatise on tuberculosis published in Philadelphia, 
stated that the disease was due to altered secretions and not to 
inflammation. He believed in the open air treatment of the 
disease. Although Kortum, 1789, first tried inoculation experi- 
ments on himself with negative results, the true experimental 
epoch began with Klenke in 1843. He first produced artificial 
tuberculosis in rabbits. He inoculated tuberculous material into 
the vein of a rabbit which was followed in 26 weeks by active 
tuberculosis. Klenke never fully realized the importance of this 
discovery and for nearly twenty years no further advance was 
made, and it was left to Villemin, 1865, fo first demonstrate the THE HISTORY OF TUBERCULOSIS 
7 
transmissibility of this disease. His discovery caused a furore 
in the medical world. He inoculated rabbits from man, from 
cows and from tuberculous rabbits, intravenously. This brought 
about a complete change in the conception of this disease. He 
demonstrated first that tuberculosis was a specific disease, second 
that it possessed an inoculable virus, third that the transmission 
from man to rabbits and other animals was positive, and fourth, 
that it was a virulent, dangerous disease, and should be classed 
with small pox, syphilis, scarlet fever, etc. 
Chaveaux, 1868, first demonstrated the transmissibility of 
Bovine tuberculosis via the alimentary canal. Weigert, 1879, 
demonstrated the positiveness of miliary tuberculosis to venous 
infection. Edwin Klebs, 1877, was able to develop on egg 
albumen an organism which he described as Monas Tuber- 
culosum, a contagion vivum. This now gave new impetus to 
the histological study of the tubercle, and the discovery of the 
giant cells followed with their multiple nuclei described by 
Rokitansky, Virchow, Klebs, etc. Next tubercles were described 
by Koster, 1876, in joints, by Schueppel in lymph glands, by 
Friedlander, 1873, in Lupus, by Lannelongue in cold abscess. 
From these numerous observations and deductions it was most 
evident that the true nature of the tuberculosis virus, the etiol- 
ogic factor of the disease, would be within human possibility of 
demonstration, and much scientific experimental work was 
undertaken by pathologists and bacteriologists all oyer the civi- 
lized world, but it remained to Robert Koch, 1882, and again in 
1884, to demonstrate positively the tubercle bacillus as the cause 
of the tuberculous disease. His memorable paper read March 
24, 1882, before the Physiological Society of Berlin was received 
with great acclaim. His was the most important contribution to 
the tuberculosis questions. He proved the presence of the 
tubercle in different pathological structures of the body to be 
anatomically the same. He proved the unity of tuberculosis, as 
first taught by Laennec, that tuberculosis of bones, joints, glands 
lungs and all other organs of the body is produced by one and 
the same organism, the tubercle bacillus, immaterial however 
different the anatomical characteristics; and when again in 1890 
he was able to demonstrate the active substance given off by the 
germ in its growth and which is now generally known as Tuber- 
culin, the medical profession hoped for a realization of that fond 
vision that at last a cure for tuberculosis had been discovered. 8 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
The fiasco and disappointment is still fresh in the minds of many 
medical men. With the discovery of the tubercle bacillus a most 
intensive study of tuberculosis began, and the names of Cornet, 
1901, Human and Bovine tuberculosis, v. Behring’s Cassel Lec- 
ture, 1903. Calmette, v. Pirquet, Mantoux, Marcus Paterson, 
Nathan Raw, Edward L. Trudeau, Theobold Smith and a host 
of others will always appear as shining lights in the study of the 
history of tuberculosis. CHAPTER 2 
THE ETIOLOGY OF TUBERCULOSIS 
THE TUBERCLE BACILLUS 
Syn.: Koch’s bacillus, Phthisis bacillus, etc. 
If Klenke in 1843 anticipated the etiology of tuberculosis and 
Villemin in 1865 definitely proved that the virus as found in 
tuberculous tissue or material was transmissable to both man and 
animals, it was left to the master mind of Robert Koch to dem- 
onstrate in 1882 the causative factor, the tubercle bacillus, as 
the active virus of the disease. This bacillus, so called from its 
rod shaped appearance, the etiological factor of all tuberculous 
disease, is a small fungus, a mushroom, a single celled plant and 
as such it is governed by the same definite laws that governs 
all plant and animal life, that is, it grows, multiplies, propagates 
the species and dies, and throughout all its growth it is governed 
also by the same laws of metabolism that obtains in all plants 
and animals. As the human being eliminates during its existence 
various toxic bodies, urea from the ingested proteins, carbonic 
acid gas from the inhaled air, so does the tubercle bacillus in its 
growth give ofif a toxic product. This product is known as tuber- 
culin. 
The tubercle bacillus has never been found to exist free in 
nature. We know not its origin and neither do we know if it 
has always existed in its present or in a different form or if it 
has assumed a different shape or form in the human or animal 
body. From our present knowledge concerning the bacillus, we 
know it to be an obligative parasite requiring for its sustenance 
and subsistence, animal and body heat and nutritious material. 
Outside of a host it can not thrive. 
Types and Varieties 
From the cultural growth and the pathogenicity of the (50) 
tubercle bacillus we now recognize about four distinct types, 
all producing tuberculous disease in man or animals; namely: 
(a) The Bacillus Tuberculosis Humanus (Homo). Found chiefly 
in the human. 
9 10 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
(b) The Bacillus Tuberculosis Bovinus (bos). Found in cattle 
and occasionally in man. 
As both human and the bovine bacilli are concerned in the 
tuberculous processes as observed in man the various char- 
acteristics of these two types will be given more in detail 
throughout this chapter. 
(c) The Bacillus Tuberculosis Avium (avis). (Producing Tuber- 
culosis Gallinarum or Fowl Tuberculosis.) This bacillus is 
found chiefly in fowl, like chickens, birds, doves, however, 
ducks and geese are comparatively free. Morphologically it 
simulates closely the human and is not pathogenic to either 
man or cattle. 
(d) The Bacillus Tuberculosis Piscium (Piscis). 
The bacillus of cold blooded animals (Poikilothermal) found 
in fish, reptiles, turtles, and occasionally in worms de- 
scribed as the blind-schleichen (a species of worm). This 
bacillus also resembles morphologically the human is, how- 
ever, avirulent to guinea pigs, rabbits and doves, virulent to 
fish, to reptiles and all amphibia; frogs are very susceptible. 
The possibility of successfully inoculating cold blooded 
animals with bacilli of the bovine or avian type is still a 
question in dispute. 
Other Varieties 
(e) The Bacillus Leprae. The leprosy bacillus also belongs to 
this, the acid fast group. This bacillus morphologically re- 
sembles very much the human type. It is found, however, 
in the diseased tissue in dense masses and intracellular 
whereas the tubercle bacillus is found in small groups and 
extracellular. As a rule animals are not sensitive to this 
bacillus. 
(f) The Bacillus Smegmatis. This bacillus resembles the human 
type, is acid fast but is less alcohol fast and is not pathogenic 
to test animals. This bacillus is frequently found about the 
genital organs of both male and female at any age and may 
then become contaminated with the urine and if so may be 
mistaken for the true tubercle bacillus. Here animal inocu- 
lation will give the differential test. This bacillus at times 
is also found in ear wax, nasal secretions, etc. THE ETIOLOGY OF TUBERCULOSIS 
11 
(g) The Bacillus Pseudotuberculosis or Pseudobacillus (also 
Bacillus tuberculoides). This bacillus is found very much 
diffused in nature, may be one and the same organism, 
saprophitic and acid fast, resembling the different varieties 
mentioned. It is variously described as milk, butter, manure, 
bowel content, grass, timothy grass No. I and timothy 
grass No. II, trumpet, earth bacillus, etc. 
Both the Pseudo and the Smegma bacillus are non-patho- 
genic. 
It is now generally recognized that a close relationship exists 
between the human and the bovine bacillus. Perhaps both (or 
may be all) have been derived from a common ancestor but 
whether they have become specialized or modified by adaptation 
to the different host can, for the present, with our knowledge 
concerning these organisms, not be definitely answered, hence, 
the question of the identity or nonidentity of human or bovine 
strains has not been definitely decided. Three views, however, 
are generally held, (1) that the human and the bovine are dis- 
tinctly different, (2) that both forms are identical, are only 
varieties of one and the same kind and (3) that they are different 
in kind but transitional in forms. 
Description and Characteristics of the Tubercle Bacillus 
(From L. Bacillus or Bacculus a stick or staff) 
Morphology. Pleomorphism. 
The tubercle bacillus is a distinct, definite and slow growing 
organism about 2.0 to 4.0 microns (millionth part of a meter), 
1/8000 of an inch in length, about 0.3 microns thick (1/100000 
inch) equal to half the diameter of a red blood corpuscle and 
about 1/8 to 1/10 as wide as it is long. (59). As we observe it, 
when stained and under the microscope, it is usually slightly 
curved, the ends somewhat rounded. When cultivated under 
various conditions, it grows with more or less vigor assuming 
various shapes. This is referred to as pleomorphism, and when 
grown under the most favorable conditions, branching threads 
are given off or clubbing may be observed at one or both ends, 
and in old lung cavities the bacillus is often found growing in 
long chains. The bacillus is a parasite midway between bacteria 
and streptothrices, is non-motile, and owing to its pleomorphism 
is considered undergoing a cycle to a higher development, a 12 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
tuberculomyces related to and approaching the ray fungus, ac- 
tinomyces. The various types with which we are familiar, 
namely, the human, bovine, avian, reptilian, are seemingly all 
interrelated. The bacillus when growing does not produce spores 
and vacuoles which have been occasionally observed are supposed 
to be due to degenerative changes. As to its viability, it is very 
little affected by cold, is very resistant to external influences, 
dies at a moist temperature of 80°C. or 175°F., or a dry heat 
of 100°C.=212°F. Direct sunlight destroys it within a few 
minutes to half an hour and diffuse day light in from half an 
hour to a day. A 95% alcohol kills the bacillus in from one to 
fifteen minutes, it dies quickly in a 5% carbolic acid, or in a 
1/10 of 1% mercuric chloride solution. In the dried sputum 
the bacillus may lose its virulence in about three months but 
under favorable condition may retain it for more than eight. 
Tinctorial Characteristics. The bacilli of this class all belong 
to what is known as the acid fast group, that is, when stained 
with aniline dyes and subjected to alcohol and acid treatment 
they do not give up the color. They have great affinity or pre- 
dilection for red dyes, particularly fuchsin, which when once 
stained they hold with great tenacity. This peculiarity is said 
to be due to the presence of a fatty acid in the body envelope. 
(Waxy body envelope is disputed by many.) 
Cultural Characteristics. By far the most interesting peculi- 
arities of the tubercle bacillus are found in its growth and by 
means of this we are able to differentiate the various types. 
The human bacillus is strictly aerobic, requiring air for its 
growth, whilst the bovine is anaerobic requiring little or no air. 
The human bacillus is somewhat longer, more slender and 
slightly curved, whereas the bovine is broader, slightly thicker 
and more plump. 
On blood serum (human) the human cultures grow vigorously 
often profusely and multiply freely while bovine colonies grow 
much more slowly and very irregularly. A vigorous growth 
of the bovine type, on a neutral 5% glycerine bullion will con- 
vert such a media into an alkaline substance, not so the human. 
If at the end of a month’s growth of the bovine type on such a 
solution an alkaline reaction is given, the growth of the human 
on a similar solution will give an acid reaction and the degree 
of acidity may reach as high as 4%, hence we notice that the THE ETIOLOGY OF TUBERCULOSIS 
13 
human grows more freely in an acid and the bovine as well as 
the avian best in an alkaline media. (Prof. Theobald Smith.) 
On a potato media with bovine bile the bovine bacillus grows 
very vigorously and both the human and avian very sparingly, 
whilst on a potato media with human bile, the human bacillus 
grows luxuriantly and the bovine and the avian poorly, on a 
similar media with avian bile all show a very vigorous growth. 
Pathogenic Characteristics. The pathogenicity of the differ- 
ent types, that is the human and the bovine, is strikingly and 
peculiarly different. We find the bovine bacillus to be highly 
toxic to rabbits and cattle, retaining this virulence even after 
prolonged cultivation, with great tenacity for these test animals. 
Not so the human, but the human is very virulent to guinea 
pigs, slightly to rabbits and seldom to cattle. In man the bovine 
bacillus may be found in glands, tonsils, in the intestines, but is 
usually not virulent and serious disease occurs but rarely. The 
human bacillus is seldom found in the carnivora, in birds, in 
fowl, in reptiles, the bovine very frequently. It is impossible 
from the lesion alone to differentiate the human from the bovine 
and vice versa, nor can we morphologically distinguish between 
human and bovine tuberculosis. The bovine bacillus is much 
more virulent to test animals than is the human, and bacilli are 
much more virulent if taken from their own source, the human 
from man, the bovine from cattle. 
Infecting Characteristics. It has repeatedly been observed 
that both the human and the bovine bacillus have a special pre- 
dilection for various organs and tissue of the human body, and 
that while the human bacillus selects such organs as the lungs, 
the pleura, the larynx, we find that the bovine bacillus usually 
spares these organs and favors the glands, the bones, the joints, 
the peritoneum, the skin, etc. 
In man pulmonary tuberculosis induced by the bovine bacillus 
is extremely infrequent. The English commission after 10 years 
of careful observation reports that in about 6/10 of 1% of all 
cases of pulmonary tuberculosis the bovine bacillus is the etiolog- 
ical factor. According to Koch human beings may become in- 
fected writh bovine bacilli but infrequently become tuberculously 
diseased. Human bacilli have not been found in cattle; bovine 
bacilli have been found in man in glands and in the intestinal 
tract, but they usually show no virulence and remain localized. 14 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
Chemical Compositions of the bacillus. On account of its 
chemical composition, richness in fat and wax the bacillus pos- 
sesses special resistance to the ordinary stains or aniline dyes, 
but if once stained it shows an exceptional tenacity or resist- 
ance to decolorization or destaining. 
The tubercle bacillus can be dissociated into its component 
parts by various methods. This is mainly affected by the use 
of diluted or weak organic acids such as lactic, malic, phos- 
phoric, etc. Careful observations and analysis have demon- 
strated the bacillus to consist of 85% of a watery substance and 
15% of a dried residue, and of this residue approximately 25% 
consists of a fatty substance soluble in alcohol and ether. Of 
this fat about *4 or 25% consist of free fatty acid and 75% of 
neutral fat or wax. Of the other constituents, a protein, (toxic) 
chiefly nucleo-albumin is the most abundant, and cellulose min- 
eral substances, potassium, sodium and calcium oxides and some 
carbo-hydrate supply the remaining constituents. On incinera- 
tion about 8% of ash remains. A small percentage of an odorif- 
erous principle is also present. 
Special Adaptation Characteristics. Bovine bacilli are differ- 
ent from the human and there are atypical types which strictly 
speaking belong neither to the human nor to the bovine; these 
types may be simply varieties of one and the same organism or 
intermediate types. The organisms evince also a special adapta- 
tion to different hosts, for we know that the strains of the hu- 
man kind may adapt themselves to the bovine organism, become 
virulent and assume the cultural characteristics of the bovine, 
and yet it is questioned if the bovine bacillus infecting man ever 
assumes the characteristics of the human. The time has not yet 
arrived when we can say positively that a transformability has 
taken place or that one strain has been converted into the other, 
the human into the bovine and vice versa; the increase or de- 
crease of virulence by passage through the body proves nothing. 
There are many aberrant types of more or less variation in their 
growths. Prof. Theobald Smith removed from the neck glands 
of a child bacilli which showed the characteristics of the bovine 
type but also showed an unusually slow growth, retaining this 
same peculiarity after 6x/2 years’ cultivation. Animal transmis- 
sions vary greatly. As a rule swine do not transmit to others 
of the same species. Again, the passage of the human type THE ETIOLOGY OF TUBERCULOSIS 
15 
through an animal, as for instance, the goat, may greatly in- 
crease its virulence.*! 
♦The tubercle bacillus is as stated a minute vegetable organism, the human, bovine and 
all others. There is no tuberculosis without the presence of this bacillus, no matter how 
susceptible the being is. Everybody is susceptible to the action of the bacilli after they 
have entered the body, but not everybody becomes tuberculously diseased. There are 
always three factors: bacillus soil and opportunity. In some the infection causes only a 
slight disturbance (30%); in some the disease becomes manifest or active (10%); and 
the remaining 60% through life are not aware of the presence of the bacillus in the body. 
tin recent years Dr. Jaime Ferran (89), Catalonia, attracted considerable attention, 
giving his views based on both clinical and laboratory observations as to the infectiousness 
of the tuberculosis virus. He maintains *that the tubercle bacillus in pure culture if inocu- 
lated into man or animal, is incapable of producing acute tuberculous disease such as is 
recognized by beginning granulation tissue or early death, but that if tuberculous sputum 
or tuberculous tissue is used as inoculating material, it will produce typical tuberculosis 
even if the tubercle bacillus can not be demonstrated to be present. In this expectorated 
material or in the tissue various non-acid fast bacteria are present which are capable of 
bringing about an acute or chronic form of tuberculosis. From the many different bac- 
teria present in a tuberculous process, the acid fast bacillus of Koch is only one of the 
many varieties derived from an ordinary non-acid fast saphrophite which can be cultivated 
and which differs materially in its tinctorial characteristic from the ordinary tubercle 
bacillus. 
Much’s Granules (89). The tubercle bacillus in granular form. It has been proved 
that occasionally in tuberculous material a virus is present which will not take the 
ordinary Ziehl-Neelsen stain but can only be stained with a modified Gram. These bacillary 
granules, remnants or salvage, are a form of tubercle bacilli which are not acid fast, they 
are, however, the normal parts of the bacillary bodies. Moreover, they represent the clin- 
ically most resistant parts of the tubercle bacillus, the parts which survived after the 
disintegration of their bodies, is usually a virulent form and a peculiar developmental stage. 
These granules found in tuberculous material are an expression of a positive reaction of 
the defense mechanism of the body. The rod shaped bacteria of less resistance or viru- 
lence have been, destroyed by this mechanism of defense and these granular bodies are 
simply the remains of this destruction, a subsequent lowering of the body’s resistance may 
again change these granules into the rod shaped form. If these granules are placed into 
the body of a susceptable animal they are again transformed into rod shaped bodies. That 
these granules do not take the ordinary Carbol-Fuchsin stain, but take up readily a modi- 
fied Gram is due to the fact that the fatty portion or envelope of the tubercle bacillus is 
absent—is. wanting in the granular form. It is this fatty component of the bacillary 
bodies which gives the acid fast character. Possibly the non-acid fast bacteria occa- 
sionally found in tuberculous material and to which Ferran alludes may after all be 
nothing more than Much’s granular form of the tubercle bacillus. CHAPTER 3 
THE PORTALS OR ATRIA OF INFECTION 
PORTA INFECTIONIS 
Query: In what way is the human body infected? How does 
the germ gain entrance into the human body? How is tuber- 
culous infection brought about? What are the possibilities of 
infection? In short, what are the avenues, atria or portals of 
infection ?x 
There are two recognized avenues of infection, an external or 
cutaneous one, that is by way of the skin, and an internal one 
through the mucous membrane. The human body consists of a 
firm bony framework to which are attached the various muscles, 
and interspersed between and throughout them are the internal 
organs, the blood vessels, glands, tissues, etc., all encased in a 
double sack of which the Lamina Externa or skin forms the outer 
investment, and the mucous membrane, the-inner, the Lamina 
Interna. If both layers of this sack, the cutaneous and the 
mucous, are perfectly intact, then, relatively speaking, all the 
various bacteria both pathogenic and non-pathogenic will be in- 
capable of entering the body, and hence will be incapable of pro- 
ducing disturbances. Infection through the skin is extremely in- 
frequent and then only after more or less denudation and a 
healthy mucous membrane is also, relatively speaking, capable 
of withstanding the entrance of bacteria. It is only when by 
means of irritants the mucous surfaces become congested, or the 
invaders are in too great a number that entrance may be gained 
The atria of infection, the primary portals, as usually observed 
may conveniently be subdivided into five routes, namely: 
1. The aerogenous, the bronchogenic route, that is by in- 
halation through the respired air; 
2. The enterogenous, the intestial route, that is by ingestion, 
by deglutition; 
lThe entrance of the tubercle bacillus into the human organism may result disastrously 
or may be perfectly innocuous depending upon many factors, namely, (1) difference in 
the degree of susceptibility in different individuals; (2) difference in the degree of 
virulence of the bacillus; (3) the number and the amount of bacilli entering the body at 
a given time; (4) if the infection was single or if it was oft repeated; (5) the age of the 
individual if healthy or not at the time of infecton, previous diseases, sanitary and 
hygienic conditions, etc. This latter is usually an acquired susceptibility or disposition; 
($) the points of entrance, if through the skin, tonsils, mouth, intestines, etc. 
16 THE PORTALS OR ATRIA OF INFECTION 
17 
3. The cutaneous route, through the skin; 
4. The genitogenetic route, congenital and inherited, includ- 
ing spermatogenous, ovagenous, germogenous, placental, etc.; 
5. The crytogenetic route, that is an obscure or unknown 
route. 
The lymphogenous and hematogenous infection so frequently spoken 
of are secondary processes of infection and not of this class. 
1.—The Aerogenous Route. The chief portals of infection are 
through the various mucous surfaces of the upper air passages, 
those of the nose, mouth, pharynx, larynx, as well as those of the 
bronchi. The vibrissae about the nasal passages mechanically 
filter the respired air and in this manner at least 95% of all dust 
and other particles are removed. Besides this, the mucous secre- 
tions possess bacteria destroying properties. The glands of the 
Waldeyer ring, tonsils, adenoids, lingual tonsil, etc., guarding 
the entrance to the lower air passages if healthy offer a barrier to 
the bacilli, but if diseased favor their entry and in this way 
bacilli may enter the cervical glands. The same holds true of all 
the mucous surfaces of the oro-pharynx. 
After careful and prolonged observations by competent 
workers, the view is now entertained that most infections, or at 
least 85% are by inhalation of air through the upper air passages. 
There are two theories as to this aerogenous infection. Fluegge 
maintains that most infection takes place by immediate and inti- 
mate contact with the active tuberculous, and that in coughing, 
sneezing, hawking and spitting, small droplets of sputum con- 
taining tubercle bacilli in greater or less number are expec- 
torated, and these droplets floating in the air are inhaled by those 
who are in close contact with the diseased individual. This 
method of infection with moist sputum is now generally ac- 
cepted. Cornet (22) on the other hand emphasizes that it is the 
dried sputum of the tuberculous which is the chief source, that 
the tuberculous individual, being frequently a very careless per- 
son, coughs and spits about the house, upon the floor and walks, 
the sputum is tracked about and dried, currents of air carrying 
the dried particles in all direction and contaminating the respira- 
tory air. In this way the bacilli enter into and find lodgment in 
the human body. It must be conceded that infection may fre- 
quently take place in that way and that infants in particular are 
infected in that manner. As to which of these two theories is 
correct can not be stated; most likely both are in part correct. 18 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
That infection takes place most frequently by the aerogenous 
route has been conclusively demonstrated first by Kiiss and later 
by Ghon (15), who out of 184 carefully conducted autopsies 
could prove that in all but one, infection took place through the 
inhaled air. It is generally conceded that the respired air, 
through the mouth or nose is, at all times, more or less laden 
with dust particles and various micro-organisms, both patho- 
genic, and non-pathogenic, which are conveyed into the bron- 
chial tubes and their ramifications constantly bathing the lungs 
with air containing many bacteria which thus reach the mucous 
surfaces where many are deposited. The greater number, how- 
ever, due to the anatomical structure of the lining membrane of 
the bronchial tubes, the ciliated epithelial cells, are again ex- 
pelled along with the bronchial secretions. Yet some will find 
suitable lodgment, produce irritation causing infection and ulti- 
mate involvement of the regional lymph nodes. Phagocytosis 
here undoubtedly also plays an important role. As has been 
stated above, in man the aerogenous route is the most frequent 
and the chief cause of almost all pulmonary tuberculosis as well 
as that of many forms of metastatic disease, all depending upon 
the virulence of the organisms and the amount of virus reaching 
the lungs, that is upon the quality and quantity of the invading 
bacilli, and also upon the sensitiveness of the host; hence, prim- 
arily, tuberculosis is both a quantity and a quality infection. 
2.—The Enterogenous Route. By ingestion, by deglutition. 
The alimentary canal is a less frequent atrium or source of tuber- 
culous infection than the aerogenous route, v. Behring (48) 
believes that the enterogenous atrium is the main source 
of infection and that by means of infected milk, meats, and other 
food stuffs infection is brought about in man by way of the 
digestive tract. It is not at all improbable that with the taking 
of infected foods through the mouth, bacilli may find entrance 
into the respiratory tract, but that must be extremely seldom and 
the food would have to be laden with bacteria. The hypothesis 
of v. Behring that pulmonary tuberculosis in children takes 
place by the aspiration of tuberculous material through the 
stomach and intestines is improbable. It is more reasonable to 
assume that with the ingestion of food particles containing tuber- 
culous material, bacilli may find entrance into the respiratory 
tract and here again, as has already been stated, the food would 
have to be saturated with the virus. THE PORTALS OR ATRIA OF INFECTION 
19 
The number of cases of primary intestinal infection must al- 
ways be relatively small, but we may assume that if tubercle 
bacilli enter the intestinal tract in large numbers, or the mucous 
membrane be irritated or not intact, that then infection may take 
place. It has never been proven satisfactorily that the ingestion 
of cow’s milk containing bovine bacilli has caused pulmonary 
tuberculosis in man, and concerning the meat of a tuberculous 
animal as a rule it does not contain living tubercle bacilli. For 
this to take place the animal must be generally infected but then 
the meat would not be saleable and even in that event the thor- 
ough boiling would kill the bacilli. In the alimentary tract many 
bacilli are killed and few if any pass into the mesenteric or 
retroperitoneal glands. It has never been proven that tubercle 
bacilli pass the normal mucous membrane of the intestines and 
infect the regional glands. A small infecting material and an in- 
tact intestinal canal will always inhibit infection and only if the 
bacilli enter the alimentary canal in large numbers or if the 
mucous surfaces be not intact will infections take place. Even 
infants are very infrequently infected from the milk of the tuber- 
culous mother, but this may take place when the glands of the 
mammae are themselves tuberculous. In about 10 to 12% the 
infection in the human is due to the bovine bacillus and then it 
is usually found in children manifested in gland, bone and joint 
tuberculosis, in about 85%, mainly in adults, it is due to the 
human bacillus. In the human, the infection takes place from 
man to man, that is from a tuberculous adult to an infant, and 
only a small percentage of children (one-eighth of all) tuber- 
culously infected show evidence of an endogenous infection. 
Intestinal tuberculosis in the adult is usually always secondary 
to pulmonary disease, but may be primary in children from milk 
containing bacilli. The oesophagus and stomach play no part in 
the way of infecting atria and we find that these organs are most 
infrequently primarily or even secondarily tuberculously dis- 
eased, however, in the active tuberculous a secondary process 
may follow an injury to these organs. It may be stated that buc- 
cal, nasal, laryngeal or pharyngeal .primary tuberculosis is also 
extremely rare. It is most difficult to prove that a tuberculously 
infected tonsil or an adenoid vegetation, as a primary infectious 
atria, could later be followed by a pulmonary lesion, although in 
manifest tuberculosis we find a very frequent tonsillar infection, 
but this is secondary. It may be worthy of note here that in 20 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
pulmonary tuberculosis the cervical lymph nodes are very infre- 
quently simultaneously involved. 
3. —The Cutaneous or Dermal Route, Through the Skin. The 
next most important route of infection. As stated above, if the 
skin is intact, bacilli can not enter the human body—an abrasion 
is always necessary to bring about infection. Abrasions are 
usually noticeable about the nose, mouth, eyes and anus, that is, 
where the cutaneous and mucous surfaces come together, and 
infection may also take place through other parts of the external 
body, the skin of the arms, hands, etc., if the cuticle is not in- 
tact. Mention may be made of the condition known as Tuber- 
culosis Verrucosa Cutis or Tuberculous Warts which may be 
observed on the hands of undertakers, embalmers, tanners, 
butchers, cattle dealers and those who handle dead bodies. Other 
cases of infection through the skin are recorded where in vac- 
cination the vaccine had been contaminated with the saliva of 
the tuberculous vaccinator, transferring in this way the tubercle 
bacillus directly into the body of the person being vaccinated. 
In medical literature (89), mention is made of tuberculosis fol- 
lowing circumcision in which the infection was brought about 
by bringing the sputum of the tuberculous individual performing 
the rite in direct contact with the wound. Very frequently in 
years gone by has tuberculosis been innocently transmitted by 
an irresponsible tattooer who carelessly and with indifference 
moistened the india ink being used with his bacilli laden sputum, 
perhaps not being aware that he was tuberculously diseased. 
Tuberculosis has also been transmitted in coition and cases of 
tuberculosis following trauma by direct infection of the wound, 
primarily, have repeatedly been proven. 
In a pathological laboratory some years ago a young physician while 
handling a flask containing live tubercle bacilli had the misfortune to 
break it and pour its contents over his bare arm. Though the arm was 
immediately washed and the skin sterilized, the incident was followed 
later by active tuberculosis. It remains still a disputed question whether 
living tubercle bacilli being present in large numbers, actually penetrated 
the intact cutaneous surface. Is it not more probable that the incident 
of breaking the flask brought about mental disturbances which caused a 
lowering of body resistance and consequent disease? 
4. —The Genitogenetic Route, Congenital or Inherited. Pla- 
cental transmission and transmission via the maternal ova pro- 
duce true congenital tuberculosis and are the only true sources THE PORTALS OR ATRIA OF INFECTION 
21 
of maternal hereditary infection. Congenital tuberculosis may 
have various atria; conceptional, germinal, spermatic, ovarian, 
placental, vaginal, uterine, etc. The spermatogenous or ovagen- 
ous route as a primary way of infection must be extremely rare. 
In fact, no direct proofs have yet been submitted as to the cer- 
tainty of infection by this means. Primary tuberculosis of the 
female genital organs, the vagina and uterus, are also infrequent, 
there being no direct proof of this mode of infection. 
Placental Transmission. Transmission may take place through 
a diseased placenta. In order to prove the congenital transmis- 
sion of the tuberculosis virus, it is not sufficient to demonstrate 
the tubercle bacilli in the placenta; the proof must show that 
bacilli have actually passed through the placenta into the organs 
of the foetus, and a negative histological examination of the foe- 
tus is insufficient to exclude placental transmission; antiformin 
methods and animal tests may be necessary. Then again, a 
tuberculous infection or transmission may take place in em- 
bryonal or foetal life through an apparently normal or perfectly 
healthy placenta. There are now two theories of this early or 
infantile infection. (1) The intrauterine, congenital or prenatal, 
which presupposes that all infection takes place before birth, 
producing a true inherited tuberculosis from the father like 
syphilis, or a congenital or hereditary infection from the mother; 
(2) Extrauterine, postgenital or postnatal, which explains that 
nearly all infection takes place after birth from a tuberculous 
adult in intimate contact with the infant immediately after birth, 
v. Baumgarten maintains that many more than we suppose are 
infected intrauterinely and yet the anatomic-pathological lesions 
are exceptionally few before birth, being greater after birth. It 
is very theoretical to suppose that tubercle bacilli have been 
transmitted into the young organism by means of the sperm or 
the ova, or through the placenta without producing any disease, 
and that they remain dormant in the child until puberty or prob- 
ably years thereafter, and only then attack the host. Particularly 
is this true when we consider that the specific tuberculin test in 
the very young, in infant life, is usually negative, and that it 
only becomes positive with advancing years, and that infants 
born with manifest disease all succumb to active generalized 
tuberculosis in the first months or within the first year of life. 
From this we must conclude what is now maintained by the 
greater number of tuberculosis workers, namely, that most in- 22 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
fection is extrauterine or postnatal and is brought about after the 
birth of the child, being only very exceptional before birth. 
5.—The Cryptogenetic Route. In a very small percentage of 
tuberculously infected infants and children at autopsy or other- 
wise (in about half of 1%), it is impossible by the most pains- 
taking procedure to demonstrate definitely in what manner in- 
fection has taken place. These cases are now usually classified 
under the heading of obscure or indefinite infection, or more 
properly as cryptogenetic. 
In this connection it may be of interest to note that v. Behring and 
his school maintain that the chief source of infection in the human is by 
the enterogenous route, this through the ingestion of milk from tuber- 
culously infected cattle. However, the consensus of opinion of most 
competent observers is that tuberculosis is an infection from man to man 
and more recent studies seem to confirm this view. 
A. Balfour states that the great frequency of tuberculosis in the Sudan 
is due to the increased number of the European people, that there exists 
relatively infrequent tuberculosis in cattle, but that dogs and apes are 
very susceptible. 
A. Calmette says that in the French colonies in Africa (89), Senegal 
gold coast, Madagascar, Algeria, tuberculosis of the black races, of the 
natives, is extremely infrequent, but the disease increases with increased 
arrivals of Europeans. These races possess no inherited immunity but 
succumb very readily to the infection. The frequency of intestinal tuber- 
culosis, as is advocated by v. Behring said to be due to infected milk, 
cannot here be accepted. 
H. Zieman finds that tuberculosis is very little disseminated in the Ger- 
man colonies in Africa at Kamerum. In many peoples it is not known 
and there is no tuberculosis in animals. Tribes exist in the interior of 
Africa which are still free from tuberculosis and that cattle are also free. 
The black races fall very easy prey to catarrhal diseases of the respiratory 
air passages; hence, to tuberculous disease. With increase of trade, social 
conditions and constant contact with the Europeans the disease increases 
most rapidly, because they possess no resistance. Chronic bone and joint 
tuberculosis and lupus are extremely seldom. The Arabians also fall 
easy prey and according to E. Smith similar conditions exist in Egypt. 
In Sicily, tuberculosis is on the increase and this is due to the returned 
Sicilians from the United States. In Turkey, tuberculosis runs a different 
course from that of the more cultured races. There tuberculosis is very 
infrequent but also very fatal, less so to the inhabitants of the larger 
cities. It is very fatal among medical students and military recruits 
from the country districts. In Palestine, the disease was introduced 
some years ago by Jews returning from Russia. In Japan, the disease 
has existed for many ages. In Scotland, tuberculosis of the bones and 
joints is very prevalent, due to the ingestion of uncooked milk, a per- 
nicious practice which is much in vogue there. In the tropics, in the West 
Indies, the death rate is from five per thousand to five per ten thousand. THE PORTALS OR ATRIA OF INFECTION 
23 
In Australia one per thousand. Bovine tuberculosis and tuberculosis of 
young children is rare in the tropics. Tuberculous meat is uncommon, 
milk is always boiled but very little is used. Natives who never came in 
contact with tuberculosis material become very easy prey to the infection. 
The natives of India living in cities are less susceptible but the inhabitants 
of the coast of Africa in the cities are the spreaders of the disease. 
There also tuberculosis in animals is very infrequent, with the exception 
of fowl. Hyman reports that in Japan, Greenland, Turkey in Asia, Rou- 
mania, Egypt, the gold coast of Africa, the infection is always from man 
to man. Tuberculosis in South Africa—the British Medical Journal, 
April 25, 1908—Tuberculosis in South Africa is rampant among the 
Kaffirs, whereas tuberculosis among cattle is unknown. McVicker, 
British Journal of Tuberculosis, April 1, 1909, speaking of tuberculosis in 
South Africa states: “The colored races in western South Africa suffer 
most severely, both those living in the towns and in the country. The 
disease is nearly as common amongst the Banta population, in Natal and 
the natives of the eastern Cape Colonies as well. It is also common 
among the India settlers in Natal and the Kaffirs, but few cattle are in- 
fected and abdominal tuberculosis is uncommon even amongst the Bantas, 
who are a milk drinking race.” In Singapore there exists a higher pro- 
portion of tuberculosis among the Chinese male than female—males 6.04, 
females 3.81. In the Malay peninsula bovine tuberculosis does not exist, 
no tuberculosis among the domesticated animals. In the abattoirs at 
Ipoh during the last four years (from 1915 to 1919) more than 250,000 
pigs have been killed and no case of tuberculosis has been found showing 
that the bovine is free from the disease. As a rule Chinese, both adults 
and children, use but little milk and yet the population of this race who 
are suffering from tuberculous disease is quite considerable, nearly 5,000 
deaths per 1,000,000 population in 1916. 
Animal Experimentation. Cattle, as a rule, with advanced pul- 
monary tuberculosis do not contaminate the milk with tubercle 
bacilli. It is only when the udder itself is diseased that the milk 
becomes contaminated. Raw milk may contain in a cc one 
thousand to fifty thousand or more tubercle bacilli and butter 
may contain as many as one hundred in each gram. In the feces 
of cattle suffering from pulmonary tuberculosis, in about 46% it 
is possible to demonstrate the presence of the tubercle bacillus, 
even here microscopic examinations are not free from error be- 
cause many saprophitic acid fast rods are present. Animal test 
only is reliable, and in the circulating blood of even the advanced 
cases, tubercle bacilli as a rule cannot be demonstrated. Bang 
states that large herds of cattle are rarely free from tuberculosis, 
that all tuberculous animals do not react to the tuberculin test 
and that in herds in which tuberculosis has existed for years, 
testing may be omitted because most full grown animals will re- 
act although they may appear perfectly healthy. CHAPTER 4 
HEREDITY, DISPOSITION, PREDISPOSITION AND 
DIATHESIS. THE TUBERCULOUS TENDENCY 
Before the etiology of tuberculous disease was well known, 
much was said and written about the diathesis, the disposition, 
predisposition and heredity, and even with a better knowledge 
concerning this disease since the discovery of the tubercle bacil- 
lus, there exists still a wide difference of opinion relative to these 
terms. These terms predisposition, heredity, diathesis or dis- 
position are all more or less vague, indefinite and misleading. 
What they really mean to convey is that the human body in 
many instances, especially in infant and young life is incapable 
of withtanding the implantation of the tubercle bacillus, is the 
possessor of a fertile soil, that is, in the individual there is a 
strong tendency toward the disease, hence all these terms are 
better expressed by the simple words, "The Tendency.” This 
tendency to tuberculosis, first to the implantation of the bacillus 
and later to tuberculous disease is said to be either an inherited 
or an acquired disposition; hence, we recognize an (89) idio- 
pathic and a toxipathic disposition or tendency. 
First: The idiopathic, the inherited, the unavoidable, the spe- 
cific disposition. The tendency to tuberculous infection. The 
direct (primary) contributory cause of tuberculosis. This pre- 
supposes a receptive condition of the body, a heightened tuber- 
culous disposition to infection. This tuberculous tendency or 
disposition is usually in early life in infants and in small chil- 
dren. There seems to be in infant life a heightened disposition 
or an hereditary predisposition to tuberculous infection and in 
later life to tuberculous disease. When a number of infants are 
exposed under identical tuberculous surroundings or environ- 
ments, some will develop manifest disease before the expiration 
of the infant years whilst others may or . may not develop the 
disease after puberty. Because the infant can not protect itself 
against the infection it is said to be unavoidable and of the 
former we would then speak as a heightened disposition or a 
24 THE TUBERCULOUS TENDENCY 
25 
predisposition and of the latter that the tendency or disposition 
has lessened. 
Second: The toxipathic, the acquired, the avoidable, the non- 
specific disposition. The tendency to tuberculous disease. This 
is the indirect (secondary) contributing cause of tuberculosis. 
The extremely great tendency of the tuberculously infected in- 
dividual to become tuberculously diseased is the tuberculous 
predisposition to the disease. This predisposition is chiefly found 
in adult life—the causative factors being many. The idiopathic 
is prone to a tuberculous infection and the toxipathic to a tuber- 
culous disease, hence in the adult a disposition is really the con- 
version of a tuberculous infection into a tuberculous disease. In 
most individuals the infection remains as it is throughout life, 
does not go further and this is due to the body resistance offered, 
but in many it does not terminate here, but after the infection it 
may develop more or less rapidly to a tuberculous disease, and 
this is really the disposition, the predisposition or diathesis. 
Strictly speaking there is no predisposition to infection because 
every human being is prone to infection, but this infection in the 
greater number of instances does not predispose to disease. A 
disposition and a diathesis are not one and the same. A diathesis 
is a form of disposition but a heightened one, an increased tend- 
ency to both infection and to disease, and then again we may say 
that there is no inherited disposition. The infant born of a tuber- 
culous mother inherits only a constitutional weakness which is 
an anomaly, a lessened resistance of the body to infection, a 
weakness to a proper functioning of the various organs and tis- 
sues of the body, hence a body or tissue weakness. An idiopathic 
disposition is of prime importance to the implantation of the 
tubercle bacillus whereas a toxipathic disposition is of prime 
importance in the development of the disease, for the entry of 
tubercle bacilli into the organism is not sufficient to produce 
tuberculosis. The essential conditions necessary are a favorable 
soil, a virulent bacillus and a receptive organism. Everybody 
without exception who receives tubercle bacilli below his cuticle, 
that is to say anywhere into his body, will react to the formation 
of tuberculous tissue, but it is not necessary that this must in- 
evitably lead to the formation of tuberculous disease. Many 
heal and again, many remain latent. This is the rule in by far 
the greater number of cases, but not an absolute rule, because, 
owing to fact that living bacilli are harbored in the organism in ACADEMIC QUESTIONS OF TUBERCULOSIS 
26 
a measure, an immunity against reinfection from without but 
not from within is offered. In a mild degree immunity is already 
acquired, or better, inherited by most infants at birth because 
nearly all parents, especially of the white race, have at some 
time in their lives come in contact with the tuberculosis virus 
and this slight immunity in infant life in a measure already gives 
to the early infection a definite phase of beginning latency. 
The important factors to the question of the idiopathic dis- 
position are the inherited body weaknesses and the inherited ex- 
haustion of the body’s power to be able to produce immune or 
antibodies. Every person possesses in a more or less degree a 
tendency to a tuberculous infection, evidenced by the fact that 
at the age of 14 nearly all children are more or less infected, but 
the tendency or disposition to tuberculous disease declines with 
advancing years. Take 100 children who are tuberculously in- 
fected in the first years of life, nearly all are made tuberculously 
sick and die; however, this tendency or disposition decreases 
rapidly with advancing years so that at the age of 6 or 7, only 
about 20%, and at the age of 14 only about 2% show manifest 
tuberculous disease, all the other remaining free. After the 14th 
year of life, towards puberty and thereafter, the acquired, the 
avoidable disposition or tendency plays the leading part, after 
this age the toxipathic factors are in the lead as the indirect 
and contributing causes of active pulmonary tuberculous disease. 
The toxipathic factors may here be mentioned in the following 
order of their importance: 
1. —Bad Housing Conditions, including poorly ventilated living 
quarters, bad air, insufficient clothing, unwholesome food, want 
of cleanliness, the underfed, the undernourished, insufficient hy- 
giene of the mouth, teeth, body, etc. 
2. —Mental Disturbances, such as grief, anxiety, worry, home- 
sickness, fatigue, overwork, overstudy, long hours with insuffi- 
cient rest, and the various psychic disturbances. 
3. —Toxic Influence Proper. Alcoholic excesses, inordinate use 
of tobacco, venereal disease, syphilis, gonorrhoea, etc. 
4. —Mechanical Causes, like ocupational diseases, inhalation of 
air laden with dust, coal dust, etc., inhalation of obnoxious gases 
and vapors, injuries to the chest wall, etc. 
5. —Infectious diseases. It is well known that after measles, 
scarlet fever, whooping cough, typhoid fever, pneumonia, etc., 
pulmonary tuberculosis is a frequent sequel. THE TUBERCULOUS TENDENCY 
27 
6. —Trauma and Shock. Accidents of every kind, railroad, 
automobile, after operations, prolonged anaesthesia, etc. 
7. —Conjugal Tuberculosis due to pregnancy, protracted lacta- 
tion, frequent miscarriages, etc. 
8. —Contact Cases. This is most infrequent, although cases do 
occur which may be traceable to intimate or close contact with a 
tuberculous, followed by infection and disease, however, these 
are extremely seldom. 
Hereditary Factors. Other predisposing factors, some of which 
will be described more in detail elsewhere, may be mentioned 
here: For instance, (1) chest deformities; (2) a small upper 
aperature of the chest; (3) the predisposition in twins; (4) the 
youngest child in a large family; (5) premature children; (6) 
children born of parents with too great a disparity in their ages; 
(7) children of the diabetic; (8) all in whom there is a defective 
development of the chest or an improper functioning of the 
various tissues and organs of the body. A small heart, imper- 
fectly developed blood vessels, such as a congenital disease of 
the aorta or pulmonary (stenosis) artery; (9) a disposition to 
demineralization in some individuals may be a predisposing 
factor and this deficiency of lime salt in the organism often con- 
stitutes a tuberculous disposition. This we find present more 
or less in all manifest tuberculosis as well as in pregnancy and in 
the diabetics giving a high tuberculous hyperreceptiveness. Oc- 
cupation and race may also, play a leading role. 
Other Noticeable Tendencies or Disposition. It is worthy of 
note, at this point, that in young life the glands, the bones, the 
joints are frequently tuberculously diseased, and this is usually 
to the exclusion of other organs, whilst in adult life the lungs are 
often the only organs which are tuberculous. This most likely 
depends upon the fact that in either the glands or in the lungs at 
these different ages there exists a heightened tendency to tuber- 
culous disease in these organs. This is a natural tendency, a 
“physiological disposition” and then again in those instances 
which are occasionally encountered in which by either lymph or 
blood stasis or by means of insufficient aeration of pulmonary 
tissue, tuberculous disease may be brought about. This is often 
referred to as a “mechanical disposition.” 
Tuberculosis when introduced into primitive races, like all other germ 
infections in these peoples is generally followed by a most disastrous 
consequence, the disease usually running a very malignant course. In 28 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
these an inherited disposition is not necessary, the bacilli gaining access 
upon strictly virgin soil and usually running a very rapid course. 
As an inherited disposition plays a great part for the tuber- 
culously infected and the acquired disposition for the tuber- 
culously diseased, our aim must be to decrease this latter disposi- 
tion, and if diseased, attempt to bring about an arrest of the 
process, increasing the body’s resistance along the line of hy- 
gienic principles. 
In conclusion let us reconsider for a moment the meaning of 
these terms, predisposition, diathesis, etc. If the terms as ex- 
pressed all point to a tissue weakness, a want of body resistance 
to the implantation of the tubercle bacillus, a favoring of the 
bacillary growth, would not the words, “a favorable soil or a 
tendency” be most expressive and synonymous? Or perhaps 
may not the want of a proper protective epithelial lining of the 
bronchial tree and which is demonstrated frequently to exist in 
the early days of infant life in the intestinal tract, favor the 
entrance of the tubercle bacillus into the organism and be 
erroneously referred to as the disposition or the diathesis? CHAPTER 5 
INFECTION AND CONTAGION 
Infectious and contagious disease (10) or more appropriately, 
communicable disease. 
Note the definition as given in the various medical diction- 
aries (11): 
Infection: The communication of disease from one person to 
another by contact, either mediate or immediate. (12) 
. ‘ v/ 
Contagion: The communication of disease by mediate or im- 
mediate contact. Communicated by direct or indirect contact. 
The words “Infection” and “Contagion,” however, are not 
synonymous; they seem to have a different meaning. May we 
perhaps assume that the word infection as we use it refers more 
to the implantation and subsequent growth of the germ and that 
contagion really relates to the disease as it is? A chronic disease 
like tuberculosis may be said to be transmitted more or less, by 
indirect contact, and hence be called infectious, while an acute 
disease may be transmitted more often by direct contact and so 
may be called contagious or better both infectious and con- 
tagious. 
Tuberculosis as we observe it clinically is a communicable 
disease; it is spread from man to man, or more correctly, from 
a tuberculously diseased adult to infants and small children with 
whom the so diseased individual may come in contact. 
Tuberculosis is rarely, directly communicated from one adult 
to another.1 For this to take place would require the most inti- 
mate contact; hence it may be stated that tuberculosis is highly 
(!) It must be conceded, however, that under certain conditions adult infectmn and 
disease may and does take place. First, the individual who has arrived at adult life and 
was never infected may become both tuberculously infected and diseased while inti- 
mately associating with an active tuberculous person. Here the spreading of the disease 
to an adult is very similar to that which is observed when primitive people come in 
contact with the virus. Second, the adult who at some previous time was tuberculously 
infected perhaps diseased as well, but who for some length of time has lived in an 
atmosphere entirely free from all tuberculous surroundings, and has for the time being 
completely lost his immunity may on returning to his former tuberculous haunts,- rapidly 
reacquire the disease and succumb to its ravages. Third, the tuberculous person only 
mildly infected may on coming in contact with an active tuberculous adult become 
massively or very virulently reinfected, and having but little resistance develop a rapidly 
progressing pulmonary tuberculosis. 
29 30 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
infectious as well as contagious to infants and small children but 
not so to adults. 
Tuberculosis, like syphilis and leprosy, can not be acquired 
simply by being in the presence of a tuberculously diseased in- 
dividual, as in the daily intercourse about the house, meeting on 
the street, in the workshops, in a street car, in an automobile or 
at social, religious or political gatherings. As previously stated, 
to bring about both infection and disease would require the most 
intimate association. 
Tuberculosis, unlike the exanthemata, small pox, scarlet fever, 
measles, etc., can not be acquired by paying a visit at the home 
of or by eating, occuping or sleeping in the same room or house 
with a person suffering from the disease. 
Tuberculosis is purely a communicable disease in the young, 
but it is not contagious to adults in a strict sense. The effect of 
shaking hands with an actively tuberculous person has fre- 
quently been made the subject of special study and usually with 
a negligible result. Further observation has also proven that on 
the hands of children living in tuberculous homes and surround- 
ings in only about 10% was it possible to find the tubercle 
bacillus notwithstanding the fact that in more than 50% of such 
cases it was possible to demonstrate the presence of the Koch’s 
bacillus on the floors. Tubercle bacilli which are expelled by 
the diseased person in the act of coughing, sneezing, hawking or 
spitting are very frequently found in the living rooms about the 
walls, curtains, bedding, clothing, draperies, etc., and most par- 
ticularly about the floors, and small children in the immediate 
vicinity may be directly infected in this way. However, these 
factors all play in adult infection but a minor role and usually do 
not lead to tuberculous disease. 
Even the probability of both infection and contagion to adults, 
and perhaps children as well, by moving into houses or rooms 
previously occupied by a consumptive must always be small, is 
considered doubtful by some and entirely denied by others. 
From the known fact that such rooms and dwellings are almost 
always renovated and cleansed after the consumptive has va- 
cated and before the new tenant takes possession makes this 
mode of contagion very doubtful. 
A tuberculous infection, as has been stated (114), is usually in 
infancy or early child life, and the frequency of this infection in 
the first year of life is only about 2%, reaching more than 90% INFECTION AND CONTAGION 
31 
at about the 14th year or at puberty. This infection is generally 
followed by manifest disease in nearly all infants during the first 
year, in 50% of children up to the third, 20% in the sixth or 
seventh and only about 2% at the age of 14; even after the age 
of 6 the infection is very seldom followed by active disease, and 
this because there is in the child at all times a strong tendency to 
healing. In early infancy the infection generally takes place 
more readily because the young organism can not protect itself 
against the infection, and many children who show a tendency 
to pulmonary disease at the time of their birth, have from birth 
a constitutional anomaly, a disposition which greatly favors the 
tuberculous infection. A primary or first infection due to the 
defence agencies induced by this first infection will give protec- 
tion to the infected organism from subsequent invasion pro- 
vided that the later invasion is not too massive nor too frequent. 
As nearly all primary infection takes place in infancy or early 
childhood and usually follows an implantation of the disease 
germs from without, a later or superinfection generally occurs 
in youth, or in young men and women. This superinfection is 
most frequently an autogenous reinfection, that is from within. 
This generally leads to active disease which is usually brought 
about by poor nutrition and a vicious life, or by overstudy and 
overwork, by grief and worry, by disease and trauma, etc. Most 
adults have been tuberculously infected in childhood, and in con- 
sequence thereof have acquired various degrees of immunity and 
a hypersensitiveness to tuberculin. Such individuals are, as a 
result, extremely seldom reinfected even in closest association 
with a tuberculous person, and never during the contact with a 
disease carrier. It has never been sufficiently recognized by the 
medical profession that in the adult the contagiousness of tuber- 
culous disease in a strict sense is not a reality, that it is only a 
theoretical expression or construction and that it is at variance 
with and contrary to all observations. (Note Saugmann’s 
Critical Study.) No proof is forthcoming that attendants, nurses 
or physicians to a tuberculosis sanatorium, or those in attend- 
ance upon the unfortunates and sick have contracted the disease, 
and such as have become tuberculously sick were undoubtedly 
tuberculously infected, perhaps slightly tuberculously diseased, 
before entering upon the services at such institutions. In our 
calling as physicians we come in constant, daily and hourly con- 
tact with both the tuberculosis carriers and the virus and do we 32 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
find the tuberculosis mortality greater amongst doctors than 
amongst those in other callings? 
In the married, tuberculosis of both husband and wife at the 
same time is very infrequent, notwithstanding the fact of closest 
contact, the infection possibility here being undoubtedly always 
present and not to be denied; however, from observations we 
must conclude that the probability is not very great. We all 
know of cases of tuberculosis in families where either the hus- 
band or the wife is suffering from pulmonary tuberculosis, but 
with how many cases are we familiar where both the husband 
and the wife are suffering from active disease at the same time? 
The estimated percentage of this family disorder is between 
6 and 8, and if we eliminate from this the percentage of men and 
women who have been infected or perhaps slightly sickened be- 
fore marriage, it leaves the percentage of those who are infected 
after marriage, say the husband from the wife, or the wife from 
the husband, as only about 2%. It is of interest to note that at 
this time in life the degree of immunity which may be acquired 
is much greater, is much faster than in child life; as evidence, 
we may be reminded that if either partner is removed from the 
environment, is sent either to a sanatorium to take the cure, or is 
called away by death, the remaining partner heals readily and 
gets quickly well. In this connection it may also be noted that 
if either husband or wife develop active pulmonary tuberculous 
disease soon after marriage, that all the children born will be 
tuberculously infected and most all will in after life become 
tuberculously diseased; if, however, in the adult the disease 
manifests itself later in life when some of the children have been 
born, then all the children who have passed the sixth year will be 
spared. 
From what has been said, we can conclude that tuberculosis 
is highly infectious and perhaps contagious to children, but in a 
sense, it is not contagious to adults; hence the frequent visiting 
of friends and relatives at the home of the tuberculously diseased 
person or at the tuberculosis sanatorium should be encouraged. 
It is wholly devoid of all danger from contagion to adults, and 
most of all such visits give much encouragement to the unfor- 
tunates, are conducive of much improvement in their health, 
ease the tuberculously diseased person’s mind, and they are 
most grateful to observe that because of their misfortune they 
are not treated like an outcast and not shunned by fellow man. INFECTION AND CONTAGION 
33 
As a resume, we can truthfully conclude that to the healthy 
adult there is usually no danger in associating with a tuber- 
culous individual,! but it can not be too strongly emphasized 
that the greatest danger lies in the surroundings of the tuber- 
culous, their homes or otherwise, to infants and small children; 
hence, the watchword must at all times be, “Keep the small chil- 
dren away.” 
Dr. Lawrason Brown, Lake Saranac, New York, only recently con- 
ducted a series of most interesting experiments at the Trudeau Tuber- 
culosis Sanatorium (56) which may be of note at this point. He first 
showed what effect room dust, collected from the tuberculous wards, 
would have on test animals, next the effect of washings from the table 
utensils, like knives, forks, spoons, cups, etc., from tuberculous patients, 
washings from tooth brushes, from door knobs, etc., even what effect 
the shaking of hands of an actively tuberculous person with a non- 
tuberculous would have. By these experiments he could prove what so 
often had been proven before, that infection by these means is very in- 
frequent. His most ingenious and unique experiments were conducted to 
see what effect kissing had on the spreading of tuberculous disease and 
he concluded from most accurate observations that kissing by an active 
tuberculous individual with positive sputum in the early morning will 
undoubtedly spread the disease but that kissing done as the day goes 
on becomes gradually less and less a source of danger and that towards 
evening kissing by the tuberculous is entirely free from infectiousness. 
Positively pulmonary tuberculous individuals, with positive sputum find- 
ings, were asked to kiss sterile petre dishes at various times during the 
day, the washings of these were at once injected into guinea pigs and 
from this experimental work he observed that the washings from the 
early morning hours were all positive, the findings becoming less posi- 
tive towards the afternoon and entirely negative from the washings of the 
sterile petre dishes kissed in the evening. See Transactions National 
Tuberculosis Association, Atlantic City, 1919. 
Any one who is doing much tuberculosis work and who has treated 
many cases of pulmonary tuberculosis and whose experience extends 
over many decades will not have failed to observe the infrequency of 
tuberculous disease of more than one adult in a given home at the same 
time. I have observed many cases of tuberculosis in homes where the 
patient and faithful wife has nursed and taken care of a sick husband for 
years, and yet in spite of the wife’s close confinement to the home, her 
+The implantation of the tubercle bacillus into or under the cuticle is not sufficient to 
bring about infection. The so deposited micro-organisms may remain quiet or dormant 
for months in no way make their presence known, and, during all this time it can not 
be said that the individual is infected. The time from implantation to actual infection 
may vary from six to eight days to three months. Even if the deposited bacilli should 
slowly multiply and spread into contiguous tissue we may still speak of non-infection if 
their presence in the organism has caused no reaction, no tissue disturbance. If, how- 
ever their presence becomes known to the body cells, the body raises a defense, protest- 
ing against the growth and spreading of the invaders, then we speak of the body’s 
defense powers and that the body is now infected. The moment the resistance begins 
infection also begins. A tuberculin application is always negative so long as the body’s 
defense powers have not been aroused, the body is then still not infected but with arousing 
the infection go hand in hand. 34 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
companionship and her most intimate association, she did not contract 
the disease nor at any time show evidence of tuberculosis. Exceptionally 
I have observed a good and kind husband wait on his sick wife after 
coming home from work, having his rest broken and disturbed the 
greater part of the night all without a murmur, perhaps occupying for 
months before the wife’s death the same bedroom or sleeping quarters, 
and this same man, now years since the death of his wife from pulmonary 
tuberculosis enjoying the very best of health. Again, a kind and affec- 
tionate sister takes into her household a worthless but unfortunate brother 
suffering from pulmonary tuberculosis, exposes her own children to the 
infection but never herself shows any symptom of disease. I can well 
recall the instance of two sisters living for many years in closest com- 
panionship, one of the sisters developing a pulmonary tuberculosis, and 
though from the onset of the disorder until death more than thirteen 
years have elapsed, these two sisters during all this time were inseparable, 
the early years and the greater portion of time being spent in travel and 
at sanatoria seeking the cure. The last year of the sick sister’s life was 
spent entirely in bed, and during the greater portion of all this time the 
healthy sister shared the same bedroom, to be at her side, to serve her 
every want, to make her last hours comfortable, and after all these years 
of sacrifice, deprivation and devotion, upon the death of the sister, the 
remaining one was in perfect health. The case of two adults in the same 
household, the one becoming sick upon the attendance of another in- 
dividual sick with pulmonary tuberculosis, must be exceedingly infre- 
quent. In all my years of experience I have never observed such a case, 
hence I ask how many cases do we see where both husband and wife are 
suffering from active pulmonary tuberculous disease at one and the same 
time? CHAPTER 6 
THE PRIMARY FOCUS OR FOCI OF INFECTION MOST 
FREQUENTLY IN THE LUNGS AND THE SUB- 
SEQUENT AFFECT ON THE PUL- 
MONARY TISSUE 0) 
As early as 1876 Parrot (15) reported from numerous au- 
topsy observations on infants and small children that in early 
infancy, in every case of pulmonary disease, tuberculous as 
well as non-tuberculous, a simultaneous involvement of the 
regional lymp nodes can be demonstrated, and, vice versa, that 
no change in the lymph nodes about the lungs can be shown 
without an analagous involvement of the lungs; that a tracheo- 
bronchial lymph gland involvement is evidence of pulmonary 
disorder and that a primary focus is invariably to be found 
somewhere in the pulmonary tissue. This became known as 
Parrot’s Law, “LaLoi des adinopathie similaires,” and it applied 
with equal force in all cases of pulmonary tuberculosis. 
Parrot, on 145 autopsy observations on tuberculosis in chil- 
dren, was always able to demonstrate in the presence of a 
tracheo-bronchial lymph gland involvement, a primary focus at 
some point in the lung, “Le foyer pulmonaire primitif.” Her- 
vouet, a student of Parrot, on further observations states that 
the changes in the lungs are not always accompanied by a sim- 
ilar change in the regional glands, but that if changes in the 
glands are demonstrable, always and invariably similar changes 
will be found in the'lungs. However, the most important and 
definite observations were those of Kuss in 1898. He confirmed 
the existence of Parrot’s Law and described in minute detail 
the portal of entry of the tubercle bacillus into the infected or- 
ganism. According to Kuss the primary invasion is character- 
ized by a small nodule situated usually subpleurally, in which 
condition it may remain for years, gradually undergoing retro- 
gressive changes, which are so frequently observed in tuber- 
culosis, or it may ulcerate, the nodule soften and its contents 
‘Under this chapter we will consider only the infection as it is brought about in the 
natural way, leaving artificial inoculation to experimental medicine. 
35 36 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
may be emptied into a bronchus. In this condition the regional 
lymph nodes are mostly always secondarily involved, showing a 
definite connection existing between the tuberculosis nodule in 
the lungs and the nearest glands. In most instances but a single 
primary process was demonstrable; two or more foci were only 
occasionally observed and the lymph tract between these pri- 
mary pulmonary foci and the regional glands remained usually 
in a healthy condition. According to Kuss, this primary pul- 
monary focus frequents both the right and left lung but favors 
in most pronounced form the lower lobes, is occasionally found 
in the upper, but never at the apex. From this he concluded 
that the current of air is capable of carrying the bacilli along the 
Fig. 1. The lung (schematic) after Ghon. Autopsy No. 444. Cause of death tuber- 
culosis meningitis, boy 7 years. Note the calcified nodule, in the lower portion of the 
left upper lobe, the lingula pulomalis, surrounded by fibroid induration, this the initial 
infection, the single primary focus. The regional lymph nodes the upper left broncho- 
pulmonary and tracheo-bronchial have undergone change, both calcification and caseation. 
The cross lines along the border of the left lung are indicative of pleurisy. 
bronchial tubes, but that they are usually deposited there where 
the current of air is vigorous and most direct. 
All this labor was later still more emphasized by E. Albrecht 
who in 1907 showed that in right sided pulmonary involvement, 
the right tracheo-bronchial glands, and in left sided disorder, the 
left regional lymph nodes become secondarily involved. He 
states further that in every case of tuberculosis of the bronchial 
glands, the corresponding nodule in either right or left lung 
should be looked for. H. Albrecht, 1909, studied the primary 
foci in 1,060 observations on children at autopsy, arriving at 
similar results. 
The most interesting, definite and conclusive labor done in 
recent years is that of Ghon, who in 1912 made known his ob- PRIMARY FOCUS OR FOCI OF INFECTION 
37 
servations on 184 carefully conducted autopsies in tuberculous 
children. He divided this number of cases into two groups, the 
larger or 170, in which he was able to demonstrate uncontro- 
vertably a primary tuberculous focus in the lung, and the smaller 
group of 14 cases in which he was not able to demonstrate posi- 
tively such a focus, although conditions existed in the pulmon- 
ary tissue which may presuppose such a focus. He further 
proved that in 142 cases out of the total of 170, only a single 
primary focus was present; in 15 cases two foci could be shown, 
in 5 cases three, in 2 cases four, in 1 case five and in 5 cases an 
indefinite number of minute foci. According to his observations, 
primary infection of the right upper lobe predominates; next 
in frequency is the left upper, followed by the right and left 
lower, and the middle lobe was found eleven times to be the 
seat of primary infection. It is worthy of note, that in nearly 
all of his observations, if the right or left lung was the seat of 
infection, the primary seat of the infection was to be found not 
in any portion of the lung tissue, but chiefly near a bronchus, 
but not in a bronchus, and only very exceptionally toward an 
apex either right or left, that is, the seat of primary infection 
was usually found near the middle portion of the lung. Ghon 
found further that the right lung was more frequently the seat 
of primary infection as compared with the left, and that the 
right upper lobe was out of choice the lobe involved. This, 
however, is contradictory to the findings of Kuss, according to 
whom a primary focus favors the right or left lung with equal 
frequency, but most particularly selects the lower lobes. 
In Ghon’s report of 184 cases, we find that the youngest tuber- 
culous child coming to autopsy was 2 months and the oldest 14 
years of age, and in addition, we find that most frequently the 
lower lobe is the seat of primary infection in the younger and 
the upper lobe in the older children. 
Perhaps the observations of Kuss were upon a greater number 
of smaller children, hence the infection was found more fre- 
quently in the lower lobes. The question now arises as to why 
a primary focus should be localized, particularly in infants, more 
frequently in a lower lobe as compared with an upper. As Kuss 
has already pointed out, and reference has already been made 
to this, the air current through the bronchial tubes is capable 
of carrying the tubercle bacilli along any part of the bronchial 
tree but they are deposited most frequently along those sur- 38 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
faces where the current is most pronounced, vigorous and direct. 
If this is true, and this has not been disproved, then the im- 
plantation of the tubercle bacillus either as a primary involve- 
ment or as a subsequent disease is simply a mechanical process, 
similar in both man and animals. This also explains the over- 
whelming frequency of tuberculous disease in the upper lobe 
in the adult and the right lobe more so than the left (65 to 75% 
right apex disease and 35 to 25% the left). This will also readily 
explain the relative pulmonary tuberculous disease in the bovine 
and other quadrupeds. In the human adult suffering from ac- 
Fig. 2. Lateral view of the bovine lung. The shaded portion, the tip indicates the 
most frequent point of election in tuberculous disease. In the bovine the apical lobe is 
also frequently involved, the cardiac the most pendent portion very rarely, this even in 
the last stages of the disease. From Sissons, J. A. M. A., p. 1513—1918. 
tive pulmonary tuberculous disease, we usually find the apices 
infrequently are the bases primarily actively diseased. In small 
children, however, we quite often find active tuberculosis of a 
lower lobe as a beginning disorder. This, as in the primary 
infection, also is brought about by mechanical means. 
The tuberculously infected individual is generally reinfected 
from within and not from without, and this leads to active dis- 
ease. This is a secondary aspiration process. The broncho- 
pulmonary glands having received the lymph flow from the pri- 
marily infected lung become secondarily infected and ultimately 
undergo either a progressive or a retrogressive change, becom- 
ing either soft and caseate or calcify or undergo fibroid changes. 
During this time the primary focus in the lungs may heal, leav- 
ing an indelible scar. If these bronchial nodes which are sec- PRIMARY FOCUS OR FOCI OF INFECTION 
39 
ondarily infected should undergo such changes, either calcifying 
or undergoing fibrosis, they may then remain quiescent for years 
without any other or perhaps slight retrogressive changes. 
Should these gland’s, however, as so often occurs, become case- 
ous and soften with accompanying irritation and inflammation 
of the surrounding tissue, then the contents of such glands may 
break through the fibrous capsule, find access into a bronchus 
through the point of least resistance and entering the lumen 
again be carried by the inhaled air in the direction of the greater 
air current. In the adult when in the upright position, this is 
Fig. 3. _ The lung (schematic) after Ghon. Autopsy No. 645. Cause of death Miliary 
tuberculosis, male, age 4 years. Note the scar in the left upper, towards the middle of 
the lobe surrounded by a secondary retraction and pleuritis. The regional lymph nodes, 
the left broncho-pulmonary and tracheo-bronchial have undergone caseation and softening. 
Note carefully the arrow showing the breaking through of a softened gland into the 
bronchus near the hilum. In such an event bacilli in the sputum may or may not be 
evidence of pulmonary tuberculosis. 
usually in the direction of one of the apices of one of the upper 
lobes, depending- upon whether or not the primary infection, fol- 
lowed by the involvement of the regional lymph node, was in 
the right or the left lung. But Ghon has shown that out of a 
total of 142 cases of pulmonary involvement, a single primary 
focus was demonstrable in the right lung 87 times or 61.27% 
as compared with the left 55 times or 38.73%. This goes to 
show that the right lung is most frequently the seat of primary 
infection, and that the regional lymph glands become secondarily 
infected, that the nearest glands to the right lung are the lymph 
nodes to the right of the bronchus and that subsequently it is 
the glands to the right that undergo changes which are ulti- 
mately followed by right sided pulmonary disease. If the left 40 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
lung is primarily infected, the lymph nodes adjacent to the left 
bronchus become secondarily infected, and this is later fol- 
lowed by active tuberculous disease of the left lung. 
In order to comprehend clearly how primary infection and 
later active pulmonary tuberculous disease takes place through 
the respired air, it will become necessary that we first consider 
the anatomical structure of the bronchial tree from its origin 
at the trachea down to its minutest ramifications in the pul- 
monary tissue, namely, (1) main trunk, (2) primary bronchi, 
(3) secondary bronchi, (4) tertiary bronchi, (5) the bronchioles, 
bronchi respiratori, (6) the terminal bronchi, the alveolar ducts, 
ductuli alveolares, and (7) the atria (vestibuli), the air sacs 
and alveoli (sacculi alveolares et alveoli pulmonum), these lat- 
ter being the last division within the pulmonary parenchyma. 
Beginning at the larynx, which may be likened to the under- 
ground portion, the root of a tree, the trachea or main trunk ex- 
tends downward, inclines a little towards the right and at a 
point on the anterior chest wall opposite Ludwig’s angle, or per- 
haps a trifle lower, on a line with the second interspace, and 
posterior on a level with the fourth dorsal spine, divides into 
two lesser trunks, the primary bronchi, one to the right, the 
other to the left, continuing to the hila of the lungs which they 
enter and almost immediately begin to again divide and sub- 
divide into smaller and smaller trunks, known as secondary and 
tertiary, and extending like the branches of a tree in all direc- 
tions, terminating towards the pulmonary periphery in most 
minute tubules known as the respiratory bronchi, at the distal 
ends of which and now in the pulmonary parenchyma are found 
the alveolar ducts and the air vesicles (59). 
The trachea, the bronchi (23), the various branches, both the 
secondary and the tertiary are not continuous straight tubes,2 
which become smaller and smaller as they approach the pulmon- 
ary periphery, but on the contrary immediately below the larynx 
the trachea is somewhat contracted, becoming wider as it ex- 
tends downward and again contracting as it approaches the 
bifurcation, at which point it again widens, continuing in this 
2Prof. W. S. Miller, of the University of Wisconsin, has conclusively demonstrated 
that the continuation of the bronchioles is not abruptly into the alveoli, but that their 
terminals are most complex bodies usually dividing into many compartments or air sacs, 
breaking up and terminating in the pulmonary parenchyma, that between these air sacs 
and the respiratory bronchi or bronchioles, we find the vestibules or atria, these in turn 
opening into minute ducts, the ductuli alveolaris, the terminal bronchi, the. continuation 
of the bronchioles. PRIMARY FOCUS OR FOCI OF INFECTION 
41 
manner throughout the primary bronchi and to some extent 
the secondary and tertiary branches. By this anatomical struc- 
ture the respired air entering is given a distinctly rotary motion. 
See Figure 4 
If we outline on the chest wall the course of the bronchial 
tree and its various branches we will observe that the latter 
Fig. 4. Representation of a Primary Lobule of the Lung (Schematic). An Anatomical 
Unit—After Prof. W. Snow Miller, University of Wisconsin. Bulletin, Chicago Tuber- 
culosis Institute 1916. 
EXPLANATORY NOTE 
b.r.—A bronchial (bronchiolus respiratorius). 
d.al.—An alveolar duct (ductulus alveolaris). 
a.—An atrium (vestibulum). 
a.p.—An alveolus (alveolus pulmonis), 
s.al.—An air sac (sacculus alveolaris). 
p.—The pleura. The lobule is represented as being situated immediately under the 
pleura. 
x. —Ring of muscle fibre. End of all muscle tissue, lymph vessels and nucleated 
epithelial cells. (See Alfred Stengel, Nothinagel’s. Practice.) 
y. —Represents the beginning of a second primary lobule, which is, however, not 
carried out in detail. 
become extremely small, terminating posteriorly on either side 
of the spine on a level with the eighth rib, anteriorly on the left 
side at the fifth rib internal to the mammary line, right side, 
fifth rib near the parasternal line, and all the tissue beyond 
and towards the lung border is occupied by the pulmonary 
parenchyma, the minute divisions of the distal ends of the termi- 42 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
nal bronchi. If next we follow along the bronchial tree, from 
the main trunk at the larynx down the primary bronchi, the 
secondary and tertiary branches to the terminal bronchi, the 
distribution of the muscular tissue, smooth muscle fibers, we 
will observe that all of this tissue becomes gradually less and 
less in amount as we proceed downward and outward ap- 
proaching the pulmonary parenchyma, and that all muscle fibres 
have entirely disappeared, with perhaps the single exception at 
the terminal bronchi, where a ring of unstriped muscle fiber, 
sphincter-like, guards the entrance to the atria at the distal ends 
of the ductuli alveolares. No muscle fiber is found beyond this 
point or in the pulmonary parenchyma, all muscle fibers stop- 
ping at the distal ends of the terminal bronchi. Now if we 
follow the bronchial lymphatics, which form a close net-work 
or mesh-like structure in the walls of the bronchial tubes, we 
will observe that they diminish in size as we proceed from the 
hilum pulmonum, becoming smaller and smaller, and terminat- 
ing with the terminal bronchi, and that no lymph vessels are 
found beyond this point, that is, beyond the ring of unstriped 
muscle fibers and that there are no lymph vessels in the walls 
of either the air sacs, atria or the alveoli, all of which are situ- 
ated in the pulmonary tissue proper. Let us now consider for 
a moment the third important factor in this anatomical picture, 
the epithelial lining of the bronchial tree from the main trunk 
to its ultimate termination in the alveoli or air sacs. From and 
including the larynx, the trachea, the primary bronchi, as well 
as the secondary and the tertiary branches and as far as the 
respiratory bronchi, we find epithelial cells of the ciliated cylin- 
drical variety lining these tubes, but on the walls of the termi- 
nal branches of the bronchioles, the alveolar ducts, we find a 
simple epithelium of the cuboidal variety, and these cells of 
cuboidal epithelium extend towards the distal ends, gradually 
becoming flatter and ultimately joining at the atria the epithel- 
ium of the flat pavement variety, polygonal cells, which line the 
atria, the air sacs and the alveoli. 
As in a tree not all the leaves are found at the outer border but many 
arise from smaller branches nearer the main body, so in the bonchial tree 
all the air sacs do not arise at the periphery, but many may arise in clus- 
ters about the smaller and the terminal bronchi. These are, however, 
found to be smaller and less numerous, though the general structural 
arrangement throughout is everywhere the same, and they are lined with PRIMARY FOCUS OR FOCI OF INFECTION 
43 
the same flat pavement epithelium as the larger and more numerous 
air cells. 
If next we study closely the structure of the cells lining the 
bronchial tree, beginning at the larynx and continuing up to 
and including those which line the terminal bronchi, we find 
that they are all of the nucleated variety, both the ciliated cylin- 
drical and the cuboidal, but that those cells which line the 
alveoli, the atria and the air sacs differ in being of the non- 
nucleated kind. 
Loeb (208) in 1899 advocated the idea that the nucleus of a 
cell is its center of oxidation, is the life of the cell, and that this 
will explain why cells without, or being deprived of, a nucleus 
are very short-lived and very easily destroyed, show no resist- 
ance and are wholly unable to regenerate missing parts. Mat- 
thews (209) in 1915 stated that the nucleus in plant cells is 
directly concerned in the oxidation process, and Spitzer (210) as 
early as 1897 reported that the nucleoprotein extract from certain 
animal tissue has the same oxidizing power as the tissue itself. 
From these observations we can conclude that the nucleus of 
the cell in both plant and animal tissue possesses highly oxidiz- 
ing properties, a power which is not possessed by the non- 
nucleated cells, and moreover, that the non-nucleated cells are 
short-lived, are easily destroyed, show no resistance and are 
wholly unable to regenerate missing parts. Now, the cells lining 
the air sacs, the terminal and distal ends of the bronchi within 
the pulmonary parenchyma are all of the non-nucleated variety, 
hence possess very little, if any, resisting power and consequently 
must be very readily destroyed by any foreign body entering the 
cells. From pathologic study we know that pulmonary tuber- 
culosis, both the primary infection and later the disease, has 
its origin, not in any part of the lung, not in the bronchial tubes, 
but in the pulmonary parenchyma surrounding the smallest 
bronchi, namely, in that portion of the lung in which the air 
sacs are situated and which are lined with non-nucleated cells. 
Parenthetically it may be stated that the assertion that free openings or 
stomata lead from the alveoli, the atria and air sacs or air cells into the 
lymph vessel of the lungs has not been confirmed, and is very improbable, 
as lymph vessels are not demonstrable in the walls of the alveoli nor in 
the atria. 
Having considered somewhat in detail the anatomical struc- 
ture of the bronchial tree, let us now consider how tuberculous 
infection has its beginning in childhood, and subsequently be- 44 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
comes active in adult life. It is necessary that we consider at 
the onset all the important factors, namely, the air currents, the 
bronchial tree, the muscle fibers along this tree, the network 
of lymph vessels in the walls of the different branches of this 
tree, the epithelial lining of these tubes and particularly those 
which line the walls of the terminal ends, the air sacs, the non- 
nucleated cells, and above all the tubercle bacillus entering the 
bronchial tubes with the respired air. 
The air on entering the main trunk is thrown into a rotary 
motion, this whirling motion is continued throughout the whole 
bronchial tract and particles of foreign matter, like minute specks 
of dirt, coal dust or bacteria, are in this manner readily carried 
along with the current. However, the greater portion of these 
foreign particles is again expelled by the motions of the ciliated 
epithelium lining the bronchial tubes and by the contractions of 
the muscle fibers accompanying them throughout, still particles 
of dust, and tubercle bacilli as well, do find lodgment on the 
bronchial mucosa, and some may gain access by penetrating the 
irritated mucous layers, and if so, they are in all probability 
taken up by the close network of lymphatics lining the entire 
inner walls of the bronchial tubes, and as all of these lymph 
vessels drain towards the lymph nodes in the hilum, the re- 
gional glands of the tubes, particles of dust, coal and tubercle 
bacilli among others are deposited in these glands. This corre- 
sponds to the findings of Kuss who showed that the lymph 
tract between the primary foci and the regional glands usually 
remained in a healthy condition. 
That tubercle bacilli are not deposited within the walls of 
the bronchial tubes per se is evidenced by the fact that a pri- 
mary tuberculous infection and a secondary reinfection as well 
are never found in these tubes. We must, then, assume that 
some, or at least a few tubercle bacilli, after passing the ring of 
muscle (3) fibers, are carried onward and outward towards the 
pulmonary periphery into the distal ends of the terminal bronchi, 
where they find prepared a portal of entry, a nidus for their depo- 
sition and further growth. 
All lymph flow in the pulmonary tissue is towards the peri- 
’That these rings of muscle fibres placed at the terminal ends of the bronchial tubes 
really guard the entrance to the air sacs can fairly well be demonstrated from observa- 
tions which have so frequently been made, namely, that when otherwise healthy coal 
miners are accidentally killed while at work, autopsy will show the bronchial tubes filled 
with coal dust, but the air vesicles will be found comparatively free. PRIMARY FOCUS OR FOCI OF INFECTION 
45 
bronchial glands.4 These become secondarily infected whilst 
the primary focus in the lung tissue often heals entirely, leav- 
ing a typical scar, often only pinhead in size—the indisputable 
evidence that this was the primary or the older infection. It 
is well to remember that the first point of tuberculous infection 
is not an involvement of the pulmonary lymph nodes, such 
gland structure, if infected, being always secondary to a pri- 
mary seat in the adjacent pulmonary parenchyma. Post mor- 
tem evidence has sustained these findings, namely, that the pul- 
monary tissue is always first infected, and that an involvement 
of the pulmonary or peribronchial glands is a subsequent in- 
fection. gB 
Fig. S, The lung (schematic) after Ghon. Autopsy No. 350. _ Cause of death scarlet 
fever, girl, 7)4 years. Note the calcified nodule, the initial lesion evidence of an old 
healed process in the middle portion of the right lower lobe with secondary calcification 
of a single regional lymph node situated in the lower right tracheo-bronchial area. 
In this connection it is interesting to note that both Kiiss and 
Ghon have observed that in the greater number of instances only 
a single primary focus is found in the lung tissue, that occa- 
sionally two foci are found and that three or more are excep- 
tional, all of which goes to prove that in the human, a natural 
infection is very similar to the artificial inoculation produced in 
the integument of animals where after a primary infection a 
subsequent reinfection is usually negative. 
After the primary foci are healed, the peribronchial, the glands 
nearest to the point of first infection, are found to be secondarily 
involved. (See Fig. 5.) If this first infection has been mild or 
4It has been repeatedly demonstrated that when live virulent tubercle bacilli are placed 
into the alimentary canal, for instance into the large bowel, that infection of the peri- 
bronchial or hilus glands may take place without previously involving the healthy lung 
structure but this is an artificial infection in an experimental animal and not the natural 
infection which we are now considering. 46 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
at any rate not massive, then these glands gradually undergo 
retrogressive changes and a period of quiescence manifests itself, 
in many instances for years (5), the lymph nodes becoming more 
and more encapsulated or undergoing calcification, no further dis- 
order being noticeable. In many instances, however, after such 
a period of either short or long quiescence, the bacilli again be- 
come active, the glands undergoing swelling and softening and 
ultimately expelling their contents in the direction of least re- 
sistance. In some instances this point of least resistance is in 
the tissues about the bronchial tubes or in the mediastinum, 
where it is quickly taken up by the lymphatics, producing a gen- 
eralized or a miliary tuberculosis, or it may break into the esoph- 
agus and the contents find their way into the alimentary canal, 
where the fate of the bacillus depends on the quantity of bac- 
teria which enter the abdomen and also upon their virulence. 
In other instances, the focus of least resistance is through a 
bronchial tube (see figure 3) from which the contents of the 
gland may simply be expectorated, healing of the lacerated gland 
and the open bronchus taking place, and here also nothing 
further being noticeable. But as frequently happens, the con- 
tents of such a gland either in part or a small quantity at a time, 
may find entrance into a bronchus, be aspirated along a bronchial 
tubes with the currents of air and ultimately find again a nidus 
now in the distal ends of the terminal bronchi, in the air sacs, the 
alveoli and infecting or better now reinfecting from within, the 
pulmonary parenchyma, this, however, is unlike the first, and is 
usually not followed by scar tissue formation but by active 
tuberculous disease, and tissue destruction. This now is the 
condition described as pulmonary tuberculosis, a secondary as- 
piration process, a disease situated about the terminal bronchi 
and the air sacs or alveoli, the distal ends of these tubes, ulti- 
mately producing a peribronchial infiltration. 
Why the tubercle bacillus in primary infection, in child life, 
should show a special predilection for the pulmonary parenchyma 
of the lower lobes (88), and in the adult, the secondary or re- 
5That a long period of quiescence often follows the implantation of the tubercle bacillus, 
that sometimes years elapse before manifestation of the disease, is now generally accepted. 
We find, however, even in the medical profession, that this is often taken somewhat 
skeptically, hence the enumeration of a few physiological instances. Histology teaches us 
that in the upper lip of the male child the roots from which the moustache grows are 
already present at birth, and yet it takes the stimulus of puberty to make them grow. 
Our dentist friends inform us that the roots from which the wisdom teeth grow are to 
be found in the jaw of the child at birth and often as much as 28 years have elapsed 
before they are erupted. Better still, from Gynecology we learn that in the female ovary 
the roots or germs of many thousands of ova are demonstrable at birth, and yet in many 
instances a Graefean follicle does not ripen until 45 or more years. PRIMARY FOCUS OR FOCI OF INFECTION 
47 
infection select the upper lobes can readily be accounted for 
when we consider the postural positions in these different years 
or ages of life. Kuss, as early as 1898, and this was later cor- 
roborated by Ghon, pointed out that the primary infection in the 
lungs in children is in the direction of the greatest and most di- 
rect air current, and undoubtedly the same applies to adult life 
and to animals as well. In cattle the point of pulmonary tuber- 
culous disease is usually found in that part of the lung which 
corresponds to the human, in what is generally known as the 
caudal portion—the tail end, that is, the base. This, in the ani- 
mal, is also a secondary infection from within, an aspiration 
Fig. 6. The Lungs in Situ in the bovine. The arrow points to the point of election 
in tuberculosis which is in the tip of the lung and which is also the highest point 
whether the animal is standing or lying. This part of the lung corresponds with the 
base or caudal portion in the human. From Sissons J. A. M. A. p. 1512—1918. 
process from a large, previously infected gland pouring its con- 
tents, laden with bacilli, into a bronchus and being carried by the 
air currents to the finest but most vulnerable tissue of the lungs. 
We note here also, that the current of air is in the direction of 
least resistance. 
It now becomes apparent why different parts of the lungs in 
both man and animal seem to exhibit a special predilection for 
the tubercule bacillus. In early childhood, in infancy, owing to 
the usual postural position of the child at that age, which is 
either lying down or on all fours about the floor in the home of 
the tuberculous adult from whom it receives its primary infec- 
tion, the most favorable point for the respired air is towards the 
base, where the air current has more free access and the same 
applies, undoubtedly, to the bovine, which throughout the 48 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
greater part of its whole life, in its natural postural position, 
places the base of the lung constantly at its highest point. This 
all favors a more direct air current and it is there that we find 
both primary infection and later active tuberculous disease. In 
the human, in adult life, the secondary or reinfection is in most 
instances towards the apices. It is there that active tuberculous 
disease first manifests itself, again in the direction of the greatest 
air currents, which in the upright postural positions during adult 
life form a more direct, a more easily accessible route, a more 
ready way to carry the aspirated tubercle bacilli mechanically 
upwards and outwards, into the most delicate and most vulner- 
able pulmonary tissue. 
Active pulmonary tuberculous disease begins as an alveolitis 
and bronchiolitis. Aspirated tuberculous material from a soft- 
ened gland is carried with the strong air current directly up into 
the pulmonary structure, along the bronchial tubes and alveolar 
ducts into the alveoli. There it meets a cellular lining, an epithe- 
lium which offers no resistance, is easily destroyed, cannot pro- 
tect itself or show any defense, and the contained bacilli—like all 
invaders—take possession of this delicate, defenseless tissue, be- 
gin the preparation of a new soil for their growth and develop- 
ment and little by little penetrate deeper and deeper into the 
contiguous tissue, surrounding more and more bronchioles and 
alveoli, gradually producing the morbid process in the lungs 
described as peribronchial tuberculosis, the subsequent growth 
and development, rapidity or retrogression, depending upon the 
fertility or non-fertility of this newly invaded soil, and upon the 
environment and age of the tuberculously affected individual. 
Recapitulation 
1. The bronchial tubes are accompanied by smooth muscle 
fibres throughout; at their distal ends all these fibres cease but 
for a ring of unstriped fibres which guards the entrance into the 
air vesicles. 
2. The walls of the bronchial tubes are lined throughout by a 
fine net-work of lymphatics, but these stop abruptly at the ring 
of muscle fibres situated at the terminal ends of the tubes. 
3. Ciliated cylindrical epithelial cells line the entire bronchial 
tubes with the exception of the alveolar ducts, the terminal bron- 
chi, which are lined with a cuboidal epithelium. Both the cili- 
ated, cylindrical and the cuboidal epithelial cells are of the nu- PRIMARY FOCUS OR FOCI OF INFECTION 
49 
cleated variety. They do not extend beyond the ring of muscle 
fibres mentioned. 
4. The epithelial cells which line the alveolar walls, the air 
sacs, distal to these rings of muscle fibres, are of the polygonal 
variety. These cells are non-nucleated, are short-lived, are eas- 
ily destroyed, have no resistance or defense power and can not 
protect themselves against foreign bodies, like bacteria, dust 
particles, tubercle bacilli, etc. 
5. It is known that on the living, healthy, nucleated epithelium 
lining the bronchial tubes, the tubercle bacillus is perfectly harm- 
less, and for that reason pulmonary tuberculosis never has its 
origin in these tubes. The epithelium of the air vesicles, how- 
ever, are all lined with polygonal cells which are non-nucleated 
and which are situated beyond the rings of muscle fibres. CHAPTER 7 
THE COURSE OF TUBERCULOUS DISEASE IN THE 
DIFFERENT AGES—FROM INFANCY TO OLD AGE 
Throughout life, at every age and at any time, that is, from 
early infancy on, up to old age, the tuberculously infected indi- 
vidual may manifest active tuberculous disease, either in one 
form or another. This tuberculous disease may show a special 
predilection for certain tissues or organs of the body to the ex- 
clusion of others, producing either a localized manifestation or 
at any time assume a virulent type, invade many organs or tis- 
sues and become generalized as is observed in miliary tubercu- 
losis (114). 
Tuberculosis (86), a disease entity, as we observe it, usually 
presents a continually changing picture beginning in the vast 
majority of cases with a primary infection in early infancy, grad- 
ually invading various organs and tissues of the body and ter- 
minating in adult life with the fully developed pulmonary tuber- 
culous disorder. 
Primary infection usually takes place after birth and is then 
spoken of as extra-uterine or post-natal in contra-distinction to 
that infection which takes place occasionally before birth which 
is known as intra-uterine or pre-natal. 
Intra-uterine Infection. Pre-natal, Congenital or unavoidable. 
A true congenital tuberculosis is a rarity and is very infrequent. 
Infants born with a tuberculous infection usually succumb early 
to a generalized tuberculosis (within the first few weeks of their 
existence) and they very rarely see the second month of life. 
It is stimated that in only about 1% of all cases the infection 
takes place intrauterinely. The mortality will always be great 
because the infant is not only suffering from intrauterine infec- 
tion but the child is actually born with an already existing tuber- 
culous disease in one organ or another. It is hardly conceivable 
how infants born with a primary tuberculous infection can carry 
that latent infection into adolescence without becoming early 
tuberculously diseased. 
Extra-Uterine Infection. Post-natal, Postgenital, avoidable, 
50 COURSE OF TUBERCULOUS DISEASE 
51 
or acquired. Most infection, about 99 percent of all takes place 
after birth, the time of infection depending upon how early or 
how late the infant comes in contact with the tuberculosis virus, 
that is, with an active tuberculous individual. As is stated above 
nearly all tuberculous infection is conveyed from man to man, 
generally from a tuberculous adult to infants or small children 
and the earlier in life of the child this infection has taken place 
the greater will be the early mortality. It is estimated that the 
number of infants infected in the very early days of their exist- 
ence is very small, that only about 2 percent of all children born 
are tuberculously infected in the first few months after birth, but 
that the mortality of all so infected is usually very great; that 
all infected in the first few months succumb to a generalized tu- 
berculosis and do not see the beginning of the second year; that, 
however, the mortality decreases as the number of days between 
birth and the first infection increases, that is in the first months 
of infant life and the question of infection also becomes a ques- 
tion of quantity, whether few or many organisms are present, 
and whether they are virulent of avirulent. If this first or pri- 
mary infection is massive, that is if many virulent tubercle ba- 
cilli enter the infant organism at a given time, or if the infec- 
tion with virulent tubercle bacilli is oft repeated for only a short 
period, then no organ or tissue is spared from the invaders and 
the child succumbs to a generalized tuberculosis and rarely sees 
the beginning of the second year. The mortality at this period 
is always great, estimated to be anywhere from 95 to 100 percent. 
It should be remembered that between a massive infection 
when great numbers of tubercle bacilli gain entrance into the in- 
fant body and definite and strong symptoms follow, and an in- 
fection consequent upon the entrance of only a few bacilli with 
none or perhaps the most mild symptoms all grades of intoxica- 
tion and disease may be noticeable. All infants only mildly in- 
fected in the first year of life as well as those who are infected 
after the first, that is during the second and third, either mass- 
ively or mildly, constitute the great army which in the subse- 
quent years are the victims of tuberculosis in one form or an- 
other. In early infancy, and this applies to both those who are 
infected before birth or intra-uterine, as well as those in whom 
a massive infection came about soon after birth or extra-uterine, 
there is a strong tendency to a generalized disease and speedy 
death; however, this tendency seems to lessen with the age of the 52 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
child and up to adolescence when it has assumed a more or less 
benign aspect, during all these years displaying a special predi- 
lection for certain organs and tissues in each decade or semi- 
decade. In the earlier years, that is from the second and up to 
the 14th the disease manifests itself chiefly in the organs and 
tissues supplied by the greater circulation, the pulmonary circu- 
lation up to this time has been comparatively free from active di- 
sease. 
Primary Tuberculous Disease. After pulmonary infection has 
taken place and the regional lymph nodes have become second- 
arily infected, a period of more or less quiescence generally su- 
pervenes, and later from various causes these glands about the 
hilum and near the bronchial bifurcation, the epibronchial, peri- 
bronchial, tracheo-bronchial, broncho-pulmonary and the tra- 
cheal as well as the mediastinal are now most frequently not only 
the seat of tuberculous infection but of tuberculous disease as 
well. In the child, this is most noticeable in the years up to and 
including the fifth year when again a decided change is ob- 
servable. 
Secondary Tuberculous Disease. Metastatic, lymphogenous 
and hematogenous. Two types may be recognized. (1) A ma- 
lignant, and (2) A more or less slow or more benign form. The 
malignant is usually hematogenous, the bacilli gaining access di- 
rectly into the blood stream from a caseous or degenerating 
gland producing miliary or basal meningeal tuberculosis. The 
second form most likely lymphogenous—many bacilli after enter- 
ing the lymph channels are held back by the nearest glands and 
only few gain access into the circulation. This, however, is then 
followed by bone, joint, spine and slow meningeal disease. 
At this point we observe a strong tendency to a less frequent 
involvement of the lymph glands but a distinct metastatic tuber- 
culosis of other tissues and organs of the greater circulation; and 
tuberculosis of bones and joints, the meninges, the skin, spine, 
etc., are now most prevalent, up to this time more or less spar- 
ing the lungs. Now the frequency of bone and joint disease pre- 
dominates and in the earlier years and up to the 6th and perhaps 
the 7th year, tuberculosis of the small bones and joints is most 
frequent, and disease of the wrist and ankle bones, the carpal 
and tarsal, the metacarpal, metatarsal and phalangeal are now 
mostly encountered and as the child advances in years and to- 
wards puberty, we find that the larger joints, the knee, the elbow, COURSE OF TUBERCULOUS DISEASE 
53 
the shoulder, the hip, etc., all of which until now have been 
spared from early involvement are most frequently the seat of 
active tuberculous disease. It is noteworthy at this point to ob- 
serve that the mortality from all forms of tuberculous disease 
has lessened, the disease having now assumed a more or less be- 
nign form and that at the age of puberty and a little beyond, up to 
the age of 14, only about 2 percent perish from tuberculosis. As 
the frequency of infection rises, the mortality decreases and the 
ratio between the tuberculosis mortality and those who are tu- 
berculously infected is in inverse proportion. In early infancy, 
the infection, as stated above, is usually estimated to be between 
1 and 2 percent with a mortality of nearly 100, whilst at the age 
of 14 with a mortality estimated at only 2 percent we find that 
the number of those who are tuberculously infected reach more 
than 90 percent. 
Tertiary Tuberculous Disease. With the beginning of life, 
that is in the first decade, tuberculosis assumes a very acute 
form, more subacute towards the middle of the decade and to- 
wards the close and beginning of the second a chronic or benign 
form and in the middle of this decade after the organs and tis- 
sues of the greater circulation have stood the brunt of the di- 
sease, have now acquired so to speak, a certain degree of immun- 
ity, we again notice a decided change in this constantly changing 
tuberculous picture, for we will observe that from now on the 
organs of the lesser circulation, the lungs, which until now have 
been comparatively spared, are most vulnerable and particularly 
these pulmonary attacks in this the middle of the second decade 
are like at the beginning of the primary infection most virulent, 
acute and fatal, becoming subacute towards the close of the de- 
cade and during the greater portion of the third, after which, 
that is during the fourth and fifth, the disease again assumes a 
chronic and benign form and as compared with the pulmonary 
tissue now involved during this time, all other forms of tubercu- 
losis are very infrequent.1 
In old age we again note a variation in the changing picture. 
We have found that in infancy the great tendency is to a very 
acute generalized form of the disease; a little later in child life, 
it becomes more subacute and towards and during adolescence, 
a more chronic, generalized form. With advancing age, there 
‘It is true that we occasionally see gland, bone and joint tuberculosis in an adult and 
we also see at times pulmonary tuberculosis in child life but not as a rule—these are 
exceptions. 54 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
is again a great tendency to the generalized form of the disease, 
now very chronic and much protracted, localized chiefly in the 
lungs but not in the apices as we find it in earlier life, but any- 
where throughout the lungs, chiefly at the bases. In the aged, 
a lessening of the body resistance becomes evident and the 
mode of living, sedentary habits, indoor life, much confinement 
in the homes or in rooms are all factors which tend to reacti- 
vate a long and insidious latent process. 
It is most interesting to note the tuberculosis mortality during 
the different periods of active disease. In early infant life the 
mortality of those who are infected is always high and all who 
are heavily infected in the first months succumb to the disease 
within the first year, the estimated percentage of death being 
anywhere from 95 to 100. At the age of 3, about 50 percent of 
all tuberculously infected children succumb to the disease in one 
form or another, 20 percent from the 5th to about the 7th and 
only about 2 percent at the age of 14. Up to this period pulmon- 
ary tuberculosis has been very infrequent, the other tissues and 
organs of the body being most frequently the seat of tuberculous 
disease, but we will observe that they seem to have now acquired 
a degree of immunity and a less frequent involvement, but a very 
perceptible increase of pulmonary tuberculosis is now apparent 
and with this increase of disease, an increase of the tuberculosis 
mortality is evident, which mortality again lessens with each 
passing decade. 
Every child which is tuberculously infected has not been prop- 
erly protected, hence it becomes necessary to guard against and 
avoid infection in early life in the young; in youth we must 
guard against a latent tuberculosis becoming active. The v. Pir- 
quet is positive in only 5 percent of all children at the end of the 
first year of life, increasing gradually so that at the end of the 5th 
year about 20 percent react and more than 90 percent at the age 
of 14. That obtains in all children infected after birth, post-natal, 
in the prenatal or congenitally tuberculous we do not know at 
which time the skin reaction is positive; it is usually negative. 
In these there is no period of latency and the absence of all al- 
lergic possibilities is due to the inability of the body cells to pro- 
duce defense agencies or antibodies. 
Resume. In early infant life a massive infection from contact 
with an active tuberculous individual is usually followed by great 
mortality; in later life however, the infection is generally more COURSE OF TUBERCULOUS DISEASE 
55 
mild, is not so massive, although it may be oft repeated, and is 
then followed by a slow chronic process. In children a tendency 
to chronic tuberculosis with connective tissue proliferation about 
the tuberculous process is extremely rare; here there is a greater 
tendency to a generalized disorder with cavity formation, which 
in very early life is quite frequent—vomicae having been found in 
the lungs of infants at autopsy. In children who have passed the 
eighth year of life the disease assumes a more chronic form like 
pulmonary tuberculosis in adult life, showing a great tendency 
in healing. Here, we usually recognize two forms of the disease 
— (1) a rapidly fatal form, a miliary tuberculosis, with symptoms 
of meningitis, pleuritis or peritonitis usually with a sub-acute pul- 
monary tuberculosis persuing a rapid course; (2) a more or less 
curable form. This may manifest itself in (a) a localized form 
with tuberculosis of the serous cavities and of the vicera; (b) 
with slight lesions in the lungs, in joints or in the pericardium; 
(c) forms without definite localization, such as may simulate ty- 
phoid, usually accompanied by peribronchial gland tuberculosis. CHAPTER 8 
HISTOLOGY AND PATHOLOGY 
Structure and Formation of the Tubercle 
Tubercule formation is evidence of a mechanical irritation, the 
presence of a foreign body in the tissue. The presence of the 
tubercle bacillus or particles of some inert foreign matter in the 
tissue may lead to the formation of tubercles but the chief cause 
of tubercle formation is the presence of the Koch’s bacillus, its 
growth and multiplication, the chemical action of its metabolic 
changes, its toxin action as a foreign protein, etc. Tubercle for- 
mation is really nature’s first effort at healing, showing a begin- 
ning immunization and a beginning chronicity of the tuberculous 
process. In all those instances in which resistance is low, viru- 
lence high and the soil propitious, no tubercle formation takes 
place. Tubercle formation is only present if the disorder shows 
a healing tendency (89). It is nature’s efforts at arresting the 
tuberculous process, is evidence of body resistance. In acute 
rapidly progressing and fatal cases of pulmonary tuberculosis, 
tubercle formation generally does not take place, is entirely 
wanting. 
Genesis of the Tubercle, v. Baumgarten’s classic experiments 
on animals, by injecting live, virulent tubercle bacilli into the 
anterior chamber of the eyes of rabbits, has clearly demonstrated 
the growth and development of the tubercle from its inception 
to its completion as a fully developed body. His technic was as 
follows: 
A number of rabbits treated in a similar manner were killed 
at various intervals and the enucleated eyes carefully studied; 
resulting in the following observations. After the first few days 
following the implantation of bacilli into the anterior chamber of 
the eye, nothing is noticeable except a slight increase in the num- 
ber, gradually invading the contiguous structure of the iris and 
cornea. About the 6th day, distinct histologic changes at the 
point of entry are noticeable and in the regions where the bacilli 
are most numerous cell proliferation and newly developed epi- 
thelioid cells from connective tissue cells are observed. As the 
56 HISTOLOGY AND PATHOLOGY 
57 
tubercle bacilli increase, the epithelioid cells increase correspond- 
ingly, and about the 7th day indirect cell division or karyokine- 
sis is noticeable in the fixed cells. This infiltration increases in 
extent and now endothelial, and connective tissue cells take part 
in the process, at this stage many bacilli within and without the 
epithelioid cells in the tubercle may be seen and now leucocytes 
also seems to take part in this process, and many bacilli are found 
within their bodies. In this way the formation of the tubercles 
spread and by coalescence may form a conglomerate mass. Pre- 
Fig. 7. Tuberculosis Giant Cell. (From Koch’s original paper 1882). Note the 
tubercle bacilli at one pole and the body cells (nuclei) at the other. (H. J. Corper 
Lectures on Tuberculosis. Bulletin Chicago Tuberculosis Institute, 1916.) 
cisely the same process of tubercle formation takes place when 
bacilli enter any part of the human body. 
The action of the tubercle bacillus on the surrounding tissue 
is found to be four-fold, namely, tissue proliferation with tubercle 
formation followed by exudative inflammation and necrosis or 
fibrosis. The tubercle as we see it consists of epithelioid, con- 
nective tissue and endothelial cells surrounding the bacilli. 
After a time cell division ceases and the bodies of isolated 58 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
epithelioid cells begin to enlarge and containing many nuclei 
(59) ; these are designated giant cells and within them few or 
many bacilli may be observed. If the process is chronic, as in 
scrofula or joint disease, only a few isolated bacilli are found, 
whereas if the process is acute, as in active pulmonary disease, 
the number of bacilli contained in a giant cell may be as many 
as 50 or more, and then again if the bacilli are few in number, 
many giant cells are usually present, but if the bacilli are many, 
only few giant cells may be observed. Another peculiarity of 
the giant cells toward the bacilli is the supposed antagonistic 
relationship existing between the nuclei of the cells and the con- 
tained bacilli. If the nuclei within the giant cell lie at the outer 
area, the bacilli will be found at the center, and if the nuclei 
are found heaped at one pole, the bacilli will be found at the 
opposite pole. In this now completed tubercle, between the 
giant and the epithelioid cells, many wandering cells, round cells 
and leucocytes with well staining nuclei are noticeable, the latter 
playing a most important part in the formation. 
Throughout all is a fine network or reticulum of fibrous bands 
consisting of threads, fibro-blasts, spindle cells and fibro-blastic 
tissue from connective tissue cells. The regional vessels now 
relax, allowing leucocytes to pass freely through their walls. 
No blood vessels are found in the tubercle, the nourishment being 
supplied from the lymph spaces. 
Encapsulation, Caseation or Softening. About the 10th or 11th 
day an inflammatory process is observed, and with the lessening 
of cell proliferation many leucocytes (lymphocytes) are seen 
passing through the capillary vessel walls into the deposited 
cells. Fibroblastic cells now predominate the whole structure. 
If many leucocytes now surround this formative process, the 
tubercle may remain of the small cell type and none or only an 
isolated giant cell be observed. The tubercle may then undergo 
further encapsulation and fibrosis or may degenerate or caseate. 
The tubercle is usually complete in about 14 days and the course 
that now follows depends upon many factors 4 retrogression, 
coagulation, necrosis or softening usually results. The bacilli 
iWith the earliest formation of the tubercle, throughout its whole existence there is a 
constant attempt at either a progression or retrogression of the process, at death or 
repair, and while the tubercle may undergo degenerative changes at its centre repair may 
take place at the periphery, hence the fate of the tubercle is entirely dependent upon the 
tissue reaction. If degenerative changes with necrosis are in the lead then the process 
will be progressive and with more or less rapidly invading and spreading into contiguous 
tissue, on the other hand if fibrosis, which is equivalent to repair, controls the situation 
then retrogression, arrest or checking of the process and healing results. HISTOLOGY AND PATHOLOGY 
59 
may die, the tubercle may become sclerotic or it may calcify, 
caseate or undergo cheesy degeneration, may soften and be ab- 
sorbed or may break down, slough be followed by pus forma- 
tion, or many tubercles may coalesce, forming a conglomerate 
mass. The tubercle in its entirety forms a small gray transparent 
nodule, in size that of a millet seed containing many or few 
bacilli and no blood vessels. If caseation takes place, the tubercle 
bacilli in the center die, the tissue undergoes retrogressive 
changes and fatty degeneration, the leucocytic protoplasm dis- 
appears, the nuclei degenerate, and with the entrance of pus 
germs and the presence of sterile pus, the process is completed. 
At this stage the nuclei have lost their staining quality and a 
more or less cellular debris is present. The caseation, softening 
and pus formation is not due to the ordinary specific pus cocci, 
staphylococci and streptococci but most probably to a proteolytic 
ferment inherent in the tubercle bacillus itself analagous to the 
softening of a pneumonic exudate by the digestive ferments of 
the dissociated leucocytes. 
The development of the tubercle may be divided into 5 phases: 
1. A sero-fibrinous exudate following the implantation of the 
bacilli, brought about by mechanical irritation. 
2. This mechanical irritation next brings about an aggrega- 
tion of many leucocytes (Polymorphonuclear) which, however, 
die in a few days, fading away without leaving a trace. 
3. Connective tissue cell reaction with formation of epithelioid 
cells, increase of nuclei and cell protoplasm with karyokinesis ; 
endothelial, and fixed connective tissue cells are all changed into 
epithelioid cells, a reticulum is noticeable and phagocytosis is 
demonstrable. 
4. Now mononuclear leucocytes at first only isolated appear 
in great number in the periphery of the tubercle. 
5. Degeneration of the tubercle and a second entrance of the 
Polymorphonuclear leucocytes. 
In both the second and fifth phases the polynuclears play a 
leading role due to cell irritation and toxic causes. The leuco- 
cytes present in the first phase are due mainly to irritation. 
Early, from his studies, Koch promulgated his views concern- 
ing the formation of the tubercle. He contended that the bacilli 
entering the body are taken up by the leucocytes, through the 
lymph and blood supply, and are deposited in the tissue. The 
leucocytes are first changed into epithelioid cells and later into 60 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
giant cells. The produced toxins change the surrounding cells 
into epithelioid cells, the tubercle ultimately undergoes necrotic 
changes or fibrosis and exudative processes from inflammatory 
surroundings join in the disorder. If the process assumes a cura- 
tive form encapsulation by means of fibroblastic tissue formation 
takes place, a fine network permeating the whole tubercle, the 
caseating mass being absorbed or undergoing calcification. 
In the tuberculous, at autopsy, histological changes are noticeable in all 
the various organs of the body and these are either typical tuberculous 
tissue or simply chronic inflammatory changes and not tuberculous lesions 
proper. 
The Usual Location of the Tubercle and Its Ultimate Fate. In 
most instances the beginning tuberculous process is in the ter- 
minal bronchioles, a bronchiolitis tuberculosa resulting. At the 
point where the cylindrical epithelium (cuboidal cells) of the 
bronchioles joins the (non-nucleated Polygonal cells) alveolar 
pavement epithelium, it is just beyond the ring of muscle fibres 
in the terminal bronchi described in Chapter 7; the alveolar 
septal walls and alveolar sacs are also with like frequency in- 
volved. The most favorable selection is along the right posterior 
bronchus, the Bronchus Apicalis Posterioris and including the 
interstitial connective tissue a peribronchiolitis is produced. If 
only a single nodule, it may be early encapsulated, then undergo 
calcarious degeneration and in time be expelled as a hard mass, 
(the so-called lung stones, pneumoliths) leaving a contracted 
scar; it may undergo cheesy degeneration, the bacilli may be 
scattered and many metastatic nodules appear, or again many 
nodules may conglomerate, degenerate, break down and lead to 
cavity formation. CHAPTER 9 
IMMUNITY 
General Consideration. The word immunity is derived from 
“Immunis” free from paying tribute (19). It simply expresses 
an idea, no well defined conception. Immunity the freedom from 
becoming sick upon the entrance of bacteria or their toxins into 
the human or animal body and the possibility of certain micro- 
organisms or their toxic products entering the body and making 
it sick or causing death is known as virulence. If, however, the 
human body resists the invasion of these various bacteria and 
thereby prevents the bringing about of disease, then we speak of 
the body’s defense forces or immunizing agencies and the forces 
necessary are known as the immunizing mechanism. On the 
other hand, if the body is passive, permits the invasion and does 
not resist implantation, then we speak of virulence of the in- 
vaders ; hence we notice that immunity and virulence are strictly 
antagonistic forces. 
In many instances immunity depends entirely upon the degree 
of virulence and the amount of disease producing germs entering 
the body; it also depends a great deal upon the individual organ- 
ism. For instance, a streptococcus strain may be highly virulent 
to a certain individual and cause death; the same strain in an- 
other individual may not even produce any symptoms of disease; 
it may be avirulent to one and highly virulent to another. If the 
body is capable of arousing the necessary defense powers when 
micro-organisms enter, the invaders become avirulent and will 
produce no disturbance; if, however, the body possesses no such 
defense powers, or perhaps the resistence is lowered by either an 
acquired or inherited disposition, then the entering bacteria will 
grow, multiply and eventually cause disease or even death. 
Again, the same individual at times may be fully capable of re- 
sisting an invasion whilst at other times he may possess no 
power whatsoever to prevent it. 
In practical medicine it has long been recognized that fatigue, 
injury, nervous shock, psychic influences, extremes of cold or 
heat, etc., play leading parts in body resistence. It will be noticed 
61 62 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
that the invading- micro-organisms and the resistance offered by 
the body cells is very similar to an invading army of an enemy 
and the resistance offered by the defenders. This simile may be 
observed in more than one way. 
It becomes apparent from this that many micro-organisms 
possess more or less, an infection possibility depending on either 
a heightened resistance or a lowered vitality, a susceptibility or 
a non-susceptibility of the body at the time of infection. How- 
ever, if the mechanism of immunity is functioning well, there 
will be no susceptibility; if not, the body is susceptible to infec- 
tion, and to disease and death as well. Usually with the entrance 
of the bacteria into the organism, immunizing activities 
brought about and directed against the invaders, and conversely, 
when micro-organisms remain for some time in the body, they 
become immunized against the body’s defense powers. Im- 
munity and virulence as well are but relative terms; there exists 
no absolute immunity; only a partial immunity can be achieved. 
Under certain conditions immunity always exists and under cer- 
tain other conditions it can always be lowered, depending upon 
whether or not at the time the immunity of a given individual is 
sufficient to be utilized for practical purposes. 
Immunity may be congenital or it may be acquired later in life. 
A congenital immunity is present in some individuals without 
having previously come in contact with the disease produc- 
ing germs. Such individuals when coming in contact with a 
pathogenic virus give no manifestation of either infection or 
disease. This is a fixed immunity and can not be transmitted to 
other or non-protected beings; not so the acquired immunity. 
This is added during life to the non-immune body as a new func- 
tion, is always specific, always for the same organism and no 
other, and may be either active or passive. 
The Acquired Tuberculous Immunity (123). It is now a wrell 
established fact that most civilized people during some time in 
their lives have become tuberculously infected and this leads us 
to recognize a second fact, namely, that in but a very small per- 
centage is this infection followed by disease. 
We are all familiar with the fact that the application of tuber- 
culin is, in most individuals, followed by a positive reaction; 
however, this is no evidence of positive disease, it only proves 
that the reacting person at some time in his life came in contact 
with the tuberculosis virus, but should we conclude from this IMMUNITY 
63 
that all who react to the tuberculin test, and show no signs of 
clinical manifestations are tuberculosis immune? 
Throughout our whole life, particularly in the large cities, we 
come constantly in touch with the tubercle bacillus, through our 
daily intercourse with one another, but these later infections are 
made perfectly negligible from the acquired immunity incident 
to a previous or earlier infection, our bodies showing an ever 
increasing defense, increasing more and more with every new 
infection, in this way increasing the immunity which with the 
defense products go hand in hand. It is not necessary that the 
established immunity destroy all the tubercle bacilli in the or- 
ganism ; it is only necessary to keep the infecting virus con- 
stantly in check. This so constantly renewed and reacquired 
immunity protects the body from infection from without and 
from within as well.1 
That recovery from a tuberculous infection offers a high degree of 
immunity was positively established by v. Behring in his epoch making 
experiments on cattle, in immunizing against bovine tuberculosis by 
intravenous injection with living human tubercle bacilli, and Koch’s early 
contention that a tuberculous infection in animals protects them from a 
subsequent reinfection has been repeatedly verified. 
In the human after the infection has passed off, the organism 
is again free to infection and although an immunity may con- 
tinue for some length of time to a high degree, it gradually 
lessens, and now a recurring or repeated infection again increases 
this immunity and so the power continues throughout the great 
part of our lives, with a constant increase and diminution of 
immunity. 
About three-fourths of all human beings have come and are 
constantly coming in contact with minute quantities of tubercle 
bacilli and in this way are continually maintaining their im- 
munity. If, however, this reinfection with the virus should be 
in too great an amount or if the virulence produced is very large, 
the body may not be capable of supplying the necessary defense 
products and so can not sustain its previously acquired im- 
munity, the infection then is soon followed by manifest tuber- 
culous disease. The human organism which has survived a 
tuberculous infection is in its behavior quite different from one 
which has never come in contact with the virus. Because of this 
the recovery from a tuberculous infection in the ordinary way will give 
relatively an immunity we have not succeeded as yet by artificial means therapeutically 
to bring about a specific immunity against infection. 64 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
so general infection in the human, most children born possess 
from birth a slight degree of tuberculous immunity and are from 
infancy already able to overcome a slight infection, not so the 
people and their children who have never come in contact with 
the virus. We frequently observe in primitive races that a 
primary infection even if this infection is very slight is often fol- 
lowed by most disasterous consequences, a rapid tuberculous 
process, and this is because they possess neither an inherited nor 
an acquired immunity. This shows that immunity is only ac- 
Fig. 8. The relative death rate in the U. S. among Indians, Colored and Whites 
(comparatively). (From the U. S. Public Health and Marine Hospital Service. Tuber- 
culosis exhibit.) (Chicago Tuberculosis Institute Film.) 
quired by years of contact with the virus. For instance, we ob- 
serve that the white race is much more resistant, is much more 
immunized to a tuberculous infection and disease than is the 
colored and the colored again more than the American Indian. 
This is most natural when we consider that the white race has 
come in contact with the tubercle bacillus for many thousands 
of years whilst the colored race began its immunization only 
since its association with the white many hundreds of years ago, 
and the Indian since the discovery of this country, some four 
hundred years.2 
2A frequently repeated but mild tuberculous infection constantly adds to the small 
capital of an inherited immunity which was given to the infant at birth. With each 
new mild infection, this capital of immunity increases so that in years after the infected 
individual can utilize the interest accrued on this capital in the form of resistance to 
protect bin* against a tuberculous disease. IMMUNITY 
65 
A tuberculous process which has been healed for some length 
of time (say for years) has left no protecting immunity and hence 
it leaves the individual liable to reinfection; it is only in the 
tuberculous organism that immunity is present. Only the tuber- 
culously infected organism is capable of immunizing against this 
disease, and not the non-infected. It is this constant reinfection 
from without which takes place in our daily life which gives us 
immunity. 
It is most probable that bacterial toxins, which are necessary 
to bring about immunity, are produced in the living body in re- 
sponse to the stimulus of the protective agencies secreted by the 
body cells. In both bacteria and body cells there exists a con- 
stant attempt at immunization, bacteria trying to make them- 
selves immune against the body cells and the body cells in turn 
endeavor to immunize against the bacteria. 
On a previous page mention has been made that Ghon in his 
184 autopsies found in by far the greater number (142) but a 
single primary focus from which he concludes that this first in- 
oculation stimulated the production of sufficient defense agencies 
to give immunity against a later or second infection. Not only 
in the experimental animal can immunity be instituted but in the 
human as well do we find an acquired, an autogenous immunity. 
This autoimmunization is brought about by the stimulating 
activities incident to the tuberculous infection, and this now 
gives to the body a relatively protecting immunity. 
The discovery of healed lesions or healing foci in about 90% 
of all autopsies and the fact that in only about 10% do we find 
tuberculous disease the cause of death shows that the greater 
majority of all human beings possess in some degree an acquired 
immunity against this disease. 
The various methods of tuberculous immunization. Many at- 
tempts at immunization in both man and animal by means of 
the human tubercle bacillus, either living or dead, by the bovine, 
the avian, the cold blooded animal bacillus, the various acid fast 
bacilli of this group as well as by the use of the artificially pro- 
duced toxins have been made. Many of this group have been 
used, tried and experimented with ever since the discovery of the 
tubercle bacillus, and from much of this experimental work we 
have learned that the highest degree of immunity for a time, 
not absolute, can best be secured by inoculating the organism 
with the living tubercle bacillus which possess a superiority over 66 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
the dead bacillus and all the recognized bacillary products for a 
protective inoculation. Usually only a minute quantity or a 
single bacillus is used, in the beginning, this dosage being gradu- 
ally increased until the experimental organism becomes tolerant 
to extremely large doses. It is supposed that the use of the 
various tuberculins for immunizing purposes are equally as effi- 
cient as the living bacteria, perhaps in a somewhat less degree 
they are at the same time less dangerous. By the use of these 
various agencies varying degrees of immunization can be 
achieved, the method of subcutaneous or intravenous injection 
being followed by the best results. By the administration of the 
bacilli by mouth, the feeding method, good results are also ob- 
tainable, and a noticeable resistance in animals to an artificial 
tuberculous infection may be brought about by feeding cattle on 
emulsion of living bovine tubercle bacilli, either virulent or modi- 
fied by heating to 70°. A single ingestion may be sufficient to 
produce an infection, and subsequent immunization, the animal 
being capable of resisting for many months a dose sufficient to 
infect a control animal; however, we must bear in mind that by 
the feeding method much larger doses must be used and that an 
initial dose of the tubercle bacillus by way of the digestive tract 
is about 6000 times that of the number inhaled. 
If to an experimental animal treated as above we give an in- 
travenous inoculation of a 5 milligram dose of virulent bovine 
bacilli and a similar dose be given to a control animal of the same 
age, the control will develop an exceedingly rapid tuberculosis 
which will prove fatal within 6 weeks, while the previously 
treated animal will remain perfectly healthy for about 8 months, 
and then lose its immunity, developing a sudden and rapidly 
fatal tuberculosis. 
Animals previously tested with tuberculin are very similar in 
their behavior to those inoculated with the living virus, and in- 
travenous injections of tuberculin will give to an animal an im- 
munity not possessed by controls. If 5 milligrams of virulent 
bovine bacilli are injected into an animal a few days after the 
tuberculin injection and the same amount be given to another 
animal as control, it will be found that the control will perish in 
about 6 weeks while the previously prepared animal will present 
a slowly progressing process. There obtains no doubt that both 
tuberculously infected and healthy animals, if previously treated IMMUNITY 
67 
with large doses of tuberculin, possess incomparably greater re- 
sistance than animals not so treated. 
A local suppurative tuberculous process occurring in a con- 
sumptive often improves the individual’s general health and 
greatly increases his resistance, raises his immunity, and con- 
versely, a person in whom pulmonary tuberculosis is running a 
rapid course rarely gives a history of a previous suppuration 
either of a gland, bone or any other form of local tuberculosis. 
This local disease has stimulated the defense powers to a relative 
immunization, and as long as this can be maintained, the in- 
dividual enjoys comparatively good health. Thus the history 
which we physicians so often hear in our daily routine work espe- 
cially from elderly people, that a long standing and discharging 
ulcer on the leg or any part of the body should not be healed 
because if cured it is often quickly followed by most disastrous 
consequences, (perhaps by active pulmonary tuberculosis) may 
not be without foundation. May we not here also consider the 
belief of the ancients in the insistence of a pre-existing catarrh 
constituting an open door to a tuberculous disease? A previously 
existing tuberculosis or a tuberculous lesion in process of evolu- 
tion gives a relative protection or immunity and prevents the 
evolution of a new or second inoculation.3 
Hypersensitiveness, Sensitization, Etc. 
If the healthy organism receives a single inoculation with sera 
or bacteria, the body becomes very much sensitized, even if the 
second injection of a similar substance has been given in very 
much smaller dosage. This phenomenon is known as “the re- 
action.” The cause of this hypersensitiveness is due to definite 
bodies in the blood serum, the result of the primary inoculation, 
which are known as lysins. If the invaders are in small number, 
they are destroyed by the lysins, and this destruction is followed 
by the reaction; if, however, the bacteria are in great numbers, 
then by means of the lysins, solutions of the invaders are brought 
about, and this may lead to most serious intoxication. 
In a sense hypersensitiveness and immunity are practically 
interdependent, there exists between them a causal relation. The 
body’s sensitiveness to the application of tuberculin is evidence 
of the body’s resistance; it shows that antibodies or protective 
3The extreme frequency of a positive tuberculin reaction, on the one hand, and the 
evidence of completely healed foci at autopsy on the other, goes to prove that already in 
the child tuberculosis is relatively a harmless disease and that tuberculosis is very 
frequently only a latent process never manifesting any symptoms. 68 
ACADEMIC QUESTIONS OF TUBERCULOSIS 
agencies are at work at the time. Sensitiveness to vaccines or 
to bacillary products is spoken of as anaphylaxis or as an anaphy- 
lactic reaction, or more correctly as allergy and the absence or 
want of this sensitiveness, which we may observe frequently in 
those who never come in contact with the virus, is known as 
anergy. (See Chapter XXXX.) 
The various tuberculins, and they are very numerous, are all 
being used to bring about active immunization in the infected and 
also the sera, Marmoreck’s, Maragliano’s, etc., with which only a 
passive immunization is aimed at. It is, however, very doubtful if 
in tuberculosis passive immunization is of any value. An activo- 
passive immunization is sought by the use of Carl Spengler’s I. K. 
or immune bodies (Immune Koerper) but it is very questionable if 
any degree of immunity can be established with any certainty in 
this way. PART TWO 
CLINICAL TUBERCULOSIS 
Having first considered the various academic questions con- 
cerning tuberculous disease we are then in a position to continue 
the subject from the clinical standpoint. Beginning, somewhat 
in detail, the study of the symptomatology, then the diagnosis, 
prognosis and treatment of pulmonary tuberculosis, as observed 
in the adult we shall continue to consider this disorder as it is 
observed in children. The consideration of Tuberculin becomes 
our next lesson. Here many of the intricate topics and questions 
as observed are really of an academic nature and for that reason 
may seem to belong more appropriately to that classification, to 
part one, however, Tuberculin, is so closely and intimately con- 
nected with the diagnosis and the treatment of tuberculosis in all 
of its various manifestations that it appeared to me better to 
consider it on the clinical side rather than on the academic. 
Some of the chapters on tuberculosis of other organs than those 
of the lungs or where pulmonary tuberculosis was complicated 
by tuberculous disease of other organs or tissues were compiled 
from lectures delivered and clinical instruction given to my 
classes, at different times during the school years by members of 
the teaching staff of Rush Medical College. CHAPTER 10 
PULMONARY TUBERCULOSIS. PHTHISIS PULMONUM. 
PHTHISIS PULMONALIS. PHTHISIS. CONSUMPTION, 
TUBERCULOSIS, ETC. SCHEMATIC CLASSIFICA- 
TION. 
Under the generally known generic term “Tuberculosis,” we 
usually designate a diseased condition of some organ or tissue of 
the body, brought about by the presence of the tubercle bacillus, 
and the name of the individual organ which is involved as the 
specific term: Phthisis (generic) Pulmonalis (specific). Every 
tissue and every organ of the human body may be the seat of the 
bacillary invasion, but in by far the greater number of instances 
we observe, especially in adult life, that these invaders have a 
decided predilection for the lungs. Besides the lungs, glands and 
perhaps the abdominal organs which are usually the seat of 
primary disease, all other organs become secondarily involved 
and only extremely seldom do we find these organs the seat of 
primary disease. 
The pulmonary form of this disease was early recognized by 
the human family and because of the slow, protracted and wast- 
ing course it so frequently persues, it was called consumption. 
Ever since the discovery of the tubercle bacillus as the causa- 
tive factor, this disease has been most intensely and thoroughly 
studied, and from the knowledge thus acquired rules have been 
arbitrarily formulated for our guidance which may enable us 
more readily to recognize the disorder. 
Pulmonary Tuberculosis is a progressive disease. In many in- 
stances the disease begins as a very slight infiltrative process ex- 
tending slowty, as there is no pain, there is usually absence of all 
subjective symptoms and in this way the disease has often spread 
and extended into neighboring tissue before the physician is con- 
sulted. In other instances, the disease runs a more rapid course, 
is more rapid in its process of invasion and produces more recog- 
nizable symptoms, both subjective and objective. Individuals 
affected with this form of the disease are more free in seeking 
medical advice. There is still another class, known as the miliary 
71 72 
CLINICAL TUBERCULOSIS 
in which the disease runs a more or less acute form and is gen- 
erally quickly fatal. 
The duration of pulmonary tuberculosis is quite variable. It 
may from the beginning manifest a very stormy scene, running 
a rapid course and exitus letalis in a few months, or it may be 
much protracted, running a slow course lasting for years. Many 
chronic cases are known to have lasted from 10 to 20 or more 
years; however, it can be stated that the average duration of pul- 
monary tuberculosis is about two years. 
Various attempts at classification of patients on examination 
have from time to time been made so as to recognize, from the 
amount of lung involvement present, to which class or group a 
certain individual belongs. Such an attempt at classification we 
already find in the pulmonary histories of the ancients, where 
mention is made of Phthisis Incipiens or beginning tuberculosis, 
Phthisis Confirmata or established phthisis, conforming to our 
now so much used term moderately advanced phthisis and 
Phthisis Desperata or grave phthisis, which we now recognize as 
the far advanced type. 
The committee on nomenclature appointed by the National 
Tuberculosis Association some years ago formulated a classifica- 
tion based on the Turban-Gerhardt Scale which is now generally 
accepted. This classification (the Turban-Gerhardt Schema) is 
as follows: 
National Tuberculosis Association Schema for the Classification 
of Patients on Examination 
The following definitions indicate the farthest extent of disease 
and the greatest severity of symptoms that a patient can pre- 
sent and still belong to the stage defined. All patients beyond 
the incipient stage (first stage) fall under the moderately ad- 
vanced stage (second stage) unless the physical signs and the 
symptoms exceed those of the moderately advanced stage, when 
they should be classified as far advanced (third stage). 
Incipient—First Stage 
Slight or no constitutional symptoms (including particularly 
gastric or intestinal disturbance, or rapid loss of weight). 
Slight or no elevation of temperature or acceleration of pulse 
at any time during the twenty-four hours. 
Expectoration usually small in amount or absent. Tubercle 
bacilli may be present or absent. PULMONARY TUBERCULOSIS 
73 
Slight infiltration limited to the apex of one or both lungs, or a 
small part of one lobe. 
No tuberculous complications. 
Moderately Advanced—Second Stage 
No marked impairment of function, either local or constitu- 
tional. 
Marked infiltration more extensive than under incipient, with 
little or no evidence of cavity formation. 
No serious tuberculous complications. 
Far Advanced—Third Stage 
Marked impairment of function, local and constitutional. 
Extensive localized infiltration or consolidation in one or more 
lobes. 
Or disseminated areas of cavity formation. 
Or serious tuberculous complications. 
Acute Miliary Tuberculosis—Generalized 
In this classification, each of the three stages is based on cer- 
tain specific pathological findings and clinical symptoms. Un- 
fortunately, however, lesions and symptoms are not interchange- 
able, but are immobilized in each of the three stages. This is 
confusing, for occasionally an advanced case may present only 
incipient symptoms, or vice versa. 
The Turban-Gerhardt Schema 
FOR THE CLASSIFICATION OF PATIENTS ON 
EXAMINATION 
I. Slight lesion extending at most to the volume of one lobe 
or two half lobes. 
II. Slight lesion extending further than I, but at most to the 
volume of two lobes; or severe lesion extending at most to the 
volume of one lobe. 
III. All lesions which in extent of the parts affected ex- 
ceed II. 74 
CLINICAL TUBERCULOSIS 
By “slight lesion” we understand disseminated centres of dis- 
ease which manifest themselves physically by slight dulness, 
by harsh, feeble, or broncho-vesicular breathing, and by rales. 
By “severe lesion” we mean cases of consolidation and excava- 
tion such as betray themselves by marked dulness, by tympanitic 
sounds, by very feeble broncho-vesicular, bronchial, or amphoric 
breathing, by rales of various kinds. 
Purely pleuritic dulness, unless marked, is to be left out of 
account; if it is serous, the pleurisy must be specially mentioned 
under the head of “tuberculous complications.” 
The volume of a single lobe is always regarded as equivalent 
to the volume of two half lobes, etc. 
“At the meeting of the Committee in New York City, on December 12th, 
1915, a rearrangement of the classification adopted by the National Tuber- 
culosis Association was presented to the members for consideration. 
Owing, however, to the limited time at their disposal, a thorough dis- 
cussion on the subject was not possible, and the President, therefore, 
appointed a Committee of three members with instructions to submit a 
report on the proposed rearrangement, at this meeting. The Committee 
realizes that frequent changing of the classification is inadvisable, and 
appreciates the necessity of maintaining a standard schema. It is also 
aware of the confusion that may arise should the text of the present 
classification be materially modified, and realizes that a radical change 
would seriously affect the past statistics of the various sanatoria. The 
Committee has, therefore, confined its proposals to a simple rearrangement, 
which will increase the flexibility of the classification, without in any way 
altering its text. The members of the Committee feel that, owing to the 
wide variation in symptomatology, which is frequently manifested by 
patients in the same stage of the disease, a rearrangement of the classifica- 
tion is advisable, and it is not possible to immobilize lesions and symptoms 
in the same stage in any schema, without decreasing its range of applica- 
tion. The present classification describes the lesions and symptoms 
presented by the general run of cases admirably, but as it confines both 
the lesions and symptoms to separate stages, it fails to classify satisfac- 
torily many cases of pulmonary tuberculosis. The proposed rearrange- 
ment divides the lesions and symptoms of the schema into separate groups 
and lists them under different headings. It offers nine combinations and 
makes possible the use of any of the three groups of symptoms with the 
lesion of any stage. It covers the borderline cases so frequently found 
in the moderately advanced class and likewise provides for the classifica- 
tion of all cases within the scope of the present schema. 
A supplemental report PULMONARY TUBERCULOSIS 
75 
The present rearrangement, which contains the same terms used in the 
former schema, with the exception of those enclosed 'in parentheses, 
follows: 
LESION 
SYMPTOMS 
A. Incipient. Slight infiltra- 
tion limited to the apex of one or 
both lungs, or a small part of one 
lobe. No tuberculous complica- 
tions. 
A. (Slight or none.) Slight or 
no constitutional symptoms in- 
cluding particularly gastric or 
intestinal disturbance, or rapid 
loss of weight; slight or no ele- 
vation of temperature or accelera- 
tion of pulse at any time during 
the twenty-four hours. 
Expectoration usually small in 
amount, or absent. Tubercle 
bacilli may be present or absent. 
B. Moderately Advanced. 
Marked infiltration more exten- 
sive than under incipient, with 
little or no evidence of cavity for- 
mation. No serious tuberculous 
complications. 
B. (Moderate.) No marked 
impairment of function, either 
local or constitutional. 
C. Far Advanced. Extensive 
localized infiltration or consolida- 
tion in one or more lobes. Or dis- 
seminated areas of cavity forma- 
tion. Or serious tuberculous com- 
plications. 
C. (Severe.) Marked impair- 
ment of function, local and con- 
stitutional. 
D. Acute (Generalized) Mili- 
ary Tuberculosis. 
Incipient A Moderately Advanced A Far Advanced A 
Incipient B Moderately Advanced B Far Advanced B 
Incipient C Moderately Advanced C Far Advanced C 
Incipient A, depicts an Incipient lesion with symptoms as found in the 
present Incipient Stage; Incipient B, an Incipient lesion with symptoms of 
the present Moderately Advanced Stage; Incipient C, an Incipient lesion 
with symptoms of the present Far Advanced Stage; Moderately Advanced 
A, a Moderately Advanced lesion with symptoms of the present Incipient 
Stage; Moderately Advanced B, a Moderately Advanced lesion with 
symptoms of the present Moderately Advanced stage, etc. 
It is recognized that an Incipient C case is a rarity, but, nevertheless, 
the condition does occur and should be covered by the classification. In- 
cipient B cases occur more frequently. Moderately Advanced A cases 
are common, and those in the Moderately Advanced C class are not fre- 
quently encountered. Patients of the Far advanced B and Far Advanced 
This schema offers the following combinations: 76 
CLINICAL TUBERCULOSIS 
A classes are abundant in hospitals for the treatment of advanced cases. 
The rearrangement gives an accurate idea, at a glance, of the amount of 
lung involvement and the symptomatic picture. Much has been said in 
the literature of late in regard to the occurrence of localized pulmonary 
miliary involvement, and it might be advisable to classify “Acute Mili- 
ary Tuberculosis” as “Acute Generalized Miliary Tuberculosis”. 
A classification which I have taught for years is based on this 
National one, but it is slightly modified for somewhat easier 
comprehension by students. It is as follows: A tuberculous 
involvement, if situated in both upper apices above the clavicles 
or posterior above the spine of the scapulae, may be spoken of 
as a first stage case; if the involvement is on one side only and 
it has not extended below the second rib, then it is also said to 
be a first stage case. Posteriorly, the involvement in such a case 
would extend slightly below the spine of the scapula, most prob- 
ably as far as the second dorsal spine. Now, as the disease 
progresses with more or less rapidity into contiguous tissue and 
at the same time downward, we usually find that where one 
apex has been primarily involved, for example, say the right, 
the apex on the opposite side, the upper, soon becomes the seat 
of secondary disease, and simultaneously with this the apex of 
the lower lobe on the side originally involved (the right). In 
exceptional instances this lower apex is not the seat of secondary 
disease, but by crossed infection both the upper and lower lobe 
of the opposite side become secondarily involved. This involve- 
ment of the lungs, that is the apex of one side primarily and the 
apex of the lower lobe of the same or the opposite side and the 
upper apex on the opposite side, if found in an individual, can 
be said to be a second stage case, and all involvement beyond 
this, that is, involvement of all the apices of the lungs as well as 
a greater portion of the body, if present, can be diagnosed as 
a third stage case. Tuberculosis known as the Generalized 
Miliary Form is considered separately on page 96. 
A classification of clinical symptoms and physical signs in 
Tuberculosis as outlined by F. M. Pottenger may be of interest 
to students and is given herewith. It offers no special advan- 
tage over the grouping into the prodromal or preactive and the 
subjective and objective or active symptoms as first given by 
me and clearly outlined in the text. (See Chapter 11.) The 
classification which he offers is as follows: 
(1) Those due to toxaemia, which fully correspond to the 
prodromal signs due to intoxication as mentioned in my classifi- PULMONARY TUBERCULOSIS 
77 
cation: (2) Those due to reflex action and (3) Those due to 
the tuberculous disease itself. The latter two correspond to 
the signs and symptoms of active disease in tuberculosis. 
Group 1. Toxaemia. Malaise, lack of endurance, loss of 
strength, appetite and weight, nervous and digestive disturb- 
ances, anemia, rapid pulse, temperature and night sweats. 
Group 2. Symptoms of Reflex Signs. Hoarseness, cough, 
irritation of the larynx, digestive, circulatory and vaso-motor 
disturbances, chest and muscle pain, loss in weight, anemia. 
Group 3. Peculiar to the disease. Frequent and protracted 
colds, hemorrhages, expectorations, pleurisies, pulse and tem- 
perature, etc. 
The National Tuberculosis Association gives the following 
definition of incipient or beginning tuberculosis: 
Slight or no constitutional symptoms (including particularly 
gastro-intestinal disturbances, or rapid loss of weight). 
Slight or no elevation of temperature or acceleration of the 
pulse at any time during the 24 hours. 
Expectoration is usually small in amount or is absent. Tu- 
bercle bacilli may or may not be present. 
Slight infiltration limited to the apex of one or both lungs or 
a small part of one lobe. 
No tuberculosis complications. 
This definition indicates the farthest extent of lesion or dis- 
ease possible to be classified as incipient tuberculosis, and cor- 
responds closely with the Turban-Gerhardt scale—(Turban 1) 
“a slight lesion extending at most to the volume of one lobe or 
two half lobes.” 
Is it not evident after scanning the above classification that 
so-called incipient pulmonary tuberculosis is now no longer a 
beginning disease, that with such findings the stage of incipi- 
ency how long since passed, and is now a fully established dis- 
order, particularly when we see it plainly stated that bacilli 
may or may not be present? The word “incipient” denotes the 
beginning of something. Accepting this definition, the term 
incipient tuberculosis as applied above should be either elimi- 
nated or used in a more restricted sense, because the disease 
is now no longer in the beginning stage. If the conditions of 78 
CLINICAL TUBERCULOSIS 
incipiency, as above outlined, have existed for months or per- 
haps years, all depending upon the extent of involvement and 
the rapidity of the pathological process, is it then logical or 
reasonable to call the stage incipient when on repeated examina- 
tions we find the same physical signs? In the history of no 
other disease do we continually speak of a beginning disorder 
when we have before us all the evidence of a long existing 
malady. 
Primary or established pulmonary disease (144) should be 
designated by such descriptive terms as “early tuberculosis/’ as 
“manifest tuberculosis” or as “first stage disorder,” and the ex- 
pression “incipient tuberculosis” used to denote a definite be- 
ginning involvement only. In speaking of early established 
pulmonary disease such descriptive terms as mentioned, no mat- 
ter how long the disease has existed or how much primary in- 
volvement may be present, are more correct, appropriate and 
less misleading than the term “incipient” now in use. 
Pulmonary tuberculosis generally after being manifested for 
some time gives evidence of body disturbances, and such dis- 
turbances are accompanied by symptoms which are either sub- 
jective or objective, that is, such as are observed by the tuber- 
culous person and such as are noticed by the examining physi- 
cian, however, we shall first consider such signs as are fre- 
quently present, but are usually not observed (for a long time), 
that is, before the disease becomes evident, and which are des- 
ignated as Prodromal “Signs and Symptoms”. CHAPTER 11 
THE SYMPTOMATOLOGY OF TUBERCULOUS 
DISEASE 
The symptoms of activity in pulmonary tuberculosis are of 
the greatest importance, even more so than are the physical 
signs. Clinical symptoms if present in a given case leave no 
doubt as to a diagnosis, whereas physical signs alone may still 
give doubtful findings. 
Pulmonary tuberculosis, as stated, is a quantity infection, 
hence the number of bacilli that have been deposited in the lung 
tissue within a given time is of primary importance. If only 
a few bacilli or only a single tubercle undergoing degeneration 
is present and the extension of the process is slow, then the 
recognizable symptoms of tuberculosis may not manifest them- 
selves in months or even years, whereas if the infection is 
massive, that is, if many bacilli enter the pulmonary tissue at 
once, producing many individual colonies and many separate 
tubercles, and because of more separate colonies produce more 
toxicity, and if these tubercles now break down rapidly, causing 
much destruction of tissue, then the accompanying symptoms 
are pronounced, and as is the case in miliary tuberculosis, be- 
come hematogenous, overwhelm the system and cause a speedy 
death. In no other disease are the symptoms so protean. They 
may be mild and insignificant, not noticeable by the patient nor 
suspected by the physician, drawn out over long periods of 
time, over months and even years, with only a slight indisposi- 
tion now and then, whilst on the other hand the symptoms may 
be so pronounced and overwhelming as to baffle botlfcthe patient 
and the physician. When the disease has been once definitely 
established, the symptoms are observed as subjective and ob- 
jective. Subjective such as are noticed by the infected indi- 
vidual, and objective, those recognized by the examining physi- 
cians. Long before the disease is clinically established in the 
lungs toxic symptoms may be observed, but only too often they 
are supposed not to relate to pulmonary disease. These symp- 
toms are known as the prodromal or premonitory. Symptoms 
may be divided into two groups: those of latency and those of 
activity. 
79 80 
CLINICAL TUBERCULOSIS 
1. The symptoms of latency; the symptoms of preactivity, the 
prodromal symptoms; symptoms of toxicity, the symptoms of 
localization, the warning symptoms; the symptoms of the first 
stage or the stage of latency; the stage of intoxication; the early 
signs and symptoms of tuberculosis. 
2. The symptoms of activity; subjective and objective. The 
symptoms of bacillary growth and development; the symptoms 
of dissemination and spreading of the tuberculous process; the 
symptoms of the stage of active pulmonary disease; the second 
stage, the stage of activity, of manifest disease, including the 
signs and symptoms of early tuberculosis. 
A. Prodromal Symptoms—Symptoms of Latency 
In the tuberculous individual that is early in the disturbance 
when the disease is still localized, perhaps confined to a single 
or at least to only a few tubercles, only few symptoms may be 
noticeable. The causes of these latent symptoms are due mainly 
to the very slight absorption of the elaborated toxins, the prod- 
ucts of bacillary metabolism, and to the presence of foreign 
particles in the pulmonary tissue, giving evidence of irritation 
and inflammation, producing the variable picture of auto-infec- 
tion. These symptoms are variously designated as latent, oc- 
cult, insidious, hidden, larval, obscure, subclinical, pretubercu- 
lous, etc. The prodromal symptoms in tuberculosis are as posi- 
tive and distinct as are the prodromal ones in the acute diseases, 
and they are always present. They dififer only in being pro- 
tracted or long drawn out, covering long periods of time, in 
many instances months and even years. 
The symptoms of intoxication are: 1. Malaise,1 a tired feeling 
11s not the very tired feeling so often observed in beginning tuberculous disease in 
reality a sign of “conservatism” to compel the patient to lie or sit down and rest? We 
know that many cases of rapidly progressing active disease have almost never shown 
prodromal symptoms, the disease having been ushered in fully developed with all the 
signs of protracted collapse which we so frequently find in terminal cases. From the 
very beginning of the tuberculous infection and showing a tendency to become active, 
the organism assumes or nature asserts through the body a conservative attitude, and at 
all times nature is trying to check the invasion. It sends out an alarm that the hidden 
foe is coming forth and that the body must give battle. The very early, the prodromal 
symptoms, are more or less signs of warning and invitation for preparedness. Early signs 
are always present if the body shows the least resistance. These signs are only the 
noticeable evidence that the body is aware of the presence of the foe and is preparing to 
give battle. In most cases, although the conflict during the course of the disease is 
noticeable even if the disease is well established, still nature’s efforts at conservation and 
resistance are always manifested. That these early or prodromal symptoms are really 
nature’s alarm signs is evident from the observations that in rapidly active cases no such 
symptoms are manifest, nor are tubercles found in the diseased tissues, which again is 
evidence that the body offered no resistance at the proper time and that now the organism 
is overwhelmed with toxins. Immobilization and retraction are both signs of conserva- 
tion and resistance, nature’s effort to put the parts at rest while the body gains sufficient 
power to cope with the invaders, for if there is no rest of the invaded organs or at least 
that part of the organ which is actively concerned in the inflammatory process, then the 
disorder extends rapidly in all directions, leading to a quickly fatal course. SYMPTOMATOLOGY OF TUBERCULOSIS 
81 
while at work, at play, taking a walk or on the least exertion; 
2. Sleeplessness, distressing and painful dreams or disturbed 
sleep, particularly noticeable in young individuals at the school 
age, and are then attributable to overstudy; 3. nervous disturb- 
ances of various kinds, particularly more or less painful and pro- 
tracted headaches lasting on and off for months or even years. 
Many cases, referred to as anemia, neurasthenia, hysteria, love- 
sickness, etc., are included in this category. 4. Cardiac disturb- 
ances, most noticeable in dizzy spells, shortness of breath on the 
least exertion, or on going up a short flight of stairs, and are 
usually referred to as heart disease, heart weakness or cardiac 
palpitation. 5. Gastro-intestinal disturbances, dyspepsia, nausea, 
vomiting, gaseous eructations, loss of appetite, hypo-acidity, all 
without any assignable cause, belong in this group. 6. Vaso- 
motor disturbances, such as cold and clammy hands, persistent 
sweating of the hands or feet, free axillary perspiration, alternate 
paling and blushing of the face; if extending over long periods, 
these symptoms are in many instances directly attributable to 
intoxication. 7. Menstrual disturbances, dysmenorrhoea, menor- 
rhagia, and particularly amenorrhoea have long been recognized 
by both the profession and the laity as probable forerunners of 
tuberculosis. 8. Rheumatism is often a symptom complex of a 
tuberculous intoxication. There are shoulder pains and usually 
one or more joints are swollen, reddened, painful and immobile 
with accompanying signs of anemia, emaciation, malaise, sweat- 
ing. 9. Thyroid disturbances. The thyroid may be enlarged or 
may even simulate Grave’s disease with slight tachycardia, palpi- 
tation, nervousness, sleeplessness, emaciation, etc. 10. Urinary 
symptoms. (73) An orthostatic albuminuria, but a complete ab- 
sence of all cellular elements, the toxines producing a kidney 
permeability, this is known as a pretuberculous albuminuria. 
That these are prodromal symptoms and are of tuberculo- 
toxic origin can be demonstrated in various ways. 1. By the 
tuberculin reaction test. Individuals giving evidence of these 
symptoms usually react quickly and vigorously to an intradermal 
tuberculin test. 2. By relieving the symptoms. If to individuals 
manifesting these symptoms small or minute doses of tuberculin 
be administered subcutaneously over long periods of time, amel- 
ioration of all symptoms results. 3. By simulating these symp- 
toms. If to individuals free from symptoms small or minute 
doses of artificial tuberculin be given hypodermically, all the 82 
CLINICAL TUBERCULOSIS 
symptoms of a natural intoxication can be produced. This latter 
has repeatedly been demonstrated on children in whom a tuber- 
culin test has been applied, for diagnostic purposes, when all the 
symptoms of a typical tuberculous rheumatism may manifest 
themselves.2 
B. Subjective and Objective Symptoms. Symptoms of Activity. 
These, in this the second stage or the stage of activity, are be- 
coming more and more distinct and definite, the signs of early 
intoxication appearing now in the background and those of active 
disease manifesting themselves. Owing to the great chronicity 
of tuberculosis, the symptoms both subjective and objective con- 
tinually change with the changed condition in the lungs, and the 
processes of latency, of activity, of quiescence, of reactivity, or 
of arrest may vary greatly, presenting a constantly changing 
clinical picture. 
The usually pronounced symptoms of activity in the order of 
their importance and frequency, are as follows: 
1. Cough. This may at first be slight or entirely absent, be- 
coming more intense and distressing as the disease advances. 
The cough may at first be dry, or non-productive, assuming later 
a distinct moist character, or it may be distinctly brassy, even 
laryngeal, particularly if the disease has assumed a sudden exa- 
cerbation or rapidity. The cough may be painful and particularly 
productive during the night, with moderate expectoration during 
the day; this order may in isolated cases be reversed. The cough 
may be increased by lying on the unaffected side, or again the 
cough may be increased on taking food, especially after break- 
fast, which is often followed by vomiting. If the parenchyma of 
the lung only is involved, cough may be entirely absent, but is 
usually always present if the disease is peribronchial. 
2. Expectoration. This may be very scanty or profuse; it may 
be scanty or wholly absent at the beginning or consist of a 
stringy mucous, later muco-purulent, more or less mixed with 
particles of dust, coal, fibres and fabrics, etc., very rarely bloody. 
If a long, protracted and painful cough is present, blood streaked 
sputa may be observed; later, as the expectoration increases, it 
assumes a more or less purulent or yellowish-gray appearance. 
In the very chronic forms of the disease, there may be very little 
*These prodromal symptoms or disturbances may manifest themselves in the tubercu- 
lously infected organism at a period when very little, or perhaps no, anatomical changes 
have yet taken place; by physical methods we are not yet in a position to demonstrate 
organic lesions and the clinical picture may still be quite negative. SYMPTOMATOLOGY OF TUBERCULOSIS 
83 
expectoration, but in the rapidly progressive form, it is usually 
very profuse. It may also be copious in the chronic form if ac- 
companied by much bronchiectasis, in which case with a sudden 
change of position the patient expectorates a large quantity of 
the sputum. 
3. Pain. A variable quantity may be very slight or absent in 
some and very intense and pronounced in others. The pain is 
usually referred to as shoulder pain, as interscapular or as inter- 
scapular backache, pain in the second and third interspaces ante- 
riorly, to a stitch in the side or a pleurisy pain, an apical or dry 
pleurisy, to myalgia or muscle pain in the pectorals, rhomboids, 
deltoids and intercostals and joint pain or arthritis as described 
by Poncet and pressure pain from contraction of the chest wall in 
chronic cases. 
4. Gastric Distress. More or less pain in the stomach after 
eating. Except for the slight nausea which is usually present at 
the beginning of the disease, it is generally a late symptom. 
Vomiting may follow the ingestion of food. In the beginning 
there may be more or less constipation, which is often followed 
later in the disease by a toxic diarrhoea, a hypo-acidity being 
usually present. 
5. Dyspnoea. This is a variable symptom. It may be slight or ab- 
sent at first, or may be present on the slightest exertion. This 
may increase as the disease progresses and this is due usually to 
the lessening of the healthy lung surface. The respiration in- 
creases from 16 to 20 to 24 to 28 or more. Vagus irritation is a 
leading cause of dyspnoea. 
6. Hemorrhage. This is usually a late symptom. (80) It 
may, however, be the initial one. A small mouthful of blood 
constitutes a pulmonary hemorrhage. A little blood or a blood 
streaked sputum is not a hemorrhage. We must be certain that 
the blood does not come from the nose, the mouth, or pharynx, 
teeth, oesophageal varicies, from heart lesions or from the stom- 
ach. A pulmonary hemorrhage is nearly always a sign of a cav- 
ity. A hemorrhage may follow exertion, a violent coughing spell 
or great excitement. In the old chronic cases there is a lessened 
tendency towards hemorrhages, in fact, slight hemorrhages in 
chronic cases is a more or less favorable sign, a sign of fibrosis 
and pulmonary contraction. A hemorrhage may be venous or 
arterial depending upon whether the blood is light or dark in 
color. 84 
CLINICAL TUBERCULOSIS 
7. Night Sweats. Early or late. These are pathognomonic 
early symptoms as a result of fever and relaxation and are en- 
countered in rapidly progressive cases, similating a crisis in the 
acute diseases. The CO2 accumulation in the circulation may 
cause an irritation of the central nervous system and this is then 
followed by sweating. It may also be due to cardiac weakness, 
to the accumulation and reabsorption of secretions in the dilated 
bronchial tubes and to the lowering of the pulse during the night. 
Mechanical heat stasis due to too much bedding and clothing 
also may be the cause of sweating. The most favorable hours are 
between 3 and 5 in the morning, due to relaxation. All grades 
of sweating may be observed from slight perspiration of the face 
or hands to that of the half or even the whole of the body. The 
nervous apparatus, the cerebro-spinal anad sympathetic play a 
great part. 
8. Temperature. This is the most important single (81) char- 
acteristic symptom. Fever is variable in type, depending upon 
whether the tuberculous process is acute or chronic, rapid or 
slow. Change in fever rate may be increased by exertion, work- 
ing, walking, etc., by both physical and mental efforts, and may 
be decreased by rest and quiet. Fever is usually present in 
nearly all advanced cases, but usually not in the fibroid. Hectic 
fever, so-called, is due to mixed infection and absorption of tox- 
ins from pus and other organisms. Extension of the tubercu- 
lous process is always accompanied by an increase in the fever 
record. There is no arrest of the tuberculous process as long as 
there is fever. Fever is always an unfavorable sign. A tempera- 
ture record of 104° is a very unfavorable sign, and one below 
100 is favorable in tuberculosis. A sudden increase in tempera- 
ture in the tuberculous is usually due to toxins of the bacteria of 
mixed infection, and less to the tubercle toxins. Absorption of 
the toxins is followed by lowering of body resistence. A rise in 
temperature may be preceded by a chill, or a chill and then a rise 
in temperature and then a drop. Usually the temperature is 
highest in the middle of the afternoon, normal towards the noon 
and evening hours and subnormal in the morning and early 
morning hours. In some inverse types, the temperature is high- 
est in the morning and gets lower as the day goes on; again oth- 
ers have a steady slow rise reaching the highest point in the eve- 
ning. These latter are more favorable cases, denoting fibrosis. 
The temperature here is usually within 100°. Again in terminal SYMPTOMATOLOGY OF TUBERCULOSIS 
85 
cases the temperature may drop to normal and remain at that 
point from 6 to 10 days and even longer before exitus, or it may 
be alternately high and normal to subnormal. The temperature 
curve may assume the remittent type. This variable temperature 
may not be known to the patient, and as dissolution is approach- 
ing for hours, the temperature may be subnormal and accom- 
panied by a slow, weak and thready pulse. 
9. Pulse. Usually rapid. Tachycardia, an increase in the 
heart’s action, a cardiac palpitation. The heart is usually normal 
while the patient is at rest. The rapidity of the heart is increased 
by exertion, excitement, emotions, while working or walking and 
after meals. The pulse is usually small, soft, compressible, of 
low tension and occasionally irregular, a symptom which is often 
very annoying to the patient. A systolic murmur at the base is 
frequently heard in beginning cases (hemic). A close relation- 
ship exists between the pulse and the temperature; if the pulse 
is too high in relation to the temperature curve, a bad prognosis 
is indicated. By the pulse rate we are in a position approxi- 
mately to estimate the amount of lung involvement. In a tuber- 
culous individual, a fairly constant pulse at 90 points to one- 
fourth of the lung being affected; a pulse of 100, half; 110, three 
fourths and 120, four fourths. 
10. Mental Symptoms. The tuberculous individual usually 
shows much indifference and is very little disturbed. This is 
most particularly true in advanced cases. He is usually optimis- 
tic to the last. At the beginning of the disease he may show 
much irritability. Some are very melancholic, but few are pessi- 
mistic. Owing to our method of treatment necessary to control 
the disease, many become extremely selfish and dependent, have 
little will power, become lazy, but always remain hopeful and 
buoyant, giving evidence of extreme intoxication. 
11. Loss in Weight, strength and courage with accompany- 
ing signs of pallor and anemia. The initial symptom in many 
cases is the recognized steady loss in body weight. The patient’s 
skin begins to look pale and anemic and a feeling of tiredness 
accompanies this loss; the skin feels flabby and dry, the muscles 
show atrophy, bony prominences begin to show, fat disappears, 
finger nails look cyanotic, lips pale, eyes sunken, etc., accom- 
panied by a gradual loss of ambition and force. 
12. Menstruation. Amenorrhea, a frequent accompanying 
symptom in the tuberculous. Many cases of dysmenorrhea are 86 
CLINICAL TUBERCULOSIS 
of tuberculous origin. Menstruation may again be regular after 
the 35th year of life. Proper hygienic measures may restore the 
normal menstrual functions. Usually with the cessation of the 
menses the tuberculous process increases, particularly in young 
adults. Ovulation may continue after the cessation of menstrua- 
tion. It is important to observe, first the effect of tuberculosis 
on the menstrual period, and second, the effect of menstruation 
on the tuberculous process. See Chapter 26—Tuberculosis and 
Pregnancy. 
13. Hoarseness. Usually a late, occasionally an early symp- 
tom. A change in the voice in some tuberculous patients is early 
noticeable. The voice is less resonant, feeble, hoarse, the vocal 
cords congested from coughing. Early hoarseness is generally 
due to thickening of the epiglottis; it may be caused by paresis 
of the recurrent laryngeal nerve, may be due to pleuretic thick- 
ening or enlarged cervical glands. Pulmonary tuberculosis in 
advanced cases is frequently followed by extension of the proc- 
ess to the larynx, producing a tuberculous laryngitis giving all 
the symptoms of pronounced hoarseness, accompanied by more 
or less severe pain on swallowing. Tuberculous laryngitis is al- 
ways secondary to a tuberculous process in the lungs. It must 
be remembered that the pulmonary tuberculous individual may 
have as an accompaniment a laryngitis which is not tuberculous 
but simply a laryngitis acuta. 
14. Blood Pressure. A lowering of the blood pressure is an 
important objective sign in the tuberculous. A low blood press- 
ure has usually a correspondingly high pulse rate. The blood 
pressure varies greatly in the tuberculous if taken in the three 
positions, lying, sitting and standing, and here also a correspond- 
ing pulse rate can be observed. It is usually observed in the 
active tuberculous individual independently of age. The systolic 
blood pressure is never much above 100 mm. However, it may 
vary between 90 and 120, with a pulse pressure about 25. In the 
tuberculous developing much fibroid tissue or bringing about an 
arrest of the tuberculous process, a steady rise in the blood press- 
ure will be observed. If the tuberculous individual has an ac- 
companying nephritis, this will necessarily increase the blood 
pressure, due to the arterial changes, and again, if in a tubercu- 
lous individual with an active process, an increase of blood press- 
ure is observed which is not accompanied by an arrest or at least 87 
SYMPTOMATOLOGY OF TUBERCULOSIS 
an improvement of his condition, an approaching hemorrhage 
may be anticipated. 
(15) Other signs that are frequently observed in the suspected 
individual and which may suggest tuberculous disease and which 
if present should demand our closest attention are: (a) Fistulae- 
in-Ano; (b) chronic discharges from the middle ear (Otitis Me- 
dia) ; (c) chronic fistulous tracts about the neck, the result of 
suppurating glands; (d) discharging sinuses about the body 
(psoas abscess) ; (e) long standing ulcers about the extremities 
(tuberculous ulcers, etc.). CHAPTER 12 
CLINICAL FORMS OF PULMONARY TUBERCULOSIS. 
CLINICAL VARIETIES 
Grouping and Classification of the Various Forms 
There are many different clinical forms of pulmonary tubercu- 
losis which are so prognostically different that it becomes neces- 
sary from a pathological and more particularly from a therapeu- 
tic viewpoint to draw a sharp line between all these different 
forms. In considering the problem of pulmonary tuberculosis 
from an anatomical standpoint, we must remember that the man- 
ifestation of the disease as we see it is only a part of the dis- 
order; there is usually a general disturbance, more or less pro- 
nounced, of all the different organs of the economy. 
In order to give the pulmonary tuberculously diseased indi- 
vidual all the chances necessary for the restoration of his physical 
well-being, to bring about, if possible, an arrest of his diseased 
process, it will be imperative that the attending physician be per- 
fectly familiar with all these pathological processes going on and 
from the pulmonary findings learn whether the process is active 
or stationary, and if stationary, whether there is a tendency to 
extension or a tendency at healing, or whether it is arrested or 
just beginning; upon the knowledge thus acquired he must base 
his prognosis. 
All pulmonary tuberculosis said to be typical has its seat in 
one of the apices, and pulmonary tuberculosis beginning in any 
other portion of the lungs than in one of the apices may be des- 
ignated as atypical. 
Ever since tuberculosis has been studied as a distinct disease 
entity it has been observed that in about 90% of all cases of pul- 
monary tuberculosis the disease has its origin in one of the 
apices. This, being the general rule, may be considered as typi- 
cal. As only exceptionally in less than 10% the disease has its 
beginning in other than the apices, these forms may be properly 
termed atypical, and the groups of these various forms of the 
disease, both the typical and the atypical, have many symptoms 
88 FORMS OF PULMONARY TUBERCULOSIS 
89 
in common. All forms may be classified as belonging to one of 
four divisions, namely, the atypical, mainly into a miliary, and 
the typical either into the exudative, proliferative or cirrhotic, de- 
pending upon the course the pathological process in the lungs 
pursues, whether more or less rapid or more or less protracted. 
Clinical Nomenclature 
Typical Types of Tuberculosis 
Early in the pathological study of pulmonary tuberculosis it 
was observed that all the typical forms of the disease, those in 
which the beginning disorder had its seat in one of the apices, 
could be placed into either one of three groups depending upon 
the course of the tuberculous process. A simple classification 
(105) based entirely upon the pathological processes going on 
in the lungs and upon the clinical findings is best expressed by 
the following grouping or classification: 
1. An exudative form. A rapidly progressing caseating 
broncho-pneumonia with a strong tendency to lung destruction. 
2. A proliferative form. Slow developing proliferative changes 
with little or no tissue destruction, and 
3. A cirrhotic form. A contracted chest, connective tissue 
hardening, with a slight tendency to extension but a strong tend- 
ency at healing. 
A. The Exudative (Caseous) Form. (Caseation—Destruc- 
tion, more or less diffuse lesions.) In this we notice a rapidly 
progressing caseating broncho-pneumonic process which is 
either acute or subacute, and like all other infectious inflamma- 
tion of the lungs, consists of an infiltrate composed of leucocytes, 
a coagulable exudate, epithelial cells derived from the lining of 
the bronchiols, alveolar ducts, alveoi, etc. This inflammatory 
infiltrate undergoes rapid caseation and by contiguity causes 
more or less destruction of lung tissue and subsequent cavity 
formation. The extension of the process into neighboring tissue 
may be rapid, the produced caseous material aspirated into 
healthy areas, new tuberculous foci developed and the surround- 
ing tissue being insufficiently aerated, breathing hampered and 
lymph flow harrassed, all producing conditions favorable to the 
extension of the process and growth of the tubercle bacillus and 
spreading of the tuberculous process, now more or less rapidly 
from above downwards. 90 
CLINICAL TUBERCULOSIS 
Various observers have from time to time applied different 
names to this form of tuberculosis, all founded upon the course 
which the disease pursues during life. As all present a similar 
and more or less progressive picture and as in all an inflamma- 
tory infiltrate occupying the air cells is found, which is more or 
less moist, representing an exudate, the name of the exudative 
form of tuberculosis is the more expressive. The disease has 
been variously designated as: Acute caseating pneumonia, tuber- 
culous caseating broncho-pneumonia, pneumonic phthisis, pneu- 
monic tuberculosis, acute or subacute pneumonic phthisis, caseous 
pneumonia, chronic catarrhal pneumonia, catarrhal phthisis, caseous 
phthisis, epithelial pneumonia, phthisis florida, acute peribronchial 
tuberculosis, tuberculo-pneumonic phthisis, acute disseminated peri- 
bronchial tuberculosis, chronic cavernous pulmonary tuberculosis, 
broncho-pneumonic phthisis, scrofulous phthisis, progressive caseat- 
ing phthisis, galloping consumption, etc. 
Characteristic Signs and Symptoms. In this variety most of 
the physical signs are distinct and definite and the clinical picture 
that of a progressive, either slow or rapid, more often rapid and 
destructive pulmonary process. The fever is usually high, run- 
ning a distinct curve high in the afternoon and a lowering in the 
early morning hours. Pulse is usually rapid and of low tension. 
There are many moist rales, a strong tendency to cavity forma- 
tion: hemoptysis is frequently present, the sputum is usually 
bacilli positive and the stereo-roentgenogram shows more or less 
scattered coarse shadows and areas of distinct motteling. The 
exudative form of pulmonary tuberculosis especially at the onset 
(or a reactivating of a quiescent focus) is very frequently con- 
fused with pneumonia, both the broncho-pneumonic and the lo- 
bar form. The following are the chief points of differentiation. 
Differentiation. (A) From Ordinary Acute Broncho-Pneu- 
monia. The catarrhal or broncho-pneumonic form of pulmonary 
tuberculosis, acute exudative tuberculosis, is often clinically 
identical with and may simulate the non-tuberculous, acute 
broncho-pneumonia. The following are the chief points of dif- 
ferentiation. In acute exudative tuberculosis, the temperature 
is usually high, with a rapid pulse of low tension and a normal 
leucocyte count, a preponderance of lymphocytes and usually a 
positive tuberculin reaction, while in the non-tuberculous bron- 
cho-pneumonia the tuberculin test is usually negative, with an 
increase of the polymorphonuclear leucocytes from 15 to 30,000. FORMS OF PULMONARY TUBERCULOSIS 
91 
(B) From Lobar or Croupous Pneumonia. The differentia- 
tion between acute caseating or exudative pulmonary tubercu- 
losis and ordinary or lobar pneumonia becomes at times very dif- 
ficult, as both may be accompanied by bloody, rusty or clear 
bloody sputa and even by hemorrhagic nephritis. The signs of 
exudative phthisis, are the following: 1. The disease attacks 
usually robust individuals. 2. A history of tuberculosis in the 
family can seldom be elicited. 3. The onset of the disease is 
slow and insidious and is not preceded by a chill. 4. The pre- 
monitory symptom of a pulmonary tuberculosis may be a hemor- 
rhage. 5. The fever usually runs a distinctly different course— 
is remittent in type, very different from that of pneumonia and is 
not accompanied by a crisis. 6. Generally the signs of dyspnoea 
and of cyanosis are slight or absent. 7. A progressive anemia 
of the skin and mucous surfaces is perceptibly noticeable. 8. 
The patient shows signs of progressive weakness. 9. The liver 
is nearer the spleen, but seldom enlarged. 10. The sputum is of- 
ten greenish yellow, but may be blood streaked or pure blood, or 
may simulate the rusty sputum of pneumonia, tubercle bacilli are 
readily demonstrable and later with destruction of lung tissue, 
also elastic fibres. 
B. The Proliferative (Nodular) Form. (Fibro-Caseous.) 
Here we observe a slower and more benign form of pulmonary 
tuberculosis and the involvement is limited mainly to the bron- 
chiols and the alveolar spaces. In this form we find the typical 
changes with tubercle formation, epitheleoid and giant cells 
mainly about the lumen of the alveolar ducts near the junction 
with the alveoli. In this form lung tissue is not destroyed and 
elastic fibres remain intact. Very seldom, less by extension of 
the tuberculous process and chiefly through the presence of sec- 
ondary organisms or caseating processes are cavities produced. 
In contra-distinction to the exudative form the development of 
larger or smaller nodules takes place, and tuberculous neoplasms 
or granuloma are demonstrable in the diseased areas. This form 
also shows a tendency to develop from above downwards and 
spreads by means of the respiratory bronchiols into neighboring 
and thence into other surrounding tissue. In this form we notice 
evidence of tissue irritation and reaction, due mainly to the 
action of the tubercle bacilli as foreign bodies. This form of 
pulmonary tuberculosis has been variously designated as: 92 
CLINICAL TUBERCULOSIS 
Tuberculosis, Consumption, Incipient tuberculosis, Incipient phthi- 
sis, Chronic phthisis, Tuberculous phthisis, Nodular phthisis, 
Nodular tuberculosis, Chronic pulmonary phthisis, Chronic peri- 
bronchial tuberculosis, Chronic ulcerative phthisis, Tuberculosis 
sicca, Tuberculosis humida, Fibro-caseous pulmonary tuberculosis, 
etc. All these terms are synonymous, however, more definitely and 
appropriately expressed by “The proliferative form.” 
Characteristic Signs and Symptoms. A common form of the 
disease, more or less chronic, is usually characterized as apical 
tuberculosis. Two sharply defined groups of this form of tuber- 
culosis may be recognized, namely, a dry and a more or less 
moist variety. In the former, secondary painful pleurisies and 
occasional friction sounds are very common, with the physical 
signs of harsh breathing, expiratory sound prolongation and 
intensification, note high and dull; crepitating sounds are not 
numerous or may be entirely absent, if much atelectasis, weak- 
ened breath sounds all showing a strong tendency at healing. 
This, the dry variety and with a good prognosis, is often referred 
to as the abortive form of tuberculosis, while in the moist group, 
assuming a position bordering on the exudative form, with occa- 
sionally slight destruction of tissue and the formation of small 
cavities and caseation, due to secondary bacteria, we find all the 
symptoms and signs as in the former variety, but accompanied 
by moist sounds, crepitant rales, and bronchial breathing, indi- 
cating a slowly progressive process which is often referred to as 
catarrhal tuberculosis or bronchial catarrh with a good prognosis. 
The physical signs are most frequently found above and below 
the clavicles, the supraspinous fossae and between the scapulae. 
The prognosis in this form of tuberculosis is always good, better 
in the sicca than in the humida variety. The third clinical group 
of pulmonary tuberculosis is: 
C. The Cirrhotic (Fibroid) Form. (Fibrosis—Healing.) 
Lesions more circumscribed or discrete. Now connective tissue 
changes predominate, encapsulating and surrounding in the 
main the specific inflammatory tuberculous area. In the exuda- 
tive or caseating form only slight if any connective tissue devel- 
opment took place, because the very rapid destructive process 
did not allow of encapsulation; in the proliferative variety this 
was somewhat in evidence but in this the cirrhotic form it is 
pronounced and definite. The conditions present in this variety FORMS OF PULMONARY TUBERCULOSIS 
93 
all favor the healing of the tuberculous process. The tissue 
outside and adjacent to the diseased bronchioles, alveolar ducts 
and alveoli is collapsed, followed by connective tissue formation, 
and this gives the area an appearance of healing in the center 
and an extension of the process at the border. Owing to the 
sluggish lumph flow throughout this fibroid connective tissue 
formation, large quantities of black dust particles and coal 
inhaled with the inspired air are deposited, giving these areas a 
dark appearance, and occasionally the bronchial tubes lying 
within this contracted area undergo bronchiectatic changes. To 
this form of pulmonary tuberculosis we also find that various 
names have been applied, all more or less indicating the forma- 
tion of scar tissue within the lung structure, a strong tendency 
at healing and contraction, all of which is best expressed in the 
cirrhotic form of pulmonary tuberculosis. The following 
synonyms are used. Fibroid phthisis, Cirrhotic phthisis, Chronic 
interstitial pneumonia, Cirrhosis of the lungs, Corrigan’s disease, 
Induration of the lungs, Chronic pneumonia, Fibroid tuberculosis, 
Bronchitic tuberculosis, Bronchitic phthisis, Emphysematous phthi- 
sis, etc. 
Characteristic Symptoms and Signs. A history of the disease 
lasting for more than two years points to chronicity. The most 
evident mark of distinctiveness of this form of tuberculosis is the 
proliferation of tuberculous processes with the formation of scar 
tissue, a recession of the destructive tendencies of the disease, 
with accompanying symptoms of tissue change and secondary 
lung contraction, a vicarious emphysema, simulating asthma, 
much dyspnoea, little or no fever and no cachexia. The notice- 
able characteristic signs may be summed up as follows: 1. re- 
traction and lessening of the intercostal spaces; 2. drooping of 
the ribs; 3. small angle at the junction of the ribs with both ster- 
num and spine; 4. lowering of the shoulder on the affected side; 
5. diaphragm high, immobile, and not influenced by breathing, 
(Williams’ Symptom) ; 6. fixation of the chest on affected side; 
7. lessening or absence of chest excursion; 8. the larynx and 
trachea are dislocated and with the heart and the great vessels, 
the mediastinum and diaphragm are drawn towards the con- 
tracted lung; 9. a high tympanitic, Wintrich’s percussion note 
over the affected side localized near the sternum; 10. a definite 
roentgen shadow. 94 
CLINICAL TUBERCULOSIS 
Owing to the lessened volume of the lung and decrease of air 
capacity, the percussion note is short and may have a tympanitic 
quality, but the vocal fremitus is distinctly impaired, and breath 
sounds usually harsh. If the lung is contracted over cavities or 
bronchiectatic areas bronchial breathing may be hard. In pro- 
nounced contractions of the lung, even of one lobe, there may be 
a heightened pressure in the pulmonary artery and consequent 
hypertrophy of the right heart. 
The main object in practice is to separate these three different 
forms of pulmonary tuberculosis, to secure a clear picture of the 
condition of the lungs, so as to formulate a judgment as to a 
possible prognosis. Very little difficulty is encountered in recog- 
nizing the cirrhotic form. The duration of the disease for two 
years or more, retraction and smallness of the involved area, a 
sunken apex, a lowering of the shoulder, retraction of the inter- 
costal spaces on breathing due to pleural adhesions, ribs prom- 
inent and drooping, diaphragm high, immobile, heart displaced, 
etc. Attention should here again be called to the percussion note 
which is usually high, due to a lessened volume of the lung and 
a consequent lessening of the amount of contained air with a 
more or less tympanitic quality like that over an infiltrated lung, 
but with a perceptible lessening of the vocal fremitus. As a rule 
on auscultation over a contracted lung, vesicular breathing of 
variable intensity is heard, and only in complete retraction over 
bronchiectatic areas or cavities is bronchial breathing audible. 
Difficulty in breathing due to pulmonary contraction is often 
followed by increased pressure in the pulmonary artery and con- 
sequent hypertrophy of the right heart, frequently developing a 
right heart insufficiency; such cases are surprisingly benefitted 
if treatment is directed towards the heart. 
It is not difficult to differentiate the progressive, caseating, the 
exudative, as well as the proliferative from the evident cirrhotic 
form by simple physical examination, but much difficulty is often 
encountered in separating the exudative from the proliferative 
form, which are so prognostically different. In both, the per- 
cussion note is high with more or less tympany, or as in the be- 
ginning of infiltration only tympany similar to that of the cir- 
rhotic form with a lessened lung volume and lessened amount of 
air is present, but on auscultation by complete infiltration bron- 
chial breathing is heard, and if much of the lung tissue is still 
normal and air cells still free, the vesicular murmur is soft with FORMS OF PULMONARY TUBERCULOSIS 
95 
a slightly blowing expiratory sound; Moist rales possessing a 
specially high note are characteristic of the progressive or exuda- 
tive form and the vocal fremitus is usually increased. The com- 
bination of the cirrhotic with the progressive infiltrative form 
with cavernous changes is difficult to separate. If over a con- 
tracted chest, indicative of fibrosis, one hears bronchial breath- 
ing, high crackling moist rales, the vesicular expiratory sound 
harsh and an increased or at least not a lessening of the vocal 
fremitus, then we can assume that upon the preexisting cirrhotic 
lung a progressive form has been implanted or that exudative 
changes exist in a cirrhotic pulmonary process. Another diffi- 
culty will be encountered in trying to separate the prognostically 
favorable proliferative form from the rapidly progressive florid 
variety. Here auscultatory and percussion differences are not 
distinct; however, a rapid progress of the disease bespeaks the 
latter form. If a whole lobe is involved and the duration of the 
disease is short, this would point to the exudative form, but a 
slow form of the disease may not exclude a rapid course because 
a proliferative process may take on a sudden activity and develop 
into the exudative. Again, the involvement of a whole or the 
greater part of a lobe speaks strongly for the florid form. 
Further, we may observe the greatest variation in isolated 
cases in which the anatomical changes are insufficient to explain 
the process. In mild, benign, not very active cases one may find 
great toxic symptoms, high fever, rapid pulse, rapid heart, diar- 
rhoea, emaciation and then requently in cases of very extensive 
involvement, fever may be entirely absent, appetite good with 
good nutrition and an absence of all general symptoms. The 
general conditions may be entirely different in two individuals 
and yet the anatomical process nearly alike. The number of 
tubercle bacilli demonstrable is also of no prognostic importance. 
Atypical or Aberrant Types 
In the above mentioned clinical classification those conditions 
alone were considered in which the disease had its beginning in 
one of the apices and which are generally known as the typical 
forms, namely, (1) and exudative form, (2) a proliferative form, 
(3) a cirrhotic form, leaving for our consideration the remaining 
or atypical forms which are only occasionally encountered and 
which comprise less than 10% of all varieties. These varieties 96 
CLINICAL TUBERCULOSIS 
are usually comprehended separately as (4) (a) miliary, and (b) 
other atypical forms. 
(A) Miliary Tuberculosis, Miliaris disseminata. Miliary tuber- 
culosis is generally the result of a sudden inflow of tubercle 
bacilli in great numbers into the circulation. From the patho- 
logic-anatomical character of the tuberculous lesion as observed 
in the organism, we may assume that very frequently and most 
readily tubercle bacilli may gain entrance into the circulation, 
and circulate in the blood stream. If, however, the entry is in 
small amounts, as so often happens, then the body is fully pre- 
pared to resist both deposition and growth. This is due to the 
existing defense agencies or antibodies within the body which 
were inaugurated at the first or primary infection. On the other 
hand, if the tubercle bacilli enter the circulation in large num- 
bers, a massive involvement, or if in small but very virulent and 
often repeated numbers, or, as may happen, there is a sudden 
outpouring of the contents of a softened gland into the blood 
stream, then all of this may speak for a resultant miliary form of 
the disease. It should be mentioned here that the demonstration 
of the tubercle bacillus in the circulating blood not only in the 
miliary form of the disease but also in active and in advanced 
pulmonary tuberculosis is always a prognostically grave symp- 
tom—a signum mali ominis. 
Miliary tuberculosis as we usually see it is a secondary process, 
the result of an active tuberculous focus somewhere within the 
body, an endogenous infection or more properly an acute auto- 
infection from a previously existing focus. Miliary tuberculosis 
as a primary affection is quite conceivable although improbable 
—must always be very exceptional, when we consider that the 
bacilli would have to enter the body in large numbers and from 
without. As to the method of miliary infection, we find that two 
views are held, namely, first that the bacilli find ready entrance 
into the various organs, but notably the lungs through the blood 
current, an hematogenous infection, usually in large numbers 
and overwhelming the system, producing as a result of this sud- 
den inflow innumerable tuberculous nodules first in the lung 
structure because this is most vulnerable, this is soon followed 
by the invasion of the other organs; the second view is that the 
bacilli find their way into the blood stream in small amounts at 
a time, but often repeated, that these oft repeated introductions 
bring about the development of tuberculous nodules in the intima FORMS OF PULMONARY TUBERCULOSIS 
97 
of blood vessels, notably that of the pulmonary veins, and that 
subsequently these tuberculous nodules in the veins undergo 
changes, becoming soft and constantly pouring their contents in 
small amounts into the blood stream. This is very reasonable to 
assume, because in 95% of all cases of miliary tuberculosis these 
tuberculous nodules situated in the vessel walls can be demon- 
strated. This is also the more probable because these nodules 
are not found in the vessel walls in tuberculosis of the non- 
miliary form. 
All forms of chronic tuberculosis, quiescent, arrested or active, 
may be followed by the acute miliary form if from any cause 
bacilli are mobilized and suddenly enter the blood stream in 
large numbers, hence all factors which favor the mobilization 
of the tubercle bacillus may bring about a miliary form of the 
disease. In youth and in young life such conditions frequently 
exist in an inflammatory infiltrate about the enlarged glands, in 
scarlet fever, in measles, etc., and in adult life we see it fre- 
quently following injuries, trauma or shock, in these latter with- 
out previous existing tuberculous disease in the vessel walls, 
both arterial or venous. We often notice that after injuries to 
enlarged and swollen glands, intestinal, mediastinal, cervical, 
etc., which rupture, their contents being poured into the circula- 
tion, after injuries or bruising of the testicle, epididymis, ovary 
or uterus, also after abortions, miscarriages, even after labor, a 
rapidly progressing miliary form of the disease has been ob- 
served. All this only goes to show, as I have so often empha- 
sized, that throughout life, that is from the first infection in early 
infancy to the fully developed disease in adult life, throughout 
the whole process of the tuberculous disease, it remains a quan- 
tity disorder; it begins as a quantity infection and ends as a 
quantity disease, that is how many bacilli have entered either the 
body or the general circulation in a given time. 
Diagnosis. Acute miliary tuberculosis has never been cured. 
We have no positive evidence that a case of acute miliary dis- 
ease was ever followed by an arrest of the pathologic process, 
and all statements to the contrary must indicate a doubtful diag- 
nosis. It is true that occasionally cases are met which assume 
a more or less chronic form, exacerbations and remissions fol- 
lowing in rapid succession. The process is somewhat drawn 
out, but death is the inevitable result. Often the diagnosis from 
the objective symptoms presents much difficulty, especially in 98 
CLINICAL TUBERCULOSIS 
children and the aged and here the pulmonary form may be sus- 
pected rather than diagnosed, and it may become necessary to 
resort to the use of the roentgen ray to confirm the findings. A 
preexisting tuberculous process either in an apex, near the hilum 
or in any other portion of the body may point strongly to a 
miliary form and examination of the blood for the presence of 
the tubercle bacillus may be necessary to clinch the diagnosis, 
that is, providing the examination is made early after the onset 
of the disorder, because the bacilli cannot be demonstrated in 
the blood if some time has elapsed since their entry. The diag- 
nostic examination of the sputum will usually be bacilli nega- 
tive, and this is to be expected as long as the tubercles are in 
process of formation. If, however, the disease has lasted for 
some time, as often happens in individuals who exhibit a slightly 
better resistance, then caseation and softening will take place, 
which generally occurs towards the close of the scene. Then if 
there is cough and expectoration, tubercle bacilli may be 
demonstrable. The disease usually terminates fatally in from 
two weeks to two or perhaps three months. The physical signs 
in miliary tuberculosis are, as a rule, not well defined but are 
more or less obscure. The percussion note is usually normal or 
hyperresonant. This is due to the distended air vesicles of the 
still normal lung structure and but for an old tuberculous 
process, healed or arrested, at one of the apices, the fremitus over 
the miliary involved area is not increased. Ausculation usually 
finds the respiratory murmurs harsh, with slight prolongation of 
the expiratory phase and rales, fine or crepitating, may or may 
not be audible. The physical signs being so much at variance 
with the clinical picture, this in itself should lead one to suspect 
miliary tuberculosis, particularly in an individual who for years 
has been sufferng from pulmonary tuberculosis which at times 
has assumed a more or less active form, or in a person who has 
tuberculosis of other organs than the lungs, like disease of the 
glands, bones and joints, of the testicles, ovary, epididymis, etc. 
Symptoms. Miliary tuberculosis may have a sudden onset, 
very stormy, or may be somewhat protracted. There is usually 
headache, malaise, high fever, loss of appetite, great depression 
and prostration, and occasionally the initial symptom may be a 
hemorrhage. Then there is generally a dry, hacking unpro- 
ductive cough, evidence of a bronchial catarrh with little or no 
expectoration, perhaps only a little clear mucous which at times FORMS OF PULMONARY TUBERCULOSIS 
99 
may be blood streaked. A most distinct symptom manifested 
from the very beginning of the disorder is shortness of breath, 
becoming gradually more and more distressing as the process 
progresses, respiration also more rapidly increasing to 40 and 
more per minute and with the progressing and growing infiltra- 
tion of the lungs, cyanosis increases in severity. On inspection 
the lips and nails are found markedly cyanotic, the sclera slightly 
bluish and even the cheeks, which are found usually flushed, are 
slightly cyanotic. Fever is always high, ranging from 101-103 
and even higher, the pulse rapid and feeble, the spleen is enlarged 
and tender and the urine is as a rule not free from albumin. 
Towards the close of the scene the patient may often manifest 
symptoms simulating a typhoid state with emaciation, delirium, 
dry and brown tongue, subsultus tendinum, etc. In miliary 
tuberculosis the symptoms often vary greatly, and may take on 
at any time the form of a typhoid, a pulmonary or meningeal 
variety, each of which has more or less definite signs and symp- 
toms. In the suspected meningeal form, an examination of the 
chorioid becomes necessary, because in more than 75% of all 
cases from 6 to 10 tubercles, clear grayish yellow, round or 
oblong spots, can be recognized. 
(B) OTHER ATYPICAL FORMS OF TUBERCULOSIS (44) 
A very small percentage of all the various forms of pulmonary 
tuberculosis belong to this group. Some are generally highly toxic 
varieties of the disease. In the order of frequency are: 
1. Typhotuberculosis (Typhobacillose of Landouzy) Tuber- 
culosis resembling typhoid. Characteristic signs are an acute 
process, high fever, duration of the disease about four weeks at- 
tacking young individuals who are usually in good health. The 
fever is continuous, somewhat irregular with a corresponding 
frequency of the pulse. Examination of the blood indicates 
leucopenia and a relative lymphocytosis. Examination of the 
lungs at the onset is usually negative. Spleen enlarged. Evi- 
dence of involvement of the lungs, pleurae and mediastinum can 
later be demonstrated. Landouzy has pointed out that a patient 
suffering from this form of tuberculosis may frequently tem- 
porarily recover and that after a lapse of perhaps a month or 
more, a sudden and quick onset, a return of the disorder with 
great severity is noticeable, which is followed by speedy death. 
2. Septic Tuberculosis. (Septicotuberculose of Neumann.) A 100 
CLINICAL TUBERCULOSIS 
severe septic condition especially observed in cases of exudative 
phthisis, with great enlargement of both liver and spleen, jaun- 
dice, an inflammation of the joints, a generalized arthritis and 
tubercle bacilli are demonstrable in the circulating fluid. Both 
of these forms indicate a high toxic condition of the individual. 
3. Tuberculosis accompanying Diabetes usually runs a very 
rapid course due to the favorable influence of the glycemia on the 
bacillary growth. 
4. Tuberculosis following trauma may assume a more or less 
uncertain course. 
5. Tuberculosis in the aged and in young infants assumes a 
more or less malignant and irregular course. 
6. Tuberculosis secondary to the other forms of pulmonary 
disease, may assume a more or less atypical course. 
7. Patients with either congenital or acquired chest deformi- 
ties, like Scoleosis, Kyphosis, Kyphoscoleosis, etc., and who are 
very infrequently disposed to pulmonary tuberculosis, should 
they develop tuberculous diseases the lesions as a rule are not 
found in the apices but in the bases of the lower lobes or in the 
middle right. 
THE DIAGNOSIS OF PULMONARY TUBER- 
CULOSIS 
Introduction into the methods of physical examination of the 
chest. Much depends in the treatment of pulmonary tuberculosis 
upon an early diagnosis. The earlier the disease is recognized in 
a given individual the better the prognosis. If pulmonary tuber- 
culosis is a curable disease, and we maintain that it is, then the 
most propitious time for bringing about an arrest and probable 
cure of the tuberculous process is at the very beginning of the 
disorder and at a time when but little invasion or destruction of 
the lung tissue has taken place, and this usually is when the 
disease is still in the first or perhaps in the preactive stage, the 
stage of latency when the symptoms are still somewhat obscure; 
it is at this stage that we can promise our patients the most hope- 
ful results. When once the disease is fully established, the prog- 
nosis can not be so favorable, although even at this stage with 
proper care and obedience, much good is often achieved.(41) 
(42) (46) 
In advanced cases when the signs and symptoms are pro- 
nounced and the physical examination positive, when the layman FORMS OF PULMONARY TUBERCULOSIS 
101 
makes the diagnosis, an exact physical diagnosis and its inter- 
pretation are of interest only to the examining physician and to 
medical students for demonstrating the tuberculous process 
going on within the chest cavity, but they are of no value, use or 
help to the unfortunate tuberculous. 
Every case presented for examination, irrespective of the stage 
of the disease, should receive full consideration; however, a be- 
ginning case should be studied with the most possible care and 
attention. First of all we must be able by physical examination 
to state definitely whether the individual is tuberculous or not 
tuberculous, for very much depends upon this. 
If in doubt about your first examination, make a second, a 
third and perhaps a fourth at short intervals. There must be no 
doubt and we must state positively and with emphasis that the 
patient is tuberculous or that he is non-tuberculous. If by phy- 
sical examination you have clearly demonstrated that the patient 
is positively tuberculous, then it is your plain duty to so inform 
him and tell him the truth; if, on the other hand, from your 
examination you have concluded that there is no tuberculous 
disease present, then again it is your duty to so inform the 
patient; this will relieve the mind and allay all fears and anxiety. 
As previousy stated, the earlier the diagnosis is made, the bet- 
ter for the patient. In the examination of a patient, the methods 
of physical diagnosis by inspection, palpation, percussion aus- 
cultation and radiography must all be most carefully considered. 
In obscure or doubtful cases, to aid me in arriving at a definite 
diagnosis I have for years followed a plan which is well known 
to most of my students. All cases of doubtful or perhaps nega- 
tive findings, after making a careful physical examination, are 
put upon a small iodide of potassium impression. I give the 
following prescription: 
Iodide of Potassium, drachms two ( 4.0) 
Tincture Cardamom compound, drachms four ( 8.0) 
Peppermint Water, sufficient to make three ounces (90.0) 
Mix. Direct that the patient take a teaspoonful in a mouthful of water 
once in three hours continuing this for three days. 
The patient retur-ns the third day and if on re-examination I 
now find constant rales over areas over which I found none at 
the previous examination, I carefully note this and make a diag- 
nosis of probable pulmonary tuberculosis. An individual in 
whom such findings were demonstrable should return for a third 102 
CLINICAL TUBERCULOSIS 
examination in about 8 or 10 days, and during this time he is to 
note carefully the temperature and pulse rate at least four times 
each day, 7 and 11a. m., 4 p. m., and at bed time. If, however, after 
the iodide of potassium administration, the signs are still negative, 
then I give intradermally a milligram of O. T. If this is followed 
by a reaction, I make a daily examination for three days, espe- 
cially at the time when the reaction is at its height, and here 
also if over an area over which at a previous examination I 
found no rales I now find permanent crackling sounds, I make 
a diagnosis of presumable tuberculosis, but if after the adminis- 
tration of a Mantoux, there is no reaction, then I give a second 
intracutaneous injection of two milligrams. If after about four 
days this should also prove negative, then a third dose of tuber- 
culin is given and no more if this also proved negative. I then 
inform the patient that in all probability he is non-tuberculous, 
and after this the radiographic chest plate may be helpful. 
Roentgenographic examinations should not be used primarily 
for diagnosis; they are only intended to confirm physical exam- 
inations, to check up the physician’s ability to make the diagnosis 
by the physical methods. 
HISTORY TAKING IN TUBERCULOSIS 
Before entering upon the study of a case of suspected tubercu- 
losis; that is, before we subject the patient to a thorough phy- 
sical examination, it is above all necessary that we take a fairly 
accurate history of the case. A good history is to the clinician 
what a roentgenographic chest plate is to the roentgenologist, 
that is, a picture, a record of the case, and the more thoroughly 
this history is taken, the more clearly this mental picture will 
appear. Not all case histories are well taken, many are utterly 
worthless. Good history taking is quite an art and, like all 
things in practical medicine, it can be acquired only by per- 
sistent and constant practice. 
History taking in Pulmonary Tuberculosis becomes quite a 
complicated affair,—there are so many angles to be considered. 
In looking over a case history sheet selected from any well con- 
ducted tuberculosis sanatorium, a striking feature is the long 
array of questions asked. This, in institutional work is found 
most satisfactory, although considerable time is usually con- 
sumed in tabulating the answers to these many questions. In 
general practice a history sheet must necessarily be somewhat FORMS OF PULMONARY TUBERCULOSIS 
103 
abbreviated, owing to the limited time allowed in each case, and 
yet a fairly good history of the case should be secured. Here 
then the outline must be more brief and to the point, yet in gen- 
eral, covering the case. This can fairly well be done according 
to the history outline as is given here: First ascertain the surname 
and the given name or names of the patient, city and street 
address, age of the patient, if single or married, vocation, occupa- 
tion, weight, height, etc. Next: 
Family History: Age of the father and mother if alive, if 
either or if both are dead, learn age at the time and the cause of 
death. Ask how many children there were in the family, whether 
all are alive and, if not, ascertain the cause and the age at the 
time of death. If there were many children in the family, as- 
certain what number in the group the patient is or, if a twin, 
about the health of the other twin; if dead, the cause and the 
age at the time of death. Inquire next about the father, if alive, 
if healthy, if dead. Is or was he subject to so-called winter 
cough? Or asthmatic, bronchitic, diabetic, etc.? Ask the same 
about the mother, perhaps either is or was tuberculous and 
the patient is quite familiar with this fact. Most particu- 
larly ascertain if there was in the household some one suffer- 
ing from lung disease while the patient was in his early child- 
hood days, when 2, 3, 4, 5, or 6 years of age. Quite frequently 
the disease is not acquired from the parents but from some one 
else about the household, and an old grandfather or grand- 
mother, a male or female servant, a relative or friend living with 
the family is often the original source of infection. Make inquiry 
if during the tender years of the patient some one about the 
household was troubled with asthma, emphyema, chronic bron- 
chitis, chronic cough, etc. Perhaps in these early years the 
patient for a shorter or longer time lived with friends away from 
home either in the city or in the country and a member of this 
household was suffering from pulmonary disorder; perhaps 
tuberculosis, and inquire if during his stay there he was very 
closely associated with this individual. As active tuberculosis 
is most frequently the aftermath of a close contact infection, 
particularly the contact of a tuberculous adult with the small 
child, the physician should be most specific to learn, how, when 
and in what manner this supposed infection took place. 
Personal History: How long has the patient been complain- 
ing? What was the first thing that he noticed about his com- 104 
CLINICAL TUBERCULOSIS 
plaint? If he had pleurisy, how recent or how many years ago? 
Ascertain whether he had measles, scarlet fever, whooping cough, 
pneumonia, typhoid, so-called walking typhoid or rheumatism. 
If so, when? Did he sustain any injury to body or mind, a 
trauma, automobile, railroad or any other accident? Any kind 
of shock? If an operation was performed, give the nature of the 
operation, was it recently or many years ago. Ascertain if al- 
coholic, if syphilitic or if gonnorrhoeal, if living quarters are 
hygienic, etc. 
Present History, Present Complaint: What was the incidence 
that caused the patient to seek medical advice? The patient in 
all probability for some time, perhaps for months, has been com- 
plaining of a troublesome cough, possibly he had an initial 
hemorrhage, this has alarmed him and he now consults his phy- 
sician. In other instances more obscure symptoms are the cause 
of his seeking aid, like headache, cardiac palpitation, nervous- 
ness, sleeplessness, gastric disturbances, extreme nervous irri- 
tability, malaise, shortness of breath, pain in the back or shoul- 
ders, etc., these almost always are the prodromal symptoms, or 
if the disease has progressed and activity is suspected, then more 
definite symptoms are present, for which he seeks relief, such as 
a warm feeling especially in the afternoon, acceleration of the 
heart’s action, loss of appetite, perhaps night sweats, much 
coughing and expectoration, emaciation and loss in weight, etc. 
Having secured a fairly good history of the case and before 
we proceed to a physical examination, it is in order that we note 
the pulse frequency, the number of beats per minute, take the 
temperature either by mouth or axilla or perhaps more accurate 
reading by rectum; note the number of respirations per minute 
and possibly take the blood pressure. 
With these preliminary and necessary data tabulated we will 
proceed somewhat in detail to consider the various methods of 
examining the chest by inspection, palpation, percussion, aus- 
cultation and radiography, beginning with inspection preceded 
by a short note on and directions, “How to Examine the Chest.” CHAPTER 13 
INSPECTION 
How to Examine the Chest. Position of Patient. (34) (40) (43). 
The person to be examined should first be stripped to the 
waist, then comfortably seated, without any restraint, on a chair, 
or preferably on a stool, sitting erect. The chest must not be 
pushed unduly forward, nor excessively drawn in, the body in a 
natural, easy and comfortable position with the hands resting in 
the lap or the arms hanging leisurely by the side, or as some pre- 
fer the arms folded over the chest, keeping the knees close to- 
gether, head erect and looking straight forward. 
The examining physician is seated in an easy and natural, in 
no way cramped position, before and on a level with the patient, 
with knees pointing in opposite direction. In fact he must be 
seated perfectly comfortable. If he desires to examine the back, 
then either the patient must be asked to turn about or the phy- 
sician takes his place behind the patient. 
All necessary instruments like fever thermometer, percussion 
hammer, stethoscope, blood pressure apparatus, as well as writ- 
ing paper, pen and ink, tape measure, tongue depressor, etc., 
should at all times be within easy reach. 
If it be desired to examine the patient in the recumbent posi- 
tion, as is often the case in listening over the heart for faint 
lesions, then the patient should be placed in a comfortable posi- 
tion on the back, preferably on an examination table or chair. 
A bed may be used, but this is usually found too low and besides 
it does not meet the requirements of the examiner so well as does 
the chair for such examinations. 
With the patient in the recumbent position either on a table, 
chair or bed, the arms should be placed at the side of the body 
or with the hands or arms resting on the head. Now with the 
patient in a comfortable and easy, either sitting up or lying posi- 
tion, the examiner at a glance must secure a relative picture of 
the external chest, if the chest appears normal or if there are any 
abnormalities and if so where. 
105 106 
CLINICAL TUBERCULOSIS 
(A) THE NORMAL CHEST ON INSPECTION 
Inspection. Observe the general contour of the chest, whether 
both sides are symmetrical. The right side may appear normally 
a trifle larger, much depending on whether the individual is right 
or left handed. Note if the excursion over both sides is free and 
equal; one shoulder may be a trifle lower than the other, usually 
the right, all within normal limits. At the same time note the 
rate of breathing. 
Next note carefully the different landmarks, first those on the 
anterior chest wall, then those posterior as well as lateral. If the 
chest wall anteriorly has been found fairly symmetrical then the 
landmarks will practically conform to normal conditions. First 
the clavicles will neither be over prominent on either side, the 
fossae above not very deep, nor very conspicious and no depres- 
sion below (Mohrenheims fossa) but possibly a slightly hollow 
or shallow appearance. Ludwig’s Angle “Angulus Ludovici,” the 
junction of the menubrium sterni with the corpora sterni must 
not protrude too prominently and the ribs must not overlap 
each other, but flare out in a graceful manner alike on both sides, 
with but slight if any depressions between. The Pectoralis 
Major muscles will be equally prominent and symmetrical on 
both sides, and the attachment to the lower border of the 5th 
rib will furnish on both sides a more or less noticeable depres- 
sion, “Sibson’s Groove.” 
The area of that part of the chest wall in the nipple line from 
the 4th rib down to the costal margin and on either side should 
be fairly full and not show much depression or retraction, ab- 
sence of “Harrison’s Groove or Sulcus,” nor a flaring upward and 
outward of the lower ribs, nor should much of a depression, if 
any, be noticeable below and about the xyphoid or ensiform 
cartilage, denoting absence of “Scrobiculus Cordis” and no de- 
pression above the xyphoid the “Pectus Excavatum” or funnel 
breast nor a sharp, protruding prominence of the breast bone, 
“Pectus Carinatum” like the keel of a boat, these if present, are 
all more or less abnormalities. The lower costal margin should 
not show a conspicuous flaring out nor should the costal angle 
be very acute and the junction of the costal cartilages and ribs 
show undue prominence, as is so frequently found in rickets or 
rachitis. The cardiac impulse should be normally visible or at 
least palpable in the 5th interspace and within the nipple line. 
The nipple, itself, particularly in the male, should be seen in INSPECTION 
107 
the 4th interspace about 4 inches (10 cm) on either side of the 
median line. In the female the presence of the mammae modifies 
somewhat the general appearance, but also here the general sym- 
metrical condition on both sides must be maintained. Note also 
in a general way if the chest appears abnormally long from the 
shoulder down to the lower costal margin or if the chest is un- 
usually wide from side to side as compared with the length. 
While making these necessary observations about the chest, 
Suprasternal 
notch 
Supraclavicu 
lar fossa 
Clavicle 
Mohrenheim’s 
fossa 
Nipple 
Ludwig’s 
Angle 
Pectus 
Excavatum 
Scrobiculus 
Cordis 
Sibson’s 
Groove 
Epigastric 
(Costal) 
Angle 
Harrison’s 
Sulcus 
Fig. 9. The natural or normal landmarks of the anterior chest. These various land- 
marks if unduly prominent, either, protruding or showing a deep hollow, must be con- 
sidered abnormal. 
the examiner should incidentally note if the suprasternal notch 
is about normal or if abnormally deep or possibly entirely ab- 
sent ; if the thyroid gland is enlarged, if much or little, if some of 
the cervical glands are enlarged on one or both sides and about 
the jaw; if scar tissue evidence of former gland disease is present 
or not, if the arms are equally developed on both sides, if 
prominent veins about the chest, neck or arms are noticeable, if 
abnormal growths. Notice the condition of the face, and whether 108 
CLINICAL TUBERCULOSIS 
the head is bald or has a healthy growth of hair, notice the color 
and appearance of the skin, of the eyes, if normal or otherwise. 
This whole picture must be reviewed at a glance and should not 
occupy more than a few seconds of time. 
Having inspected the chest anteriorly, an examination of the 
posterior aspect should be made and the landmarks, mainly the 
scapulae and their relation to the vertebral column observed. 
Normally the scapulae are situated on either side and parallel to 
the spine and at about an ecpial distance from the vertebral 
Vertebra 
Prominens 
Spine of the 
Scapula 
Mid spinal 
line 
Scapula 
Angle of the 
Scapula 
Margin of 
the Lungs 
Twelfth rib 
(Base of the 
thorax 
Fig. 10. The natural or normal landmarks of the posterior chest. 
column. Has the vertebrarium its natural contour, neither deviating 
to the right nor to the left, absence of “Scoliosis,” nor projecting 
unduly outward, absence of “Kyphosis” or being drawn notice- 
ably inward, absence of “Lordosis,” or perhaps one or more of 
the vertebrae may show a more or less sharp projecting angle of 
bone, presence of tuberculous disease, “Gibbus.” Note the scap- 
ulae if they are an equal distance from the spine. Note the spine 
of the scapulae, if both are equal, if the depressions above the INSPECTION 
109 
spine are not unduly prominent and equal in appearance on both 
sides. Next note the lower angles of the scapulae, if they are 
equal or perhaps one more conspicuous than the other; then 
notice the area between the scapulae and along the spine, if sym- 
metrical, if the muscular development of the rhomboideus the trap- 
ezius and the levator anguli scapulae, are alike on both sides and 
if the excursion of the chest is uniform and symmetrical over 
both sides. The appearance of the skin if healthy or if flabby, if 
veins or perhaps minute venules are conspicuously noticeable. 
Next notice if the lateral surfaces are symmetrical. A descrip- 
tion or picture of the normal chest must not be taken too criti- 
cally but only within certain limits, because we all know the 
difference in appearance of the chest of an exceedingly fat per- 
son as contrasted with that of a very thin individual. A chest to 
be considered normal must be fairly well symmetrical and that 
applies equally to the fat as well as the thin. 
(B) THE ABNORMAL CHEST ON INSPECTION 
Inspection. If in the ordinary examination of the chest much 
deviation from the normal has been observed, or if various parts 
show some abnormality, then a special and more careful exam- 
ination is required. This brings us to a consideration of ab- 
normal findings on an inspection of the chest, the picture as 
being presented at a glance, a first view, or what is generally 
described as Prima Vista Diagnosis. 
General consideration. In basing a diagnosis on inspection it 
becomes necessary that all the various methods of examination 
be made available, for instance, the relation of body weight to 
height, the circumference of the chest, etc. In a large number 
of chest examinations made, and noting the average, it has been 
observed that not only does the individual suffering from active 
pulmonary tuberculosis and its complications show a perceptible 
loss in body weight, but that many persons who possess a sub- 
normal body weight and are not already suffering from tuber- 
culous disease become easy prey to its ravages. Attention 
should be given then first of all to the circumference of the chest 
in the adult. At birth and for years thereafter the general ap- 
pearance of the chest is more or less cylindrical assuming 
towards puberty and remaining for years thereafter the oval 
type, to resume again in old age or reverting back to the cylin- 
drical or “infantile” type. In the normal adult the chest is oval 110 
CLINICAL TUBERCULOSIS 
in outline, the antero-posterior diameter is less than the lateral 
in proportions nearly as is 1 to 2. In the individual suffering 
from long standing or chronic pulmonary tuberculosis and in 
those predisposed to the disease, the chest is usually flat antero- 
posteriorly, wide laterally and long from above down. Again, 
the relation of body weight to height; in the average normal 
male for every foot in height 25 pounds should be added, and in 
the female about 23. A man whose height is 5 ft. 6 inches, (168 
cm.) should weigh within 138 pounds (65 kilos). In the person 
suffering from tuberculous disease, either active or of long 
standing, this relationship is often greatly disturbed. Next note 
the circumference of the chest to body height. Normally the 
circumference of the chest in inches should be at least half that of 
the body height. A healthy individual whose height is 5 foot 
6 inches (168 cm.) should have a chest excursion of more than 33 
(84 cm.) inches or at least 33 (84 cm.) inches when at rest. 
These variations must always be great and can not be applied in 
all individual cases and are considered more or less crude 
methods in diagnosis; nevertheless they point to abnormal chest 
probabilities. 
The chest on inspection may show definite signs of an existing 
disease. This is often noticeable, and particularly in children. 
It may present evidence that the disease has existed at some time 
and that the process is now healed, or that the formation of the 
chest is such that the individual who possesses such a chest falls 
easy prey to tuberculosis. It may also give evidence that the 
possessor of such a chest early in life came in contact with tuber- 
culous disease but has weathered and braved the storm, hence 
from these observations we assume that certain signs in an in- 
dividual may stigmatize the possessor as being classed as tuber- 
culous, either past, present or future. 
Stigmata of Tuberculosis. Early in the study of the subject 
of pulmonary tuberculosis, the careful and observing physicians 
were impressed by the facts that certain individuals or even 
groups of individuals, possessing chest formations which showed 
a more or less distinct type, were either already suffering from 
tuberculous disease or later developed a tuberculosis, and these 
types were described as having many signs in common and yet 
were capable of a distinctly separate classification. 
(A) Chest Deformities which point to a tuberculous disease, 
past, present or future—The chest as a whole. (44) INSPECTION 
111 
1. The Stenotic or Contracted Chest. Children and adults as 
well possessing this type of chest are predisposed to tuberculosis. 
In this form of chest development we find the upper aperture, 
that is the first rib and its cartilage, small and contracted. The 
first ring is small, the cartilage also small and early ossified, and 
the rib is but imperfectly developed. This causes contraction of 
the apices and deformation, accompanied by early stasis, insuffi- 
cient blood and lymph supply with faulty aeration. This type of 
chest offers a mechanical disposition to a tuberculous disease 
which is manifested by two clinical varieties, according as the 
cause is a disturbance in the development and contraction of the 
above described first rib and cartilage, or is a congenital or more 
or less acquired scoleosis of the upper spine in the paravertebral 
area. This type of chest formation which was first described by 
Freund and further enhanced by the labors of his pupil, Hart, is 
now recognized by most observers as a distinct form of the 
chest predisposing to tuberculous disease. Classic pictures of this 
form of chest development are frequently seen in art galleries, 
and paintings, portraits and figures of the fair sex, depicted with 
long, scrawny and conical necks, small upper chests are of this 
type. 
That the contraction of the upper aperture incident to early 
ossification of the usually small cartilage of the first rib, and the 
faulty development of the rib itself are important contributing 
factors in tuberculosis is now generally recognized. In an in- 
tensive study of 394 roentgenographic chest plates, 221 of which 
were those of male and 173 of female patients, ossification of this 
first cartilage was demonstrable in 58%, and in addition in 48% 
it was possible to show definite tuberculous shadows in the lung 
structure, and it was also shown that the frequency of ossifica- 
tion of the first cartilage increased with age and that in youth 
only in about 10% was this present and then usually un- 
ilaterally, becoming more bilateral with mature years, all proving 
that tuberculous disease has a special predilection for the apices 
if the first rib and the ring are small and the cartilage is early 
ossified. 
2. The Thorax Infantilis, Infantile type of Chest. In this form 
of the chest, predisposing to tuberculosis, the round form, com- 
mon in infant life is still retained. In children and young adults 
possessing this type of chest, the gradual change from the infant 
to the adult type has not taken place, the infantile form still 112 
CLINICAL TUBERCULOSIS 
maintaining, and possessors of this form of chest are very prone 
to pulmonary tuberculous disease. In this form, as in the pre- 
ceding, faulty aeration plays a prominent role, and enlarged ton- 
sils, adenoid vegetation, obstruction to the upper air passages, 
insufficient circulation and aeration, accompanied by rickets, 
drooping of the ribs, narrow intercostal spaces, large lower 
aperture and possibly a high palatal arch generally completes 
the picture. This type predisposes relatively less frequently to 
tuberculous disease than does the former. 
3. The Phthisical Chest—Thorax Phthisicus, seu Paralyticus, 
Habitus Phthisicus, Habitus paralyticus. 
The long, narrow and flat chest. A close relationship to 
heredity, a simple form of the hereditary chest, and the chest de- 
formity which gives evidence of a previous tuberculous process, 
a tuberculosis having preceded or accompanied this type of chest 
development. This form of chest, however, gives no absolute 
proof of any connection between the phthisical chest and tuber- 
culosis, because, as is well-known, tuberculosis is often, found in 
individuals with perfectly normal chests; nevertheless an etio- 
logical connection between this form of chest and tuberculosis 
must be admitted from the fact that pulmonary tuberculosis de- 
velops surprisingly rapid in chests hindered from free and 
full expansion because here the function of the lungs is hampered 
by physical disturbances, and such an unexpanded and illy ven- 
tilated lung, particularly that portion in the contracted upper 
aperture offers a nidus for the growth and development of the 
tubercule bacillus. The classic picture of this form of the con- 
tracted chest is due to a deficient blood and lymph supply and 
insufficient aeration, thereby furnishing a very favorable 
mechanical disposition to a tuberculous infection, which is early 
followed by active tuberculous diseases and speedy death. 
Thorax phthisicus embraces more or less nearly all the stig- 
mata of the stenotic and infantile type, with the addition of loss 
of fat, muscle degeneration, emaciation, cachexia, etc. 
The chest deformity generally known as “Habitus Phthisicus” 
was very early recognized and is even at length described in the 
writings of the ancients, who at that early time had noticed the 
fact that this condition predisposed to early tuberculosis. Such 
individuals are usually thin, slender and scrawny, sitting and 
walking much stooped, have but little if any adipose tissue, 
muscles are poorly developed and flabby, with a dry and pale INSPECTION 
113 
skin, throughout which, mainly over the anterior and upper 
posterior chest, minute venules are noticeable. The neck is thin 
and long, cheeks hollow and flushed, the chest flat and long from 
above down, and narrow from side to side, hands and arms 
emaciated, the face presenting a tired expression, and with uually 
long lashes the eye presents that condition known as the appeal- 
ing eye. 
(B) General Observation. Suspicious signs pointing to tuber- 
culous disease, past, present or future. 
Prima Vista Diagnosis. 
A first view impression or diagnosis. In itself a crude method, 
nevertheless pointing to some abnormality. The picture which 
impresses itself upon our mind when we see or examine the chest 
for the first time. If at this examination the chest is found ab- 
normal, especially the chest of the youth, it may correspond to 
one or other of the three types described above, or it may be a 
composite of all. Most signs as observed are those of a chronic 
condition of the lungs, healed or arrested lesions, or those of a 
functional disturbance consequent to a faulty chest development. 
However, abnormalities are also observable in some instances at 
the beginning of the pulmonary tuberculous process, particularly 
that of the slow or benign form. Singly, these signs may be of 
no value, but in correlation with others they bear evidence that 
at some time in the life of the infected individual a pulmonary 
disturbance, functional or otherwise, has taken place. The fol- 
lowing are some of the more important signs now generally 
recognized, a few of which have been previously mentioned in 
connection with the abnormal chest types described above. 
1. Chest measurements: 
a. Abnormal length. The measurement of the chest from the 
neck above to the costal margins below (the cranio-caudal 
measurement) is usually greater than normal (is longer). 
b. Abnormal diameter. The measurement of the antero- 
posterior diameter of the chest (The sterno-spinal measurement) 
is generally less than normal (is shorter). 
c. Abnormal circumference. The circumference of the chest 
as compared to body length is smaller than normal. (The cir- 
cumference should be at least one-half the body length.) 
2. Kyphosis. Slight or pronounced. Probably also a scolesosis 
(Kypho-Scoleosis) mainly of the upper dorsal area, may be pres- 
ent. 114 
CLINICAL TUBERCULOSIS 
3. Conspicuous and prominent protruding Ludwig’s angle. 
(Angulus Ludovici prominens.) 
4. Drooping of the shoulder on the involved side. 
5. Early ossification of the first cartilage and a secondary 
shortening of the first ring already described above. 
6. The clavicle. Abnormalities of this important landmark 
are most interesting. (54) The clavicle as a whole may be much 
displaced, may be very prominent or project conspicuously, or 
may remain fixed on inspiration. This usually is due to shrink- 
age of the cupula pleura and adhesion to the first rib. In chronic 
apical tuberculosis of one lung only the clavicle on the healthy 
side may be perfectly normal, showing a distinctly contrasted 
appearance as compared with the diseased apex. The sternal 
end of the clavicle may be noticeably lower over the affected 
than on the healthy side. This can be readily demonstrated by 
placing the index fingers of both hands on the sternal end of the 
clavicles when the difference between the healthy and the dis- 
eased side can be recognized. On the affected side the clavicle 
is lower. The acromial end may be much more prominent, 
showing many bony prominences and deep depressions above 
and below, as compared with the opposite, if healthy side, and 
the body of the clavicle itself as compared with its mate on the 
opposite or healthy side may be thicker than normal.1 
7. The supraclavicular and infraclavicular fossae. In old, 
chronic, healed or arrested cases, the fossa above the clavicle will 
be found abnormally deep as compared with the opposite side. 
If the other side has not been the seat of disease, the contrast 
will be particularly noticeable. Usually in such cases the de- 
pression below the clavicle (Mohrenheim’s fossa) will also be 
more prominent. 
8. Visible retraction, immobility, emaciation, muscular atrophy 
and flatness over the affected area. 
9. The intercostal spaces on the affected side will be found 
deep and narrow and the ribs overlapping and drooping. 
10. The cardiac impulse may be diffuse, rapid, circumscribed, 
or visible to the right of the sternum or displaced upwards. 
iThis thickness of the body of the clavicle and often of the sternal portion as well 
bears a close relationship to an old tuberculous process in the apex. If both apices 
have for some time been the seat of tuberculous disease and the involvement of one has 
been secondary upon a slow and chronic process in the other, then the clavicle over that 
apex which was the seat of primary lesions will be the thicker. Also the clavicle on the 
affected side will be found to slope more than its mate on the healthy or opposite side. INSPECTION 
115 
11. The epigastric or subcostal angle. This angle which in 
the normal chest is usually broad and wide, filled by the ab- 
dominal muscles and the viscera in the tuberculous chest is found 
to be narrow and high, showing more or less contraction of the 
soft parts, giving the costal margins and the ribs usually a 
prominent appearance. 
12. The tenth, a floating rib. Costa fluctuans decima. The 
ribs from the first to the sixth are attached to the sternum each 
by its separate cartilage and the seventh, eighth, ninth and tenth 
by a common cartilage. In some individuals this tenth rib is not 
attached to this cartilage, is free from all connection with the 
sternum, similar to the eleventh and twelfth, hence such persons 
possess three floating ribs instead of only two as is the general 
rule. According to Stiller, people with such an abnormality gen- 
erally suffer from tissue relaxation, nervous dyspepsia, neuras- 
thenia, from enteroptosis, gastric immotility, the stomach is 
never empty and splashing sounds are often elicited, in short, 
they suffer from general asthenia, a constitutional anomaly, and 
consequently fall easy prey to accompanying tuberculous com- 
plications (a habitus asthenicus.) 
13. The Scapulae. The scapula on the affected side may show 
undue prominence and flare outward, giving it a winged appear- 
ance, the scapula alata, or may approximate closely towards the 
median line. In the beginning of the tuberculous process the 
rhomboideus may be in a state of spasticity and this condition 
has a great tendency to push the scapula outwards; with the con- 
tinuation of the disease muscle relaxation follows in the usual 
train, the muscle degenerates and having lost its tone the scapula 
nowT lies passively by the side of the spine. This again denotes 
an old or chronic process. 
14. Respiratory Excursion. A more or less pronounced lag- 
ging of the affected side on deep inspiration is noticeable in all 
chronic forms of tuberculosis. In a recent tuberculous involve- 
ment, lagging of the affected side will be often observed if an 
inflamed pleura mechanically interferes with free breathing, the 
patient suppressing the respiratory movements on the affected 
side as much as possible. 
15. Veins and Venules. Enlarged veins over the anterior 
chest wall, (compression of vena azygos) prominent venules pos- 
teriorly on the upper chest on one or both sides of the spine and 
above the spine of the scapula and over the anterior chest on 116 
CLINICAL TUBERCULOSIS 
either or both sides of the median line over the 6th, 7th and 8th 
ribs and interspaces and towards the axillae are evidence of pul- 
monary stasis. If veins are enlarged or venules prominent, uni- 
laterally they present strong diagnostic evidence of either pul- 
monary disease or mediastinal gland enlargement. 
16. The Mammae and the Nipples. In the male the nipple is 
found in the 4th interspace normally, and with contraction of the 
chest, consequent to tuberculous disease, the nipple may be dis- 
placed. The mammae in the female modifies conditions, depend- 
ing upon the size. Here, usually, we find the mamma on the 
affected side smaller and less developed than the one over the 
healthy side, the nipple itself is smaller and less fully developed 
and the areola also is smaller and is less pigmented over the 
affected side. 
17. The Pupil. The pupil is often dilated on the affected side. 
Apical pleurisies accompanying apical tuberculosis, or enlarged 
tuberculous glands causing irritation or pressure upon the fibres 
of the sympathetic nerve, is usually the cause of this dilitation. 
18. Red Line along the Gums. (Steger) As evidence of 
toxicity. A red line is sometimes seen in tuberculous individuals 
following the gums, similar to the blue line in lead or the black 
line in bismuth poisoning. Its significance is not well under- 
stood. 
19. Muscular Spasticity and Atrophy. (Pottenger’s Sign.) 
In beginning tuberculosis the various muscles of the upper 
chest, those overlying the pulmonary tuberculous process, like 
the trapezi, the pectorals, the sterno-cleido mastoids, the Sca- 
leni, the rhomboidei and others are often found in a state of 
spasticity. This muscular rigidity persists until the tuberculous 
condition has lasted for some time, when a change in the muscle 
substance takes place and the fibers undergo degenerative 
changes which in chronic cases are evidenced by distinct atrophy 
clearly visible on inspection (and by palpation as well). 
20. Finger Nails. Distinct trophic changes are often notice- 
able in most cases of chronic pulmonary as well as cardiac 
lesions. In pulmonary tuberculosis which is assuming slowly 
the chronic form, distinct changes are observed, which begin 
with a slight hyperemia and then thickening and glistening of 
the nail matrix. The nail then gradually assumes an antero- 
posterior curve similar to the lateral, a gradual thickening of the INSPECTION 
117 
bulbs of the finger ends until the fingers are curved, cyanotic, and 
enlarged, being then described as “clubbed” fingers. 
21. Skin and Hair. The skin in the tuberculous person has 
also undergone some changes, taking part in the general trophic 
disturbance incident to the disease. The skin is usually pale, 
and anemic, or slightly yellow or even brown and lichens, pity- 
riasis and psoriasis are not infrequent. The skin is dry to the 
palpating hand, has lost its moist and unctuous feel, is somewhat 
scaly, and may even feel feverish. The hair on the chest seems 
to appear disordered, irregular in growth, in children downy, 
showing a lack of luster, evidence of faulty nutrition and trophic 
changes. 
22. Mouth. In examining the mouth by inspection, one is 
often impressed, in young individuals suffering from tuberculosis, 
that the palatal arch is unusually high. This is akin to those 
nose and mouth disturbances incident to enlarged tonsils, adenoid 
vegetations, or hypertrophic turbinates. These obstructions to 
the upper air passages often bring about faulty aeration, par- 
ticularly to the apex of right lung and thus favoring tuberculous 
disease. In addition, in active pulmonary tuberculosis, the 
uvula, soft palate and pillars are often pale and anemic. 
23. Litten’s Phenomenon. Absence of the phrenic shadow, 
or Litten’s Sign, a diminution in the excursion of the diaphragm 
on the affected side of the tuberculous. The phrenic wave, the 
peeling off of the diaphragm during inspiration. If a person with 
normal chest, lying on his back, chest bared to the waist, feet 
pointing towards a window, is asked to inhale, the examiner 
standing at the patient’s side will observe a narrow shadow in 
the axillary line from the seventh to the tenth rib, about 2 to 
2y2 inches of excursion, moving down with inspiration and again 
up with expiration. The absence of this shadow on either or 
both sides indicates some previous disturbance in the pleura or 
lung. In beginning tuberculosis the shadow is often diminished 
or absent owing to the lessened elasticity in the affected lung and 
probably also to pleuritic thickening and adhesions. 
24. Integument Atrophy. When an apex has become (64) 
tuberculously invaded, a peculiar phenomenon manifests itself 
as soon as the process is well established. Nature, here, as in 
every other form of tuberculosis, endeavors to put the parts at 
rest, and we notice that the fascia, subcutaneous fat, muscles, 
(Panniculus adiposus et carnosus), and integument, give way 118 
CLINICAL TUBERCULOSIS 
early to trophic changes. If, over the anterior chest wall in the 
parasternal line, we pick up the overlying skin with the thumb 
and middle or index finger and pull it towards us, we very 
readily observe that the tissue has entirely lost its elasticity, the 
skin feels lifeless, and we quickly notice that the amount of skin 
held between thumb and finger is perceptibly less when compared 
with the other, perhaps still healthy side. If both sides are the 
seat of tuberculous involvement, the greater amount of atrophy 
Fig. 11. Integument Atrophy. (Demonstrating Integument Atrophy.) 
will be noticeable over the apex which was the seat of primary- 
disease. (This is particularly noticeable when we combine In- 
spection with palpation.) Wheaton directed attention to this in- 
teresting- phenomenon as early as 1910. 
25. The phthisical facies. Last, the facial expression of the 
phthisical subject, the usually characteristic oval face, the 
pinched features, the dilated pupils, the whitish-blue sclera and 
the appealing eyes must be mentioned. In such a picture one 
can readily observe in one’s mind the rapid, shallow, unconscious 
breathing all bespeaking the gravity of the disorder. CHAPTER 14 
PALPATION 
Definition: The word Palpation as defined means to feel with 
the hands or with the tip of the fingers, the laying on of the 
hands; in practice it is the application of the examiner’s hand, 
hands or fingers over various parts of the chest wall of the 
patient, the patient being asked to speak at the same time. It is 
next to inspection the most important method of physical exam- 
ination when the hand is placed flat on the chest wall of the person 
to be examined and the patient is then asked to speak or count out 
loud, a peculiar vibratory sensation is communicated to the 
palpating hand. This is usually described as fremitus, thrill or 
tactile fremitus or more correctly as vocal fremitus. Normally, 
if the palpating hand is applied, this vibratory murmur is felt 
with more or less intensity over certain areas and entirely absent 
or nearly so over others. All things being equal, in palpation 
much depends upon the voice of the individual to be palpated. A 
high pitched voice will give little or no fremitus whereas a low 
pitched voice will produce a fremitus which is palpable over the 
greater part of the whole chest and it is because of the voice that 
women and children usually give less vocal fremitus than do 
men. The more sonorous the voice the greater and better the 
vocal fremitus and vice versa. 
Methods of Palpation 
The simplest method of practicing palpation, the one most in 
vogue, is by applying the palm of the hand firmly against the 
chest wall, at the same time asking the patient to count aloud 
and repeatedly, 1, 2, 3 or 99 or 66. It is essential that the hand 
be placed firmly against the chest wall, allowing no hollow space 
between the palpating hand and the thoracic wall. Another 
method in great favor with many is to palpate with the lateral 
margin of the hand along with the little finger while the patient 
counts or speaks. Still another method and one which I consider 
of particular importance because of its subtle manner is finger 
palpation. This is practiced, and is particularly applicable in 
the examinations of small infiltrated areas in the apices of the 
119 120 
CLINICAL TUBERCULOSIS 
lungs, by placing the thumb of the right hand over the right 
upper and posterior lobe of the lung of the patient to be exam- 
ined, the thumb of the left over the left upper, the right and left 
index finger in the right and left supraclavicular fossae, respec- 
tively, and the middle finger of each hand placed in the depres- 
sions below the clavicles. If the patient now is asked to speak 
while the fingers are in this position, a peculiar but definite sen- 
sation is imparted through the palpating fingers. This is espe- 
cially acutely noticeable over the upper and posterior chest 
through the palpating pulp or ball of the thumb. Another 
method of palpation often practiced is by grasping the upper 
apices posterior with the ball of either hand resting firmly against 
the muscular tissue above the spine of the scapulae, the fingers 
firmly grasping the tissue above or below the clavicles. In prac- 
ticing palpation by this method, a method in high favor by many 
lung specialists, while the patient is asked to speak, the apices are 
firmly grasped, at the same time making slight pressure with the 
palpating fingers toward the ball of the hand. All the above 
mentioned methods are usually known as immediate palpation 
in contra-distinction to mediate palpation, that is by means of a 
media between the chest to be palpated and the palpating ob- 
server. Mediate palpation is also known as osteal palpation, and 
for sensitiveness as a method of palpation it has no equal. 
Mediate or osteal palpation is generally practiced by the examin- 
ing physician, either sitting or standing behind the patient, plac- 
ing the hand over the upper chest, over the apex, and then plac- 
ing his forehead directly and firmly upon his hand, at the same 
time asking the patient to speak or count aloud. By this method 
a distinctly definite and sharp vibratory sensation is communi- 
cated to the forehead through the hand and even the slightest 
variation in the two sides can most readily be recognized by this 
method. Fremitus is often described as subjective and ob- 
jective; subjective as observed by the patient himself and ob- 
jective, that which is elicited by the palpating hand of the 
physician. 
Palpation of the Normal Chest. As a coarse, sonorous voice 
will give an amplitude of sound waves of greater intensity and 
larger volume than a high and feeble voice, it becomes evident 
that the fremitus must be greatly influenced by different voices. 
The fremitus is also greatly influenced by the thickness of the 
muscular development, by the amount of adipose tissue, whether PALPATION 
121 
the chest to be examined is that of a fat or fleshy or that of a 
thin and scrawny person, whether the chest be that of a child or 
of a woman or that of a man old or young, hence, the voice, the 
sex, the age, the chest formations, all must be considered while 
practicing palpation. 
In placing the palpating hand on the normal chest, the vi- 
bratory impulses imparted to the hand differ over different areas. 
Usually the fremitus is most pronounced and definite over the 
right chest, both anterior and posterior, and over the right apex 
more than over the other portions of the lung, and over the left 
lung the fremitus is usually much in abeyance or may be entirely 
wanting or only slightly felt over the apex. Various reasons are 
given for the greater fremitus over the right as compared with 
the left side. (1) The greater number of right handed people 
and thicker muscular development; (2) the larger lumen of the 
right bronchus; (3) the more direct access of air and sounds to 
the right upper lobe; (4) the usually somewhat contracted upper 
right lobe, the right apex being more conical and the left more 
dome shaped (see Figs. 14 and 15); (5) the right lung lies in closer 
proximity to the trachea and larynx than does the left; (6) the large 
organ at the base of the lung, the liver, acting as a sounding board, 
etc. 
Palpation of the Abnormal Chest (17). The normal lung, as 
we observe it, is usually a poor conductor of sounds, and any- 
thing which will replace the air contained in the alveolar cells, 
bronchials and small bronchial tubes by solid or semi-solid ma- 
terial will convert it into a better conductor. If the parenchyma 
of the lung becomes airless, the normally inhibitive influences of 
the sound conveying conditions are lost and in place of a poor 
sound conducting medium we now have one which is a fairly 
good conductor, the conduction depending more or less upon the 
amount and extent of airless lung structure. The more intensely 
airless this air contained area is made, the more pronounced is 
the tactile or vocal fremitus, and anything which will make a 
good conductor out of the normally poor conducting lung tissue 
will in that proportion increase the fremitus. 
In palpating a lung or an apex to ascertain the extent of in- 
filtration or involvement of the underlying lung structure, it is 
equally important that in addition to observing the fremitus we 
note also most carefully the amount of resistance. An infiltrated 
condition of the lung will generally be accompanied by a vocal 122 
CLINICAL TUBERCULOSIS 
fremitus and an increased muscular resistance, and if an area 
of the thorax which under normal conditions is negative as to 
fremitus should give an increased resistance and a vocal fremitus, 
that is always a sign of a pathological lesion. The fremitus being 
normally greater over the right upper lobe, if in a given case the 
fremitus is greater over the left apex or if only equal to that of 
the right or apparently equal, then we have positive evidence of 
left sided apical involvement, and if, in addition, the palpated 
muscles are more rigid on the one side and more relaxed over 
the other, then we most likely have additional evidence that on 
the one side over the rigid muscle the process is probably active 
whilst on the side where the muscle is relaxed the process is old 
or arrested. If an apex is infiltrated only recently, is not a very 
old process but an active one, then all the muscles over and 
about this active area are in a state of spasticity, and we find the 
sterno-cleido-mastoids, the scaleni, the intercostals, in a less de- 
gree the pectorals anteriorly, and posteriorly the trapezi the 
rhomboidei, the levator anguli scapulae all more or less resistant 
to the touch. This spastic condition may last for some time, being 
more prolonged if the pulmonary process is slow, but ultimately 
the muscle rigidity will lessen and later degenerative changes 
will appear, and then to the palpating finger a sense of lessening 
of resistance, a lack of muscle tone, is imparted until gradually 
the muscle becomes more and more relaxed and now nothing 
remains but a few fibrous bands. The muscle spasm (35) or 
rigidity noticed in many conditions of acute inflammation of 
various organs of the body, for instance, the rectus over an acute 
appendicitis, the various abdominal muscles over an acute pan- 
creatitis and the muscle spasm so frequently observed in acute 
bone and joint disease are all of like nature. In these conditions 
the muscle spasm is more readily observable because the onset 
is more acute, is sudden, whereas in a tuberculous infiltration of an 
apex the process is slow, protracted, even chronic and insiduous, 
and the condition of the overlying muscles often goes unnoticed. 
In pulmonary tuberculosis which in the greater number of 
instances begins in the apices, the right more frequently than the 
left, an increase of the vocal fremitus is most important in diag- 
nosis. If an individual with an apparently normal chest and 
pitch of voice not too high or low be asked to count 1, 2, 3 or 
repeat 33, 66 or 99, a very distinct fremitus is conveyed to the 
palpating hand or finger, and if wrhile comparing the fremitus of PALPATION 
123 
one side with that of the other we notice a distinct difference in 
the normal relationship of the two sides, if there is a plus fremi- 
tus, a fremitus more than normal, and if at the same time the 
overlying- or contiguous muscles are in a state of spasticity or 
rigidity or perhaps the muscles over the side where the fremitus 
is increased have already become soft and relaxed, again we 
have evidence which points to a tuberculous process active, 
recent, old or arrested, depending upon the area over which we 
find spasticity or degenerative changes. Fremitus over the base 
of the lung is felt most distinctly when the lower lobe, either 
right or left, is the seat of inflammatory changes, and here also 
muscle resistance and relaxation are noticeable, and the inter- 
costals being either stiff and spastic or distinctly relaxed and 
soft, depending on wdiether the pulmonary process is early, recent 
or late. 
Painful and tender points. In some instances of beginning 
pulmonary tuberculosis as well as in some cases in which the 
process has existed for some time, perhaps a long time, espe- 
cially if the seat of the disease is in one apex, pain can be often 
elicited by the palpating finger. Begin palpation with the tip of 
the index or middle finger at the lower angle of the scapula and 
by making gentle pressure follow along the inner margin, up- 
wards to the spine of the scapula, and in the course a point may 
be reached which is more or less painful. If, while making light 
pressure, a strict watch is kept to see the expression on the face 
of the individual being examined, we can often observe that 
when a certain spot is reached there is a sudden expression of 
pain, the person seeming to flinch. The painful spot is usually 
permanent, is usually posterior over either the right or left apex 
or it may be demonstrated over both apices. With the palpating 
finger following up along the scapula, first on one side then on 
the other, this phenomenon can easily be elicited. This sensa- 
tion of pain, hyperesthesia or algesia, the demonstration of 
which is described as algoscopy, is usually due to an apical 
pleuritis which often accompanies the tuberculous process. 
In the early beginning of tuberculous infiltration, due to the 
collapsed condition of the air cells surrounding the initial tuber- 
culous process, the vocal fremitus may be somewhat decreased 
as it is also in the old and chronic form of the disease when the 
pulmonary tuberculous process is accompanied by much con- 
traction. The fremitus also is often found to be decreased owing 124 
CLINICAL TUBERCULOSIS 
to the emphysematous condition of that portion of the lung 
surrounding the contracted tuberculous area. 
If while palpating the chest of the patient, he has a fit of coughing, 
then frequently a peculiar sensation is carried to the palpating hand; 
this is known as tussic fremitus. If he is suffering from much secre- 
tion in the bronchial tubes or a bronchitis, then the respired air 
passing through the tubes will produce a murmur which is im- 
parted to the palpating hand and this is described as rhonchial 
or bronchial fremitus. In practicing palpation it is most im- 
portant always to remember that the palpating hand must lie 
firmly against the chest wall of the person to be palpated. 
Attention should here be directed to the fact that in muscle 
spasm demonstrable at the apices that the upper border of the trap- 
ezius extending from the occiput down to the shoulder feels 
thicker, more spastic to the fingers, and that in grasping the 
thickened upper border between the thumb and the index or 
middle finger, a perceptibly larger amount of muscle tissue is 
noticeable as compared with the opposite or still unaffected 
side. It seems as if the palpating fingers pick up a greater 
volume of muscle tissue and integument in a given time. CHAPTER 15 
PERCUSSION 
Percussion as practiced as an aid to physical diagnosis con- 
sists in gently, striking or tapping the chest wall, either directly 
or indirectly, by means of the tips of the fingers, with a force 
sufficient to throw into vibration the underlying structure to be 
examined. The method of percussion as applied in the examina- 
tion of the chest is of comparatively recent adaptation, and, 
although percussion had been practiced in various industries for 
many years, as, for instance, the carpenter percussing the wall 
with a hammer in looking for a suitable place to drive a nail, 
etc., it was not until 1761, that Leopold Auengrubber of Vienna, 
in a classic description, first clearly defined this method of phy- 
sical examination. With the aid of percussion it is possible to 
outline perfectly, on the outer chest wall, the apices of the lungs 
and the heart, the large blood vessels and the anatomical borders 
of the healthy, as well as the diseased lung, and by the nature of 
the sound elicited to determine the density of the parts per- 
cussed. (2) (4) 
Topography of the Thoracic Organs. (31) A study of pul- 
monary tuberculosis or of the general pathology of the lungs 
presupposes a thorough knowledge of the position of the normal 
lungs within the chest cavity, and the ability to outline on the 
thoracic wall the various parts of the lungs, the position of the 
heart and its borders, the divisions and the borders of the lungs 
on inspiration, on expiration, etc. In order to simplify this study, 
the chest is primarily divided into the anterior, the posteror, and 
the two lateral surfaces, each again being arbitrarily subdivided 
in order to facilitate memorizing of the parts and convenience 
of study. 
The anterior surface of the chest wall is divided and sub- 
divided by a series of lines from above downwards, intersected 
at right angles from side to side. A line drawn from the supra- 
sternal notch over the center of the sternum down to the ensi- 
form cartilage and beyond is known as the midsternal line. This 
line divides the chest into equal halves, the right and the left. 
125 126 
CLINICAL TUBERCULOSIS 
A similar line drawn parallel and following the junction of the 
ribs with the sternum is designated as the costo-sternal line, and 
another line from the middle of the clavicle down to the lower 
costal border and through the nipple is generally known as the 
mid-clavicular, mammary, or nipple line, an outer line dropped 
from the shoulder down to the lower margin of the ribs, parallel 
Mid-sternal 
line 
Costo-sternal 
line 
Supraclav- 
icular area 
Parasternal 
line 
Infraclav- 
icular area 
Midclavicular 
line 
Anterior 
Lower border 
third rib 
Axillary line 
Mammary 
area 
Lower border 
sixth rib 
Inframam- 
mary area 
Fig. 12. The topographic area of the thorax (Anterior). The areas of the lungs as 
outlined on the anterior chest—right and left. 
A. 1. 1. 1. 1. Infraclavicular area. The clavicle above, third rib below, costo-sternal line 
inner and anterior axillary line outer. 
B. 2. 2. 2. 2. Mammary area. Third rib above, sixth rib below, costo-sternal line inner 
and anterior axillary line outer. 
C. 3. 3. 3. 3. Inframammary area. Sixth rib above, costal arch below, costo-sternal 
line inner and anterior axillary line outer. 
to the nipple line, and about 10 cm. to the outer aspect is called 
the anterior axillary line, and a vertical line midway to the 
mammary or nipple line and the costo-sternal line, is spoken of 
as the para-sternal line. All these parallel lines are intersected 
at right angles by two horizontal ones, one on a level with the 
lower margin of the third rib, the other that.of the sixth rib, and 
these two lines with the parallel mid-sternal and anterior axillary 
lines divide the anterior chest into six nearly equal divisions, PERCUSSION 
127 
three on either side, a right and a left upper infraclavicular, a mid- 
dle or mammary, and a lower or inframammary area. 
The posterior surface is divided as follows: a vertical line 
along the center of the spine divides the posterior chest into two 
equal halves; this line is designated as the vertebral line. An- 
other line drawn from the middle of the shoulder down and 
Midspinal or 
midvertebral 
line 
Para vertebral 
line 
Mid-scapular 
line 
Posterior 
axilliary line 
A. Suprascap- 
ular area 
Suprascapu- 
lar line 
B. Scapular 
area 
D. Interscap- 
ular area 
Infrascapular 
line 
C. Infrascap- 
ular area 
Basel line 
(ribs) 
Fig. 13. The topographic area of the thorax, posterior. The area of the Lungs as out- 
lined on the posterior chest, right and left. 
B. 2. 2. 2. 2. The scapular area. From the spine of the scapula to the angle of the 
scapula and from the paravertebral line to the posterior axillary line. 
C. 3. 3. 3. The infrascapular area. From the angle of the scapula to the lower bor- 
der of the lungs and from the vertebral line to the posterior axillary line. 
D. 4. 4. 4. 4. The interscapular area. From the line along the spines of the scapulas 
and the line horizontal to the angles of the scapulae and the paravertebral lines right and 
left, (or more correctly the area between the inner margins of both the right and left 
scapulae). 
parallel to the vertebral, to the angle of the scapula, is known as 
the scapular line, a line from the shoulder along the axilla, the 
posterior axillary line, and a line midway and parallel to the 
vertebral and mid-scapular line, the paravertebral line. These 
posterior thoracic lines are intersected at right angles by an 
upper one along the spines of the scapulae, and a lower one on a 
level with the angles of the scapulae. These lines divide the 128 
CLINICAL TUBERCULOSIS 
posterior surface of the chest also into six but unequal divisions, 
a right and left upper, or supra-spinous, a mid-scapular, and a 
lower or infrascapular. The area between the inner borders of 
the scapulae on either side and from about the first thoracic spine 
down to the seventh; or eighth is also known as the interscapular. 
The lateral surfaces of the chest wall on each side are divided 
by a horizontal line along the lower border of the sixth rib, the 
anterior axillary line of the anterior division of the chest, and 
the posterior axillary line of the posterior division, forming the 
vertical boundary lines of this area; this area is again divided by 
a vertical line through the center, the “mid-axillary line.” These 
lines divide the axillary area into the supra-axillary, the area 
above the sixth rib, a right and a left, and all that portion below 
this rib into the infra-axillary, also a right and a left. 
The area over the sternum anteriorly is divided into the upper 
sternal, mid-sternal, and xiphoid, and by the mid-sternal line into 
a right and a left sternal. 
The triangular area above the clavicle is known as the supra- 
clavicular, bounded by the clavicle below and inside by a line 
running upwards and outwards along the border of the sterno- 
cleido-mastoid muscle; the outer margain of this triangle is a 
line running from the middle of the clavicle upwards and in- 
wards, meeting this first mentioned line about two inches above 
the clavicle. This area is occupied on either side by the apices 
of the lungs; the right apex is supposed to be slightly lower 
than the left, although this is considered pathological by some. 
An area on either side bounded above by the clavicle, below by 
the lower border of the third rib, internally by the costo-sternal 
line, and externally by the anterior axillary line is known as the 
infraclavicular area in which pure lung structure is found. 
The area from the lower border of the third rib to the lower 
border of the sixth, and from the costo-sternal line to the anterior 
axillary line is the mammary area. This area on the right is 
covered by lung structure throughout, the dome of the liver ex- 
tends into this area as high as the fourth rib, still covered by lung 
tissue, and on the left side in this area the heart lies super- 
ficially, being only partly covered by lung tissue. That part of 
this area between the heart and the anterior axillary line is 
covered by normal lung structure. The area below the sixth rib 
on either side and as far as the lower costal arch, is the inframam- 
mary; and here the right side is covered by the liver, very little if PERCUSSION 
129 
any lung structure extending below the sixth rib, and on the left 
by the stomach, where Traube’s crescent shaped space can be 
demonstrated. Posteriorly in the area above the spine of the 
scapula, the supra-scapular, over the scapulae, the scapular, be- 
Fig. 14. The viscera of the thoracic cavity right side (R) in situ. Note that the apex 
of the right lung is conical. 
tween the scapulae, the interscapular, and below the angle of the 
scapulae, the infra-scapular, and extending from the first dorsal 
spine above to the tenth rib below, is normal lung tissue covered 
by the bony and fleshy structures of the posterior thoracic wall. 
In the axillae both right and left that part known as the supra- 130 
CLINICAL TUBERCULOSIS 
axillary above the sixth rib is covered by lung structure, and 
the area below the sixth rib on the right side by the liver, on the 
left by part of the stomach and the anterior portion of the spleen 
between the ninth and eleventh ribs, the posterior portion lying 
Fig. 15. The viscera of the thoracic cavity left side (L) in situ. Note that apex of the 
left lung is dome shaped. 
in the left infra-scapular area. The lung's themselves, as stated 
above, are usually divided into the right and the left lobe, the 
right being again divided into an upper, middle and lower, the 
left into an upper and a lower. These divisions, dividing the 
lobes of the lungs into smaller lobes, three on the right half, and PERCUSSION 
131 
two on the left, are known as the fissurae or incisurae, the in- 
cis.urae interlobares, and they begin posteriorly on either side of 
the spine on a level with the cartilage between the second and 
third thoracic vertebrae, the right fissure or incisor running for- 
ward and downward in the right axillary area along the fourth 
rib, then dividing, the short branch following the course of the 
rib, terminating at the edge of the lung just behind the junction 
of the rib with the sternum, the other, the longer branch running 
downward, forward and inward, terminating opposite the mid- 
clavicular line, these fissures thus dividing the right lung into an 
upper, a middle, and a lower lobe; on the left side the fissure 
begins opposite the right, and running forward and obliquely 
downward, terminates near the lower border of the lung behind 
the parasternal line, dividing the left lung into an upper and a 
lower lobe. The lungs normally extend about an inch and a 
half to two inches above the clavicles, the left a trifle higher than 
the right, the lower margin extending in the mammary, or mid- 
clavicular line to the sixth rib in the midaxillary, to the eighth, 
and in the scapular to the tenth rib, the complemental pleural 
space about two inches below the margin of the lungs, and with 
the exception of a small portion of the left mammary area which 
is occupied by the heart, the lungs fill all this cavity, or at least 
the lungs lie in close contact with the entire surface of the 
thoracic wall. 
The Borders of the Lungs. On the posterior chest wall the 
inner border of both the right and the left lung extend parallel 
on either side of the spine from the tenth rib upwards to the 
second thoracic vertebra, from which points they deviate, run- 
ning upwards and outwards, reaching the highest point on a line 
opposite the lower margin of the vertebra prominence. The an- 
terior borders of the lungs in the supraclavicular area corre- 
spond closely to the outer margin of the sterno-cleido-mastoid, 
on either side extending downwards and inwards, converging to 
a point opposite Ludwig’s angle or a trifle below, whence they 
run parallel to the fourth rib, the right continuing down to the 
sixth and joining the lower border on a level with the mid- 
clavicular line, the left border at the fourth rib running outward 
and downwards, leaving the heart exposed, then turning inwards 
and downwards, joining the lower margin on a level with the left 
mid-clavicular line. This lapet of lung structure at this point is 
described as the Lingula Pulmonalis and the depression or 132 
CLINICAL TUBERCULOSIS 
hollow where the heart is free is known as the cardiac depression 
or hollow indentation. (Incisura Cardiaca.) 
Methods of Percussion. As in all other methods of chest exam- 
ination, so also while practicing percussion the patient must be 
in an easy and comfortable position. The anterior chest wall is 
best percussed with the patient in a sitting or standing position, 
the arms hanging leisurely by the side of the body; for posterior 
percussion the patient either sits or stands, with arms folded 
over the chest or resting in the lap, the body leaning slightly 
forward; for lateral percussion the patient’s arms should be rest- 
ing upon the head. 
Percussion is usually practiced by gently striking or tapping 
the thoracic wall with the tip or tips of the fingers, at the same 
time listening carefully to the sound produced, and noting the 
resistance offered to the percussing fingers. If the chest wall is 
tapped directly with the finger, like in striking the clavicle with 
the tip of the finger, it is known as immediate percussion; if, 
however, something is placed between the chest and the percus- 
sing finger, and the blow directed upon this, it is known as 
mediate percussion. Immediate percussion is now only applied 
when percussing the clavicles; over all other portions of the 
chest mediate percussion is practiced. The usual instruments 
necessary for mediate percussion are the plexor or hammer, and 
pleximeter or anvil; however, the best and simplest means al- 
ways at hand, is to make use of the middle finger of the left hand 
placed in close contact with the_ thoracic wall as a pleximeter, 
using the middle finger of the right hand bent at right angle at 
the second joint as the plexor or hammer. Some examiners 
use the index, middle, or ring finger, or may use two or three 
fingers jointly as a plexor. 
In beginning to percuss, the student should always remember 
to percuss very lightly at first, to practice light percussion at 
all times; heavy percussion is needed only if the area to be per- 
cussed and to be vibrated is deep seated, or we have reason to 
suspect that healthy lung tissue overlies an infiltrated area which 
we wish to throw into vibration. If a small infiltrated area 
should lie near the surface and much healthy lung tissue below 
this, then heavy percussion would vibrate this healthy tissue, 
and we could not gain a clear conception of the tissue overlying 
the healthy lung. Percuss lightly and with a force sufficient to 
vibrate the underlying tissue at a depth and a circumference of PERCUSSION 
133 
about 5 to 8 cm.= 2 or 3 inches, and if in doubt about the area 
being more deeply involved, resort to heavy percussion. On the 
average, we find that most physicians percuss too heavily, 
but long experience in teaching has convinced me that the 
proper way of percussing can only be acquired by long practice, 
like all the other methods of physical examination. It is most 
important here to again remind the student in physical diagnosis 
that in the science of percussion it is necessary to carefully note 
the sound elicited, as to its pitch, quality, duration, etc., and the 
amount of resistance offered to the percussing finger. 
Percussion of the Normal Chest. It might not have been 
necessary to have gone into details of how to percuss, as the 
technic is supposed to have been sufficiently mastered by all, 
while students in physical diagnosis. The object of giving the 
method of percussion here at some length is intended simply to 
refresh the memory of the student or physician who is doing 
tuberculosis work, to again remind him of the conditions of these 
sounds which he is expected to find over normal lung tissue, and 
to enable him to compare these sounds and the resistance, if any, 
with the sounds produced by the altered condition of the lungs, 
the tuberculous infiltrate. 
Always begin percussion on the anterior chest wall, left side, 
just below the clavicle, in the mid-clavicular line. The note 
which is there elicited on percussion is called the normal reson- 
ant; it is soft and low in pitch, accompanied by a certain degree 
of resiliency. It is the given individual’s most resonant note, 
more so at this point than over any other part of the thoracic 
wall. This normal resonant note obtained below the left clavicle 
should at once be compared with the note obtained over the 
corresponding area below the right clavicle, and the difference 
noted; here the note although resonant is normally found some- 
what higher in pitch, and slightly more resistant. Next by im- 
mediate percussion tap the left clavicle above this point and at 
once compare it with a similar point on the right clavicle, and 
again note the slight difference in pitch and resistance and now 
percuss tfie lung apices above the clavicles, first the left apex, 
and then the right, and again note the normal differences. Next 
percuss the left chest below the clavicle down to the third rib, 
mid-clavicular line, and then compare it with its mate the right. 
Throughout the whole upper portion of the left lung and down 
as far as the third rib this normal resonant note will appear soft, 134 
CLINICAL TUBERCULOSIS 
and the tissue slightly more elastic to the touch, than that of 
the right. As each individual has his or her own special note, we 
cannot know in advance what that normal note is, nor can this 
note be described, but must be learned in each new case by com- 
paring the left most normal with the right less normal area. 
Each individual has a resonant percussion note distinct and 
definite. A percussion note of the greatest acuity can be elicited 
in the spaces between the heads of the sterno-cleido-mastoid 
muscles, just above the sternal end of the clavicles. Here per- 
cussion must be practiced in the direction of the lungs, and not 
towards the trachea. Insert the tip of the middle finger of the 
left hand between the heads of the muscles, the finger being bent 
at right angle at the second joint, as a pleximeter, and with the 
middle finger of the right hand as a plexor, percuss upon the 
knuckle of the inserted finger, keeping the finger well in the direc- 
tion of either the right or left shoulder. The slightest difference 
in the percussion note, here directly upon the lung tissue is then 
very readily discernible. The normal difference in the percussion 
note of the left and right sides, as well as the normal difference 
of the same side, may readily be observed, next by percussing 
first on one side and then on the other, beginning at the median 
lung border below the clavicle near the sternum and percussing 
outward and towards the shoulder along a line below the clav- 
icle. A perceptible but normal difference is then observed, being 
higher towards the shoulder but lower towards the sternum. 
Percussion sounds may be much enhanced by placing the patient 
whose chest we desire to percuss with his back against a door, 
hollow wall, or anything which may act as a sounding board, 
when by fairly heavy percussion the difference between the two 
sides is distinctly noticeable. 
After having percussed the left apex anteriorly and having 
compared the note obtained with that of its mate on the opposite 
side, the right apex, percuss the left lung from the apex down to 
the lower margin about to the sixth rib, first along the mid- 
clavicular line, and then along a line midway between this and 
the anterior axillary line. In the mid-clavicular line a change of 
note is observed below the fourth rib, where the heart is first en- 
countered deeply situated, the note still having a resonant qual- 
ity but becoming more and more dull with continuous downward 
percussion, and gradually completely flat where the heart lies 
superficially and as the area over the heart is passed, the note PERCUSSION 
135 
again changes now to tympany, indicating the location of the 
stomach. The percussion note from the apex of the left lung 
down to the lower border along the line parallel to the anterior 
axillary line is usually clear and resonant, and though slightly 
modified by the proximity of the heart and the stomach below, 
and over the right half of the chest anteriorly, as already has 
been stated, the note is slightly higher, on percussion from 
above down, when at the fourth rib, the note changes, becoming 
higher on fairly firm percussion, where the dome of the liver lies, 
deep and continuing percussion downward the note gradually 
blends into flatness or complete absence of resonance over the 
liver at the lower margins of the lungs. We next percuss the 
posterior thorax, beginning at the upper part of the chest along 
the paravertebral line from above down to the lower margin of 
the lungs, usually on a level with the tenth rib, percussing first 
over the left, then over the right lobe, and here, as on the anterior 
chest wall, the difference over the two sides is again apparent, 
the note being more resonant, less high, softer, but resilient 
over the left and less so over the right, where it is slightly less 
resonant, somewhat higher, and less resilient. 
In percussing the axillary area, the spleen is encountered at the 
left, between the ninth and eleventh ribs, extending anteriorly as 
far as the midaxillary line. Over this area the note is flat, but 
being resonant over all the other portion and over the right ax- 
illary area it is slightly higher, changing to flatness at the lower 
border where the liver lies superficially. In percussing the upper 
axillary area, high up in the axilla, the method in use on the 
anterior chest, as between the heads of the sterno-cleido-mastoid 
muscles, should be practiced, putting the tip of the middle finger 
of the left hand as a pleximeter well up into the axillary 
space. (44) 'Deep inspiration and full expiration greatly modify 
the percussion note, making it more resonant, even tympanitic on 
full inspiration, and correspondingly less resonant, slightly 
higher on expiration. The student should always bear in mind 
that in the normal over all that area over which lung tissue lies 
in close proximity to the walls of the inner thoracic cavity, a 
normal resonant percussion note can be elicited, modified by the 
overlying bony structure, by the sternum anteriorly, and the 
scapulae posteriorly and by the region over the heart, liver and 
spleen. He should also remember that this percussion note finds 
its most normal and natural expression over the apex of the left 136 
CLINICAL TUBERCULOSIS 
lung, particularly anteriorly below the clavicle, that over the 
right apex a mixture of resonance with dulness can always be 
elicited as normal, that the excursion and aeration of the upper 
apices of the lungs, especially the right, is usually very slight, 
that in the respiratory movements the apices expand only a few 
millimetres, that the excursion is mainly in a lateral and ante- 
rior direction, and that it is over this area that the percussion 
note can best be studied; and that posteriorly in the adult the 
lung extends upward on a level with the spinous process of the 
first dorsal vertebrae but that in the newly born the apices lie 
somewhat lower, more on a level with the tracheo-bronchial 
lymph glands. 
Percussion, of the Abnormal Chest. A tuberculous process 
consists either in the filling up of the alveolar spaces with an 
inflammatory exudate, as in beginning or acute disease, or in 
fibroid changes gradually taking place in the pulmonary tissue, 
as in the chronic form. This lessens the normal air content of 
the lungs, in consequence of which the normal resonant, low, 
soft, full percussion note becomes less intense, but shorter and 
higher in pitch. If the tuberculous process is not extensive, as 
is frequently the case, the surrounding healthy lung tissue may 
become collapsed and be then accompanied by a tympanitic 
quality of the percussion note, tympany being higher in propor- 
tion to the size of the collapsed area, but if the tuberculous 
process is extensive, then the percussion note becomes more or 
less dull, and in proportion to the extent and the nature of the 
diseased process, all gradations from normal to tympanitic and 
from dull to even flat can be demonstrated. It is evident from 
this that especial importance must.be placed on the early recog- 
nition of the primary changes in the note from the normal. 
On the anterior chest begin percussion, as has been stated, on 
the left side below the clavicle, mid-clavicular line, making a few 
soft taps and then compare it with the opposite right side over a 
corresponding area. If the note over these areas is alike in 
resonance on both sides, or perhaps the left a trifle higher, then 
we have fairly positive evidence that the left apex is infiltrated. 
It is understood that we consider the normal differences in the 
muscular development in left handed people, etc. To compare 
slight differences between the two sides, percuss first the left 
side by making but a single tap, using fairly firm percussion, and 
then percuss immediately a similar area over the right chest, PERCUSSION 
137 
or percuss directly upon the clavicle, first upon the left, then 
the right. This single tap percussion should be repeated quite 
quickly from left to right, like, one two, one two, one two, etc., 
making about six to ten single taps in quick succession on both 
sides, the slightest difference between the two sides being readily 
recognized in this way. This is far superior to the method of 
making six or eight strokes first upon one side, then upon the 
other, at the same time trying to carry in your mind the note 
observed first upon the left, then upon the right. Having found 
here a difference in the percussion note, as compared with the 
normal, next percuss from the inner margin of the lung, near 
the sternal end of the clavicle, towards Mohrenheim’s fossa 
along the lower border of the clavicle, and observe the change 
in note. In the normal, the note changes as we percuss towards 
the shoulder, becoming less resonant, but at the sternal end 
a slight tympanitic quality accompanies the note. If. how- 
ever, either lung is infiltrated, the note does not change, as we 
percuss from left to right or right to left. Percuss in the direc- 
tion of the lungs not towards the trachea nor towards the shoul- 
der. Having found an apical involvement, next percuss down- 
wards in order to outline the extent of infiltration, and here again 
the percussion note will change from dull to resonant and re- 
siliency, as we approach normal lung structure. If only one apex 
is involved, then percuss this apex, first on full inspiration, while 
the patient takes a deep breath, and still holds the breath, then 
on full expiration, the patient again holding the breath, and 
compare this with the note obtained over the healthy side under 
similar conditions. Over the healthy side a decided difference in 
the percussion note on deep inspiration and full expiration is 
most distinctly noticeable, the note becoming higher with full 
expiration, and more resonant, even tympanitic on inspiration, 
but no such change will be observed over the infiltrated area.1 
If a less amount of air enters the lungs on inspiration than in the 
normal respiratory act, the difference in the percussion note between 
that obtained on deep inspiration and full expiration may be very little, 
or may be entirely lost, or if but very little air enters on inspiration, 
then the difference between the inspiratory and the expiratory percussion 
IThe difference in the percussion note over various parts of the chest can more readily 
be noted and studied by means of stethoscopic percussions. Place the bell of the stetho- 
scope anteriorly on the sternum or posteriorly over the spine and note carefully the sound 
produced while percussing different areas of the chest. This is best done while one or 
more students are listening, the instructor doing the percussion. For instance, first per- 
cuss the left and then the right clavicle, next the area below the clavicles, mid-clavicular 
line, then percuss any part of the neck lateral or posterior, or perhaps the shoulder, then 
the chest over normal lung structure, and the difference in the percussion note between 
high and low will become readily apparent. 138 
CLINICAL TUBERCULOSIS 
note may be very faint, usually there being no difference at all. Fre- 
quently in beginning apical involvement the percussion note during in- 
spiration is low, and high during expiration. On very light percussion, 
however, we usually find the reverse, the percussion note being higher 
on inspiration. 
The difference in the percussion note, when one apex is infil- 
trated and the other is still free from the disease, can be more 
distinctly elicited as has been stated previously if the patient’s 
chest is percussed while his back is firmly placed against a panel 
door, hollow wall, or box to act as a sounding board. In be- 
-5. Manubrium 
Sterni - Percuss 
from this point 
right to left or 
left to right be- 
low the clavicles 
as far as Mohr- 
enheim’s fossa. 
On the left side 
the note changes 
almost immedi- 
ately, becomes 
softer when the 
lung border is 
passed; not so 
on the right; 
here the note 
becomes softer 
after we pass x. 
Also note the 
change in breath- 
ing and in the 
■ whispering voice. 
1. Upper border 
of the right lung 
(apex). 
2. Percussion note 
breath sounds 
and whispering 
voice change 
(from this point). 
3. Inner margin 
of the right lung. 
4. Lower border 
of the right lung. 
6. Inner margin 
of the left lung. 
7. Lower border 
of the left lung. 
Fig. 16. The normal Lung borders of the anterior chest. Showing the normal variations 
in the percussion note, the stethoscopic changes in the breath sounds and in the whispering 
voice (normal). 
ginning apical disease, if the area above the clavicle is percussed, 
the lower position of the apex and the lessened amount of lung 
volume on the affected side is also readily demonstrable. Next 
percuss the apices posteriorly and compare the infiltrated side 
with the normal, remembering always the normal difference be- 
tween the right and left side, and as over the anterior chest the 
diagnosis by percussion could most readily be made if the left PERCUSSION 
139 
apex is primarily involved, so can also the posterior upper lobe, 
the left sided infiltration, be more easily recognized by percus- 
sion. The involvement of one or both apices may fairly well be 
outlined by the following method: 
At the second thoracic vertebra, on either side, the inner mar- 
gin of the lungs approach, and from this point run parallel along 
6. Pectoriloquy. 
Heard here fre- 
quently in some 
individuals per- 
haps somewhat 
distant and not 
very intense. 
1. Upper level of 
lung on a line 
with the carti- 
lage below the 
7th cervical ver- 
tebra. 
7. Bronchophony. 
8. Vertebra 
Prominens. 
2. Inner margin 
of left lung. 
9. Upper margin 
(apex) of the 
lung. Above this 
the breath sounds 
are bronchial. 
3. Area of nor- 
mal, vocal or 
voice resonance. 
4. Lower border 
of the lung, or- 
dinary breathing. 
10. Second dorsal 
spine. 
5. Lower border 
of the lung, deep 
breathing. 
11. X. Between 
this and the up- 
per border of 
the lung breath- 
ing is broncho- 
vesicular. 
12. Inner border 
of the right lung. 
Fig. 17. The normal Lung Borders of the posterior chest. Showing the change of note 
in the normal when percussing from an airless to an air containing structure. This 
becomes still more definite when we auscultate the breath sounds and the whispering voice. 
Arrow Left. Percuss paravertebral line—the note changes almost immediately when the 
upper margin of the lung has been passed. Also note the change in the breath sounds, 
particularly note the change in the whispering voice. 
Arrow Right. Percuss diagonally. Here the note does not change as abruptly when 
the lung border is passed, it only becomes soft when we pass X. Here also note the 
gradual change in the breath sounds and the whispering voice. 
the spine to the lower border at about the tenth rib. The upper 
border or highest point of the lung in the paravertebral line is 
on a level with the upper border of the cartilage, of the first 
dorsal vertebra. Here let us draw a horizontal line. If from the 
second dorsal vertebra a line is drawn upwards and outwards 
crossing the paravertebral on a level with the first dorsal verte- 
bra and continuing upwards and outwards to the horizontal line 140 
CLINICAL TUBERCULOSIS 
we will form a line which runs quite parallel with the upper lung 
border. If now we percuss above this line, we are percussing 
over airless tissue, over the neck, bone and muscles, and we 
elicit a note which is distinctly high pitched, short, very resist- 
ant, and flat. If we then percuss downwards a perceptable 
change is noticeable as we pass this line in the normal, the note 
becoming soft, low, accompanied by a palpable resiliency; how- 
ever, if the area is infiltrated, there is only a slight or no change 
when we cross this line, depending mainly on whether the area 
is intensely consolidated, or if the involvement is but slight. 
Now, if a primary involvement should be below this line, say 
from three to five cm, the lung being still normal up to this line, 
then as we percuss from above down and approach this line, the 
Fig. 18. Isthmus percussion in health according to Kroenig (Schematic). Anterior and 
posterior view. (Normal.) The narrowest part is about 4 cm in width, equal on both 
sides. (Here a perceptible difference in one sided tuberculous infiltration is noticeable on 
percussion.) 
note does not blend into the flat note, as it would if the extreme 
upper lung margin were involved, but we perceive a resonant and 
lower note, changing as we continue downward and reach the 
seat of infiltration, to high and short, its intensity depending, as 
in all pulmonary consolidation, upon complete or partial involve- 
ment. If in doubt, percuss first about two to four cm, above this 
line and then immediately over the supposed infiltrated area as a 
comparison, and the great similiarity of the percussion note in 
both will become apparent, perhaps slightly modified if the dis- 
eased process is not entirely airless. The note percussed above 
this line, as well as the note percussed over the supposedly 
infiltrated area, should next be compared with a normal lung 
area, so as to fix definitely in the mind of the student the differ- 
ence between the normal flat note above this line, the abnormal 
flat note below this line, and the normal soft, resonant note 
audible over healthy lung structure. Next, should the flat note PERCUSSION 
141 
above this line blend with a similar flat note below the line, 
then continue percussion in a downward direction until a de- 
cided change to resonance has been secured, and now draw a 
line at this point, and the extent of infiltration reaches from this 
point up to the line indicating the upper lung border, and now, 
on percussing this area in either direction from right to left, or 
left to right, the extent of the consolidation may be outlined. 
Next continue percussion in a downward direction along the 
paravertebral line to the base of the lungs. Percussion of the 
lower lung borders should never be omitted, although in by far 
the greater number, the primary tuberculous process in adults 
is in one or both apices; however, tuberculosis of the lower lobes 
as a beginning disease is sometimes encountered. This is particu- 
larly so in children and occasionally in adults. It is also of impor- 
tance to remember in this connection that in individuals suffer- 
ing from diabetes, if complicated with pulmonary tuberculosis, 
the primary process in the lung is often found in the lower por- 
tion of the upper lobe and not in the apices of the right, middle 
nor in the upper portion of the lower lobe. In patients suffering 
from chest deformities, the primary process is usually in the 
lower or middle right lobe. One must remember, however, that 
notwithstanding much thoracic deformity, such as scoleosis, 
kyphosis, etc., that in children, as well as adults afflicted with 
such deformities pulmonary tuberculosis is very infrequent. 
The upper lung structure about the shoulder, known as the 
isthmus of the lungs, can also, according to the methods of 
Kroenig and Goldscheider, (44) be distinctly outlined, and per- 
cussion should be here of the mildest type, the sound produced 
by the percussing finger should scarcely be audible, and the re- 
sistance and the faint note should be observed particularly. In 
pulmonary tuberculosis, owing to early contraction of the pul- 
monary tissue, the isthmus over the affected side is less in 
extent, from 1 to 2 cm, depending upon the tissue involved. In 
the normal, both sides are about alike, varying in different indi- 
viduals, from 5 to 6, and more cm. The isthmus, or the nar- 
rowest part of the lungs can be outlined here on the anterior 
as well as the posterior wall of the chest. 
In practicing percussion, the axillary area, especially the upper, 
should never be omitted and with the patient’s arm resting well 
on the head, the tip of the examiner’s finger should be placed 
way up in the axillary groove as a pleximeter. 142 
CLINICAL TUBERCULOSIS 
Aberrations. The note on percussion may frequently be com- 
plicated by various aberrations, to which attention may be 
directed, as for instance, by emphysema, by pleurisy, by cavities, 
etc. If emphysema surrounds a tuberculous area, the note then 
will be low, somewhat hyperresonant, or, as frequently happens, 
if a whole lobe becomes tuberculous, the remaining healthy side 
will do compensatory work, giving a more or less tympanitic 
note. If a pleurisy accompanies the tuberculous process, the 
acute onset, the pain, the flat note, evidence of a compressed 
lung above the fluid, can be utilized in making the diagnosis, 
and when cavity formation has taken place the evidence of 
vomicae is easily demonstrable by percussion, the difference in 
the percussion note with the mouth of the patient open and 
closed being often readily demonstrated. Wintrich’s note in the 
presence of a cavity, the patient breathing in and out with the 
mouth wide open, the percussion note will be high and loud, 
becoming low and soft with the mouth closed and breathing in 
and out through the nose. Cavities are usually sharply defined 
and outlined over small areas. Cracked pot sounds are best 
demonstrable while percussing quickly and heavily, the patient 
keeping the mouth wide open. A natural pneumothorax occa- 
sionally accompanies an active case of pulmonary tuberculosis, 
particularly if one side is extensively involved. This and a 
band-box percussion note, great resistance to the percussing 
finger due to the compressed air in the chest cavity, are evidence 
of a collapsed lung. Immobility of the diaphragm on the affected 
side, (William’s Symptom) should be mentioned, being higher 
on the diseased, as compared with the healthy side, and may aid 
in the diagnosis of tuberculosis by the method of percussion. 
Sources of Error. Percussion sounds which may be mistaken 
for tuberculous infiltration. Over different areas of the thoracic 
cavity over which we expect to find a normal note, on percus- 
sion we may at times find some changes, and this may lead to 
wrong deductions, unless we bear in mind that something other 
than a pulmonary tuberculous process may admit a change in 
the percussion note, which may often resemble that of tubercu- 
losis. This particularly is to be borne in mind when percussing 
the chest wall in children. Error in percussion may also be due 
to a faulty technic, or to the variations in the anatomical rela- 
tionship existing between the two sides, hence: 
(1) Attention should be directed to the difference in the mus- PERCUSSION 
143 
cular development on the two sides, the somewhat greater mus- 
cular development in right handed or left handed people, all of 
which may greatly influence the note being higher over the 
thicker muscle. 
'(2) In scoleosis, kyphosis, etc., due to the contour of the 
spine, the note is higher over the muscle on the bulging side and 
lower over the retracted or atrophied area. 
(3) In percussing the clavicles too near the sternal end, too 
far inward where a tracheal note is added, or again too far out- 
wards, towards the shoulder and beyond lung tissue, the note 
may be flat. 
(4) Percussing over enlarged bronchial glands, on either side 
of the spine and upwards towards the apices a dull note is elicited 
which may be mistaken for pulmonary involvement. A similar 
note is frequently noticed anteriorly in the parasternal line right 
side in the second and third interspaces. 
(5) In children a collapse induration of the lung, as first pointed 
out by Kroenig, due to insufficient aeration and usually, the re- 
sult of nasal or mouth obstruction, adenoid vegetations, hyper- 
trophic turbinates, tonsillar hypertrophy, etc., may give signs 
which simulate infiltration. That this is not due to tuberculosis 
the clinical picture can prove and besides, the student must re- 
member that pulmonary tuberculosis in children is comparatively 
infrequent. This condition is also occasionally found in adults 
as the result of early nasal trouble. 
(6) Chronic bronchial inflammation, particularly bronchiec- 
tasis in children, due to compression of the upper lung, may give 
rise to consolidation, and on percussion give a high pitched re- 
sistant note, not due to tuberculosis. 
(7) In pneumoconiosis, siderosis, chalicosis, etc., the percus- 
sion note is more diffuse than in pulmonary tuberculosis, due to 
early retraction but without destruction of lung tissue. 
(8) Neoplasms, carcinoma, sarcoma, syphilis, actinomycosis, 
etc., may all, if involving the lung, give a percussion note which 
may simulate that of pulmonary tuberculosis, but the general 
history of the case and the cause of the disease will make the 
differential diagnosis definitely. 
(9) Apical bronchitis, a chronic pneumonic process, etc., may 
all modify the percussion note from the normal, and it should 
also be remembered that apical percussion dulness has been 
occasionally observed in perfectly healthy lung tissue and con- 
firmed by autopsy findings. 144 
CLINICAL TUBERCULOSIS 
Palpatory Percussion. The subject of percussion can not be 
passed, would be but incomplete, if reference were not made to 
Palpatory Percussion. Notwithstanding the fact that a most 
able writer on physical diagnosis refers to it in very slight terms 
as of “very little value in diagnosis,” if properly understood and 
carefully practiced it becomes one of the most valuable aids in 
our armamentarium. Palpatory percussion is practiced by mak- 
ing a few firm taps directly over various parts of the chest wall 
with the tips of the four fingers of either the right or left hand in 
quick succession, from the wrist and not from the elbow or 
shoulder, observing the note produced and the resistance offered. 
Chronic pneumonic processes, old pleural thickenings, muscular 
spasticity and atrophy, empyaema, pleurisy with effusion, em- 
physema, intra-pulmonary thickening due to neoplasms, etc., can 
most readily and quickly be discerned by palpatory percussion. 
It may, as compared with the ordinary method of percussion, be 
considered a crude method of diagnosis; it remains, nevertheless, 
if faithfully practiced and thoroughly mastered, a most valuable 
aid, and the student in physical diagnosis is well rewarded, and 
the time well spent for its mastery, continuous practice alone 
leading to its thorough comprehension. One must remember 
that, as in all other methods of physical examination, only con- 
tinuous and faithful practice and repetition will lead to a thor- 
ough understanding. 
THE (TUBERCULOUSLY) INFILTRATED LUNG. (SCHEMATIC.) 
Explanatory remarks concerning the infiltrated pulmonary tissue, as is 
indicated by the shaded areas in Figures 19 and 20. 
A study of the tuberculous lung by means of the physical signs of (1) 
Percussion; (2) Auscultation and (3) Whispering Bronchophony. 
(1) Percussion: Begin percussion at A (Fig. 19) along the shoulder 
where the note usually is dull or flat; as we approach the upper, lateral 
border of the lung the note begins to change and as we pass the border 
the note becomes distinctly resonant; at the same time a resiliency is 
noticeable. This change would be still more in evidence if we percussed 
along the line B, and the pulmonary tissue were normal. Here, in Figure 
19, however, the apex appears pathologic, and as we approach the lung 
border the note does not change to resonant as in the normal, but remains 
dull and continues so till we pass the dark area which in the Figure indi- 
cates the region over the second or third rib and interspaces, below which 
the note again becomes distinctly resonant. On the opposite side, the 
right lung, the extreme apex is still free, but an area of infiltration is in- 
dicated by the dark area towards the shoulder, extending, perhaps, from 
the second to the fourth rib. Now, if we percuss at C or, better perhaps, 
about 6 cm towards the right and percuss downwards, the note will PERCUSSION 
145 
change from dull to resonant as we pass the upper lung border, differing 
greatly in this respect from the note elicited over the opposite, the left, 
apex. If next we percuss in the direction of D, we shall again notice that 
the percussion note does not change; we pass the lateral border of the lung 
as we find in the normal or as we found when percussing the opposite 
lung or from A down and inward but the note only begins to change from 
dull to resonant when we have passed the darkened, the infiltrated area 
and are again percussing over normal lung structure, where the note again 
becomes resonant and more resilient to the palpating finger. This from 
the shaded area in the figure would be at about the fourth rib and inter- 
space. Again percuss at B and downwards, approximately following the 
left paravertebral line to the fourth or fifth rib, and then along a similar 
line on the opposite side (right paravertebral line), and the difference in 
the percussion note can be distinctly and clearly noted. Along the right 
paravertebral line the note changes almost abruptly as we pass from neck 
percussion, which is dull or flat, over to percussion of the normal lung 
area, that is, when we have passed the upper lung border, but not so when 
we percuss the corresponding area on the left side. Here the note does 
not change when we pass the left upper lung border, only when we have 
passed the shaded area does the note become again resonant. This same 
applies to Fig. 20 where the le-tters E, F, G and H indicate the direction of 
percussion over healthy tissue or from an infiltrated area through to 
normal lung structure. Here the changes in the percussion note are not 
so clearly demonstrable, that is, in comparing the area of the anterior with 
that of the posterior chest, excepting in the parts below the clavicles. 
Over the areas below the clavicles, begin percussion at the middle of the 
manubrium at X, percuss in a lateral direction following the arrows, from 
the sternum towards the shoulder. Over the left, the most normal side, 
where the tissue below the clavicle is still in great part normal, the note 
does not differ much from the full normal (here the proximity of the 
infiltrated to the normal lung changes the percussion note but slightly), 
the normal being very resonant in the mid-clavicular line, slightly so 
towards the shoulder, higher over the sternum. (For description, see text 
above, (this chapter), where the normal percussion note elicited over both 
right and left areas below the clavicles is given in full detail.) 
(2) Auscultation. Placing the bell of the stethoscope anywhere along 
the neck, we usually hear a coarse sound, described as tracheal breathing. 
This sound in the normal continues until we pass the margin of the lung 
(left apex), when tracheal or bronchial sound ceases, to be displaced by 
soft vesicular breathing. Here, in Figure 19 at B, as we pass the lung 
border (left apex) the breath sounds do not change (do not become soft 
but remain harsh), but owing to tuberculous infiltration continue harsh 
till we have passed the darkened area, where at about the third inter- 
space the breath sounds gradually change from the coarse inspiratory and 
prolonged expiratory to the soft inspiratory and still softer and shorter 
expiratory sounds. The same difference in the breath sounds can be 
demonstrated when we move the bell of the stethoscope in the direction 
of the arrow D. At C, however, the normal sounds become somewhat 
more apparent when we listen a little more to the right in the direction 146 
CLINICAL TUBERCULOSIS 
of the right paravertebral line. This also applies to Figure 20 in the direc- 
tions of the arrows E, F, G, H. Now place the bell of the stethoscope 
over the middle of the manubrium at X, where tubular breathing is dis- 
tinctly heard. Next place the bell a few centimeters towards the left, and 
we note that the breath sounds begin to change, and as we pass the lung 
margin, over that portion where the lung is still free from tuberculosis 
we hear a distinctly vesicular sound, soft though continued with less in- 
tensity, perhaps slightly harsher in the infraclavicular fossa. Having 
studied the left area below the clavicle and having interpreted the sounds, 
we place the bell of the stethoscope for a second time at X, gradually 
carrying it towards the right lung border, in the direction of the arrows, 
Fig. 19. Posterior view of the thorax showing tuberculous involvement of the upper lobes 
(schematic). The darkened areas indicate pulmonary pathology. 
and we note that the sounds here differ much from the sound which we 
heard while listening along the lower border of the left clavicle. Here 
bronchial breathing is distinct at X and continues so as we proceed to the 
right, the breath sounds do not change as we approach the shaded area, 
there is perhaps a greater accentuation as we enter the densely infiltrated 
area. (Compare these findings with the breath sounds in the normal lung.) 
(This is fully described in Chapter 16—Auscultation.) 
(3) Whispering Bronchophony. The Whispering Voice. Again place 
the bell of the stethoscope at B along the neck (Fig. 19) and follow the 
arrow in the downward direction, note that the whispering voice is dis- 
tinctly transmitted to the ear. This in the normal should cease when we 
pass the lung border, the voice being heard but faintly or not at all. Here, PERCUSSION 
147 
however, as we pass the lung margin the voice sounds are carried with the 
same intensity over this border and only begin to change when the 
darkened or infiltrated zone has been passed, where again the intense 
whispering sound stops almost abruptly, to pass into a faintly audible 
sound (or perhaps no sound at all). A similar study can be made at D, 
when following the direction of the arrow; here, also, the whispering 
voice changes when the darkened area has been passed, this at about the 
fourth interspace, paravertebral line. At A and at C a few centimeters to 
the right along the paravertebral line, the faintly, indistinct, or absent 
whispering sounds over normal lung structure can readily be studied so 
Fig. 20. Anterior view of the chest showing tuberculous involvement of both apices 
(schematic). The darkened areas represent the tuberculous pathology. 
as to differentiate them from the pathological whispering sounds heard in 
the direction of arrows B and D. Next place the stethoscope on the 
anterior chest over the middle of the manubrium at X (Fig. 20) and care- 
fully note the whispering voice as heard there, and gradually carry the 
bell first from X to the left shoulder and then from X to the right and 
note the difference in intensity of the whispering voice as heard toward 
the right infraclavicular fossa, where in the normal this sound should not 
be heard at all. (See Auscultation, page 157.) 
The student’s attention is specifically directed to these figures. The 
darkened zones here indicate a tuberculous infiltration, schematically. A 
tuberculous involvement of any part of a lung, be it at the apices, at the 
bases or in the middle lobe, can be outlined by percussion, auscultation and 
by the whispering voice and will conform with the changes as given in 
these schematic pictures. CHAPTER 16 
AUSCULTATION 
(Including the Mechanism of Breathing) 
General Considerations. After having made a thorough in- 
spection of the chest, followed by careful palpation and percus- 
sion, we must then be in a position to state definitely whether 
the findings are those of a healthy or a diseased individual, 
whether they show a strictly normal or a pathological lung, be- 
fore we resort to auscultation. Inspection, palpation and percus- 
sion have shown that changes have taken place in the underlying 
lung structure, but auscultation tells us what these pathological 
processes are, the kind and nature of these changes and whether 
these processes are active, arrested or healed. In a true sense 
auscultation is employed simply to confirm our previous findings, 
to clinch the diagnosis, and it should not be used, as it so fre- 
quently is in routine examinations, as the chief or sole method 
of physical examinations, but only as a confirmatory aid. 
Auscultation as an aid in the early diagnosis of pulmonary 
tuberculosis depends upon the initial pathologic changes going 
on about the alveoli, alveolar ducts and the bronchiols. As this 
is usually accompanied by a more or less exudative infiltrate and 
as by means of these changes which are generally of a catarrhal 
nature, the free access of air to the periphery of the lung meets 
with an obstruction, followed by productive foreign sounds, 
such as are never found in the normal, and as the initial tuber- 
culous process gradually extends and advances into neighboring 
and contiguous tissue, becoming more and more definitely catar- 
rhal, primarily normal lung sounds give way to these changes, 
and from the vesicular one passes to the impure vesicular, to the 
bronchial and ultimately to the cavernous, accompanied at first 
by very fine but numerous crackling sounds, then more coarse, 
less numerous, more mucous and finely to amphoric, presenting 
a continuously changing picture. 
Methods of Auscultation. Auscultation is defined (31) as the 
method of listening over the surface of the thoracic cavity to the 
148 AUSCULTATION 
149 
sounds produced within the chest wall during both the phase of 
inspiration and expiration. If in examining the chest of a patient 
the physician places his ear directly upon the chest wall while 
the patient breathes or speaks, it is known as immediate auscul- 
tation; if, however, the sounds produced within the chest are 
studied by means of an instrument known as the stethoscope, 
and this is the method now almost exclusively in use, it is known 
as mediate auscultation, that is, a medium is placed between the 
patient’s chest and the ear of the examining physician. Auscul- 
tation or proper mediate auscultation was introduced to the 
profession by Laennec, Rene Theophile Hyacinthe, a most 
distinguished French physician, about 100 years ago, namely in 
1821, since which time it has been constantly in use. To men- 
tion the various instruments recommended for making aus- 
cultory examinations does not properly fall within the province 
of this work. Suffice to state, however, that every student 
should select the make of stethoscope most suitable to his hear- 
ing, because a certain instrument may be well adapted to the 
hearing of one while entirely useless to another. 
The Normal Breath Sounds. The Normal Auscultatory Sounds. 
If we note carefully the respiratory movements of a healthy adult 
while asleep, we will observe that he breathes from 18 to 20 
times per minute or that he performs that many cycles of breath- 
ing, and we will note further that each cycle of breathing is divis- 
ible into three distinct phases, the phase of inspiration, of ex- 
piration, and of rest, and that the phase of rest is equal to and 
even a trifle longer than both inspiration and expiration. With 
advancing years a slight change in each cycle is noticeable; this 
is the addition of a fourth phase, a short period of rest between 
inspiration and expiration. In the infant we often observe in the 
normal only two phases—inspiratory and expiratory. 
If we place the bell of the stethoscope above the upper margin 
of the lung border, that is along the neck, either right or left 
side, and listen, we will hear a coarse inspiratory sound not 
unlike that of blowing through a tube, of high pitch, but no 
other sound; with expiration we will hear a nearly equal coarse 
but less intense expiratory sound a trifle longer than the in- 
spiratory and a little higher in pitch; this is next followed by a 
period of rest during which no sound whatever is heard. This 
Auscultation of the Normal Thoracic Sounds 150 
CLINICAL TUBERCULOSIS 
is then immediately followed by another cycle of equal time and 
duration as the preceding one and so on. 
These sounds which we hear at these points over various parts 
of the neck are designated as tracheal breathing but may also 
be described as intense tubular or bronchial, being produced in 
the largest bronchial tubes. Similar sounds, though of less in- 
tensity, are heard above the clavicles, over lung structure on the 
upper portion of the sternum, and in children may frequently be 
heard along either side of the spine as far down as the fifth or 
sixth dorsal vertebrae, but usually bronchial sounds about the 
thoracic wall over normal lung tissue are heard over a very lim- 
ited area and throughout the greater portion of the chest cavity 
we hear a soft inspiratory sound low in pitch, followed imme- 
diately by a still softer, still lower and shorter expiratory sound. 
The duration of these sounds is usually described as 4 to 1, the 
expiratory only one fourth as long as the inspiratory. This is 
usually known as the normal vesicular murmur. This sound or 
murmur has been likened to the rustling of the leaves in the 
forests by the winds, but to my mind the best simile in nature is 
the sound produced by the waves along the shores of a lake, the 
waters rushing shoreward with a coarse sound (active motion), 
flowing back (passive motion) with a softer, less audible and 
shorter, often scarcely heard sound. This is then followed by a 
period of quiesence or rest after which the next wave occurs and 
so on. 
Pure normal vesicular breathing as a physical symptom is an 
expansion murmur of the healthy pulmonary air cells. It is 
heard wherever healthy lung tissue is found underlying the 
bony frame work of the chest wall and it predominates greatly. 
To a limited extent only do we find different sounds over this 
area and these different sounds are usually described either as 
bronchial or broncho-vesicular. These three different sounds are 
the sounds heard over a normal lung and all other sounds heard 
are abnormal or pathological. Even these normal sounds, if 
heard over portions of the chest wall over which they are usually 
not heard, must be considered as pathological. For instance, 
hearing the vesicular sound over the heart area is just as patho- 
logical as hearing the bronchial at the base of the lung. Over 
the anterior portion of the chest wall the normal vesicular mur- 
mur is heard from the clavicles to the lower border of the lung, 
and posterior from the apex to the base, modified over the area AUSCULTATION 
151 
where the heart is superficial, over the liver, and by the thick- 
ness of the chest wall, the muscular development, the fatty in- 
filtration of the skin, etc. 
As in percussion, so also in auscultation, we find the area be- 
low the left clavicle the most normal in each individual and here 
in the mid-clavicular line the vesicular murmur is normally soft, 
a harsher quality being added as we listen on the right corre- 
sponding area. A distinctly harsher quality is also heard even 
over the left side, as wre place the stethoscope more towards the 
sternal end of the clavicle, but it appears softer if we listen below 
the clavicle and towards the shoulder. As already stated, over 
the right lung below the clavicle, the inspiratory sound is 
harsher than over the left lung, less vesicular, but the expiratory 
is still more harsh and less vesicular when compared with the 
left and is at the same time slightly prolonged and high. This 
is known as the broncho-vesicular murmur. It is a sound mid- 
way between the soft normal vesicular murmur and the presently 
to be described normal bronchial. Over the posterior chest wall 
the normal vesicular sound is also heard best over the left apex, 
a slightly harsher quality being added over the right. 
Over the upper portion of the sternum, the upper portion of 
the spine, to a slight extent near the bifurcation of the trachea, 
the 3rd and 4th dorsal vertebrae and perhaps a little on either 
side, as well as above the clavicles, the predominating sound is 
distinctly tubular, a high and intense inspiratory, and a higher 
and more prolonged but less intense expiratory murmur; this is 
bronchial or tubular breathing. This sound particularly if heard 
over an area over which it is normally not heard, is a true indica- 
tion of pulmonary infiltration. Bronchial breathing if heard over 
otherwise healthy lung structure indicates a compact infiltration 
of parts of the pulmonary tissue or the communication of an air 
containing hollow space with a bronchus. 
Next, if we outline the upper lung border as we have done in 
percussion, (see figures 16 and 17) and place the bell of the 
stethoscope above this line posteriorly where there is no lung 
structure, beginning, as is proper, over the left side, we note dis- 
tinct bronchial or tubular breathing, and having obtained a clear 
idea of bronchial breathing in the individual we are examining, 
we place the stethoscope a few cm lower, approaching the line 
and again carefully listening. We now note as we reach the lung 
border that the murmur begins to change, so that when we have 152 
CLINICAL TUBERCULOSIS 
passed this line the murmur becomes distinctly vesicular, being 
entirely devoid of its bronchial quality. If now we compare 
these findings, that is the left side with the opposite, the right, 
we note that there is no such distinct and abrupt change when 
we pass the lung border on this, the right side, but that a dis- 
tinctly bronchial quality is still heard with the vesicular and as 
we reach a point about 2 to 3 cm below the lung border the 
murmur again becomes distinctly vesicular; the murmur heard 
distinctly between these two points is the broncho-vesicular. 
This is normal in the right upper lung but never over the left if . 
strictly normal. The same applies anteriorly below the clavicles, 
and in the mid-clavicular line of the left and right side. Other 
areas over which a more or less intensely bronchial quality may 
be added to the vesicular or a vesicular to the bronchial, depend- 
ing upon which may predominate, are anteriorly over the body 
of the manubrium and on either side along the sternal end down 
to the 3rd rib and occasionally a few cm to either side, pos- 
teriorly in the interscapular area as far as the 3rd and 4th dorsal 
spine, and outward, perhaps a little beyond the paravertebral 
line and upwards to the upper margin of the lung. With the ex- 
ception of this area posteriorly, and the area described an- 
teriorly, and that portion of the lung extending above the clavi- 
cles over which broncho-vesicular or mainly bronchial is heard, 
over all other portions of the chest wall the vesicular murmur is 
in evidence, and any change from this indicates some patho- 
logical condition; any murmur heard over an area over which 
it is not heard in the normal indicates that something has taken 
place within the lung structure. As the normal lung is a poor 
conductor of sound, any infiltration will make out of this poor 
conducting media, the lungs, a good conductor, transmitting 
sounds more readily to the surface. 
Abnormal auscultatory murmurs in pulmonary tuberculosis. 
The abnormal chest sounds heard in pulmonary tuberculosis are 
symptoms of infiltration. In the very beginning of pulmonary 
involvement the vesicular breath sounds begin to change. At 
first they may be accompanied by a decided weakening; this is 
soon followed by a distinct harshness and prolongation of the 
inspiratory murmur, the note acquiring a slightly higher pitch, 
the expiratory being still unchanged. However, a gradual and a 
greater change is soon noticeable in the expiratory sound which 
becomes still higher and more prolonged than the inspiratory, AUSCULTATION 
153 
the whole displacing entirely the soft inspiratory and still softer 
and much shorter expiratory of the normal vesicular. This is 
due, as has already been stated, to the changes in the lumen of 
the bronchiols, alveolar ducts and in the alveolar spaces, the 
infiltrate materially interfering with the free access of air, weak- 
ening first the vesicular murmur until it becomes gradually 
entirely lost.1 
In the examination of the chest abnormal auscultatory sounds 
cannot always be diagnostically utilized, for in many women and 
quite a few men who are physically weak, abnormal sounds over 
the chest are often heard, for even the normal breath sounds are 
not always the same or heard with equal intensity over both 
sides in the same individual, even in perfect health. Attention 
must here again be called to the fact that the expiratory sound in 
the normal is higher over the right upper lobe both anterior and 
posterior especially on deep and full breathing. With deep and 
full inspiration over the upper left lobe posterior a slight pro- 
longation of the expiratory sound also may be observed, which 
is not found on slightly superficial or moderate breathing. This 
expiratory phenomenon can only be utilized as a clinical sign 
when over the left apex posteriorly; over that portion over which 
the note was found high on percussion, the respiratory murmur 
is prolonged and harsh during very slight or moderate breathing 
or if it is heard only over a small and circumscribed area, as over 
healed lesions. In fibroid conditions the breath sounds also are 
intensified and prolonged and bronchial breathing frequently 
heard in the interscapular areas, over the upper sternum, about 
the trachea and above the clavicles has already been mentioned. 
Auscultatory Catarrhal Signs. Dry and Moist Rales. Adventi- 
tious Sounds. Abnormal Chest Sounds. Catarrhal signs, usually 
crackling, heard over the chest are always foreign sounds and 
are produced by the respired air coming in contact with either 
abundant secretion or little moisture in either the bronchial tubes 
and their divisions or in the bronchiols, the terminal bronchi and 
the alveolar spaces. 
In the very beginning of the disease numerous fine crackling 
lln the very beginning, the inspiratory sounds become weakened and impure, but with 
very little if any effect on the expiratory. As the process continues, the expiratory sound 
also begins to change, becoming gradually more and more prolonged, more harsh and 
devoid of all soft quality; the pitch rises when eventually the process is complete; the 
vesicular sound has been completely displaced by the bronchial which is now higher in 
note than the inspiratory and as long or longer in duration. The student should remem- 
ber at this point that the expiratory sound is the key to the diagnosis, not only in pul- 
monary tuberculosis but in all the other forms of pulmonary disease of whatever origin, 
whatever cause or nature. 154 
CLINICAL TUBERCULOSIS 
sounds are heard which at the height of inspiration bespeak 
their catarrhal nature, especially if these sounds are heard over 
small circumscribed areas. Pulmonary tuberculosis is primarily 
a localized bronchitis, but not in the ordinary sense, being con- 
fined to the smallest tubes; more correctly is it a bronchiolitis, a 
bronchitis of the capillary bronchi. These numerous sounds, at 
first crepitating and fine crackling, usually heard at the height 
Fig. 21. Adventitious Sounds or Murmurs. (Rales, Rhonchi, friction rubs, etc.) A 
schematic representation of the various sounds heard over the chest cavity (abnormal). 
The nature and quality of these sounds indicate the particular location in the lungs in 
which those sounds are produced. 
of inspiration, are known as crepitant rales. As the process ex- 
tends to other tissues surrounding the initial involvement, in- 
vading contiguous tissue, the sounds begin to lose their fine 
crackling quality and at the same time lessen in the number 
of crackles. Fewer crackling sounds, known as subcrepitant 
rales, both inspiratory and expiratory, are now heard (in both 
phases of breathing), becoming larger, moist, and more of a 
mucous variety, and as the catarrhal process extends a cough, 
resulting from the heightened bronchial tube irritation, accom- 
panies these sounds, and dry and moist rales are now clearly aud- AUSCULTATION 
155 
ible and sonorous and sibilant, mucous, subcrepitant and crepi- 
tant sound rapidly follow in ever changing order. 
An explanation may not be out of place at this point. Sounds pro- 
duced in the bronchial tubes of various calibre are often referred to 
by writers on physical diagnosis as musical rales. Admitting that the 
sounds produced in these tubes possess a musical quality, the time worn 
terms, sibilant and sonorous, although very old, and perhaps a little 
obsolete, are still better and more descriptive. If I am told by a student 
that over a certain area over the chest wall sibilant or sonorous rales (197) 
are heard, I know in what portion of the bronchial tubes and also in what 
size tubes these sounds have been produced, if in tubes of smaller or of 
larger calibre, but if I have been told that musical sounds were heard I 
must inquire about the quality of these sounds, if they were very high 
in note or very low, in order to orient myself. 
Coarse rales having a metallic or coarse, crackling or creaking 
sound are usually evidence of small cavities, especially if accom- 
panied by an expiratory prolongation and of low, hollow note; 
with large cavities the note becomes more amphoric or like the 
sound produced by blowing over the mouth of a bottle. These 
crackling or creaking sounds are heard usually in both the phases 
of inspiration and of expiration, but they are usually louder and 
more numerous with inspiration, more crackling, fewer and long 
drawn out with expiration. All fine crepitating as well as 
crackling sounds bear evidence of the catarrhal process in the 
small air spaces, the alveoli, the bronchiols and terminal bronchi 
whilst coarse and piping sounds produced in the larger tubes 
bear evidence of inflammatory secretions in these tubes. 
Tuberculosis in the beginning is an alveolitis, and a bronchiol- 
itis per se, and sibilant and sonorous rales if present are only 
evidence of an accompanying bronchitis or tracheitis. With the 
formation of cavities, these sounds change to creaking, short, 
sharp, crackling sounds, circumscribed, with the expiratory sound 
much prolonged, but not now as in early consolidation high 
pitched but low pitched and amphoric, that is, a bronchial, high 
pitched, expiratory sound speaks for consolidation but an am- 
phoric, low pitched, expiratory for cavities. 
In the opinion of some authors, a systolic murmur, which if heard 
over the subclavian artery on one side, especially if heard with expiration 
only, pr if it becomes more intense in this phase is a sign which be- 
speaks of early pulmonary tuberculosis. The cause of this murmur is 
supposed to be due to adhesions of the apical pleura. A similar murmur, 
often in anemia, is heard in the supraclavicular fossa, but the sound is 
more intense with inspiration or it may be heard at the height of inspira- 
tion only. 156 
CLINICAL TUBERCULOSIS 
Normal Vocal Sounds. Voice Resonance or Vocal Resonance. 
If we listen with the stethoscope placed over any portion of the 
chest wall over lung tissue both anteriorly and posteriorly, while 
the patient speaks or counts aloud, a peculiar vibratory sound 
is conveyed to the ear; this is known as the normal vocal or 
voice resonance. If next we place the bell of the stethoscope 
over portions of the chest behind which there is no lung tissue, 
but near which the bronchial tubes lie, a very harsh but muffled 
sound is carried to the ear; this is known as bronchophony or 
the bronchophonic voice. If now we ask the patient to whisper 
one, two, three while we are listening over the bronchial tubes, a 
distinct but less harsh sound is heard which is known as the 
whispering voice or whispering bronchophony. 
These three sounds, normal vocal resonance, bronchophony 
or loud voice and whispering voice or whispering bronchophony 
in health, are heard distinctly over sharply defined areas, but if 
heard outside of these areas they usually indicate a condition of 
pathological lung change. As the normal vocal resonance is 
heard best over that area of the lung over which the vesicular 
breath sound is clearly heard, and bronchophony and whispered 
bronchophony over that part of the chest wall over which bron- 
chial or tubular breathing is best heard, we can again make use 
of the outline of the upper and posterior lung border on the 
chest wall, as we did when considering the subject of percussion. 
(See figures 16 and 17.) 
As has already been pointed out, on the posterior upper chest, 
the right and left lung, borders meet on a level with the second 
dorsal spine, extending from this point upwards and outwards 
on a level with the first and running from the second dorsal 
downwards and parallel with the spine to the 10th rib, in the 
axillary area to the 8th, and on the anterior chest to the 6th, and 
running thence upwards, the right from the 6th, and the left at 
the 4th, following behind the sternum, where at the junction 
with the manubrium, they again separate, running upwards and 
outwards and extending from an inch and a half to two inches 
above the clavicles. Over all this area, over which the lung 
structure lies superficially with the exception of that portion of 
the lung which lies above the clavicles, the normal vocal resonant 
sound is more or less distinctly heard, modified somewhat by the 
thickness of the chest wall, difference in muscular development, 
deposit of fat, bony framework, pitch of the voice, etc. This AUSCULTATION 
157 
resonant murmur is a muffled, humming, more or less loud 
sound, but over the trachea, bronchi and about the neck both the 
loud and whispering bronchial sounds are heard in the normal. 
If we draw a line along the posterior upper border of the lung 
from the second dorsal spine where both lungs come in close 
apposition, upwards and outwards on a level with the upper 
border of the first dorsal spine, we will outline, as has already 
been stated (on page 139) the upper margin of the lung. We 
draw a similar line over both the right and left side. If now 
we place the bell of the stethoscope anywhere above this line 
along the neck and ask the patient to whisper one, two, three or 
use the words, 99, 66, 33, the whispering voice or whispering 
bronchophony will be distinctly heard. This sound will continue 
over every square inch of surface above this line, but a decided 
change is observed when we pass this line. On the left side 
usually as we pass this line the change is abrupt, no whispering 
voice will be audible below this line but over the right side the 
sound is carried, though with less and less intensity, for about 
2 or 3 cm below this line, when it also can no longer be heard.2 
Abnormal Vocal Sounds. Whispering Bronchophony in Pul- 
monary Tuberculosis. The whispering voice sound in consolida- 
tion of the lungs is one of the most distinct and definite of all the 
physical signs; in fact, I consider it the most distinct single sign, 
and throughout the whole tuberculous process with the very 
beginning of the infiltration, with the earliest incipiency, the 
whispering bronchophony manifests itself, even long after the 
disease has been arrested or even if healed, the whispering voice 
will still be distinctly heard. The whispering voice is the very 
first sign to appear in pulmonary tuberculosis and the last to 
disappear. Whispering bronchophony heard anywhere over an 
area where normal lung structure is usually found indicates in- 
filtration. To this there may be some exceptions, but careful 
examination will avoid errors. In beginning pleurisy, with effu- 
sion for instance, or even if the pleurisy has lasted for some 
time and the pleura is still thin, sounds are often conveyed which 
simulate consolidation. This will be described more in detail in 
the discussion of the subject of “Tuberculosis and Pleurisy.” 
In children the whispering voice is usually heard well between 
2Caution, The student must learn to differentiate between the whispering sound heard 
through the stethoscope and that extraneous sound of the voice heard when the bell of 
the stethoscope is placed over any portion of the chest and the individual is asked to 
whisper. Practice alone will teach how to obviate such errors. 158 
CLINICAL TUBERCULOSIS 
the scapulae, more particularly when the mediastinal glands are 
enlarged. This also will be referred to more in detail when the 
subject of gland tuberculosis is considered. On the anterior 
chest along the sternum occasionally to the right over the second 
and third interspaces, parasternal line and above the clavicles the 
whispering voice is also heard as normal. 
Normal vocal resonance, as has previously been stated, is 
heard over healthy lung tissue as a dull, humming, low pitched 
sound; in healthy individuals the sound varies greatly in pitch 
and in intensity, is more feeble or diminished in women and 
children than in men and like all sounds produced depends 
greatly upon whether the voice is high or sibilant or screeching, 
or low, sonorous, a basso profunda. If the stethoscope is placed 
above the line so often referred to while on the subject of per- 
cussion and auscultation, say along the neck, about the larynx, 
trachea, thyroid, etc., and the person is asked to speak or count 
out loud, a most intense, a more or less painful sound is dis- 
tinctly heard. This is normal bronchophony; the words are still 
confused, not perfectly clear. Over slightly consolidated and 
infiltrated lung areas, similar sounds are usually heard, still 
muffled, but with complete consolidation or with the formation 
of cavities, these sounds may again change and the voice is then 
distinctly and clearly transmitted through the stethoscope to the 
ear; this is described as pectoriloquy or clear voice conduction. 
Generally in consolidation, pectoriloquy is heard more sharply 
and over larger areas, high in pitch, more intense and nearer to 
the ear, while pectoriloquy heard over cavities is more circum- 
scribed, over smaller areas, lower in pitch, less intense, more 
distant from the ear. If such conditions are present then both 
forms of pectoriloquy can usually be demontrated about these 
areas, because the area surrounding cavities is usually densely 
consolidated and a good conductor of sound. Here also the 
whispered voice or whispering pectoriloquy is most definite and 
distinct as in simple voice conduction.3 
How and When to Auscultate. It is most important that aus- 
3lt is often very easy to demonstrate on many healthy and normal individuals normal 
vocal resonance, bronchophony and pectoriloquy. Place the bell of the stethoscope on 
any part of the posterior chest, say, near or below the angle of the scapula and listen 
while the patient speaks; this low muffled sound heard is the normal vocal resonant. Next 
place the bell anywhere about the neck, say, above the line so often mentioned and the 
loud sound heard is the bronchphonic voice or simply bronchophony, the voice less muf- 
fled more intense than the former but still not quite clear; now carry the bell of the 
stethoscope to the occiput or even on top of the head and the sound heard there is the 
clear and distinct voice, perhaps somewhat distant and faint; that is pectoriloquy. (See 
Figure 17, page 139.) AUSCULTATION 
159 
cultation be practiced at a time when we may anticipate the best 
results, especially in beginning cases of pulmonary disease when 
the adventitious sounds can be definitely located. This time is 
usually best in the early morning when the patient is endeavor- 
ing to clear the bronchial tubes from the secretions which have 
accumulated during the night. The patient should then be exam- 
ined first under ordinary breathing, then under forced or deep 
breathing, paying close attention to the first sounds or rales 
which may be heard at the height of inspiration. Next, carefully 
auscultate the cough. No examination can be said to be well 
done if this has been omitted. The patient is asked to take a 
deep breath, a full inspiration, and at once to exhale or breathe 
out, coughing just before he again takes another breath, then 
immediately to follow this by a deep inspiration, when crackling 
sounds may be heard with the height of the inspiratory phase. It 
is really not auscultating the cough, but the inspiratory phase 
immediately following. Coughing quickly at the end of expirat- 
ing expells a great amount of residual air, collapsing the small 
bronchial tubes, the bronchiols, the terminal bronchi and aveoli 
which in the next, the inspiratory phase, are forced asunder by 
the entering air and due to the sticky mucous contained within 
their lumen, produce crackling sounds of various sizes. Aus- 
cultation of the mouth may furnish in some cases very reliable 
data. By placing the bell of the stethoscope before the mouth of 
the patient while breathing in slowly and quietly, but deeply, 
crackling sounds are often distinctly heard which usually point 
to a deep seated or central lesion. It is advisable that women be 
examined during the absence of the menstrual period. 
Errors in Auscultatory Sounds. Not all sounds which are 
heard with the stethoscope when listening over the thoracic wall 
can be construed as having their origin in a normal or patho- 
logical chest. The student can learn only from constant observa- 
tion to know the difference between these various sounds pro- 
duced. Many such sounds heard over a part of the chest wall 
are extraneous and are usually produced at a point more or less 
remote from the point at which they are heard. Some such 
sounds, for instance, may be produced over the opposite side, 
but conveyed to the side over which we are listening; again, 
sounds produced in the upper air passages during the act of 
breathing, in the nose, the mouth, the pharynx or the larynx, 
may also be distinctly heard over the chest and may be construed 160 
CLINICAL TUBERCULOSIS 
as being produced just below the point over which we are listen- 
ing. Still other sounds leading to error are such as may be pro- 
duced by the bell of the stethoscope pressing against the skin, 
especially in such cases in which the skin is dry or rough, by the 
rubbing of the hair or by the movements of the muscles. These 
latter the so-called muscle sounds are usually lost if the muscle 
producing the sound is made to relax, as, for instance, if the 
muscle sound is heard posteriorly in the upper portion of the 
chest; if we change the position of the arm either up or down or 
sideways, the muscle sound will be lost. These muscle sounds 
are very frequently mistaken for pleuritic friction rubs, but their 
inconstant nature and very superficial sound are sufficient for 
identification. Further, muscle sounds are usually present dur- 
ing inspiration and decreased or entirely absent during expira- 
tion. The muscles of the back and shoulders, by contraction and 
movement of the scapulae may all simulate muscle sounds; these 
also are often lost by a changed position of the arm on the side 
where these sounds are produced. 
The sounds of tracheal breathing are heard chiefly along the 
spine and with equal intensity over both sides. Harsh breath 
sounds are also often heard over normal lungs if breathing be 
continued while the mouth is closed, if the chink at the larynx is 
much contracted or abnormally small; if free breathing is inter- 
fered with by pushing the head too far forward or downward 
during the examination, or by the noise made while breathing 
through the nose, usually at the nasal opening anteriorly. It 
must also be noted that in contracted bronchiectatic conditions 
which are usually the result of a healed tuberculous process, 
crackling rales simulating a recent tuberculous process may be 
heard almost indefinitely; at the base of the lungs fine, crackling 
inspiratory rales are frequently heard, due to pulmonary ate- 
lectasis, which after repeated and deep inspiration usually wholly 
disappear. These atelectatic rales may not be heard only at the 
base but along any border of the lung if the free excursion is in- 
terfered with from any cause. 
The student is here again to be reminded that in the diagnosis 
of pulmonary tuberculosis, the evanescent or changing rales are 
of no import, that permanent crackling sounds only must and 
can be utilized because evanescent sounds or rales as we hear 
them in atelectasis, in which by insufficiently deep breathing the 
lower margin of the lung structure has not been separate for AUSCULTATION 
161 
some time, usually clear up upon a few full and deep inspirations. 
This also applies to the crackling sounds occasionally heard at 
the apices of the lungs in acute and in chronic catarrh, in emphy- 
sema, etc., which are not always due to tuberculosis, but to 
simple catarrhal conditions; here again the evanescent nature of 
the rales is of prime importance. In collapse induration of the 
lungs, the result of faulty breathing in the upper air passages, 
the tonsils, adenoids, turbinates, etc., crepitating and crackling 
sounds are also heard over the collapsed area. These also are 
of a more or less evanescent nature, the patient presenting a 
very different clinical picture from the tuberculous.4 
In examining individuals for tuberculosis we are constantly making use 
of the physical sensitiveness of feeling, seeing and hearing, but the sense 
of smelling and tasting are not applied. If not the sense of taste, has 
not the sense of smell a place in physical diagnosis? Many persons suf- 
fering from active tuberculosis have about their person an odor which is 
quite characteristic. In the exudative form of the disease with high fever 
and rapid pulse this odor is particularly noticeable. To my sense of 
smell this odor is akin to tuberculin which for some time has been 
exposed to atmospheric air (rancid). This odor is so distinct and defi- 
nite that if recognized at a physical examination I state that it is path- 
ognomonic of active pulmonary tuberculosis. I am so positive of this 
that in preparing a patient for examination (stripping to the waist) if I 
recognize this odor I make in my mind a positive diagnosis of active 
pulmonary tuberculosis without physical examination. This has often 
been confirmed by the subsequent course of the disease. 
The Mechanism of Breathing5 
The mechanism of breathing and the respiratory sounds pro- 
duced during the act of breathing have often lead to misinter- 
pretations. If we observe a normal, healthy adult while asleep 
or resting, we will note that breathing begins with a moderately 
full inspiratory phase; this is immediately followed by one of 
expiration, then a pause, a rest, then the beginning of another 
inspiratory phase, etc. This inspiratory phase, followed by an 
expiratory one, and then by a period of rest is known as a cycle 
of breathing, and the whole is spoken of as the Mechanism of 
Breathing. We will also note that the inspiratory phase is a 
short one, the expiratory a trifle longer, and that the period of 
4The pitch, duration and intensity of the sound waves may best be exemplified by the 
following simile. A large steamer is approaching the harbor. It makes its presence known 
by blowing a steam whistle which gives a sound of deep, low, sonorous tone and which is 
heard at a great distance. A little tug in the harbor answers the signal by a whistling but 
sibilant sound, short, quick, high. Its waves are carried but a short distance. 
5To make clear to the student the factors concerned in the physical examination of the 
chest by means of sight and hearing. 162 
CLINICAL TUBERCULOSIS 
rest is a little longer than both inspiration and expiration com- 
bined. These cycles of breathing are rhythmical and are re- 
peated in the normal subject about sixteen to twenty times a 
minute, with about four heart beats to each cycle of breathing. 
This is what we observe on inspection, and it should not be con- 
fused with what we hear on auscultation. 
On auscultation over the normal chest, we hear different and 
distinct breathing sounds during each cycle, over different parts 
of the chest. Placing the bell of a stethoscope over the upper 
sternum or spine, we hear a harsh high-pitched inspiratory mur- 
mur during the whole of the inspiratory phase, and an equally 
harsh murmur, not so intense, higher-pitched, slightly longer 
during the whole of the expiratory act after which nothing is 
heard during the period of rest until, with the beginning of the 
next cycle, similar sounds are again heard; and so on with each 
following cycle. This is known as bronchial breathing. 
If in another cycle we place the stethoscope below the clavicle 
on the left side, about the second rib in the mid-clavicular line or, 
posteriorly, near the angle of the scapula either right or left, 
we will hear with beginning breathing, an inspiratory sound 
much softer and lower in pitch than the one we heard over the 
upper sternum or spine. This sound is also heard during the 
whole of the inspiratory act; with expiration a still softer and 
lower sound is heard. This expiratory sound is not heard during 
the whole of the expiratory act as we found when listening over 
the upper sternum. It is heard only during one-fourth or one- 
third of the act, when all sounds cease, though the act of expira- 
tion is still going on; after this follows the period of rest. Now, 
if we compare the area over the upper sternum with the one be- 
low the left clavicle, and study the sounds carefully, we will ob- 
tain a good picture of what is meant by bronchial breathing and 
by vesicular breathing. 
After we have a clear conception in our mind concerning these 
two phases of breathing we next place the stethoscope below the 
clavicle on the right side towards the parasternal line and pay 
close attention to the sounds we hear there. We will notice that 
during the inspiratory phase we hear a sound that is not quite 
so harsh nor as high and intense as the bronchial, nor quite so 
soft and low as the vesicular. This is the broncho-vesicular in- 
spiratory sound. The expiratory sound heard immediately fol- 
lowing is also not so high as the expiratory bronchial, nor so soft AUSCULTATION 
163 
or as short as the expiratory vesicular and is known as the bron- 
cho-vesicular expiratory sound. The broncho-vesicular mur- 
murs are generally of two types; if the bronchial sounds pre- 
dominate they are broncho-vesicular; if the vesicular are most 
prominent, they are vesiculo-bronchial. 
The student should remember that the cycle of breathing is 
what he sees on inspection, but the breath sound produced dur- 
ing each cycle of breathing is what he hears through the stetho- 
scope. This is all graphically outlined in the following diagram 
in which the two circles represent a cycle of breathing, and the 
three unequal semicircles within these circles represent bronchial, 
broncho-vesicular and vesicular breathing. 
A Cycle of Breathing. Normal Breathing Rhythm 
(A) The two circles represent a complete cycle of breathing. This is what we see 
when we observe breathing in a healthy adult. 
The three semicircles within represent the sounds which we hear when the bell of 
a stethoscope is placed over the chest of the normal adult during respiration. 
The longest semicircle shows bronchial breathing, heard during the entire respiratory 
act. Inbreathing is harsh, high pitched and prolonged, outbreathing less harsh, higher 
pitched and slightly longer. The shortest semicircle represents vesicular breathing. Here 
also the sound is heard during the whole of the inspiratory act, but it is very soft as 
compared with the bronchial, lower in pitch and of equal duration, the expiratory sound, 
however, differs greatly from the expiratory bronchial. Here the sound is found very 
soft, very low in pitch and of very short duration. As compared with the bronchial it 
is only about one-fourth as long and is heard during a very short period after beginning 
expiration. Broncho-vesicular, also known as atypical intermediate or indeterminate 
breathing is midway between, is represented by the middle semicircle and may give the 
quality of one or the other depending upon which predominates the vesicular or the 
bronchial. 
(B) A cycle of breathing as is usually expressed by two vertical lines and a horizontal 
line. [Inspiration 5, Expiration 6, Rest (apnea) 13.] 
Fig. 22 CHAPTER 17 
ROENTGENOLOGY 
The Relation of X-Ray to the Diagnosis of Pulmonary 
Tuberculosis 
Historical Data. The value of X-ray in the examination of 
chest conditions was recognized very soon after Prof. Wm. K. 
Roentgen discovered this form of radiation in December, 1895. 
Due to the long exposure necessary, at that time, to obtain 
plates, only gross changes could be demonstrated. Interpreta- 
tion of these plates was often difficult because the shadows were 
blurred by respiratory movements. 
In 1905, Rieder and Rosenthal (189) exhibited X-ray plates 
taken while the patient held his breath. With this began a new 
era in the X-ray diagnosis of chest conditions. Fine details were 
shown on plates and slight changes recognized. The use of the 
Roentgen ray in chest examinations spread quickly, and instead 
of its occasional employment, it is now depended upon in a large 
percentage of cases. 
General Consideration. Knowledge of the X-ray interpreta- 
tion of pulmonary conditions has been acquired by carefully 
checking the fluorescent screen and plate findings with those of 
the clinical, physical, and laboratory examinations, and by au- 
topsy study, both gross and microscopic. Withal it is still 
fallacious to believe that the X-ray furnishes the method par 
excellence for making the diagnosis of all chest conditions. It is 
sometimes the means of arousing suspicion and stimulating 
further clinical study, and it may be the only means for discover- 
ing intrathoracic pathology, as, for example, an early central 
pneumonia, an incipient pneumothorax, or a foreign body. 
A complete X-ray examination of the thorax is best done by 
fluoroscopy and plates, preferably stereoscopic. Each examina- 
tion has its own specific value, and each supplements the other. 
Fluoroscopy permits, by changing the position of the patient, 
a view of the thoracic viscera and their movements from differ- 
ent angles. Especially noticeable are the movements of the 
164 ROENTGENOLOGY 
165 
heart and diaphragm. Pathological conditions which make rela- 
tively gross changes may also be noted and an idea of their loca- 
tion obtained. Certain changes are better shown by fluoroscopy 
than by plates, such as hydro-pneumothorax or irregularities of 
the diaphragm and its movements. 
Plates bring out much finer detail and furnish a permanent 
record so important for comparison in repeated examinations. A 
plate shows only the condition present at the instant of the ex- 
posure, and additional plates must be taken to show changes in 
position or motion. Stereoscopic plates add the factor of per- 
spective and permit fairly definite localization of thoracic lesions. 
An X-ray plate is a record of the differences in density of the 
objects rayed. The denser the object, the more it obstructs the 
ray, and the more definite, or heavier, will be the shadow cast on 
the plate. If, during plate exposure, a direct ray must pass a 
dense object overlying one less dense, the latter is obscured more 
or less completely by the former, as, for example, the heart over- 
shadows certain of the bronchial markings. If two practically 
equal densities have certain portions in line with a direct ray, 
their combined density in that particular area will cast a con- 
siderably heavier shadow, as, for example, the area of inter- 
secting rib shadows. 
(A) The Normal Chest Plate. Markings, Shadows and Find- 
ings 
It is very important to know the normal shadows on a plate 
or screen in order to recognize a deviation therefrom. A sys- 
tematic routine is needed in X-ray interpretation to avoid over- 
looking apparently minor, but often important, details. The 
following outline is suggested: 
1. —The diagnostic quality of plate or screen. 
2. —Contour and subcutaneous structures. 
3. —Bony structures. 
4. —The diaphragm. 
5. —Mediastinum, including cardio-vascular apparatus. 
6. —The hilus shadows. 
7. —The lung markings. 
Plates of adults are here considered and will be described with 
interpolation of screen findings. 
Normal Findings 
1. The diagnostic quality of plate or screen. The diagnostic 
quality of a plate depends upon the technic used. Plates should 166 
CLINICAL TUBERCULOSIS 
be taken while the patient holds the breath to avoid blurring by 
respiratory movements. Forty to sixty milliamperes, Al/2 to 5 
inch spark gap, 28 to 30 inch distance from target to plate, and 
1 to 2 or 3 seconds’ time will give a good plate. The higher 
settings, longer time, and greater distance are used with thick 
patients. Some feel that as nearly an instantaneous exposure as 
possible is preferable in all cases which require even higher 
settings than close given time. 
Routine plates are better taken in the postero-anterior posi- 
tion, preferably with the patient sitting so that the diaphragm 
Fig. 23. The normal chest plate. Explanatory note: (a) Trachea; (b) Clavicles; (c) 
Scapulae; (d) Rib; (e) Calcification of costo-chondral junction; (f) Diaphragm; _ (g) 
Aortic Arch; (h) Pulmonary Artery and Appendix of the left auricle; (i) Left Ventricle; 
(j) Ascending Aorta; (k) Left Auricle; (1) Hilum; (m) Lung Markings. 
and heart descend. The arms should be elevated to remove the 
scapulae as far as possible from the lung fields. The tube is cen- 
tered over the spine at the level of the lower borders of the 
scapulae. For stereoscopic plates, the tube is shifted six cm 
upward for the second exposure. Parts nearer the plate are more 
clearly shown, hence the postero-anterior position gives a better 
view of the interior of the thorax, especially the apices. The 
posterior parts of the ribs, the scapulae, and the upper dorsal 
and neck muscles are then farther from the plate and their 
shadows therefore less distinct. The anterior intercostal spaces 
are wider than the posterior, and the cartilaginous portions of 
the ribs (unless calcified) do not cast a shadow, hence a less ob- ROENTGENOLOGY 
167 
structed view of the intrathoracic shadows is obtained on postero- 
anterior plates. 
A successful screen examination depends upon the proper 
amount of X-ray penetration for the thickness of the patient 
rayed. Two to four milliamperes and 5 to 6 inch spark gap are 
usually sufficient. Thick patients require more penetration, 
even up to 5 milliamperes and 6 inch spark gap. Very thick 
patients are poor subjects for fluoroscopy. Care must be taken 
to avoid burns. A one to two millimeter aluminum filter on* the 
fluoroscopic table is a wise precaution. 
The examiner’s eyes must be thoroughly accommodated to the 
dark, as otherwise many details escape notice. The average per- 
son should remain in the dark five to ten minutes, or until, for 
example, small dots on a “radio” watch are seen to illuminate 
brilliantly. 
2. Contour and subcutaneous structures. The contour of the 
two sides of the thorax is equal and symmetrical. The thickness 
of the subcutaneous structures can be determined only at the 
lateral margins of the thoracic shadow, and is an indicator of the 
state of nutrition of the individual rayed. On plates of females 
the breasts cast rounded sharply defined shadows (See Fig. 24-a). 
If large they may interfere with a clear view of the diaphragm 
and lower parts of the lungs. During fluoroscopy, they may be 
pushed aside. 
3. —The bony structures. Normally the spine appears straight 
in postero-anterior and antero-posterior views. The vertebral 
bodies are seen fairly distinctly in the region of the trachea, less 
distinctly or not at all in the portion overshadowed by the 
sternum and cardio-vascular apparatus. 
The trachea (Fig. 23-a) is represented by an area of decreased 
density, 1 to 2 cm wide with straight margins, seen in the mid- 
line of the cervical and upper dorsal spine. Under favorable 
conditions, the bifurcation of the trachea and even the large 
bronchi may be made out. The upper portion of the trachea is 
deviated to the right or left of the spine if the patient’s head is 
turned to the corresponding side during the exposure. 
The clavicles (Fig. 23-b) extend upward and outward from the 
sternum to the shoulders. The right is nearly always a trifle 
higher than the left. The inferior angles and lateral borders of 
the scapulae (Fig. 23-c) are seen outside the thoracic margin if 
the patient’s arm were elevated during the exposure. The verte- 168 
CLINICAL TUBERCULOSIS 
bral borders and especially the spines of the scapulae are not so 
well seen in the postero-anterior position as in the reverse. Re- 
membering these findings makes it easy to determine the position 
of the plate during exposure. The ribs (Fig. 23-d) are distinctly 
outlined and symmetrically placed. The width of the interspaces 
gradually increases from above downward, and is wider an- 
teriorly than posteriorly. Due to their curve around the thoracic 
wall, the rib shadows on the flat plate intersect, giving a latticed 
effect. On stereoscopic view the ribs assume their normal per- 
spective. Trabeculae are usually seen in the parts nearest the 
plate. Only on very favorable plates do parts farther from the 
plate show trabeculae. 
Calcification, if present, makes either a dense line at the costo- 
chondral junctions (Fig. 23-e), or an irregular shadow in the 
cartilage. Calcification is often present in adults, usually in- 
creasing with the age of the patient. The cartilage of the first 
rib may be the only one involved, or, if all are involved, the first 
is usually more densely calcified than the others. 
Plates taken with the patient’s left side against the plate (ex- 
posure through the right oblique) give a lateral view of the spine 
and bring out the thoracic curve, and each vertebral body is then 
quite distinct. The prevertebral space, or posterior mediastinum, 
through which the oesophagus passes, is clear. In plates made 
with the patient’s right side against the plate (that is through 
the left oblique) the heart shadow covers the spine and obscures 
the prevertebral space in the lower thoracic portion. 
On screen examination, the respiratory mobility of the bony 
structures can be determined. Bone, detail, however, is less dis- 
tinct than on plates. The clavicles and anterior portions of the 
ribs move through a range of about two centimeters on deep 
respiration. The posterior portions of the ribs move but little. 
Elevation of the arms of the patient gives a clearer view of the 
lungs by partly removing the scapulae from the field. 
4.—The Diaphragm. In the postero-anterior view, the dia- 
phragm (Fig. 23-f), as seen in each lateral half of the thorax, is 
dome-shaped, smooth, and higher on the right side—in this plate, 
1.5 cm. It forms an acute angle on each side with the lateral 
thoracic wall. The angle formed with the heart shadow on either 
side is less acute, in some chests even slightly obtuse. 
Movements of the diaphragm are observed during screen ex- 
amination. On quiet respiration its excursion is 1 to 2 cm. In ROENTGENOLOGY 
169 
patients with the thoracic type of respiration, the movements 
of the diaphragm are but slightly increased on deep inspiration. 
In those having the abdominal type of breathing, the diaphragm 
descends uniformly 5 to 7 cm on deep inspiration. The angles 
with the lateral walls remain acute, the angles with the heart 
become more obtuse. 
5.—Mediastinum, including cardio-vascular apparatus. The 
chief mediastinal shadows are those of the heart and great ves- 
sels. Normally, these vary in size and shape within rather wide 
limits depending upon the height and weight of the individual. 
The two extremes are the long, narrow, “drop” heart, and the 
transverse or “squat” type. Variations between these are within 
the range of normal. The more frequent type, is here described. 
Just below the sterno-clavicular junctions, and on a level with 
the fourth and fifth thoracic vetebrae, lies the aortic arch (Fig. 
23-g). Its shadow is rounded and definitely outlined and it 
covers and extends a little beyond the spine shadow on each side, 
forming a knob-like projection on the left. The width of the 
aortic arch shadow is approximately one and one-half times that 
of the spine. 
On the left, just below the aortic knob, is a second, smaller 
shadow (Fig. 23-h) with a slightly more elongated curved out- 
line, (or rarely, normally, two smaller successive curves), caused 
by the pulmonary artery and appendix of the left auricle. This 
shadow merges with that of the left ventricle (Fig. 22-i) to form 
the major portion of the heart shadow. The left ventricle out- 
line is curved and extends downward and outward till the apex 
lies at the apparent intersection of the fifth rib anteriorly with 
the ninth rib posteriorly—in this case 9.5 cm to the left of the 
midline of the spine. From this point, it curves again toward 
the spine, and meets the diaphragm shadow near the midpart of 
its dome. The descending portion of the aorta passes downward 
from the arch to the diaphragm. The left margin of its shadow 
is sometimes seen through the heart area—the right margin is 
hidden by the spinal density. 
On the right, the nearly straight edged shadow of the ascend- 
ing portion of the aorta (Fig. 23-j) lies close to the right margin 
of the spine (here within 1-1.5 cm). At the level of the eighth 
dorsal vertebra, the right auricle outline (Fig. 23-k) curves be- 
yond the margin of the ascending aorta and downward to the 
diaphragm. It extends outward to the right of the spinal margin 170 
CLINICAL TUBERCULOSIS 
approximately 4 cm in the widest portion. The right ventricle 
outline is not seen. The vena cava is sometimes seen as a 
straight shadow crossing the right cardio-diaphragmatic angle 
close to the spine. 
During the fluoroscopy the pulsation of the heart is seen as a 
rhythmic movement of its shadow. The aortic pulsation is also 
seen. It has less excursion than that of the heart. During full 
expiration, the heart shadow is pushed upward and is widened, 
thus assuming a more transverse position due to the elevation of 
the diaphragm. On deep inspiration, the heart shadow becomes 
longer, and more perpendicular, and narrower, due to the de- 
pression of the diaphragm and consequent change in the position 
of the heart. At the same time, a narrow, clear space appears be- 
tween the left side of the diaphragm and the lower border of the 
heart. 
Viewing the patient from in front through the right oblique, 
the cardio-vascular shadow is separated from that of the spine 
and is seen in almost directly lateral view. The aortic arch then 
appears longer and narrower, about one-half to two-thirds the 
former size. The right margin of the heart follows practically 
the same curve as the spine. The left heart border is distorted 
and extends outward well toward the lateral thoracic wall, usual- 
ly to within 2 to 3 cm. 
6.—The Hilus Shadows. The hilus shadows (Fig. 23-1) are 
masses of density lying in each half of the chest near the midline 
and at the level of the sixth and seventh thoracic vertebrae, or 
in other words, at the lung roots. They are composed of the 
conglomerate mass of shadows of the large bronchi, arteries, 
veins, and peribronchial lymph glands. The outer edges have a 
tendency to linear radiation, corresponding to the heavier bron- 
chial trunks. Normally, hilus shadows vary considerably in size 
and density in different individuals. Both generally increase 
with the age of the patient. Very dense rounded shadows are 
also frequently present, and correspond to the calcified peri- 
bronchial glands found in nearly all persons at autopsy. Hence, 
on plates they have the same significance. In Fig. 23, one large 
and one small dense, rounded shadow is present on each side. 
The large one (1 cm diameter) on the right is made up of a 
cluster of smaller shadows. 
On screen examination, hilus shadows are irregular masses of 
more or less heavy density about the lung roots. If the patient ROENTGENOLOGY 
171 
is turned to the left, semilaterally, the right hilus density is usual- 
ly lost in the spine shadow and the left hilus density is lost in 
the heart shadow. If, however, the hila are large and dense, or 
if the patient is turned farther to the left, their shadows may be 
seen in the region of the posterior mediastinum. 
7.—The Lung Markings. Lung markings (Fig. 23-m) are 
quite distinctly seen on plates and consist of branching linear 
shadows caused by the bronchial tree and its neighboring struc- 
tures. 
Beginning at each hilum, the right and left bronchi divide into 
their main trunks, usually three on the right and two on the left 
side. The shadows of these with their spreading subdivisions 
extend outward in a triangular arrangement, apex to hilum and 
base toward periphery—the arrangement sometimes called a 
“fan.” . 
The first trunk on either side divides into the vertebral and 
first, second, and third interspace branches. The shadow of the 
vertebral branch extends upward toward the apex. On the right 
it lies close to the spine, on the left it is a little farther out, due 
to the fact that the left bronchus divides after curving under the 
arch of the aorta. The shadows of the next three branches on 
either side lie in the plane of the first, second, and third inter- 
costal spaces, and are named from these positions. The finer 
branches more or less intermingle or overlap, especially those of 
the second and third interspace branches. The middle trunk on 
the right supplies the middle lobe, while on either side the re- 
maining trunk divides into the lower lobe branches, which as 
seen on plates, radiate downward and outward. All branches are 
best made out on stereoscopic plates, together with some addi- 
tional (127) details not otherwise observable. 
Normally the shadows of the various bronchial branches can 
be followed about two-thirds the distance toward the periphery 
beyond which the branches become so fine and so nearly the 
same density as the surrounding lung tissue that they do not 
cast a distinct shadow on the plate. Lung markings are practi- 
cally equal in density from above downward and in correspond- 
ing positions in either lung, except that the lower lobe branches 
are large and heavy near the spine. They are harder to see on 
the left because they are overshadowed by the heart. The apices 
(within the circle of the first rib) are clear and show either no, 
or but faint, markings of the bronchi. It is especially to be noted 172 
CLINICAL TUBERCULOSIS 
that no fan stands out as heavier than the one above or below. 
With advancing- age of the individual rayed, all branches are 
more dense and extend nearer to the periphery, including the 
apices. 
On screen examination the lung areas are practically clear 
from apex to base. The density of corresponding portions of the 
two sides is equal. If conditions are very favorable, some of the 
coarser lung markings are distinguished as linear strands radiat- 
ing outward from the hila. Finer markings are lost on fluor- 
oscopy. On deep inspiration, the lung areas “light-up” or appear 
less dense practically equally on the two sides. 
(B)—Variations from Normal. Interpretation of pathological 
chest findings in tuberculosis. (167) 
Variations from normal plate shadows consist in either in- 
creased or decreased density, with or without distortion of the 
outlines or organs. Variations producing an increased density 
may be due to pathological changes which have taken place, 
either within the lung parenchyma or along the bronchi. 
The type of the variations giving an increase in density, and 
due to pathological conditions along the bronchial tree and its 
surrounding parenchymal structures, may or may not produce 
on plates shadows which follow closely the bronchial branches. 
The shadows which do follow the bronchial branches give a tri- 
angular or fan-shaped arrangement, with base toward the peri- 
phery and apex toward the hilum. If such shadows are in upper 
lobes, if their density is mottled and extends well toward the 
periphery, and if one or more heavy bronchial shadows connect 
with the hilum—which also shows increased density—a tuber- 
culous infiltration of the lung is suggested (142). 
When the linear markings of one or two upper bronchial 
branches are slightly heavier than those of the neighboring 
branches and when the peripheral portion shows a hazy and 
slightly stippled, or mottled appearance, an incipient or very 
early tuberculosis is to be considered. Such changes are fre- 
quently at the level of the first or second anterior interspace. In 
other cases, the increased linear markings extend into one or both 
apices, and may, or may not, end in small, rounded, denser 
shadows. In still other cases, the increased density of the linear 
markings is absent and only a haziness or clouding of one or both 
apices is found. If both apices are involved, the shadow in one is 
usually denser than in the other. Dunham (146) stated (103) ROENTGENOLOGY 
173 
that the right apex is involved before the left, judging by its 
heavier density as seen on X-ray plates, in the proportion of 55% 
to 45%. 
Associated with any of these variations, the corresponding 
part of the hilus shadow may be increased in density and often 
includes small, round, dense shadows due to tuberculous changes. 
In cases with clouding of the apices only, other reasons for the 
clouding must be considered, such as shadows caused by heavy 
neck muscles, thickened pleura, supra and infra-clavicular glands, 
struma, scoliosis, cervical ribs, movements, or an artifact. Clini- 
cal findings are, therefore, of great importance in the interpre- 
tation. 
If the shadows in or near the apex are due to an active tuber- 
Fig. 24. Early Tubercu’osis. First Stage, (a) Breasts; (b) Heavy Lung Markings. 
culosis, corresponding physical findings are present, such as dul- 
ness, harsh or bronchial breathing, and rales, also general symp- 
toms, such as cough, loss of weight, failing appetite, etc. The 
slight changes so far described are rarely, if ever, recognized on 
screen examination. 
Fig. 24 illustrates a typical case of slight variation from nor- 
mal. The right apex is hazy. No linear markings extend into it. 
The linear shadows of the bronchial branch in the right first in- 
terspace are heavier and extend farther toward the periphery than 
those of any other branch in either lung. Near the periphery, the 
markings are not well defined, but are hazy and somewhat 174 
CLINICAL TUBERCULOSIS 
stippled. The bronchial markings in the left first interspace are 
nearly as heavy and extend nearly as far towards the periphery 
as those of the right, but here is neither haziness or stippling. 
A heavy linear marking is present on the right side (Figure 
24-b), and extends downward from the hilum well toward the 
diaphragm. The hilus region on either side is moderately heavy 
and contains three or four dense rounded shadows in each. These 
lie near the apices of the triangular areas of increased density 
just described. 
On physical examination, fine crepitant and subcrepitant rales were 
heard anteriorly and posteriorly over the area corresponding to the shadow 
in the right first interspace. On the left, over a small area in the third and 
fourth interspaces near the sternum, occasional subcrepitant rales were 
heard. A friction rub was present at the lower border of the left lung. 
(Left sided pleurisy was present six months previously. No correspond- 
ing pleural shadow is made out on the plate.) There was no cough or 
expectoration, temperature to 99.6°, pulse 70-80. Complement fixation 
test for tuberculosis + + +. Diagnosis, based on the combined findings 
—early tuberculosis. 
Increased density of the bronchial markings is also found in 
other chronic inflammatory processes, such as bronchitis and 
asthma, or due to long continued inhalation of coal-dust or simi- 
lar material. In plates of such cases, the linear markings are in- 
creased in density and extend farther toward the periphery than 
normal, but in distinction to tuberculosis, no one or two branches 
stand out as heavier than all others; instead, the markings are 
practically uniform throughout both lungs, though occasionally 
the markings of one lung are a little heavier than those of the 
other. Haziness of the peripheral portion of the bronchial branch 
shadows is absent, or, rarely, very slight. Stippling, when pres- 
ent, is uniformly distributed, and occurs in small, rounded, fairly 
dense spots, with little or no surrounding haziness. 
Advance of the tuberculous process accentuates the previously 
described plate findings. Increased density is seen in several of 
the bronchial branches, usually of the upper lobes, with varia- 
tion in the degree of density in the different triangular areas. 
The lung markings appear more broken and irregular, due to 
being overshadowed by larger flake-like spots. The general ap- 
pearance of these shadows is that of a heavy snowstorm which 
grows lighter toward the lower lobes. Increase of the density 
and of the size of the flakes bespeaks the advancement of the 
process. In general, those bronchial branches first affected cast ROENTGENOLOGY 
175 
the heaviest shadows. Rarely are the shadows in the different 
areas uniform. In fact, the irregularity speaks strongly for 
tuberculosis. (Areas in which the density is heavy need not 
necessarily be “active” in a clinical sense, but may be of long 
standing, or partly healed). 
The corresponding areas of the hilum show heavier shadows 
somewhat in proportion to the increase in density elsewhere in 
the lungs. Usually there are one or several rounded, very dense 
shadows in the hilum, due to the affected lymph glands. It is 
not unusual to find a high position of the diaphragm on the af- 
fected side. 
A tuberculous process, sufficiently advanced to give such plate 
findings as are here described, also gives definite clinical findings, 
such as productive cough with tubercle bacilli in the sputum, 
fever, rapid fiulse, emaciation, night sweats, etc., also dulness, 
bronchial breathing, and rales. The greater dulness, tubular 
breathing, and coarser rales go with the greater density and 
stippling in larger, heavier flakes. The slight dulness, slight 
bronchial breathing, and fine, crepitant and subcrepitant rales are 
associated with the slight increase in density, slight haziness, and 
stippling in small, not very heavy spots. In general, the latter 
findings thus become evidence of a more recent or acute process, 
while the former are evidence of one older or more advanced. 
On screen examination, the density of the lung field varies in 
the affected areas from heavier than normal to very dense. Often 
there is also a blotched or spotted appearance consisting of 
lighter and darker areas. These variations in density correspond 
to the amount of infiltration of the affected bronchial branches. 
Limited respiratory excursion and irregularity in outline of the 
diaphragm are also frequently seen. 
Figures 25 and 26 are from plates of the same individual. 
The patient’s main complaints were difficulty in swallowing, associated 
with shortness of breath on exertion, persistent cough and expectoration, 
some loss in weight, and profuse night sweats. The difficulty in swallow- 
ing was due to cardiospasm with retention of as much as 375 cc of food 
and mucus in the oesophagus. Lung expansion was poor, and dulness 
was present over both upper lobes. Many rales were heard on both sides 
anteriorly and along both sides of the spine. Tubercle bacilli were found 
in the sputum. 
A plate taken at this time (Fig. 25) shows a triangular, uneven 
density on the right side, in the region of the apex and first and 
second interspaces. The peripheral portion of this shadow is 176 
CLINICAL TUBERCULOSIS 
denser and more hazy than elsewhere, and is densest in the sec- 
ond interspace. Extending downward from the apex to the dia- 
phragm is a snowstorm of moderately large, flake-like spots 
which grow progressively lighter and smaller toward the base. 
A similar triangular, uneven density is present on the left side, 
also involving the apex and first and second interspaces, but is 
not so heavy as on the right. Smaller, less dense, flake-like spots 
are present. These are scarcely noticeable below the level of the 
third rib anteriorly. About half way to the periphery in the left 
second interspace is a pear-shaped area of decreased density, 
(2x4cm) with the narrowed portion outward. This area is sur- 
rounded by a fairly dense, slightly irregular margin. These find- 
Fig. 25. Advancing Tuberculosis. Cavity Formation. (A) Cavity. 
ings are characteristic of a cavity. On screen examination a 
heavy, mottled density was present, especially in the upper 
lobes. 
After receiving treatment for the cardiospasm, the patient 
gained thirteen pounds in five weeks. In the plate taken at this 
time (Fig. 26) the general density of the triangular shadows in 
the upper lobes is heavier than in the previous plate (Fig. 25). 
The flake-like spots, giving the snowstorm appearance, are larger 
and denser, and are seen throughout the right side and extend 
a little farther down on the left. The left lower lobe is still prac- 
tically clear. In the left second interspace, there is a heavy, 
nearly solid density, somewhat triangular in shape, with apex ROENTGENOLOGY 
177 
outward, extending from the hilum about two-thirds the distance 
toward the periphery. (This is the area in which the decreased 
density—cavity—was seen on the previous plate.) 
Since the snowstorm appearance in Fig. 26 involves a greater 
area of the lung fields than in Fig. 25, an advancement of the 
process is clearly indicated. The increase in density of the upper 
lobes is difficult to interpret from the plate alone. It may be due 
entirely to advancement of the tuberculous process, or may be 
due in part at least, to healing. Since eleven months later this 
patient had gained 33 pounds and was “feeling fine,” it is reason- 
able to believe that a healing process had begun at the time Fig. 
25 was taken. This brings out the difficulty of correctly inter- 
Fig. 26. Active Tuberculosis. Far Advanced. Note area of cavitation. (A) Cavity Area 
preting the condition of the patient from plates alone, and em- 
phasizes the importance of combining the clinical evidence with 
the plate findings. 
(C) Differential Diagnosis. 
In the differential diagnosis the pneumonias are chiefly to be 
considered. 
The shadow of lobar pneumonia is a uniform “pneumonic” 
haze, veiling the lung markings more or less completely, (Fig. 
27-a). The shadow is triangular in shape with apex outward, and 
usually with at least one straight, sharply defined margin cor- 
responding to an interlobar septum. Part of a lobe, especially in 
the early stages of the disease, later an entire lobe, or more than 178 
CLINICAL TUBERCULOSIS 
one lobe may be involved—lower lobes more frequently than 
upper. The shadow varies markedly on re-examination within 
a few days, due to the rapidly changing stages of the pneumonia. 
The history and physical findings are usually characteristic for 
a pneumonia. In clinically atypical cases, the plates findings 
may speak definitely for pneumonia, especially an early central 
pneumonia, some time before other findings warrant such a 
diagnosis. 
The shadows of an unresolved pneumonia, or one in which 
resolution is irregular or delayed, may very closely simulate 
those of tuberculosis, especially if involving an upper lobe. In 
such cases the differentiation must be by clinical means! 
Fig. 27. Pneumonia. Note area of congestion. (A) Area of Congestion. 
Shadows due to broncho-pneumonia are similar in character 
to those of the lobar type, except that they are not confined to 
one lobe, but are of an irregular or patchy distribution—often 
in the lower lung. Its X-ray appearance may simulate tuber- 
culosis. The rapid change in plate findings, the fact that it is 
usually in a lower lobe, the history and clinical and laboratory 
findings make the differentiation. 
The shadows due to influenza-pneumonia are not characteris- 
tic, and their distribution is variable. These shadows are of a 
hazy and mottled appearance, which may be localized to one or 
two bronchial branches, or may be very extensive. Here again, ROENTGENOLOGY 
179 
the rapid change in plate findings, together with the history and 
clinical findings are essential for a diagnosis. 
For some time after the active process has subsided, any of the 
pneumonias may leave changes in the lung which on plates give 
an increased density of the linear markings very similar to that 
seen in the chronic inflammatory conditions, such as bronchitis 
and asthma. 
The plate in Fig. 28 was taken twelve days after the fever of a 
severe influenza had subsided, and illustrates early post-influenzal 
changes. Throughout both lung fields, the linear markings show 
a uniform increase in density which is fairly heavy. Very similar 
Fig. 28. Post-influenzal changes. Increase in density of lung markings simulating a 
chronic inflammatory process. 
plate findings may also be seen several weeks or months after an 
attack of either influenza or pneumonia. 
In tuberculosis, in contradistinction to the pneumonias, the 
densities are uneven and are more frequently located in the upper 
lobes, and the findings are constant on repeated examination 
even after relatively long intervals. 
Miliary tuberculosis gives shadows of increased density due 
to pathology in the lung parenchyma which obscure, rather than 
follow, the triangular or fan-shaped arrangement of the bronchial 
branches. Myriads of small, fairly dense spots, each with a hazy 
halo, are scattered promiscuously, usually throughout both lungs. 
These hide the lung markings and give a hazy, stippled appear- 
ance which suggests a fine snowstorm on a gray day. The gen- 180 
CLINICAL TUBERCULOSIS 
eral density may be a little heavier in the upper than in the 
lower lobes. The size of the flake-like spots may vary slightly 
in different cases, but is practically uniform in each individual 
case. There is usually little or no apparent increase in the 
density of the hilus shadows. 
Figure 29 illustrates a case of miliary tuberculosis. Here the 
stippling is in small flake-like spots, each with a hazy halo, scat- 
tered very profusely throughout both lungs. A heavy, triangular 
shadow extends to the periphery in the left second and third in- 
terspaces and is covered by larger flakes. It is reasonable to as- 
sume that this area is the site of an earlier tuberculosis, from 
Fig. 29. Miliary Tuberculosis. 
which the miliary dissemination took place. The patient died 
with the clinical picture of miliary tuberculosis a week after this 
plate was taken. An autopsy was not obtained. On screen ex- 
amination, there is an increase in density, quite uniform through- 
out the area involved, often with a blotched or spotted appear- 
ance. Diaphragm excursion may be limited. 
The shadows of miliary tuberculosis are rather typical on 
plates and their differentiation is often necessary. The plate, 
on the contrary, becomes of diagnostic importance because the 
clinical and physical findings are often absent or indefinite. 
A few other lesions have a miliary distribution of their shad- 
ows on X-ray plates. They are not very likely, however, to be 
confused with miliary tuberculosis. ROENTGENOLOGY 
181 
In advanced cases, the nodular type of metastatic carcinoma 
appears on plates in a miliary distribution so profuse that both 
lung fields are covered by rounded shadows due to the meta- 
static nodules. On the same plate, these shadows may vary in 
size from very small up to two centimeters in diameter, and in 
density from very faint up to the density of the heart shadow. 
There is a fuzzy or “Cotton-ball” appearance about the periphery 
of each spot which is quite characteristic. 
Figure 30 illustrates a plate of metastatic carcinoma of the 
lungs. This patient had had a breast amputation for carcinoma 
some time before, with recurrence and evidence of lung meta- 
Fig. 30. Metastatic Carcinoma. Nodular Type. 
stases at the time the plate was taken. The plate shows all the 
characteristics of the shadows just described. 
The shadows due to sarcoma of the lungs are occasionally 
numerous enough to be considered of miliary distribution and be 
confused with miliary tuberculosis (113). More usually they 
appear on plates as one or several widely separated spots of vari- 
able size and density, the peripheral margins of which, in con- 
tradistinction to carcinoma, are sharply defined. The plate in 
Fig. 31 illustrates a case of the latter type of sarcoma. In this 
plate, one large and three smaller, fairly dense, rounded, sharply 
defined shadows are present on the right side. These are due to 
the sarcomatous nodules. The left lung is not involved. 
The shadows of multiple gummata of the lungs are said to 182 
CLINICAL TUBERCULOSIS 
have much the same appearance as sarcoma; here serological 
and therapeutic tests are needed. 
The type of plate shadows appearing in the region of the lung 
parenchyma as an increased density, which veils the linear mark- 
ings, but may or may not follow the triangular arrangement of 
the bronchial branches, is that due to pulmonary hemorrhage. 
In this type, a cloud-like shadow appears which may be localized 
or extensive, and which may vary somewhat in density in dif- 
ferent parts of the cloud. Lung markings may or may not be 
seen, or, in places, may seem to show through this cloud of in- 
creased density. Variations due to hemorrhage depend not so 
much on the total quantity of blood lost, as on the position of 
Fig. 31. Metastatic Sarcoma. (A) Areas representing metastatic nodules. 
the blood retained in the bronchi, and also the amount and type 
of reaction which may have taken place in the lungs. 
Figure 32 is the plate of a medical student, who without warn- 
ing or previously recognized symptoms, had a severe hemor- 
rhage, followed by a second hemorrhage the next day. The total 
quantity of blood lost was estimated as two quarts. A few tu- 
bercle bacilli were found. This plate, taken three days after the 
second hemorrhage, shows a heavy fan-shaped cloud of increased 
density covering the left hilum, and extending well to the pe- 
riphery in the left first and second interspaces. Almost no lung 
markings are seen in this area. In the right hilum is a mass of 
rather heavy, rounded shadows. The findings elsewhere in both ROENTGENOLOGY 
183 
lungs are practically negative. On fluoroscopy, there is simply 
an increased density, often very heavy, in the region of the 
hemorrhage. 
A hemorrhage shadow may be quite similar to that of a pneu- 
monic consolidation. Hemorrhage appears at once as a heavy 
shadow, and is less rapid in its subsequent change—here the his- 
tory and clinical findings are of great value. 
Still another type of increased density, due to tuberculosis, 
which on plates is in the region of the lung parenchyma, which 
blurs or obscures lung markings, and which may or may not 
follow the fan-shaped arrangement of the bronchial branches, 
is that due to healing processes, such as scar tissue or fibrosis. 
Fig. 32. Pulmonary Hemorrhage. 
These shadows are of an even or “solid” density which may 
appear in localized streaks or bands, small spots or larger masses. 
The fan-shaped shadow of the healing tuberculous lesion be- 
comes denser than in the more active stage. Its linear markings 
become more definite and a little wider. The stippling either 
disappears or changes to small, dense, even calcified spots, 
which, scattered through the area, add to its density. A small, 
healing, fan-shaped area may thus seem to be a small, almost 
solid mass, streak, or band on the plate. 
Small cavities may be lost by contraction of the scar tissue, or 
obscured by the shadow of the thickened wall, giving the ap- 184 
CLINICAL TUBERCULOSIS 
pearance of a smaller or larger dense spot as was pointed out 
under Fig. 25. 
In marked cases of fibrosis, the shadow is a heavy density, 
often more or less irregular in outline, and in the degree of its 
density. Such a shadow may be dense enough to blot out all 
the lung markings in a lobe, the greater part of a lung, or parts 
of both lungs. The heart shadow may be pulled completely 
to one side or its outline lost in the general density. The shad- 
ows of the aorta and trachea are frequently pulled far to one side. 
The diaphragm may be drawn upward or made irregular in ap- 
pearance. Even the chest wall may be contracted. 
Figure 33 is shown as an example of marked fibroid phthisis 
Fig. 33. Fibroid Phthisis, (a) Mass of heavy streaks and bands; (b) Oval, relatively 
clear, area; (c) Trachea; (d) Left Bronchus. 
with distortion of the outlines of viscera. In this plate, there is 
a heavy density throughout the right side. It is practically solid 
in the lower half, obscuring the diaphragm and lung markings. 
Even bone density is lost except for parts of the ribs near the 
lateral margin. The heart shadow must lie within this solid 
density, for it is not made out elsewhere on the plate. In the 
upper half of the right lung the density is not so uniformly solid 
and rib outlines can be followed, though lung markings cannot. 
Just below the mid-portion of the clavicle and above the level of 
the third rib anteriorly (Fig. 33-a), the density is made up of a 
compact mass of heavy streaks and band-like shadows, none of ROENTGENOLOGY 
185 
which can be traced for more than a short distance. These are 
a part of the fibrosis. An oval, relatively clear area (Fig. 33-b) 
lies in the first interspace and overlaps the first and second ribs 
anteriorly. This is probably due to partial pneumothorax. The 
shadow of the trachea (Fig. 33-c), is curved and lies to the right 
of the spinal margin from the second to the sixth dorsal vertebra. 
There the left bronochus (Fig. 33-d) crosses the spine shadow. 
The left lung is relatively clear, although its linear markings 
are uniformly intensified, extend well to the periphery, and have 
a somewhat flaky or beaded appearance. The hilus shadows 
are fairly heavy, and several heavy bronchial branch shadows 
extend downward. The intercostal spaces are narrower on the 
right than on the left indicating some retraction of the chest 
wall. 
This patient had a long history of cough, loss in weight, etc., 
and tubercle bacilli were found in the sputum. On screen exam- 
ination, the shadow of such fibrosis is dense, even solid. The 
position of the distorted viscera can usually be made out. These 
shadows are to be differentiated from those which appear to 
occupy the lung field by virtue of their position, but which are 
due to pathology outside of the lung. 
A uniformly increased density, covering the region of the lung 
field and varying from a faint haze to so dense a shadow that 
lung markings are obscured, may speak either for fluid in the 
pleural cavity, or for thickened pleura. If the shadow is faint, 
it is more often due to thickened pleura, as the fluid shadow is 
usually, though not always, heavy. Given a heavy shadow, if 
the contour of the chest wall on the affected side is contracted, 
as shown by narrowing of the intercostal spaces at the lateral 
margin, and if the mediastinal viscera are not displaced toward 
the opposite side, then the increased density is very probably 
due to thickened pleura. A displacement of the mediastinal vis- 
cera, en masse, toward the opposite side without narrowing of 
the intercostal spaces, speaks strongly for the increase in density 
being due to fluid. If the shadow is uniformly dense, the inter- 
costal spaces narrowed, and the viscera as a whole pushed to- 
ward the opposite side, there is probably a combination of fluid 
and thickened pleura. This combination is not infrequently 
seen in tuberculosis, but may also be due to other causes, as 
empyema, or carcinoma of the pleura by direct extension. 186 
CLINICAL TUBERCULOSIS 
Small amounts of free fluid obscure the costo-phrenic angle 
only, larger amounts extend higher in the pleural cavity, and 
hence obscure more of the lung field. The upper border of these 
fluid shadows has a definite outline, which curves upward at the 
outer or peripheral margin, unless the fluid so completely fills 
the chest that the upper border is lost under the clavicle and 
first rib. Exudative pleurisy, or hydrothorax, is so frequently 
associated with tuberculosis that, with such plate findings, it 
must always be kept in mind. 
Figure 34 illustrates the plate findings of hydrothorax. 
On the left, extending upward to the level of the second in- 
terspace anteriorly is a uniform, very dense shadow, with a well 
Fig. 34. Hydrothorax. 
defined, upper border, which curves upward at the outer margin. 
The diaphragm, left heart outline, and lung markings are hidden 
by it. The right border of the cardio-vascular shadow is seen 
farther to the right than normally. The lung markings which 
lie above this shadow, and also those of the right side are normal. 
These findings alone are not diagnostic for tuberculosis, but are 
suspicious for it. 
On fluoroscopic examination, hydrothorax appears as a solid 
density which curves upward at the outer margin, and which 
is not movable on respiration or with change of position of the 
patient. (The fluid associated with certain tumors may be slowly ROENTGENOLOGY 
187 
movable. If air is also present, the fluid is freely movable.) 
The relative position of small amounts of fluid in the chest may 
be determined by viewing the patient from different directions 
during the fluoroscopy. Increased density due to localized thick- 
ening of the pleura, may also frequently be an associated finding 
in tuberculosis. 
If the angle of the diaphragm with the chest wall is clouded 
by a rather dense, more or less irregular, shadow, without the 
sharply defined upper margin due to fluid, although there may 
be an upward extension of the shadow at the lateral margin, a 
localized thickening of the pleura with adhesions to the dia- 
phragm is definitely suggested. The dome of the diaphragm 
then appears flattened, or is irregular in outline, while the lat- 
eral portion is fixed. This fixation is best brought out by the 
limitation of the respiratory mobility of the diaphragm as seen 
on fluoroscopic examination. Fluid may obscure or limit the 
movements of the diaphragm but does not make it irregular. 
A dense line a little inside of, and parallel to, the lateral thor- 
acic wall is due to a localized pleural thickening, causing re- 
traction of the lung and consequent small pneumothorax. The 
intercostal spaces in this region may also be narrowed. These 
findings are not uncommon in tuberculosis. Similar findings, a 
little larger in area, are associated with “walled off” pockets of 
fluid or pus occurring about the lung surface but not extending 
to the diaphragm. In such cases, however, the fluid level mav 
often be made out. 
If either a dense line, or a relatively small, fan-shaped, uni- 
form density with base to hilum extends transversely across the 
lung field in a position corresponding to a lobe interspace, an 
interlobar pleural thickening is to be considered. Such findings 
accompany tuberculosis, as well as pneumonia, localized empy- 
ema, etc. Their position helps to differentiate them from the 
lines due to fibrosis or healing described above. 
Very dense, irregular shadows which are well localized, or 
fairly extensive, and due to calcification of the pleura, may ap- 
pear to occupy any part of the lung field by virtue of their posi- 
tion in the pleura. These shadows may follow, or be associated 
with, tuberculosis, an old empyema, a lung abscess, or, occa- 
sionally, old age. To determine their relative position stereo- 
scopic plates are necessary. 
On fluoroscopy, localized pleural thickening appears as a 188 
CLINICAL TUBERCULOSIS 
heavy density in the region of the lung field. Its diagnosis and 
localization are aided by viewing the patient from different an- 
gles, and also by noting any limitation or irregularity in the ex- 
cursion of the diaphragm. 
Certain tumor masses, such as primary mediastinal malig- 
nancy and the infiltrating type of metastatic carcinoma, may give 
heavy shadows in the region of the lung field which involve the 
portion of the lung nearer the spine, instead of the peripheral 
portion as in tuberculosis. A mediastinal tumor casts a heavy, 
rounded shadow, usually in the upper portion of the lung field, 
and appears to be a single mass rather than a group of several 
smaller shadows. There is often considerable thickening of the 
lung markings about the tumor, but in contradistinction to tu- 
berculosis, they decrease, rather than increase in density toward 
the periphery. If lying in the region of the aortic arch, a tumor 
is differentiated from an aneurysm by the fact that its margin 
is not so sharply outlined as the aortic shadow, and can nearly 
always be seen to lie in a different plane. On lateral plates, 
tumors usually extend into the posterior mediastinum; aneur- 
ysms extend anteriorly. 
The infiltrative type of metastatic carcinoma might be mis- 
taken for one of those relatively rare cases of basal tuberculosis. 
Carcinoma, however, is heaviest near the spine with a tendency 
to linear radiation of its markings, and a decrease in the general 
density toward the periphery; the opposite is true of tuber- 
culosis. History and clinical and physical findings are again 
very valuable aids in diagnosis. 
Figure 35 illustrates such a case. Here the density is very 
heavy and mass-like near the spine, from the arch of the aorta to 
the diaphragm, on the right side, but grows less dense as it ex- 
tends outward, and practically ceases about half way to the peri- 
phery. This metastatic growth followed a breast amputation for 
carcinoma, and was confirmed at autopsy. 
Decreased density in the region of the lung field may, on 
plates, be (a) localized or (b) generalized. 
A. Localized. A localized or circumscribed decrease in density 
due to tuberculosis is that produced by cavity formation. Cavities 
are usually in upper lobes, may be single or multiple, and may 
vary in size from very small up to several centimeters in diam- 
eter. They are usually rounded in outline, with a margin which 
varies from very thin to very broad and dense. The area of de- ROENTGENOLOGY 
189 
creased density due to the cavity may be more or less mottled 
depending upon the density of the lung markings in front or back 
of it. Cavities show an increase in density when they are filled 
with fluid. Occasionally, a definite fluid level with an overlying 
clear air space may be seen. A cavity is illustrated in Figures 25 
and 26. Heise describes annular shadows very similar in appear- 
ance to true intrapulmonary cavities but which may change in 
size and shape rapidly. In some, a fluid level has been seen. He 
believes these are due to localized pneumothoracies and indicate 
pleural softening with rupture of the lung. They are rarely diag- 
nosed clinically. 
Cavities are not always made out on screen examination, espe- 
Fig. 35. Metastatic Carcinoma. Infiltrative type. 
dally if small. The surrounding density may be the only thing 
which attracts attention. On deep inspiration, an open cavity 
may grow clearer and a trifle larger. Fluid appears, as on plates, 
as a definite density and may be demonstrated by its mobility, if 
air is also present. Rotation of the patient aids in the localiza- 
tion of the cavity. 
A bronchiectatic cavity or a lung abscess is most often in a 
lower lobe. The shadow of either is that of a rounded, hazy, or 
“pneumonic” area usually connected with the hilum by several 
heavy bronchial branches. This area is usually surrounded by a 
fairly well circumscribed zone in which the lung markings are 
much increased in density. Shadows of enlarged or dilated 190 
CLINICAL TUBERCULOSIS 
bronchi speak strongly for bronchiectasis. These conditions are 
rarely due to tuberculosis. 
B. Generalized. One type of generalized decrease in density, 
not a feature of tuberculosis, is briefly mentioned here for the 
sake of the differential diagnosis. In such cases, there is an in- 
creased transmission of the rays throughout the lung fields, due 
to an increase in the size of the air spaces of the lung. There is 
little change otherwise in the lung markings. A “barrel-shaped” 
chest with widened intercostal spaces and a depressed, flattened 
diaphragm are usually associated findings. Such X-ray findings 
speak strongly for emphysema. 
A generalized decrease in density which, on plates, appears in 
the region of the lung field, and which is frequently found in 
cases of tuberculosis, is that due to pneumothorax. This condi- 
tion often develops spontaneously in the course of a tuberculous 
process, or is produced artificially as a therapeutic measure. 
On plates, pneumothorax gives an area of decreased density 
between the border of the collapsed lung and the lateral thoracic 
wall. The size of this area corresponds to the amount of air 
present, or conversely, the lung is compressed in proportion to 
the amount of air in the pleural cavity. The area between the 
lung margin and the chest wall is clear, and, of course, is devoid 
of lung markings. The compression of the lung may be slight, 
or so marked that the lung appears as a small mass about the 
hilum. If pleural adhesions exist, the compression of the lung 
is irregular, depending upon the size and position of the adhesive 
bands. The markings of the compressed lung appear to be in- 
creased in density because more compact, aside from any other 
lung pathology which may also be present. 
Figure 36 is the plate of a patient in whom a spontaneous 
pneumothorax developed. Here, the left lung is compressed to 
about half its normal size. The space beyond the smooth, 
sharply defined, undulating lung margin is clear, and devoid of 
all lung markings. The lower half of the left lung is practically 
a solid density and some very dense markings are visible in the 
upper lobe. The increased density in the left lung is due to 
compression. The left diaphragm is depressed and flattened. 
On the right side, the lung markings are uniformly intensified, 
somewhat beaded in appearance, and extend well to the peri- 
phery and into the apex. 
If artificial pneumothorax is considered as a therapeutic ROENTGENOLOGY 
191 
measure in a given case, the X-ray plate should always be 
studied before making the final decision. A plate is the best 
means of determining the real extent of the process, and, in cases 
of bilateral involvement, warns against compression of one lung 
if too great an area of the opposite side is involved. A plate aids 
in determining the best site for the injection, and also acts as a 
check on the results of the pneumothorax, by showing at once 
the amount of compression obtained, and, later, by showing the 
effect on the tuberculous process. 
On fluoroscopy, the clear area of the pneumothorax is easily 
seen, while the area of the compressed lung is relatively dense. 
Fig. 36. Pneumothorax. 
Pleural adhesions, especially if fairly dense, are quite easily made 
out. 
Plate findings due to hydro-pneumothorax are a combination 
of increased and decreased density since both fluid and air are 
present in this condition. The dense shadow of the fluid in such 
a case has a straight upper border, which is superimposed by the 
clear air space. Lung markings are wholly or partially obscured 
in the region of the fluid, are absent in the region of the! air, and 
are compressed through the rest of the lung field. Pleural thick- 
ening may be present, which, of itself, or perhaps by adhesions 
which pull the lung slightly upward, may give the appearance of 
an upward outer curve of the otherwise level fluid surface. 192 
CLINICAL TUBERCULOSIS 
Changes in the fluid level may be demonstrated by plates taken 
in different positions. With the patient horizontal, however, on 
postero-anterior plates or the reverse, the shadow of the fluid 
spreads out and obscures the clear air space. 
Figure 37 is a plate, illustrating hydro-pneumothorax. In this 
plate the lower part of the left lung field and the left diaphragm 
are completely obscured by a dense shadow which extends up- 
ward as high as the level of the fourth rib anteriorly. At its 
upper margin this shadow is very sharply outlined, and forms a 
straight line transversely across the lung field from the spine to 
the lateral wall. The area above this line is clear due to the 
presence of air, and the lung markings are absent. The heart 
Fig. 37. Hydro-pneumothorax 
and aorta are pushed slightly to the right. The right lung 
markings are moderately intensified, and may be seen extending, 
practically uniformly, well toward the periphery. The right 
diaphragm is normal. 
There are several small, dense shadows on the left side in the 
region of the lower lung field and upper abdomen, due to shell 
fragments. Clinically, the case was hemo-pneumo-thorax, due to 
war injury. 
On fluoroscopic examination, hydro-pneumo-thorax presents 
a dense shadow due to the fluid, which is superimposed by a clear 
air space. The upper margin of the fluid is very freely movable ROENTGENOLOGY 
193 
by slightly shaking the patient. Viewing the patient from differ- 
ent angles aids in determining the amount of fluid and air pres- 
ent, and their relative location in the chest. 
It is hoped that the difficulties in the diagnosis of tuberculosis 
from the plate alone have been brought out. There are a few 
rather characteristic findings, such as shadows of calcified tuber- 
culous glands, and of miliary tuberculosis, and some which are 
always very suggestive, such as the fan-shaped, hazy, rather 
heavily mottled shadows near the periphery in the upper lobes. 
But with all this it is to be emphasized that the relation of X-ray 
to the diagnosis of pulmonary tuberculosis is that of an adjunct, 
rather than the only means, or even the best method, of making 
the diagnosis. C. B. R. CHAPTER 18 
MENSURATION, SUCCUSSION, VITAL CAPACITY, ETC. 
(a) Mensuration. Measurements of the Chest. Thoracometry. 
Physical exploration by inspection may reveal that the chest as 
a whole is abnormally long from the neck down to the costal 
arch, or abnormally flat, or perhaps disproportioned, is not sym- 
metrical, one half of the chest may bulge or protrude, or the other 
half be much retracted, is much smaller than the opposite half. 
These abnormalities or chest deformities may point to some dis- 
turbance in the thoracic cavity, perhaps, a tuberculous process; 
the retraction, to an old chronic fibroid phthisis, empyema, or 
pleurisy; an over distension of one half of the chest, to a vicarious 
emphysema, so that exact measurements are often necessary. 
In tuberculous individuals, even with apparently perfectly nor- 
mal chests, measurements are often resorted to, to learn the 
amount of chest excursion. A normal, healthy individual usually 
gives a chest excursion anywhere from three to five or more 
inches. The individual in whom free in and out breathing is 
hampered by pulmonary disease often shows no chest expansion 
or, if any, but very little. 
Chest measurements are usually undertaken as to circumfer- 
ence and diameter. The circumference of the thorax is generally 
measured with an ordinary tape measure graduated in centi- 
meters and inches, usually on a level with the nipples in front 
and the angles of the scapulae behind with the arms outstretched 
or resting on the head. The circumference of the chest should 
be one-half that of the body length or height and the measure- 
ment should be taken while the subject is holding the breath. In 
old age, the ordinary chest measurements along the upper part 
diminish, and the lower chest circumference becomes greater. 
Normally the right chest is from 1 to 3 cm (one half to one inch) 
greater than the left. The diameter of the thorax, the long 
diameter, cranio-caudal measurement, the measurements from 
the clavicle to the base of the chest are very variable. It is 
scarcely possible to fix any one number as expressing its normal 
length; the appearance by inspection, however, often suffices. 
194 MENSURATION, SUCCUSSION, VITAL CAPACITY, ETC. 
195 
The transverse diameter (the breadth), from the right axilla 
through to the left or vice versa in the upper part of the chest of 
the male adult, is about 25 cm or 10 inches, in the female about 
23 cm, approximately 9 inches. The antero-posterior diameter, 
the sterno-vertebral (the depth), is about 19 cm or inches 
through the middle of the chest. 
An asymmetrical chest, one in which there is on inspection a 
perceptible difference in the two sides, may best be measured by 
making a small ink mark over the midsternum on a level with 
the nipple and another in the centre of the spine on a line with 
the angles of the scapulae and measuring each half of the chest 
separately and carefully noting the difference. Various instru- 
ments for measuring chest deformities have been devised but 
few are in general use; a good steel tape line will answer all the 
necessary requirements. 
In great chest deformities, as in scoliosis, kyphosis, or kypho- 
scoleosis, chest measurements must be undertaken at different 
levels along nearly horizontal lines and the different measure- 
ment of the two sides of the thorax carefully noted. The student 
is here again to be reminded that although there may be much 
chest deformity due to a distorted or twisted spine, tuberculous 
disease is extremely infrequently as accompanying disorder. 
(b) Succussion. Succussion Sounds or Murmurs. Splashing 
Sounds. This method of physical exploration was well known 
to the ancients. It is closely described by Hippocrates and in the 
older writings it is frequently referred to as the Hippocratic 
succussion sound. Laennec, however, recognized it in associa- 
tion with pneumothorax, and gave us the first accurate descrip- 
tion of this phenomenon. 
Succussion is here briefly considered because it frequently is 
a symptom-complex of a pre-existing pulmonary tuberculous 
process. Succussion sounds can only be elicited if the fluid is 
free in the pleural cavity and then only when both air and fluid 
are within the chest cavity. Succussion sounds are produced by 
suddenly shaking the body of a tuberculous person suspected of 
having a pneumothorax, when if air and water are present in the 
pleural sac, a splashing sound becomes audible if the examiner’s 
ear is placed directly against the chest. A stethoscope may be 
used but the splashing sounds do not become so pronounced. In 
exceptional instances, intrapleural succussion sounds may be 
recognized by the palpating hand when it is referred to as “sue- 196 
CLINICAL TUBERCULOSIS 
cussion fremitus.” A fairly good representation of this sign may 
be obtained by placing a rubber hot water bottle partially filled 
with water against the ear and shaking. An ordinary glass 
bottle or jug will answer the purpose fairly well. 
(c) Vital Capacity. Spirometry. Estimation of the vital capac- 
ity. (32) The vital capacity of the lungs is the measurement of 
the greatest volume or quantity of air which is exhaled after the 
fullest inspiration followed by the most forced expiration. The 
total capacity is the vital capacity plus the quantity of air still 
remaining in the lungs after the most complete expiration. On 
ordinary inspiration and expiration, the “tidal air,” amounts to 
about 500 ccm or 30 cubic inches. The “reserve” or “supple- 
mental” air, that is, the amount of air which, after ordinary ex- 
piration, may be expelled by forced expiration is about 1500 
ccm or 90 cubic inches. “Complemental air” or the amount of 
air which after ordinary inspiration may be inhaled by forced 
inspiration and the “residual air,” the quantity of air which after 
forced expiration still remains in the lungs, are each estimated 
to be about 1500 ccm or 90 cubic inches. The vital capacity is 
variously given by different authors and while some limit it to 
2500 ccm others estimate it as high as 3800 ccm. In a perfectly 
healthy man it amounts to about 2>y2 litre of air, approximately 
one gallon (231 cubic inches). 
The vital capacity is proportional to body length, is influenced 
by sex, age, height of the individual, and it increases at the rate 
of 60 ccm for every cm of height above 155. The minimum 
vital capacity of a man of 155 cm (about 5 feet) is about 3000 
ccm (or 180 cubic inches), and if 5 cm (2 inches) is added to 
body height, the vital capacity will be 3300 ccm, etc. As to age, 
the vital capacity increases about 160 ccm from the 15th to the 
35th year and decreases about 500 ccm from the 40th to the 65th 
year. It also becomes less in the extremely aged and is less in 
the very young. The vital capacity is also increased in health as 
well as in disease by residence in a high altitude, that is, in moun- 
tainous countries. Sedentary occupations and defective nutrition 
lower and the opposite conditions increase the vital capacity. 
As a rule, men between 20 and 40 years of age of medium 
height have a vital capacity of about 3600 ccm (230 to 240 cubic 
inches) and women about 2500 ccm (150 cubic inches) short 
people about 3000 and tall about 4000 ccm. Cornet places the 
minimum amount in healthy men as 1 to 20 and in women as 1 MENSURATION, SUCCUSSION, VITAL CAPACITY, ETC. 
197 
to 17, that is, 1 cm in body length (or 7/16th inch) in men is 
equal to 20 ccm (or about 4 cubic inches) of vital capacity, and 
in women 1 cm of body length (or 7/16th inch) to 17 ccm (or 
3% cubic inches). All these figures vary considerably and can 
only be given approximately. They vary greatly as to age, the 
expiratory efforts and muscular force, fulness or emptiness of 
the stomach, etc. Any interference with the full or free ex- 
pansibility of the lungs, such as diseases of the respiratory or- 
gans, will diminish the vital capacity. In advanced pulmonary 
tuberculosis accompanied by much tissue destruction, this may 
be reduced by one half and even more. 
In beginning cases or early tuberculosis, the method is not al- 
ways applicable as a diagnostic aid because the physical signs of 
palpation and percussion are positive long before there is a lower- 
ing of the vital capacity. Then again, the lessening of the vital 
capacity does not always run parallel to the amount of lung 
which is incapacitated, for in pleurisy with effusion when half of 
the lung is compressed the vital capacity does not drop to one- 
half because the functioning lung is doing compensatory work, 
which makes up somewhat for the loss encountered by the af- 
fected member. There is also an element of danger in spiro- 
metry in the active tuberculous because the forced inspiration 
and expiration may carry infectious material up into otherwise 
healthy portions of the lungs; then, there is also danger from 
hemorrhage by forcibly compressing or expanding a cavernous 
lung. Pleurisies, pericardial disease, emphysema, etc., all lower 
the vital capacity, and not only the diseases of the intrathoraic 
organs but muscular weakness may lower it. 
Vital capacity, like blood pressure observations, can not be 
gauged by a single test; in fact, the first experiment is usually 
wholly unreliable because the patient has not learned how to 
breathe. It is only after repeated attempts that one succeeds in 
securing reliable data as to the vital capacity. If the free excur- 
sion of the lungs is prevented, that is, when breathing is accom- 
panied by pain, when respirations are abnormally frequent, or 
when the patient is weak, vital capacity is not available as a 
diagnostic measure. In the beginning stage of suspected pul- 
monary tuberculosis, when the process is still quiescent, is not 
very active, is of the slow or proliferative type, the patient is not 
yet showing any or perhaps little loss in weight, has few clinical 
symptoms, the diagnosis not quite definite, the low vital capacity 198 
CLINICAL TUBERCULOSIS 
in an individual when compared to height, sex, weight may be- 
come a valuable aid as a diagnostic measure, whilst in the ac- 
tively tuberculous with positive physical findings and clinical 
picture, vital capacity can be of no value because here the diag- 
nosis can be definitely made by physical examinations, besides, 
it may become a source of grave danger. CHAPTER 19 
THE CARE OF THE TUBERCULOUS 
The Treatment of Pulmonary Tuberculosis. General Therapy, 
Ambulatory, Home, Sanatorium, Dietetic-hygienic, Medical, 
Tuberculin, etc. 
General Consideration. Health and Disease. (20) 
A human being- is said to be in perfect health when there is per- 
fect co-ordination of all the organs and tissues of the body, no 
functional disturbances; the direct opposite of this state is known 
as disease. Disease as we know it today is not, as was believed by 
the ancients, a visitation from heaven which must be borne with 
patience, nor an infliction from an evil spirit. It is brought about 
by our mode of living, our environments, our social relationship, 
and more than that it is the direct result of the violation of in- 
flexible, inalterable and immutable laws which have been violated 
by the afflicted individual. In no other disease can this, the 
violation of these laws, be traced back to a period of trans- 
gression as in pulmonary tuberculosis, if we only persist in a 
diligent search. 
Diseases have been variously classified as to duration. We 
speak of acute diseases when the onset is sudden, as in scarlet 
fever, measles, small pox, etc., and the duration is short; sub- 
acute when the onset is somewhat protracted, as in pleurisy, and 
chronic when the disorder is drawn out over more or less long 
periods, as is generally observed in syphilis, leprosy or tuber- 
culosis. 
We also speak of pulmonary tuberculosis, the disease now 
under consideration, as the most chronic of all, and we say that 
it is primarily a house or home disease, which it is in more than 
one sense. We all know that the.primary infection, in by far the 
greater number of cases, is brought about in the home, being 
transmitted from the tuberculous adult to the child, that subse- 
quently the disease is fostered in the home, and that the actively 
diseased individual constantly frequents the home. It seems that 
throughout the whole period of the affliction he is wedded to the 
home, is anxious to become well but only in the home. 
199 200 
CLINICAL TUBERCULOSIS 
Tuberculosis is spoken of as a preventable, (21) a curable dis- 
ease, that the infection could have been prevented but was not, 
that even if once the infection is followed by manifest disorder 
it is still curable, provided the disorder has not existed too long 
and the damage inflicted is not too great. Pulmonary tubercu- 
losis, as has been stated, is a chronic disorder, a scourge, a plague, 
the mortality and morbidity exceeding that of all other diseases. 
Fig. 38. Comparing the death rate from tuberculosis in the U. S. in one year with 
that of yellow fever in 115 years. (From the U. S. Public Health and Marine Hospital 
Service. Tuberculosis Exhibit, 1908.) 
In the United States more than 160,000 (1908) succumb annually, 
and more than 800,000 are constantly sickened from this disorder. 
(The U. S. Census for 1920 shows the tuberculosis mortality to 
be 114 per 100,000, an unusually low death rate.) In the city of 
Chicago the annual mortality from tuberculosis is, in round num- 
bers, approximately 4000, with a constant morbidity of more 
than 20,000. It is most frequently a disease of young or middle 
life, exacting in the latter its greatest toll at a time when the CARE OF THE TUBERCULOUS 
201 
earning capacity should be at its best and in the former at that 
period when the afflicted youth should be in a position to earn 
or at least to repay either to his parents or to his benefactors 
some of the interest accrued on the amount of money which was 
necessarily expended for his care, schooling, teaching, clothing 
and raising, etc. 
Sources of Infection. If, as so often has been stated, every- 
body has at some time become infected, that in a certain propor- 
tion only of those infected the disease becomes manifest, that the 
problem has become a family or home infection, whence the 
propitious source of all this disorder? Close observation has 
demonstrated definitely that there are three chief sources— 
namely: 
(1) Infection from the unknown tuberculous. We will find 
in many homes individuals suffering from so-called chronic 
bronchitis, chronic catarrah, from asthma, from emphysema, etc. 
In these, owing to the generally good physical appearance, tuber- 
culosis is not suspected and many a good and kind old grand- 
father or grandmother suffering from these disorders, upon close 
examination, will be found afflicted with chronic pulmonary 
tuberculosis, and being unfortunately in constant companionship 
with the infants or small children in the household, will often be 
the source of a tuberculous infection. Again, a hired person 
about the home, either male or female, may be suffering every 
winter from a slight cough, and here also, owing to the healthy 
appearance, tuberculosis is not suspected. Often parents, either 
the father or the mother, have a slight cough or cold, especially 
if the onset is slow, causing little or no disturbance, general ap- 
pearance is good, there is no loss in weight, tuberculosis is not 
suspected and even if a diagnosis of pulmonary tuberculosis has 
been made, it is not believed and the given instructions are not 
heeded. In such homes the disease is very often spread to all 
the young members of the household. 
(2) As a second source of tuberculous infection and disease are 
the known tuberculous. First those living and belonging to the 
household, who are known to be suffering from pulmonary tuber- 
culosis, but are careless about their person, do not keep clean, 
do not take proper care of their sputum, insist upon the freedom 
of the house, upon eating with the family at the family table and 
in other ways insistent on doing as they please about the home; 
they are a most prolific source of tuberculous dissemination. 202 
CLINICAL TUBERCULOSIS 
Second: the homeless consumptive. A kind hearted sister or 
brother takes the homeless member of the family into the home, 
gladly provides a willing shelter, and themselves having families, 
expose their small children to a positive infection. Many a home- 
less and drunken father or a shiftless mother, being taken into 
the home of a dutiful and loving daughter has often repaid this 
act of kindness and duty by making the little ones of the house- 
hold tuberculous. 
(3) The third great source of tuberculosis is the discharged 
sanatorium patient. It is greatly to be deplored that in many 
instances the sanatorium patients leave these institutions with 
the firm belief, or at least make themselves believe, that a cure 
has been effected, return to their former homes or to the homes 
of acquaintances or friends to which they have free access, and 
now become the source of continuous infection. Often this un- 
fortunate class of individuals is unjustly condemned for the in- 
jury which it has done and for which it was not at fault. Had 
these individuals been taught while at the sanatorium that the 
disease is not cured—that the process is only arrested, that at 
any time, if indiscreet, the disease may break out again and 
perhaps many times more active than the first, they would per- 
haps have been more careful and would have tried at least to 
avoid the spreading of tuberculosis. 
The General Care of the Tuberculous. In caring for the tuber- 
culous three classes or groups of consumptives are usually en- 
countered: (1) the ambulatory, which comprises generally the 
first stage cases; (2) the bedfast or home cases, second and third 
stage, and (3) the sanatorium cases, consisting of some first 
stage, usually second and third stage cases, 
(1) The Ambulatory Cases. These are usually under the care 
of the family physician. These patients generally consult the 
doctor, chiefly at the office, and it is this class which we so fre- 
quently see at the dispensaries. In these beginning cases, par- 
ticularly when diagnosis has been positively made, it becomes 
the physician’s duty to instruct the patient, truthfully, tell him 
what he has and teach him how to live to bring about an arrest 
of his tuberculous process. Many of these patients as a rule be- 
long to the poorer classes, depending upon their daily labor for 
the support of themselves and their families. If the work is not 
too strenuous, they may be allowed to continue their vocation; if. 
however, it is very laborious, then lighter employment must be CARE OF THE TUBERCULOUS 
203 
secured. They must be incessantly encouraged to spend much of 
their time out of doors, rest a great deal out in the open, live in 
the outskirts of the city rather than in the congested districts, 
avoiding as much as possible much walking, observing the strict- 
est rules of cleanliness and the proper hygiene about themselves 
and their homes or rooms, avoiding all excitement, being most 
abstemious in their habits, desist from the use of whiskey, wine, 
beer or tobacco, and be regular about their diet which must be 
good, wholesome and nutritious. The sleeping quarters and the 
sleeping rooms must be well ventilated, the windows open day 
and night. They must be told to remember at all times that the 
same good Lord who made the day air also made the night air, 
and that they must permit it to come freely into their houses and 
homes. These patients must be told that they must sleep alone 
and that the freedom of the house is only permissible if the case is 
a closed one and no tubercle bacilli have been found in the 
sputum. If, however, bacilli are present and the case then is an 
open one, they must spend most of their time in their rooms if 
they be not out in the open. If such individuals cough and ex- 
pectorate, they must be taught how to take care of the sputum 
so as to avoid as much as possible a spreading of the disease. They 
must be told frankly that in their association with their fellow 
workers while exercising proper precautions, they are in no way 
a menace and they must be greatly encouraged to continue in 
their daily work. This tends to take the mind off their troubles 
and to bring ease of mind. As these patients usually at the very 
beginning of the disease consult the family doctor, he should 
evince the greatest interest in the case; this has a most favorable 
influence and a strong tendency to lessen fear in these beginning 
cases of pulmonary tuberculosis. While under the family phy- 
sician’s care, if the tuberculous process does not become 
promptly arrested, they sooner or later drift into one of the other 
two classes—either the home or bedfast or the sanatorium cases. 
(2) The Bedfast, the Home or House Cases. This comprises 
both the second and third stage cases. In tuberculosis the home 
treatment is the most important of all, and at this stage the old 
family doctor is again looked to for advice. From the very be- 
ginning of the disease, from incipiency and up to the far ad- 
vanced stage, even to exitus, he is asked to minister to this un- 
fortunate class and his opinion usually carries great weight. 
Long before the case becomes bedfast the doctor, if he wishes 204 
CLINICAL TUBERCULOSIS 
to do his full duty, should suggest sanatorium care. He must 
explain the method in use at such institutions, how these patients 
are being cared for and how by this method of treatment the 
disease becomes arrested. These patients at first are usually 
very much adverse to going and he must make clear to them 
what a sanatorium is. As about 9/10 of all pulmonary tuber- 
culous individuals are not able, willing nor inclined to go to the 
sanatorium, the greater number will continue to be in the care 
of the family doctor, that is at the homes; this now becomes a 
most serious educational problem. From the very beginning 
these patients must be taught how to get well, how to make 
their surroundings safe for themselves as well as for others, par- 
ticularly in the open cases. The sleeping rooms or preferably 
sleeping porches must be so situated that they can be readily 
aired and ventilated. A most desirable room is one with a south- 
east exposure, there must be little drapings or furnishings in such 
quarters and the bed must be comfortable and have sufficient 
coverings. Body cleanliness, bathing and sponging are most 
essential—if much fever and rapid pulse, absolute rest and quiet 
must be instituted. The diet should be wholesome and well 
cooked, bowels kept soluble and such symptoms as from time to 
time arise must be met by proper medication. Living in the 
open with much sunlight should be encouraged. 
(3) The Sanatorium Cases. Considering the extremely great 
frequency of pulmonary tuberculous disease, there remains after 
all only a very small percentage, about 1/10, of all the afflicted 
who wish or are willing and anxious to go to a sanatorium—by 
far the greater number preferring to take the treatment at the 
home under the care of the old family doctor; nevertheless, the 
family doctor, as has been already stated, should in every in- 
stance at the very beginning, suggest the sanatorium. This, on 
the part of the doctor, often requires a great deal of tact, and 
owing to the patient’s peculiar psychic state, becoming easily 
irritated, even the allusion to a sanatorium may be sufficient to 
cause a change of medical attendant. 
The physician from the very onset must impress upon the patient’s 
mind the importance of knowing that a tuberculosis sanatorium is in no 
sense a hospital but only a school in which the afflicted person is taught 
how to get well and how to remain so. It may be stated here paren- 
thetically that it is true that a tuberculosis sanatorium is a school, but it is 
in no sense an ordinary school. It is strictly a reform school, in every 
way and only if the strictest rules are lived up to and the most rigid CARE OF THE TUBERCULOUS 
205 
discipline instituted, will the patient get well; this requires on the patient’s 
part the most passive obedience. 
The patient should next be informed of the simple fact that at 
the sanatorium he is under constant observation—daily and 
hourly—that there he will be taught the conditions of his disease, 
that a strict record of his case is kept at all times, that he is sub- 
mitted to a periodic examination, as his case may require, that 
when it is deemed advisable he will be forced to take the neces- 
sary rest, and that his presence at the sanatorium brings about 
a change of surroundings, and as he notices and observes the 
steady improvement in others he becomes gradually more en- 
couraged about his own case and that by these favorable environ- 
ments he becomes more and more obedient, more so than at 
home, where he wants to do as he pleases. Throughout his stay 
at the sanatorium he will then become more and more impressed 
with the truism that “no tuberculously diseased individual ever 
became well or had his tuberculous process arrested, who wanted 
his own way.” Observe the regularity in the diet, the mode of 
living, the medication, the treatment, the very atmosphere at a 
sanatorium. They are all factors which lead to an arrest of the 
tuberculous process. 
The question is often asked, “How long should a tuberculously 
diseased person remain at the sanatorium?” Until the process 
is surely arrested, until he has learned his lessons well and has 
come to believe that in the future and at all times he must prac- 
tice vigilance, that any indiscretion on his part may reactivate 
his old trouble and that when he returns to his home he must 
be willing and determined to lead a regulated, orderly and ab- 
stentious life. The old adage, “Once tuberculous always tuber- 
culous” perhaps may not be literally true; nevertheless, the 
healed or arrested tuberculous individual should shape his mode 
of living as though it were true. 
We have observed that when the tuberculously afflicted in- 
dividual first begins to sicken of the disease he consults his fam- 
ily doctor, and now upon his return from the sanatorium to his 
home, we observe again that the old family doctor is the first to 
be consulted; hence, it becomes the doctor’s duty to constantly 
remind the patient not to forget his institutional training. This 
is most important. The returned sanatorium patient needs much 
encouragement and this should be freely allotted to him by all, 
the physician, the nurse, the social worker, fellow workmen and 206 
CLINICAL TUBERCULOSIS 
his associates. The aim of these patients should be to main- 
tain their restored health and in this the family doctor will be the 
most important councilor. The next important problem for the 
patient to consider is his ability to again provide for himself and 
for his family. Here again the family doctor must advise. This 
necessitates work in which he needs the encouragement and sup- 
port of every one. 
The tuberculous patient returned from the sanatorium usually 
has been well trained, knows a great deal about tuberculosis, 
about the difference between infection and disease, and is in gen- 
eral a good disciple of the anti-tuberculosis gospel. He generally 
desires to remain much out of doors, preaches the doctrine of 
out-of-door life, the use of wholesome, good food and much rest, 
of diet, of retiring early and sleeping late. He generally submits 
every thirty days to a re-examination, knows well the meaning 
of a rapid pulse, watches closely the temperature curve, leads a 
quiet and unexcitable life, avoids excesses of all kinds and aims 
in general to maintain his body resistance, all of which, however, 
often has a strong tendency to make these individuals lazy, yes, 
even sluggards, and here again the physician has a great task to 
perform in preventing these returned sanatorium patients from 
becoming chronic sitters. Too much lounging about the house 
must be discouraged. The patient must become from day to 
day more reliant upon himself just as he was before he was made 
sick. 
Tuberculosis a Threefold Problem. Pulmonary tuberculosis 
as we see it is a threefold problem, a social, and economic and 
a medical one, and to bring about healing, relief and betterment 
of surroundings it is required that the whole community become 
interested. Being a community question all have a duty to per- 
form, not only the physician and perhaps the nurse but the com- 
munity as well. The physician’s duties have already been de- 
scribed somewhat in detail, namely, care of the patient from the 
medical standpoint, advice as to rest, order, adequate and whole- 
some nourishment, regulation of the home life and treatment of 
the symptoms as they arise. Then there is the duty of the at- 
tendant or nurse as to the housing conditions, seeing that the 
sleeping rooms and sleeping quarters are properly ventilated, 
that for the taking of food the open tuberculous is supplied with 
individual dishes, knives, forks and spoons, which are to be kept 
entirely separate from those in use by the other members of the 
household. The nurse must further teach the patient how to CARE OF THE TUBERCULOUS 
207 
take care of the sputum, how to gather and to destroy it so as 
to guard the spreading of the disease, how to keep a record of 
the daily doings, to regulate the time for visitors, she must en- 
courage frequent bathing and sponging, in fact, everything must 
be done to keep up and increase body immunity. 
A still greater duty to perform is that of the community at 
large towards the tuberculous. The tuberculously afflicted in- 
dividual, in whatever walk of life, needs much encouragement, 
needs assistance, and he must be made to feel that because of his 
affliction he is not treated as an outcast but that the whole com- 
munity is greatly interested in his welfare. If he is in poor or 
needy circumstances and is willing to go to a sanatorium, pro- 
visions must be made by the community to provide what is 
necessary for the care and comfort of his family while he is 
away from home and taking the cure. This can only be done by 
the community as a whole; however, charity organizations, wel- 
fare workers, insurance companies and associations, and philan- 
thropists are generally the proper source for relief and they will 
take care of this class of cases if only their attention is directed 
toward them. If the patient is not willing to go to a sanatorium 
and wishes to take the cure at the home, then again these various 
organized bodies must come to the relief and suitable sleeping 
porches, blankets, bedding, food and care be provided. In every 
individual instance either at the sanatorium or at the home 
everything must be done with the sole object of returning the 
tuberculous back to the community as a fairly capable working 
unit. 
The Treatment of the Tuberculous. General Therapy. (50) 
Tuberculosis is a constitutional disturbance in which both the 
body and mind require special care hence we must institute both 
a somatic and a psychic therapy. From the very beginning of 
the treatment our aim must be to endeavor to bring the diseased 
individual back to normal. In almost every case of pulmonary 
tuberculosis, if the process is not too extensive often even in 
cases of more or less extensive involvement, an arrest and even 
an apparent cure may be brought about if in the treatment we 
can correlate six well known and well established factors, namely, 
(1) ease of mind; (2) wholesome fresh air; (3) rest and appro- 
priate exercise; (4) the diet, the dietetic-hygienic treatment; (5) 208 
CLINICAL TUBERCULOSIS 
time; (6) obedience. These six factors and no others are always 
necessary to bring about in a tuberculous individual an arrest of 
the diseased process—all depending upon their proper harmoniz- 
ing. If either one is wanting our efforts will be of no purpose. 
(See illustration, page 543.) 
(1) The Psychic Factor. Contentment or Ease of Mind. Educa- 
tion. From the very beginning it must be our aim to educate the 
patient and to explain to him the nature of the disease. We must 
speak the truth, we must not tell him that he is simply suffering 
from a little catarrh, when we positively know that he has active 
tuberculous disease. On the other hand, we must not frighten 
him but on the contrary convince him that although he is suffer- 
ing from pulmonary tuberculosis he is not condemned to die and 
that by having confidence in his physician he must follow his in- 
structions to the letter and in that way he will get well. In 
patients suffering from far advanced pulmonary tuberculosis it 
is above all essential that we ease or relieve the despondent mind 
even to a point of shading the truth, because here speaking the 
whole truth would be cruel, nay, criminal. From the long drawn 
out, chronic condition of this disorder many patients become quite 
hopeful and buoyant even to the last, and here it becomes the 
physician’s imperative duty to encourage this buoyancy. Some 
tuberculous patients become very despondent when they observe 
their helpless condition and the conditions about the home, about 
the care of their families, etc. Here ease of mind is often most 
helpful if aid is offered by the community, the charity organiza- 
tions and allied bodies, knowing that suitable measures assure 
prompt relief and much comfort to his dependents. This also 
applies to individuals who are taking the cure at a sanatorium 
where either the husband or the wife should be assured that 
during their stay at the institution and while they are taking 
the cure, the other members of the family, those remaining at 
home, will not want for anything. 
This principle of “Contentment,” however, finds its most ap- 
propriate application in those cases for which it has originally 
been advised, namely, for the youth suffering from pulmonary tu- 
berculosis and who is taking the cure in a more equable climate, 
perhaps thousands of miles away from home where owing to the 
want of “ease of mind,” by far the greater number become victims CARE OF THE TUBERCULOUS 
209 
of nostalgia, become homesick and succumb early to the disease. 
If, for instance, a tuberculosis patient be advised to go away from 
home, that a change of climate be desired to effect a cure then 
one or more of those who are near and dear must make the 
sacrifice and accompany the sick member of the family. Do not 
send him or her alone out into a strange land, perhaps many 
hundreds of miles away from home, from friends, from those 
who are near and dear when the thoughts and the mind of these 
unfortunates during the long nights of vigil are constantly about 
the home, the friends, the dear ones, the always earnest desire 
and longing to be with the loved ones. Admitting that climate 
is a factor in hastening the cure, it should be weighed well before 
the afflicted person is sent away—only when the physician has 
the positive assurance that the patient’s mind is at ease should 
this be allowed. Since the establishing in every community of 
tuberculosis sanatoria which are easily accessible and not too 
far from the homes of the afflicted, the leaving of home to go 
many hundreds of miles can be discouraged, as these institutions 
being near to the homes can readily be visited by relatives and 
friends on proper visiting days. The patients look forward to 
these days, and being encouraged in this way “ease of mind” is 
brought about. 
(2) Wholesome Fresh Air. The second necessary factor is 
out-of-door living with plenty of fresh air. It is not necessary 
that the consumptive, in order to take the cure, must go up into 
the mountains or live in the valleys, in either a high or a low 
altitude, it is most essential that wherever he takes the cure 
that the air is pure, is free from dust and dirt and free from ob- 
noxious gases or coal dust; nor must the humidity in the air be 
too great. The air must be wholesome and fresh, but it is not 
necessary that it be icy cold, for warm air will do just as well and 
perhaps better, provided it is pure. The air warmed by the sun’s 
ray is most ideal, and inhaling pure air while there is much sun- 
shine is most valuable—that is, combining a mild sunbath while 
taking pure air and remaining much out in the open, away from 
dusty air, free from obnoxious gases, where there is no noise 
and no excitement, out in the open, winter and summer, is the 
ideal way to take the open air treatment. 210 
CLINICAL TUBERCULOSIS 
(3) Rest and Appropriate Exercise. In the treatment of the 
various conditions in pulmonary tuberculosis it is necessary that 
at times we apply absolute rest and that we institute when neces- 
sary gradual and graduated exercises with much rest in the open 
and out of door sleeping. With much rest in bed, or graduated 
rest like graduated exercise, often very much can be accom- 
plished. As a rule febrile cases require absolute rest while in 
afebrile cases graduated and gradually active exercises favor auto- 
inoculation. Absolute rest, only during the active, febrile stage, 
is the treatment in this the first stage. In the second and third 
stages if afebrile regulated exercise and a physical and an occu- 
pational therapy. If the pulse is rapid, the temperature about 
100 or more, during the 24 hours, then absolute body rest must 
be instituted. The patient should be placed in the recumbent 
position, in bed, and must remain lying mainly on the involved 
side until his temperature approximates the normal and remains 
normal for a week, perhaps varying in the afternoon to about 99. 
It can not be too earnestly emphasized that under absolute rest 
we understand that the patient must remain in bed the whole 24 
hours of each day. He must take his meals in bed and for toilet 
purposes he must make use of the bed pan. A patient suffering 
from active pulmonary tuberculosis, with a fast pulse and high 
temperature, must be treated just like one who is suffering from 
an acute disease like typhoid, pneumonia, etc., and absolute 
rest must strictly be insisted upon. For a patient with a daily 
temperature above 100 and rapid pulse, a 15 minute stay out 
of bed would completely inhibit or negatate the good work which 
was accomplished by remaining in bed the other hours. 
Only the most strict adherence to this rule of absolute rest leads 
to success. If, in the treatment of our home cases we could in- 
stitute the principles of absolute rest, often for weeks or months, 
so admirably enforced in a sanatorium, much better results would 
be obtained and many more cases would get well. If in a given 
case the temperature approaches the normal and the pulse wave 
begins to lessen, then graduated rest can be directed, but always 
bearing in mind that the moment fever again becomes high we 
must at once return to the absolute rest treatment. Rest lowers 
fever and activity, reduces the rate of breathing towards the nor- 
mal, increases the appetite, inhibits night sweats, exerts a favor- CARE OF THE TUBERCULOUS 
211 
able influence upon the skin, lessens the cough and has a most 
salutary tendency on the condition of the lungs. In some pul- 
monary cases showing much activity, rapid pulse and high fever, 
often much good can be accomplished if the tuberculous individ- 
ual, whilst at rest, is placed with the head and chest on a near 
level, slightly elevating the abdomen and lower extremities, when 
by means of autotransfusion and passive hyperemia the tuber- 
culous processes seem to show a greater healing tendency. With 
graduated rest, graduated exercise go hand in hand. If the 
patient manifests much improvement after beneficent rest, then 
sitting up for % to y2 hour is advisable; if no fever follows the 
time out of bed may gradually be extended and perhaps it might 
also be well to exercise slightly, taking a little walk about the 
room, always observing closely above all the temperature and 
the pulse. The patient should be told to rest a great deal in the 
open and to walk very little or not at all. The notion common 
among the public that the tuberculously diseased person should 
take long walks in the open is most pernicious and more damage 
than good has resulted from this practice. Walk very little, only 
as the case may require, and here as in all other diseases we must 
individualize. Tuberculous patients who are improving, and the 
conditions seeming to approach the normal should walk before 
meals and rest after. Rest from one to two hours after each meal 
and take a short walk before meals. Here again we must be 
cautious and careful in our advice, because too much rest is just 
as injurious as is too much exercise. We must aim to strike a 
happy medium. Then again, the amount of rest and exercise 
ought to be regulated according to the seasons, more rest 
in summer with less exercise and in winter the reverse — 
a trifle more exercise and perhaps less rest. The temperature 
curve and the pulse rate must be our guide, and from putting the 
patient to doing a little light work and gradually changing to 
heavier, or perhaps first from light sports, croquet, etc., gradu- 
ally to tennis, golf, etc., we often observe a steady improvement 
and so the tuberculously diseased individual not infrequently 
finds himself gradually restored as a former working unit being 
again capable of resuming his previous vocation. Last the pa- 
tient should continually bear in mind that it is indeed a long 212 
CLINICAL TUBERCULOSIS 
drawn out process and that only obedience and perseverance on 
his part will lead to a triumphant issue.1 
(4) Diet. (A) The Dietetic-Hygienic Treatment. Diet is the 
basis, is the fundation of all treatment in tuberculosis, or more 
properly the dietetic-hygienic, as first applied in the middle of 
the last century by Brehmer (1859) and later by Dettweiler. As 
the digestive apparatus in the normal is of the greatest impor- 
tance in maintaining the body in a healthy condition, so it be- 
comes the first and foremost in the diseased condition, to aid in 
bringing the body back to health. In the dietetic care of the 
tuberculous no special food is prescribed. The rule is to give 
what the stomach can easily digest, to give it with regularity, 
but always to save the stomach. Give the stomach sufficient 
rest; do not overeat but rather undereat; eat only such food as 
the system craves and then only in moderation and do not recom- 
mend foods which are most obnoxious to the patient. Eat with 
great regularity and at meal time only, allowing the stomach 
sufficient rest between the meals. The stomach like every other 
organ of the body partakes of the general tuberculous disturb- 
ance and if we institute general body rest in the treatment of 
tuberculous disease, why not stomach rest? Eat nothing be- 
tween meals; if, however, the meals are very small, eating be- 
tween meals may be advantageous. In health, we usually give 
*The great importance of absolute body rest in the treatment of pulmonary tuberculosis 
can not be sufficiently emphasized. Even with the instituting of most complete rest, it is 
after all only relative. Where complete rest is possible it often requires years to effect 
a cure, how much longer time must then be required to arrest a tuberculous process in 
which complete rest is a physical impossibility. A child suffering from tuberculosis of the 
spine is put upon a. Bradford frame and securely strapped; the parts are put to absolute 
rest and even here it often requires after complete immobilization years to effect a cure. 
This inhibition of motion is readily applicable in most cases of tuberculous disease of 
bones and joints, but it cannot be applied in disease of the kidneys, larynx, lungs, etc. In 
lung tuberculosis, the inhibition of pulmonary motion is a physical impossibility, and yet 
we must recommend absolute rest for the cure of all active cases. 
A healthy individual under ordinary conditions breathes about 20 times a minute, 1,200 
in an hour, 28,800 in a day, 864,000 in a month, and 10,368,000 in a year, and even 
here we observe that deep or full compensatory breathing is occasionally required. The 
pulmonary tuberculous patient during the period of his activity, often greatly increases 
his breathing cycles by additional thousands each day, his number of full or deep 
breaths is also increased, and the toxins circulating in the blood stream irritate the 
circulatory apparatus, causing increased cardiac action; this all lends additional motion 
throughout the pulmonary tissue, thus decreasing the amount of rest; besides, emotion, 
excitement, nervousness, are all additional factors in this lessening of rest. 
As it is a physical impossibility in the treatment of pulmonary tuberculosis, to put 
the lung absolutely at rest, we must aim to bring about at least a maximum amount of 
rest with a minimum amount of exercise or lung excursion. At the same time, all such 
factors which tend to disturb this necessary rest must be removed as much as possible. 
We frequently observe, in a child who is suffering from joint disease, that its parents 
are perfectly contented when told that with absolute rest the child can make a complete 
recovery, although this may take years, but when we are treating a young individual 
suffering from pulmonary tuberculosis and in whom pulmonary rest can onlv be rela- 
tively instituted, parents generally expect a cure in a few months. The only rational 
method for the cure of pulmonary tuberculosis, if the process is active, is to insist upon 
absolute body rest, in the recumbent position with the patient lying on the affected side, 
thus controlling the breathing motions by giving the lungs the maximum amount of rest 
with the minimum amount of motion consistent with life. To accomplish this fully we 
must, in addition, insist upon very little or no talking, the control of coughing and the 
avoidance of all excitement or emotional disturbances. CARE OF THE TUBERCULOUS 
213 
the stomach an hour or so rest after having digested a full 
meal, and this generally requires about 3 to hours, why 
should we not give sufficient rest to a weakened and irritated 
stomach, which is usually an accompaniment in the tuberculous? 
Forced feeding or stuffing so much in vogue a few decades ago 
is with our present knowledge concerning the treatment of this 
disease no longer tenable. Besides, it is harmful as the stomach 
is wholly incapable of digesting a large quantity of food at a 
single ingestion. 
The tuberculous patient who under a properly regulated diet 
gains slowly and steadily in weight presages a favorable prog- 
nosis ; a rapid gain is not a good sign as this does not indicate 
energy but simply fat and water. Our aim in the treatment is 
not to make the afflicted person fat, as body fat or increase in 
weight alone usually consists only of water, but to produce 
strength of muscle, healthy blood and energy—not quantity of 
cells, but quality. The best, not the greatest, must be our wish 
and aim and for the achieving of this, a well regulated diet, 
well prepared and wholesome, must be secured, preferably a 
mixed one consisting of animal and vegetable food with sufficient 
heat units or calories to maintain the patient’s present condition 
and at the same time secure a steady and gradual increase of his 
body cells. This is done by building up and increasing his body 
strength. In order to assure this the various foodstuffs consist- 
ing of proteins, fats, carbohydrates, etc., must contain a suffi- 
cient number of heat units or calories to supply the output of 
heat and to equalize the body metabolism. Proteins, fats and 
carbohydrates each have food values estimated in calories and a 
sufficient number of each is necessary for the proper mainte- 
nance of life. Protein is an absolute essential for tissue building 
and repair; heat and energy of the body can be developed from 
the carbohydrates and fats. In food values 1 gram of protein 
equals 4, 1 gram of fat equals 9 and 1 gram of carbohydrate 
equals to 4 heat units or calories. (See Chapter 39.) The 
requirements of a healthy individual’s intake in proteins, fats and 
carbohydrates (an individual weighing about 150 pounds) while 
at rest will approximate very close to 3000 calories per day; for 
light work it may be increased to 3500 or 3600 and this will re- 
quire about 120 grams of protein—4 ounces equal 480 calories, 
60 grams of fat—2 ounces equal 540 calories, and 500 grams car- 
bohydrate—17 ounces equal 2000 calories, a total of 3020 calories. 214 
CLINICAL TUBERCULOSIS 
The tuberculous individual while taking the rest cure would 
require daily about 3000 calories, whereas a man doing heavy 
manual labor would require about 4000 or about 196 grams of 
protein (or 6]/2 ounces) equal 784; 126 grams of fat (or 4 ounces) 
equal 1134 and 522 grams of carbohydrate (or 17l/2 ounces) equal 
2088, equal almost 4000 calories. The necessary foods should 
consist of meats, fish, poultry, eggs, cheese, eggnogs, butter, fats, 
and oils,(71) milk, whey, koumiss, bread, potatoes, puddings, 
fruit, nuts, vegetables like cabbage, spinach, etc. Aim to reduce 
the output rather than the intake. Further, throughout the treat- 
ment we must strictly inhibit the use of alcoholic beverages and 
the use of tobacco, and limit the intake of coffee or tea. In order 
to outline a proper dietetic course for the tuberculous and to 
estimate the necessary food values we ought to make a thorough 
study of each patient’s case. Every patient’s requirements in pro- 
teins, carbohydrates and fats should be carefully ascertained so 
that the daily amount of intake does not exceed the individual’s 
tolerance. Proteins above all should constitute a fair proportion 
of this advised diet, but not more than the organism can take 
care of. In many instances in order to supply the immediate 
wants of the economy the nitrogenous food must be increased. 
This, however, requires often a great deal of good judgment not 
to go beyond the patient’s protein tolerance. Nitrogenous food 
intake relative to tissue metabolism has received much attention 
particularly from dietitians, but not the over intake, that is, that 
amount over and above the necessary tissue waste and repair. 
Too much protein intake causes either too much renal work or 
the unutilized nitrogenous material may be the cause of intestinal 
putrefaction and disturbances followed by additional toxin ab- 
sorption; hence a wholesome and generous diet, consisting of 
carbohydrates, fats and proteins, in such varying proportions, in 
amounts sufficient and suitable, just like the patient enjoyed 
when he was still in perfect health, will be found the most ser- 
viceable and appropriate in his diseased condition. It should be 
allowed with the same regularity and prescribed intervals as in 
health, at meal time only, giving nothing between meals. Thanks 
to a better understanding of the underlying principles which 
govern the processes of this disease, the pendulum has swung 
back and forced or over feeding and stuffing is now obsolete, 
but we must be guarded not to go to the opposite extreme and ad- 
vocate underfeeding as the panacea in this tuberculosis problem. CARE OF THE TUBERCULOUS 
215 
In the dietetic treatment particular attention must be paid to the 
conservation of the digestive integrity of the stomach and in- 
testinal tract, constantly bearing in mind that in health the 
gastro-intestinal organs offer the greatest protection against 
diseases of the lungs and that the digestive apparatus also offers 
the first aid and is chiefly to be relied upon when the lungs are 
diseased. 
Therapeutically then, it may be stated that an increase of nitro- 
genous material in the diet of the tuberculous may be of un- 
doubted value, but we must not lose sight of the fact that this 
must be kept within the patient’s albumin tolerance, that a high 
protein diet over and above that used in tissue metabolism may 
cause in the intestines a rapid bacterial increase, intestinal putre- 
faction with toxin production and toxin absorption, and that this 
intestinal autointoxication is usually proportional to the nitrog- 
enous intake. 
(B) Zomotherapy. From Zomos, Meat Juice.(125) (139) The 
treatment of pulmonary tuberculosis by means of the freshly ex- 
pressed meat juice. A strictly protein therapy. It has long been 
observed that meat is almost indispensable in the treatment of 
pulmonary tuberculosis and that raw meat or preferably raw 
meat juice is a most readily digestible and assimilable nutriment, 
a nerve stimulant, and that it is particularly indicated for 
the anemic, the convalescent, the undernourished, the chlorotic 
and the hemorrhagic and that with a patient in bed on a raw 
meat diet the temperature often becomes reduced. For a weak 
stomach the expressed meat juice is most suitable, particularly 
the muscular plasma of horse meat a most excellent therapeutic 
agent, being rich in both haemoglobin and glycogen. This ex- 
pressed juice found much favor and soon became known as Hors- 
ine and it was but a step from taking freshly expressed meat juice 
to that of fresh blood, and the drinking of beeves blood for a time 
became quite popular. The drinking of fresh meat juice for the 
cure of pulmonary tuberculosis was introduced by French phthis- 
otherapeutists; this was soon followed by drinking fresh beeves 
blood and at the abattoirs in Paris the daily attendance soon be- 
came very large and the drinking of one p2 litre (or 1 pint) of 
fresh blood once or twice a day became a common practice 
among the tuberculous visiting these institutions, taking the 
supposed cure. It only began to decline and ultimately was 
abandoned when it became apparent that the treatment, how- 216 
CLINICAL TUBERCULOSIS 
ever faithfully and persistently it was followed, would not af- 
fect a cure. Today it is only a memory of one of the many 
thing's which have been recommended as a cure for tuberculosis 
and have fallen by the wayside as of no special value. 
(C) Lactotherapy. Milk Cure. (62) The milk cure in Pul- 
monary Tuberculosis. Since time immemorial the use of fresh 
cow’s milk has always been highly recommended for the treat- 
ment of pulmonary tuberculosis, and at the present time, cow’s 
milk is the most important single article of diet in the treat- 
ment of this disease. While some clinicians have advocated 
its use in large quantities, others again have recommended it in 
small amounts, as the latter say not to overtax an already dis- 
turbed heart and from giving a few glasses daily to that of a 
quart or more, varying amounts are used. Recently the use of 
cow’s milk in enormously large quantities in the treatment of 
pulmonary and the various other forms of tuberculosis has at- 
tracted a good deal of attention and from some quarters very 
favorable results have been reported. It is generally conceded 
that in milk we have the most nutritious single food known, but 
some maintain that if given in too large an amount it may do 
harm, that although we have in milk all the units necessary to 
sustain life and to build up the body, that the quantity of fluid 
given in milk is generally too great to be taken care of by the 
heart of the tuberculous individual. That this contention can 
not be supported we may conclude from the fact that many a 
tuberculous individual even in an advanced stage of the disease 
has taken an exclusive milk diet for months at a time without 
embarrassing the heart. 
We must remember that in taking the milk cure it must be 
an exclusive milk diet — nothing but milk. Pure, unskimmed 
cow’s milk is usually given, and almost from the very beginning 
of the treatment the patient drinks large amounts, taking it at 
regular intervals. Usually the patient begins the treatment at 
7 o’clock in the morning, drinking a glass of milk every half 
hour, continuing this during the day until 9 o’clock in the 
evening. It is a strictly milk diet, incurs no hardship after the 
first few days, and the taking of a quart to six or more quarts a 
day causes no discomfort and patients being known to have 
taken from two and as high as three gallons a day without any 
inconvenience. To keep the bowels soluble these patients re- 
ceive a daily enema of salt water, and to favor the elimination CARE OF THE TUBERCULOUS 
217 
of such large quantities of water a daily warm bath and rub 
down is advised. Some patients taking the exclusive milk diet 
complain of slight pain in the stomach or of distress in the ab- 
domen, of nausea and even vomiting is occasionally complained 
of. In such cases the eating of an orange, sucking of a lemon 
or eating some grapefruit, by inhibiting the formation of hard, 
cheesy curds, often gives prompt relief. The citrate solutions 
like sodium or potassium citrate have long been in use as drugs 
which favor the formation of light, floculent, cheesy particles 
when given with milk; these are more readily digested. In 
taking the cure, pure full milk is usually recommended; how- 
ever, occasionally the course may be varied, giving at times 
skimmed milk, then changing off to buttermilk for a day. 
The milk given should not be too rich in butter fat and for that 
purpose the milk obtained from a Holstein herd will be more 
suitable than that from the Jersey cow. Holstein milk contains 
about 3.5% of butter fat against the Jersey 5%. Milk contains 
all the necessary requirements of a perfect diet. 100 grams of 
fresh cow’s milk contain 87 grams of water, 3.5 fat, 5. sugar, 3. 
casein, 0.5 albumin, 0.75 salt and .24 milligrams of iron. As the 
human body requires from 12 to 15 milligrams of iron in the 
daily diet, in about six quarts of milk this amount of iron is 
present, and as the body while at rest requires about 3000 
calories, with light exercise about 3500, this number of heat units 
is also found in about 6 quarts of milk, and as every quart of 
good Holstein milk contains about 600 calories, 6 quarts will just 
equalize the daily waste and repair of the human body. The ex- 
clusive milk diet must continue daily for months, sometimes the 
regular diet is substituted for a month or so and then a return to 
the milk diet and so on. The milk diet is said to be very suc- 
cessful in arresting or checking the tuberculous process. Many 
cases are put on a fast for 24 to 36 hours before beginning the 
exclusive milk.diet. An -exclusive milk diet may be very helpful 
in carefully selected cases, and here as in everything else, in 
every other treatment of pulmonary tuberculosis, we must in- 
dividualize. 
(5) Time. Of the necessary factors to bring about an arrest 
of the tuberculous process, the fifth is time. As the tuberculous 
disorder usually comes on slowly and insiduously, so the arrest 
of the process also becomes slow and long protracted. It is esti- 
mated that the average duration of a case of pulmonary tuber- 218 
CLINICAL TUBERCULOSIS 
culosis is about two years and it takes also approximately about 
that length of time to bring about healing. This long drawn out 
course often becomes very discouraging to the patient when he 
observes how long it takes to bring about a cure. I frequently 
draw a simile, namely, that of moving a mountain of sand with 
a teaspoon, that after days of toil the mountain does not appear 
smaller, but just continue in the work and you will observe that 
the pile of sand which you are taking away steadily grows and 
so it is with taking the tuberculosis cure, it will take a long, 
long time to notice any change but keep on and persevere and 
you will observe that first some improvement and finally an 
arrest of the tuberculous process has been achieved. The patient 
from the very onset when he begins taking the cure must be 
thoroughly informed of this fact, that it is a long drawn out 
affair; he must be constantly encouraged by the physician in 
attendance, by the nurses, by attendants and visiting friends and 
he will soon begin to realize the truth—that time plays a most 
important role and he gradually becomes reconciled to this fact. 
(6) Obedience. Discipline. The sixth and last but equally 
necessary factor to bring about an arrest of the tuberculous 
process is obedience, that is strict obedience on the part of the 
patient, a perfect submission, the ignoring of which generally 
spells a grave prognosis. The tuberculous individual must have 
full confidence in his medical adviser and follow implicitly the 
given instructions. The psychology of the tuberculous subject 
is frequently most peculiar. He wants to get well, is very 
anxious, but usually wants his own way in getting well. He 
must from the onset be told that he can get well but that no 
tuberculous patient ever got well who wanted his own way. The 
physician should know what is best for the patient and he must 
follow the given directions to the letter. It is only by such 
means that a healing of the disease is brought about. 
In beginning the treatment in a case of pulmonary tuberculosis 
in whatever stage, be it incipient or advanced, it becomes the 
physician’s imperative duty to co-ordinate these six necessary 
factors for bringing about an arrest or possible cure of the dis- 
ease ; however, should he not be successful in co-ordinating all 
six, his efforts will be futile. He must from the very beginning 
impress the patient with the importance of these six necessary 
factors in order to have a hearty co-operation and a perfect har- 
monizing of all. CARE OF THE TUBERCULOUS 
219 
Symptomatic Treatment. While the tuberculously diseased 
individual is being cared for, is taking the cure, is trying to 
bring about an arrest of his disorder, be it while he is still able 
to be about and coming to the physician’s office or to the dis- 
pensary, is still ambulatory, or perhaps he is taking the house, 
bedfast or the sanatorium treatment, certain definite symptoms 
will arise and must be combated as they manifest themselves. 
A symptom which is usually present from the onset of the 
disease and generally tends to remain up to the close of the 
scene is: 
(1) Fever. A temperature ranging daily from 99 to 102° and 
over; here absolute rest finds its greatest application. If the 
temperature is 102° and over, sponging with cold water or an 
alcohol rub may be directed. In some instances the temperature 
reading when taken by mouth may appear normal or but slightly 
above, but the palpating hand of the examining physician demon- 
strates that there is fever; in such instances the rectal tempera- 
ture reading will be the correct one. I have very frequently 
observed especially at the bedside when the tuberculous in- 
dividual has been taking the rest cure for some time that the 
mouth temperature reading is or approximates the normal but 
that the body warmth and the rapid pulse attracted my suspicion 
that the reading was faulty and that when a thermometer was 
placed into the rectum it registered from 1 to 3 degrees 
more. I firmly believe that in pulmonary tuberculosis the rectal 
temperature reading is the only correct one. I have often ob- 
served in cases with a rapid pulse and a temperature reading by 
mouth of 99° that a rectal reading frequently showed 101.5 to 
102.5° and more. 
If there is much temperature, it is always advisable to give a 
small amount of calomel, say about 1/10 grain every three 
hours for a few days. A small amount of calomel may be very 
conveniently given by combining it with a number of antipy- 
retics, as for instance, 1/10 grain of calomel with 2 grains of 
quinine given in a capsule or with 2 grains of sodium salicylate 
or two grains of each with a quarter grain of calomel if there is 
constipation or if the abdomen feels bloated. As a combatant for 
fever in the tuberculous Pyramidon is the antipyretic par ex- 
cellence, a 5 grain tablet being given once in three hours. This 
with cold sponging if the fever is high is usually followed by 
good results. Of the coal-tar products, if given, some have a 220 
CLINICAL TUBERCULOSIS 
decidedly depressing effect on many tuberculous subjects; hence 
they should be given with caution. Salol particularly has a 
tendency to show this in a most pronounced way in individual 
cases. Aspirin, antipyren or phenacetin may be given in small 
doses, not to exceed 5 grains, and if not given for too long a 
period may all be very serviceable. The ordinary fever mixtures 
so much in use in the treatment of the acute diseases, the liquor 
amtnonii acetatis in teaspoonful doses, citrate of potassium in 
10 grain doses, sweet spirits of nitre in 10 minimum doses are 
all very useful. The following combination makes a most grate- 
ful fever mixture: 
Potassium Citrate 3ii (8.0 gm.) 
Sweet Spirits of Nitre 3ii (8.0 cc ) 
Liquor Ammonii Acetatis sufficient to make 3 ounces.. (90.0 cc ) 
Give a teaspoonful in a mouthful of water, sweetened, every three hours. 
Tincture aconite root, tincture gelsemium or tincture veratrum 
viride most favorable remedies in the high fevers of the exanthe- 
mata, are of little value in the treatment of tuberculosis; how- 
ever, in this the pulse must be the guide. In tuberculosis the 
pulse is usually of low tension; should, nevertheless, the tension 
be high and bounding, then they may be administered. If the 
fever is high and tuberculosis complicated by cardiac disease 
then the tincture of digitalis in 10 minim doses should be given. 
Frequently after the meal the temperature rises in the tuber- 
culous; in such cases the giving of antipyretic remedies some 
hours before the taking of food often checks the rise. Fever 
usually results from the presence of secondary organisms and 
their toxins in the body and these with the products of bacillary 
growth and perhaps some tissue destruction and the absorption 
of all these toxic products bring about a rise in temperature; for 
this absolute rest is the ideal remedy. Altitude is one of the 
surest methods for combating fever. In about 70% of all cases 
of pulmonary tuberculosis with high fever, the temperature is 
reduced very quickly while residing up in the mountains and 
patients with high temperature, in whom the fever is not reduced 
after a two months’ stay in the mountains usually presages a 
grave prognosis unless there are other causes than tuberculosis 
which keep up the temperature. The 30% of cases which do not 
improve while residing in the mountains should be removed to 
the seashore or into the valleys or at any rate a change should 
be suggested. CARE OF THE TUBERCULOUS 
221 
(2) Pulse. A rapid or fast pulse ranging anywhere from 100 
to 120 or more, a tachycardiac, is generally present with the 
fever. The pulse is usually rapid, readily compressible, there is 
a want of force and it is very weak. This often becomes a very 
distressing symptom which greatly alarms the patient and here 
sedatives are mostly indicated. The giving of an 54 or a 54 grain 
of morphine, hypodermically, gives prompt relief, or codeine in 
54 to 54 grain doses either by mouth or subcutaneously, may be 
substituted, however, all sedatives should be given most cau- 
tiously and only in extreme instances. Sodium bromide in 10 to 20 
grain doses once m three hours is often very beneficial. Tinctura 
opii deodorati, in 5 to 10 drop doses, tinctura hyoscyami in 10 
drop doses every three hours with perhaps the addition of 5 
drops of the tincture of digitalis may be of good service in 
slowing the heart’s action and the giving of cold drinks and the 
application of the ice bag over the heart is much in favor in 
some quarters. Avoid all excitement, inhibit the use of intoxi- 
cants in all forms and do not give hot or warm drinks, but give 
freely of cold water. 
(3) Cough. This in pulmonary tuberculosis is the most dis- 
tressing of all symptoms. What to give to relieve the cough 
often taxes the skill of the attending physician to the utmost. 
In the very active and progressive vases cough is usually a con- 
stant and very annoying symptom whilst in other cases the 
cough pursues a more quiet course, but we must also remember 
that in some cases of pulmonary tuberculosis this one symptom 
of cough may be entirely absent. The cough may be dry or 
moist, productive or non-productive, and the expectorations be 
very slight on the one hand and very profuse on the other. The 
treatment here consists of much rest in bed, and as the air about 
the room is usually very dry, and this has a tendency to irritate 
the throat and this increases the cough, the aim should be to 
keep the air a little moist; this is best accomplished by placing 
about the room and near the bed a basin of hot water. The 
giving of morphine in very small doses 1/20 to 1/16 grain or 
codeine in 1/12 to 1/8 or heroin hydrochlorate in 1/24 grain dose 
is always indicated. Always be cautious in giving opium or its 
derivatives. Tincture of hyoscyamus in 10 minum, tincture of 
cannabis indicae in 5 drop, terpin hydrate, sodium salicylate, 
aspirin, ammonium chloride or carbonate either separate or 
combined in 1 or 2 grain doses every 2 or 3 hours have found 222 
CLINICAL TUBERCULOSIS 
much favor. The well known pharmacopeal preparation, the 
Mistura Glycyrrhizae Composita, compound licorice or brown 
mixture, given in one or two teaspoonful doses is a most valu- 
able, reliable and dependable cough medicine. This can be some- 
what improved by the addition of two to five grains of either 
ammonium chloride or carbonate to each teaspoonful. The old 
household remedy known as paregoric, the Tinctura Opii Cam- 
phorata of the pharmacopea in one or two teaspoonful doses 
is equally a reliable remedy. The various combinations of ter- 
pin hydrate with codeine or heroin, the different compounds of 
White Pine Syrup offered for sale, the syrup of tar, of ipecac, 
of squill are all more or less valuable as preparations for the 
relief of cough. Some of the cough preparations or mixtures 
which I am wont to prescribe are the following: 
(a) Ammonium Chloride drachm one (4.0 gm.) 
Syrup of Senega, 
Syrup of Ipecac each drachms four ( 15. cc ) 
Mixtura Glycyrrhizae Composita sufficient to make three 
ounces (90.0 cc ) 
Directions: A teaspoonful with water once in two or three hours. 
(b) Ammonium Chloride drachm one (4.0 gm.) 
Syrup of Senega, 
Syrup of Squill each drachms four (15. cc ) 
Elixir Terpin Hydrate and Heroin sufficient to make three 
ounces (90.0 cc ) 
Directions: A teaspoonful every two to four hours in water. 
(c) Ammonium Carbonate, 
Terpin Hydrate each drachm one (4.0 gm.) 
Elixir Terpin Hydrate and Codeine, 
Compound, Mixtura Glycyrrhizae of each sufficient to make 
three ounces (90.0 cc ) 
Directions: Give a teaspoonful with water every two or three hours. 
(d) Ammonium Carbonate, 
Ammonium Chloride each one drachm (4.0 gm.) 
Syrup of Senega, 
Syrup of Squill Compound, each three drachms.... (12.0 cc ) 
Syrup of Tolu or 
Syrup of Wild Cherry Bark sufficient to make three ounces.. 
(90.0 cc ) 
Directions: One teaspoonful with a mouthful of water every three 
hours. 
Many other efficient combinations could be enumerated here, 
but the physician will have to prescribe as each case requires. CARE OF THE TUBERCULOUS 
223 
In the old chronic forms of cough, not painful or distressing but 
perhaps copious, I much favor the following: 
Take: Creosote (Beechwood). 
Guaiacol, pure. 
Oil of Cinnamon. 
Oil of Cloves, each one half or one drachm (2.0 cc) or (4.0 cc) 
Give 2, 3 or 4 drops on loaf sugar every 2, 3 or 4 hours. 
Creosote or its derivatives, Guaiacol, Thicol may be given. 
Avoid as much as possible the giving of narcotics or better 
give them sparingly. The physician must always bear in mind 
the nature of the drug which he is using for the allaying of 
cough, that there is always a strong tendency to give the drugs 
wffiich enslave, because it is these that seem to give most relief 
and for which the patient will repeatedly ask; if given at all 
they must only be used in most minute doses. 
(4) Night Sweats. A most distressing, annoying and alarming 
symptom coming on usually about midnight or towards the early 
morning hours, about 4 o’clock, when tissue relaxation is at its 
height. This symptom is often caused by the toxins present in 
the organism. It may also at times be due directly to mechanical 
causes, such as too much bedding, or clothing, to overheated 
rooms or insufficient and poor ventilation or again the patient 
may be tucked in too close in bed, or it may be due to extreme 
nervous depression. Whatever may be the cause, this should 
first be ascertained, if possible corrected, and the patient made 
comfortable. If from nervous causes the administration of a 
sedative % grain morphine with perhaps 20 grain sodium brom- 
ide is often efficacious, inducing rest and sleep. Often thorough 
ventilation of the rooms will inhibit the night sweats; however, 
the most common cause is from the disorder itself, from the 
elaborated toxins and from the toxins of tissue destruction 
causing the low tensioned pulse and the low blood pressure, 
all combine to produce vaso-motor disturbance, capillary relax- 
ation, stasis and sweating. As these patients in addition to the 
sweating have a slightly accelerated pulse and a temperature, 
alcohol sponging often gives much relief. In those who are 
somewhat advanced in years, a teaspoonful of whiskey or 
brandy given in a little hot water, sweetened to suit the taste, 
at bed time, will very frequently retard the sweating. Drink- 
ing a cupful of hot sage tea prepared by steeping an ounce of 
sage leaves or sage tea in a pint of hot water and then allowed 224 
CLINICAL TUBERCULOSIS 
to simmer for about five minutes strained and sweetened to 
suit the taste, will frequently be found very satisfactory. 
Many prefer giving the sage tea as a cold infusion, and then 
in some again a glass of cold milk taken at night will give 
relief. However, here the use of drugs will find its must suit- 
able application in these symptomatic disturbances if given in 
appropriate dosage, foremost of which will be found atropine 
sulphate in 1/200, 1/150 or 1/100 of a grain given either by 
mouth or more efficiently hypodermically. If much restless- 
ness or nervousness is present the addition of a little Morphine 
sulphate in 1/16 to 1/8 grain doses is indicated. The aromatic 
sulphuric acid given in to 1 teaspoonful doses, well diluted 
with pure cold water, and drank during the evening hours is very 
often sufficient and useful. Agaracin, a glucoside prepared from 
a fungus, the Agaricus Albus, given in 1/10 grain doses at bed 
time will be found a most reliable drug in many cases of ex- 
cessive night sweats. Camphoric acid in 2 to 5 grain doses by 
mouth, giving a few doses during the evening hours is with many 
a most favorite drug. Many use the newer hypnotic drugs like 
veronal, adalin, sulphonal, trional, etc., in 5 grain doses. 
Sodium bromide in 20 grain doses dissolved in a mouthful of 
water and given during the evening is often most helpful. The 
various preparations of valerian, the tincture, the fluid extract, 
elixir of ammonium valarianate, etc., may all be employed. 
(5) Dyspnoea. Shortness of Breath. A very annoying symp- 
tom. Here again as in the general treatment of tuberculosis, 
rest is the most effective and prompt therapeutic remedy. At 
the very onset we must try and ascertain the cause of this short- 
ness of breath. It is often due to an accompanying cardiac dis- 
order or perhaps a kidney complication, or it is simply because 
the pulmonary parenchyma is greatly destroyed or contracted, 
is perhaps distended, emphysematous or atelectatic, all condi- 
tions which greatly interfere with the free access of air to the 
alveoli. If the cause can be ascertained, the proper remedy may 
often be very promptly applied; however, no matter what may be 
the cause of the dyspnoea, a small dose of morphine is usually the 
drug which gives prompt relief. Should much cough accompany 
the dyspnoea, the addition of a small amount of atropine sulphate 
1/200 or 1/150 grain is very useful, or a hypodermic tablet may 
be given or administered by mouth. If much nervousness accom- 
panies this distressing symptom,. Sodium Bromide in 15 or 20 CARE OF THE TUBERCULOUS 
225 
grain doses is indicated. The following is a most admirable 
combination: 
Sodium Bromide drachms four (15.0 gm.) 
Morphine Sulphate grain one (0.06 gm.) 
Essence of Pepsin sufficient to make two ounces (60.0 cc ) 
Directions: Give one teaspoonful in a little water at once, repeat in 2 
or 3 hours if necessary. 
If the shortness of breath is due to an accompanying cardiac 
disturbance, then the addition of tincture of digitalis in 5 to 10 
drop doses added to the ordinary mixtures is advisable. If the 
heart’s action is feeble, pulse scarcely palpable, with little 
force, then the use of strychnine in 1/60 to 1/40 grain doses 
hypodermatically is often most useful. Aromatic spirits of am- 
monia in y2 to 1 teaspoonful doses given in a few mouthfuls of 
water, or a little whiskey or brandy, is often found to be a most 
helpful remedy, and alcohol sponging especially if there is fever 
will often be followed by better breathing conditions. A most 
souverain remedy, one of much value for the relief of shortness 
of breath is oxygen gas. This gas should be inhaled through 
the nostrils by means of a rubber tube tipped with glass tubing. 
If the dyspnoea is not very urgent this gas may be given inter- 
ruptedly, but not if the shortness of breath is lasting; it should 
then be given continuously for hours, even for days, and the 
patient should be asked to inhale deeply in order to force the 
oxygen gas into the very recesses of the lungs so as to become 
more readily effective. 
(6) Sleeplessness. Another very annoying, even painful 
symptom. Here again the anodynes and sedatives take the lead- 
ing role, of which may first be mentioned morphine sulphate 
given hypodermically in 1/12 to 1/4 grain dose according to the 
exigency of the case. Sodium bromide in 10 to 20 grain doses 
dissolved in a few tablespoonfuls of water given every two or 
three hours for two or three doses, beginning the administration 
in the middle of the afternoon, will often induce refreshing sleep. 
Trional, sulphonal or veronal in 5 grain tablets once in three 
hours for a few doses, Dover’s Powder in 10 grain doses, Tinc- 
tura opii deodorati in 5 to 10 minim doses, camphorated tinc- 
ture of opium or ordinary paregoric in one or two teaspoonful 
doses given in cold water are all more or less useful and helpful. 
In elderly individuals a teaspoonful of whiskey or brandy given 226 
CLINICAL TUBERCULOSIS 
in a little hot water and sweetened to suit the taste is often fol- 
lowed by restful sleep. 
(7) Gastro-Intestinal Disturbances in the tuberculous are often 
very distressing. Nausea, vomiting, dyspepsia, constipation, etc. 
The use of ice, by mouth, in small pieces will often allay the 
sickening stomach symptoms of nausea or vomiting. The giving 
of essence of Pepsin in Y teaspoonful doses every Y\ to y2 hour 
without water will be found very serviceable, and if much dis- 
tress from gaseous eructations after eating then the various com- 
binations of sodium bicarbonate will be found beneficial. 
Sodium Bicarbonate ounce one (30.0 gra.) 
Magnesium Calcined ounces two (60.0 gm.) 
Oil of Peppermint drops three ( 0.2 cc ) 
Mix well. Give one half to one teaspoonful in glass water, repeat in 
%. or J4 hour if necessary. 
Many tuberculously diseased individuals are also suffering 
from a hypoacidity and consequently after the ingestion of a 
meal, particularly if rich in protein, have much gastric distress. 
Here the giving of a small amount of diluted hydrochloric acid 
often gives relief. The following can be offered as a reliable 
combination: 
Acid Nitro-muriatic, diluted 
Tincture of Nux Vomica, each drachms two ( 8.0 cc) 
Tincture of Gentian Compound ounce one (30.0 cc) 
Glycerine sufficient to make three ounces (90.0 cc) 
Directions: Give a teaspoonful in y2 glass of water y2 hour after meals. 
For constipation, the aromatic fluid extract of Cascara Sa- 
grada in teaspoonful doses in y2 glass of water at bed time or a 
pill of Aloin, Strychnine, Belladonna and Ipecac given alone or 
with a 1/20 or 1/10 grain calomel is often very efficient. Although 
constipation is not a frequent symptom accompanying tubercu- 
lous disease, if present it is always better to regulate it by an 
appropriate diet. To accomplish this a liberal supply of vege- 
tables like spinach, cabbage, celery, lettuce, etc., or what is known 
as rough food should constitute a large part of the principal daily 
meal. The addition of a few tablespoonfuls of ground linseed or 
flax seed meal or bran to the ordinary breakfast foods will be 
found most serviceable in all constipated conditions in the tuber- 
culous as well as the non-tuberculous individual. The newer 
preparations, the liquid petrolatum extensively recommended for CARE OF THE TUBERCULOUS 
227 
the cure of constipation, are also very valuable and reliable in 
some individual cases, in appropriate doses and salt water enemas 
are freely recommended if applied by a trained person. Avoid 
above all the giving of active cathartics. 
(8) Diarrhoea. This symptom is frequently present when 
tuberculous peritonitis or enteritis accompanies the pulmonary 
disorder. It is fully described in Chapter 29—Tuberculous 
Peritonitis, page 388. 
(9) Pleurisy Pain. For the relief of pleurisy pain. See Tu- 
berculosis and Pleurisy, page 335. 
(10) Tachycardiac. See Tuberculosis and the Cardio-vascu- 
lar System, page 450. 
(11) Urinary Distress. See Tuberculosis of the Genito- 
urinary Organs, page 410. 
(12) Abdominal Pain. See Tuberculous Peritonitis, page 388. 
(13) Sore Throat. See Tuberculous Laryngitis, page 369. 
(14) Hemorrhage. See Tuberculosis and Pulmonary Hemor- 
rhage, page 362. 
Note. Tuberculin as a therapeutic remedy in the treatment 
of pulmonary tuberculosis it is now somewhat obsolete, however, 
in some quarters it is still used and as stated with very satis- 
factory results. The opinion of many phthisotherapeutists is 
that what effect for the better in the use of tuberculin may be 
observable in pulmonary tuberculosis must be attributed chiefly 
to a psychologic influence per se, and in no way to the drug in 
question. The use of tuberculin in the treatment of pulmonary 
tuberculosis may be found in Chapter XXIV—Tuberculin: In- 
dications and Contraindications, page 316, to which the reader 
is referred. CHAPTER 20 
THE CARE OF THE TUBERCULOUS—(Continued) 
The Surgical Treatment of Pulmonary Tuberculosis (33) 
Introduction. Under surgical treatment of pulmonary tuber- 
culosis should be considered all those methods of procedure 
where by means of surgical measures we aim to give the tuber- 
culous individual relief, either from pain or suffering or from 
excessive fluid in the chest cavffy, if by its presence the lung 
becomes crowded and breathing is strikingly interfered with; 
for the relief of urgent dyspnoea; for the relief of uncontrollable 
hemorrhages, but perhaps most frequently for the purpose of 
bringing about, if possible, an arrest or cure of a pulmonary 
tuberculous process and this chiefly by putting the lungs at 
rest. 
The simplest method, and the one now in general use, for 
bringing about an immobilization of the lungs for the treat- 
ment of pulmonary tuberculous disease is by means of artificial 
pneumothorax. If from extensive pleural adhesions this pro- 
cedure is not possible, then the other, the more difficult and 
more serious thoracoplastic operation may be advocated. It 
seems that the effect of lung compression is a lowering or lessen- 
ing of the circulatory lymph flow through the collapsed lung, a 
lessening of the amount of oxygen and an increase in the CO„ 
content, all of which is unfavorable to bacillary growth and the 
spreading of the bacilli through the blood or lymph stream, 
inhibiting the flooding of the organism with toxins. 
The various operative methods in vogue in the treatment of 
pulmonary tuberculosis, namely, artificial pneumothorax, pneu- 
monectomy, phrenicotomy, thoracoplasty, chondrotomy, etc., 
when compared with the dietetic-hygienic and medicinal will 
always be considered secondary and the suggestion made that all 
pulmonary cases be treated surgically can not be applied in prac- 
tice. 
Artificial Pneumothorax or Compression of the Lung. (61) 
Historical Notes. Early in the study of pulmonary tuberculous 
disease it was noticed by close observers that many cases of 
228 CARE OF THE TUBERCULOUS—(SURGICAL) 
229 
tuberculosis showed a healing tendency if the lung was com- 
pressed by mechanical ways, either by fluid or by air; that many 
cases if accompanied by a severe pleurisy or if the pleural cavity 
contained both fluid and air and that if this was maintained for 
some time a healing of the tuberculous process usually resulted. 
Baglivi as early as 1669 reported his observations on the frequent 
healing of pulmonary tuberculosis after injuries to the chest wall 
and opening of the pleural cavity, and William Hewson, 1739-74, 
made the observation that air is contained in the pleural cavity 
in pneumothorax. He was one of the first to perform the opera- 
tion of paracentesis, and Laennec described and differentiated 
spontaneous pneumothorax from the other pulmonary disorders. 
It became apparent from these observations that if nature 
effected a healing by putting the lung at rest, an artificial com- 
pression of the lung may be equally as efficient. Although the 
signs and symptoms of a spontaneous compression of the lungs 
had been known since the time of Hippocrates, nothing definite 
is recorded until the beginning of the 18th century when Jean 
Marie Gaspard Itard, a French surgeon (born at Oraisio in 1775, 
died in Paris in 1838), wrote a treatise on pneumothorax. He 
was the first to investigate the causes of natural pneumothorax 
and he has given us a clear description of a number of cases in 
which both air and water were present in the thorax during the 
course of tuberculous disease. About the same time James 
Carson* read before the London Medical Society (namely on 
November 25, 1819) a paper “On the elasticity of the lungs.” 
He was the first to study and to note the contractive power 
and elastic quality of the lung. Both Itard and Carson make 
mention of the fact, although this had been noted before their 
time, that injuries to the chest wall like stab wounds about the 
thorax of tuberculous soldiers were often followed by a trau- 
matic pneumothorax which generally would show a marked heal- 
ing tendency and even often effected a cure of the pulmonary 
tuberculous process. Carson’s observation led him to intensive 
work and we find that in 1822 he published his first papers giving 
the results of puncturing the chest wall in rabbits. Although his 
technic from present knowledge of paracentesis may be consid- 
ered somewhat crude, still he gives us a very clear picture of the 
behavior of these animals during the ordeal. Making an incision 
*(Essays, Physiological and Practical by Janies Carson, M. D., physician in Liverpool, 
appeared in 1822.) 230 
CLINICAL TUBERCULOSIS 
between the ribs he notes that the animals remained for a few 
seconds as if stunned but that at the end of a few hours they 
would resume their usual normal state. He concluded from this 
that collapse of one lung may be done with perfect safety on the 
human and suggested the possibility of treating pulmonary 
hemorrhage by lung compression, that it would be equally as 
efficacious in controlling bleeding of the lung as contraction of 
uterus would be in uterine hemorrhage. It is stated, supposedly 
authoritatively, that Carson assisted by Bickersteth actually 
treated pulmonary tuberculosis by artificial compression. 
Ramadge in 1836, advocated puncture and compression of the 
pleural cavity as the best remedy for the treatment of pulmonary 
tuberculosis and reported that his patient was doing well at the 
end of two years following the operation. Houghton, a co- 
worker with Ramadge, states: “The constant movement of the 
lungs, the entering air during the respiratory act keeps up a con- 
tinuous stimulation and an increase of blood to the tuberculous 
tissue, this favors growth and extension of the tuberculous 
process. In immobilization of the lung this ceases nearly alto- 
gether because the organ is put to complete rest and now lies in 
a more or less anemic condition close to the spine.” Luigi 
Parola, physician at the hospital at Cuneo, Italy, published in 
1849 a 700 page volume on pulmonary tuberculosis in which he 
mentions the work of Carson and of Barry of one hundred years 
ago and refers to this treatment. Constatt, 1843; Wunderlich, 
1856; Ehler, 1867; all mention Carson’s work and they all men- 
tion his animal experimentation but we glean nowhere that 
artificial compression of the lungs was actually performed by 
him on man. Although he suggested the procedure in 1821 and 
it was again advocated by Spaeth, a German physician in 1870, 
no artificial lung compression was attempted on the living human 
until the time of Forlanini of Padua who first put this method 
of treatment into actual practice, reporting his observations 
first in 1882 and after years of close labor publishing his results 
at the International Tuberculosis Congress at Rome in 1894. In 
America up to the close of the last century nothing was done 
along these lines with the exception of the work done by J. B. 
Murphy (67) and his associate, A. F. Lemke (66) of Chicago, the 
former reporting their observations in 1898 and the latter his in 
1899. J. B. Murphy in his oration, “Surgery of the Lung,” de- 
livered at the 49th annual meeting of the American Medical CARE OF THE TUBERCULOUS—(SURGICAL) 
231 
Association at Denver, Colorado, June 1898, described the 
method of procedure in detail and reported five cases in two of 
which they were not successful owing to pleural adhesions. The 
time of observation after compressing of the three successful 
cases was only two and one-half months before the reporting— 
too short a time to be of much clinical importance. A. F. Lemke, 
associated in the work with J. B. Murphy, reported the following 
year his observations on fifty-three cases of pulmonary tuber- 
culosis, giving his findings in a paper read at the Fiftieth Annual 
Meeting of the American Medical Association held at Columbus, 
Ohio, June 1899, entitled “Pulmonary tuberculosis treated with 
intrapleural injection of nitrogen with a consideration of the 
pathology of compression of the tuberculous lung.” His ob- 
servations were on fifty-three patients from September, 1898. to 
April, 1899, covering a period of about eight months. He also 
encountered in some of his cases a thickened pleura, conse- 
quently was unable to pass the gas or collapse the lung. 
Owing to the untimely death of Dr. Lemke (he being himself 
a victim of the white plague soon after the reading of his paper) 
nothing more was heard in American Medical Society meetings 
about pneumothorax until about 1911 when the subject was 
again brought forth as a curative measure in pulmonary tuber- 
culosis. 
During the earlier years of this century much intensive work 
on lung compression was done in Europe, and in 1906 Prof. 
Ludolph Brauer, Marburg, published his report of the most 
brilliant experimental and clinical work along these lines, and in 
1908 Dr. Fr. v. Sauerbruch,(147) Marburg, “Surgical treatment 
of pulmonary tuberculosis”—Page 82, Vol. 11, Sec. Ill; Dr. 
Hermann v. Schroetter, (140) Vienna,—“Recognition of pure 
pneumothorax without exudate in pulmonary tuberculosis”— 
Page 1165, Vol. 1, Sec. 11; Dr. Lucius Spengler,(152) Davos, 
“The course of the tuberculous disease under the influence of 
artificial pneumothorax,”—Page 1169, Vol. 1, Sec. 11; presented 
most interesting clinical observations on artificial collapse of the 
lung, the reports of which were read and well received at the 
Sixth International Tuberculosis Congress, Washington, D. C., 
1908. At this meeting no other papers on pneumothorax in the 
treatment of pulmonary tuberculosis were read or offered by 
either American or other European clinicians. The real and per- 
manent interest taken in artificial pneumothorax by clinicians 232 
CLINICAL TUBERCULOSIS 
and surgeons of our country dates back to 1912 when Louis 
Hamman and Martin T. Sloan,(55) Baltimore, and Mary E. 
Lapham, Highland, N. C., presented their observation on col- 
lapse of the lung before the annual meeting of the Association 
for the Study and Prevention of Tuberculosis at Washington, 
D. C., the latter reporting her observations on thirty-one cases 
of pulmonary tuberculosis treated by compression of the lung, 
the former fifteen cases divided into four groups. These papers, 
the pioneer papers on pneumothorax by American physicians, 
excepting the papers by Murphy and Lemke, did not receive 
sufficient encouragement in the discussion and the paper by Mary 
E. Lapham which was also read at the meeting of the A. M. A., 
at Atlantic City a short time after was even severely criticised 
as being of little importance and of doubtful value. It wras 
not until two years after when Gerald Webb of Colorado 
Springs,(55) Colorado, read a paper at the meeting of the Na- 
tional Tuberculosis Association that phthisotherapeutists be- 
came thoroughly aroused to the importance of this valuable 
therapeutic measure; fourteen leading clinicians participated in 
a lively discussion and since that time up to the present at 
every meeting of the National Tuberculosis Associations one or 
more papers were presented. 
These were the first papers presented on the subject of pneu- 
mothorax since the organization of the National Association for 
the Study and Prevention of Tuberculosis in 1904. In the tran- 
sactions of the Association issued annually since the first meet- 
ing at Washington, D. C., in the spring of 1905 until the gather- 
ing in 1912, mention is nowhere made of any observation on 
this method of treatment. 
It appears that Rothschild (170) (San Francisco, Cal.) in 1911 reported 
eighteen cases of pulmonary tuberculosis treated by lung compression 
and Robinson and Floyd in the Archives for Internal Medicine in April, 
1912, described artificial pneumothorax more in detail. 
Resume from historical data. The idea of compression of the 
lung for the probable arrest of the tuberculous process originated 
with Carson, although his suggestion applied to what is known 
as open pneumothorax in distinction to what is now practiced 
as closed lung compression, but to Forlanini belongs the credit 
and the original idea of a pneumothoraxtherapy under aseptic 
conditions, rather than to Carson who suggested simple or open 
pneumothorax. Following Carson comes Piorry who suggested CARE OF THE TUBERCULOUS—(SURGICAL) 
233 
a compression of the chest wall for the treatment of pulmonary 
disease by means of a tight binder or adhesive plaster. By these 
external means he aimed to bring the walls of cavities into close 
apposition and he even applied heavy weights, as much as 14 
pounds, securely fastened over circumscribed spots, to compress 
the thorax so as to immobilize the diseased and not the healthy 
portion of the lung, that this might have a tendency to bring 
about scar tissue formation. The idea of Carson and the sugges- 
tion of Piorry were both rejected by the profession, at the time, 
as being entirely impractical. No definite data as to Carson’s 
work on produced lung compression on the human are obtain- 
able and for more than a half century the method was nearly 
entirely forgotten until reintroduced by Prof. Carlo Forlanini, 
University of Pavia (Padua) who in 1882 again called attention 
to lung collapse by closed pneumothorax, reporting in 1894 his 
observation to the International Tuberculosis Conference at 
Rome on the healing and cure of pulmonary tuberculosis by 
means of artificial pneumothorax. Between the year 1821, that 
is, from the time of Carson until 1882 when Forlanini redis- 
covered immobilization of the lung for the arrest of a tubercu- 
lous process very little work was done and that only in isolated 
instances. Forlanini’s observations and study form the basis 
of the present applied method for the arrest of pulmonary tuber- 
culosis by means of an induced pneumothorax. He pointed out 
that a complete inhibition of functioning is necessary, that there 
must be an absolutely complete uninterrupted and continuous 
immobilization and that a simple lessening of pulmonary 
motility favors an extension of the process. As to priority, we 
may state the words of Forlanini: “It is not a matter of priority, 
—that belongs to Carson. No doubt that Carson in 1821, I (For- 
lanini) in 1882 and Murphy in 1898 had the same identical 
thought or idea and that it may be said there are indeed three 
priorities, that the first belongs without doubt to Carson, that 
his suggestion was lost for more than a half century and was 
then rediscovered by me (Forlanini) who may be credited with 
the second priority, and that the third priority is due to Murphy 
assuming that he had no knowledge of my (Forlanini) work.” 
Forlanini’s (the latter’s) paper was read in 1894 before the 
International Tuberculosis Conference in Rome and appeared 
right after in full detail in the Muenchner Mediciniche Wochn- 
schrift. See spirited controversy as to priority. Forlanini- 234 
CLINICAL TUBERCULOSIS 
Padua, Daus—Gentrogotz, Berlin. Die Therapie der Gegenwart 
1910. 
Observations on compression of the lung by means of gas, air 
or by fluids; serous, seropurulent or purulent. The respiratory 
act and the bony framework of the chest offer a constant resist- 
ance against pulmonary cicatrization and rest. This resistance 
to nature’s efforts at repair exists about every pathologic pul- 
monary cavity. If, however, we can compel the abscess cavity 
to collapse and to empty its contents, it will heal; an observed 
physiologic phenomenon. If an abscess cavity can be obliterated 
and subsequently healed by forcing it to collapse, might not pul- 
monary tuberculous processes be arrested on similar lines by 
mechanical immobilization, collapse and enforced rest? This 
was the argument advanced by those intensely interested in the 
pulmonary tuberculosis problem. This led up to the induction 
of the artificial collapse of the lung so much now in favor. 
Quoting from Murphy’s paper, “Have we any evidence from 
postmortem records that will support the principles of lung im- 
mobilization and physiologic rest, and which would favor the 
healing of the pulmonary process? Yes we have, namely, (1) 
lungs that have been severely involved in a tuberculous process 
when repaired show a contraction of the overlying chest wall in 
proportion to the degree of tissue involved; (2) tuberculous 
lungs compressed by pleural exudates generally heal during the 
collapse if the compression is maintained for a sufficient length 
of time, and, (3) lungs allowed to be collapsed following an op- 
eration for empyema have usually healed during the resting 
process.* 
*Attention is directed here to the clinical observation that more than 
80% of empyemas in the adult are secondary to a primary pulmonary 
tuberculous involvement. 
Every general practitioner can recall cases of tuberculosis of 
the lung resulting in empyema1 or hydrothorax in which there 
was complete recovery of the tuberculous process when the 
empyema or hydrothorax was operated at the proper time. This 
may not apply to those cases of advanced pulmonary tubercu- 
losis in which much tissue has been destroyed and in which much 
cavity formation or consolidation and fibrosis has taken place, 
iThe most probable reason why empyema is more curative in pulmonary tuberculosis is 
the fact that the pus is never absorbed but may increase and continue the lung compres- 
sion more evenly, whilst in pleurisy with effusion there is always a tendency at absorp- 
tion and consequently a relaxation from the compression. CARE OF THE TUBERCULOUS—(SURGICAL) 
235 
so that the resultant pleurisy or empyema is not capable of pro- 
ducing sufficient contraction or collapse of the pulmonary struc- 
ture. The number of cases of operated pleurisies or empyemas 
which present cures of the primary tuberculous process of the 
lungs carry conviction that compression and collapse of the lung 
favor a reparative process.” 
Pulmonary collapse or quiescence may be obtained in three 
ways: (1) by collapse of the lung by intrapleural injection of 
nitrogen gas or air. This is generally known as intrapleural 
pneumothorax or simply artificial pneumothorax; (2) by forcing 
the collapse of the lung by separation of the parietal pleura and 
by intrathoracic compression. This is known as extrapleural 
pneumothorax, and (3) by removing the bony resistance, the ribs, 
and allowing the collapse of the chest wall, thus favoring con- 
traction and cicatrization. This is known as Thoracoplasty. 
To insure a rapid contraction of the lung to favor early cica- 
trization and to put the lung at rest irritants have at various 
times been used. Iodine, in the form of the tincture, solution of 
iodide of potassium, and of carbolic acid, mercuric and other 
chlorides and many others have been tried with more or less sat- 
isfactory results. These solutions were directly injected into 
the diseased pulmonary tissue anticipating that by their presence 
sufficient irritation would be brought about to ultimately favor 
cicatrization. By some surgeons the use of the actual cautery 
has been advocated. Most all these therapeutic measures have 
been abandoned for the much simpler, less painful, and more 
natural method of putting the lungs to rest by means of nitro- 
gen gas or filtered air. 
Compression of the lung obstructs mechanically the various 
avenues through which the infection is transmitted to other 
parts, the most important of which are the air vesicles, the vesi- 
cular ducts, and the smaller bronchi as well as the lymphatic cir- 
culation which plays a great part in the spreading of the disease. 
That compression of the lung aids the natural forces which are con- 
stantly at work in the effort to arrest the tuberculous process we see 
frequently, as when the disease is complicated by either pleurisy, empyema 
or a natural pneumo-thorax, and also in the permanent retraction of the 
chest wall often observed in old and long quiescent or arrested pulmonary 
processes. The effect of a natural immobilization of the lungs had been 
observed by clinicians for centuries and even the ancients noted the 
beneficial result, but the practical application of these observations had 
not been attempted, and only within very recent years have the principles 236 
CLINICAL TUBERCULOSIS 
observed been applied by clinicians in the treatment of pulmonary 
tuberculosis. 
A spontaneous pneumothorax developing in the course of pulmonary 
tuberculosis seems to arrest or check the progress of the disease. Some 
tissues resist completely a tuberculous invasion as, for instance, the 
fibrous tissue of tendons and fascia; others when attacked never tend to 
repair, such as the tuberculous ulcer in the intestine, and again others, 
such as the peritoneum offer great reparative powers or resistance to the 
advancement or spread of the disease. A comparison of the postmortem 
evidences of repair of tuberculosis in the various tissues shows that the 
lungs far exceed any other tissue in the body in its ability to overcome the 
effects of a tuberculous inoculation. 
From the beginning of the tuberculous nodule, the solitary tubercle in 
the lung which is the first evidence of the body’s defense activities, down 
to active pulmonary tuberculosis there is a constant attempt at histologic 
repair to check the advance of the disease and to put the diseased parts at 
rest. A spontaneous pneumothorax in the course of a tuberculous process 
is usually most effective in producing this, an empyema as a concomitant 
symptom in tuberculosis has a similar effect and in a less degree a pleurisy 
with effusion. If we observe carefully we will notice nature’s effort at 
rest in most every case of pulmonary tuberculosis. About the first thing 
we observe by inspection is a lessening of motion on the affected side to 
spare the lung, an inhibition of the excursion over the diseased side; the 
muscles are rigid over the involved areas and there is a contraction or 
more properly the retraction of the diseased side, all evidence that nature 
is endeavoring to put the injured parts at rest till she has completed the 
reparative work. We notice the same in tuberculosis of all the other 
organs and tissues of the body. 
Cases of pulmonary tuberculosis suitable for lung compression. 
The indications and contraindications. Selection of cases. 
It has long been an undecided, and judging from the literature 
on the subject, still an open question as to what really does con- 
stitute a suitable case for immobilization of the lung. In the 
selection of cases from the incipient to the far advanced and from 
the fibroid to the hemorrhagic there exists a great difference of 
opinion. It was early recognized as an established fact in tuber- 
culosis treatment, dietetic, hygienic and otherwise, that the 
earlier the treatment is begun the more favorable the prognosis 
and this undoubtedly also applies to the surgical treatment of 
the disease. In the beginning, advocating compression of the lung 
for the cure of the diseased organ, the selection of cases was con- 
fined chiefly to those in which the other or opposite lung was in 
apparent perfect health. To show how cautiously then this selec- 
tion was made we may mention that an experienced operator in 
selecting his first cases for collapse carefully studied the case CARE OF THE TUBERCULOUS—(SURGICAL) 
237 
histories of ninety-six patients in the male receiving wards of a 
large tuberculosis sanatorium and found only seventeen indi- 
viduals in which the disease appeared to be confined to one side 
only. From that number two were selected for compression. 
All others were considered not suitable. With our present 
knowledge a goodly number of the others perhaps would have 
been urged to take the treatment and today the consensus of 
opinion is that many cases of pulmonary tuberculosis are suitable 
for collapse providing the involvement is not too extensive, 
or if extensive, confined mainly to one lung; that the tubercu- 
lous process is not running a very rapid course; and that the 
patient is not already in a moribund condition. In short, it may 
be stated as a rule that all cases of pulmonary tuberculosis that 
are not terminal, or that are not too active and that when under 
observation for some time show no improvement in the general 
condition, seem unable to be arrested, where the pulse remains 
fast and temperature about 101-102 and higher, and perhaps cases 
which under long observation seem to show no further progres- 
sion nor retrogression, may be suitable for attempted lung com- 
pression. If, after months of conservative and careful treatment, 
hygienic, dietetic, medicinal, tuberculin, etc., no satisfactory 
progress can be recorded, then compression or collapse of the 
lung should be attempted. 
Early in the study it became evident that the most favorable 
and typical cases for compression were the unilateral, although 
pure unilateral pulmonary tuberculosis is a rarity, and that next 
are those bilateral cases in which the involvement is not too great 
on the opposite side. If there is much evidence on physical ex- 
amination that both lungs are involved, usually the lung selected 
for compression is the one in which the disease appears to be 
the more active. In bilateral pulmonary tuberculosis, particu- 
larly in the somewhat advanced cases, attempts at compression 
of both lungs have been made by first collapsing fully the most 
involved or active and later by partial immobilization of the op- 
posite lung. This method in the hands of competent surgeons 
has given most gratifying results. By this procedure the medi- 
astinum is more completely put to rest, inhibiting in a measure 
mediastinal motion and enabling the remaining healthy lung to 
perform more quiet breathing. 
The most favorable application of lung collapse offering the 
most gratifying results is in recent and uncontrollable pulmo- 238 
CLINICAL TUBERCULOSIS 
nary hemorrhage accompanying tuberculous disease. In con- 
templating a compression of the lung for the control of pulmo- 
nary hemorrhage the surgeon must be sure from careful physical 
examintion from which lung the blood comes, so as not to col- 
lapse the freely functioning or healthy one, and incidently must 
be sure that it is a pulmonary and not a gastric, oesophageal, 
buccal or nasal hemorrhage. This compression for the arrest of 
pulmonary hemorrhage may best be done by slow collapse dur- 
ing the interval of bleeding to assure more lasting results. How- 
ever, if the hemorrhage is very severe and profuse, more rapid 
and quick compression is desired. The question has often been 
asked, what effect compression of one lung has on the opposite 
or non-compressed lung which is generally already and. slightly 
involved? If the functioning lung is slightly diseased compres- 
sion of the opposite lung or putting it at rest will not overtax 
this lung. Most likely the increased functioning of this lung will 
increase the blood and lymph flow, and congestion or hyperemia 
will favor rather a healing of the pulmonary lesion than an ex- 
tension. » 
To summarize: Pneumothorax indications and contraindica- 
tions. Indications: (1) In all chronic destructive processes lim- 
ited to one lobe; (2) in very acute exudative and infiltrative 
cases;'(3) chronic infiltrative processes with tissue destruction 
showing a progressive character and which are not influenced 
by the generally applied therapeutic methods; (4) owing to the 
unfavorable prognosis basal tuberculosis complicated by bron- 
chiectasis may be considered suitable in some selected cases; 
(5) as an indicatio vitalis in frequent profuse pulmonary hemor- 
rhages. Contraindications: Basal tuberculosis generally when 
both sides are extensively involved, tuberculous peritonitis and 
enteritis, complicating heart and kidney disease, non-tuberculous 
affections, abscess, gangrene, foetid bronchitis, bronchiectasis, 
etc., are all unsuitable for lung compression. The contra- 
indications then for the induction of artificial pneumothorax are 
in terminal cases, in the miliary form, in chronic contracted 
fibroid phthisis, in pulmonary cases accompanied by serious 
heart and kidney disorder and in tuberculous enteritis and peri- 
tonitis. 
A sufficient period of trial without improvement should be the basis or 
the failure of progressive cases of pulmonary tuberculosis to respond to 
the ordinary methods of treatment, regardless of the stage, before com- CARE OF THE TUBERCULOUS—(SURGICAL) 
239 
pression is considered. Numerous factors will determine the decision, 
such as a rapid extension of the process, marked constitutional dis- 
turbances, rapid impairment of the general conditions, etc. 
It is the gradually formulating consensus of opinion among the 
majority of observers that the best results can be obtained before the 
occurence of extensive adhesions, marked involvement of the opposite 
lung and the irreparable deterioration of the general resistance. 
Fig. 39. (a) The Floyd-Robinsor. Apparatus for Compression of the Lungs; (b) The 
Floyd-Robinson Needle. 
The Apparatus and the Technic for the Induction of Lung 
Compression. 
The induction of artificial pneumothorax or lung compression 
to put the diseased organ to rest requires usually only a very 
simple apparatus. The apparatus originally used in this country, 
devised by the late Dr. J. B. Murphy of Chicago, answered all 240 
CLINICAL TUBERCULOSIS 
requirements. This apparatus provides means for noting the 
escaping gas, measuring its volume in cubic inches and using 
pure nitrogen gas for the compression. At the present time ni- 
trogen is but little employed, having been superseded by the use 
of sterile and filtered atmospheric air and the volume of air used 
for compression is now measured in units of ccm. There are 
now many different makes of apparatus to be had. The Floyd- 
Robinson (98) outfit originally described in the journal of the A. 
M.A., in March 21, 1914, will answer all purposes. Every apparatus 
offered is simply a modification of the Murphy-Brauer-Forlanini 
type to which a water monometre has been attached, as had 
been suggested by Prof. Chr. Saugmann of Christiania in 1907. 
This is by all means the most important addition, for it registers 
with exactness the location of the end of the needle and by its 
use the amount and flow of the entering gas or air can be regu- 
lated with perfect accuracy. A good and complete apparatus 
may be purchased from any dealer in surgical instruments. As 
already stated the original compression (99) was done with pure 
nitrogen gas. This was generally supplied by dealers, deliver- 
ing it in steel tanks, but now most operators are using pure and 
filtered atmospheric air which is generally prepared either before 
or while the operation is proceeding by the following method. 
A long rubber tube is connected at one end with an intake valve 
of an ordinary aspirating pump and at the other with a metallic 
bathroom spray loosely filled with sterile cotton. This end is 
placed in the outside air which is then pumped through a bottle 
of sterile cotton, thence into one filled with a 1-1000 bichloride of 
mercury solution and from this into the inverted cylinder sur- 
rounded by boiling water. Another and simpler device for the 
preparing of the atmospheric air for use in lung compression is 
by means of two bottles, a few glass tubes, rubber tubing and 
an ordinary atomizer bulb or pump forcing the air through a 
solution of carbolic qcid and then through sterile absorbent 
cotton. 
T he technic for the induction of Pneumothorax is as follows: 
(63). The necessary apparatus is placed on a solid, well-sup- 
ported table. The operator and his assistants must be surgically 
clean. To conserve time one nurse remains sterile while an- 
other gets the patient into the operating room and takes care of 
other details. An assistant or nurse operates the apparatus, 
reads and records the pressure, the site of injection, incidents, CARE OF THE TUBERCULOUS—(SURGICAL) 
241 
etc. As a certain number of cases of serous effusion often com- 
plicate this treatment, strict observation of the principles of 
surgical asepsis is imperative. The needles used are 18 gauge 
aspirating, the ends of which are filed to an angle of 45 degrees 
and about 1/16 of an inch from the end a nick is filed. These 
needles are carefully cleansed after use by running cold water 
and a stiletto put through them several times in order to re- 
move any coagulated blood or tissue. They are then dried by 
compressed air, stilettos replaced, wrapped in gauze, then cov- 
ered with muslin and sterilized under high pressure for an hour. 
A number of needles must be kept on hand to eliminate steriliza- 
tion during the procedure. A hypodermic syringe filled with 
camphorated oil should be a part of the equipment. All treat- 
ments, initial as well as refills, must be preceded by a thorough 
physical examination. The patient is stripped to the waist, 
placed on the operating table lying with the side to be operated 
uppermost. A sheet is placed over the body below the waist 
line, then the sides of the chest are thoroughly cleansed from the 
sternum to the posterior axillary line and from the 4th to the 7th 
interspace and covered over with two sterile towels. The oper- 
ator usually selects the site for puncture by means of percussion 
and his previous observation. The site is usually in the 5th or 
6th interspace about the anterior axillary line or perhaps slightly 
farther back, particularly when the left side is to be injected. 
The site is then painted over with tincture of iodine and the 
operator introduces a hypodermic needle so as to make a bleb 
with a small amount of 0.5 per cent solution of novocaine. After 
a few seconds the needle is slowly reintroduced perpendicularly 
and Schleich’s infiltration method employed. Care is neces- 
sary in order not to puncture the parietal layer of the pleura. 
The next step is to pick up the integument surrounding the site 
between the thumb and forefinger of the left hand with consid- 
erable pressure, and with a cataract knife puncture the layers of 
the skin; frequently no hemorrhage follows the pressure method. 
The index finger is then placed over the interspace so that its 
tip almost covers the incision. The needle is next held perpen- 
dicularly between the tips of the fingers and thumb of the right 
hand, the wrist resting upon the patient’s chest to steady the 
movement. It is then slowly introduced, the index finger on the 
wound acting as a guide and the nail as a brake. Occasionally 
slight negative oscillations are observed in the monometer when 242 
CLINICAL TUBERCULOSIS 
the point of the needle reaches the parietal layer of the pleura, 
but as soon as the needle passes through this layer into the free 
pleural space the suction, or negative pressure, immediately 
causes2 oscillations varying between 10 or more to 1 or 2 cm 
Such oscillations of water, even with much less amplitude, give 
the assurance that the end of the needle is in the free pleural 
space and that now air may be allowed to flow into it without 
danger. It is best to wait a few moments in order that the os- 
cillations may become stable before they are recorded and air is 
admitted. In working without a monometer, and this is ex- 
tremely infrequent at the present time, to assure oneself that the 
end of the needle is in the pleural cavity, the patient is in- 
structed to take a few deep inspirations and if the needle is 
within the pleural space a current of air will be heard rushing 
in. During the initial operation air should be given at short in- 
tervals and no more than 100 cc at a time, the column of water 
being watched continuously. When the total number of cubic 
centimetres has been given this is recorded along with the read- 
ings following. After the needle is withdrawn the puncture is 
immediately touched with tincture of iodine and pressure ap- 
plied, the wound dressed with sterile gauze and the patient in- 
structed to continue pressure for a few moments and, by having 
the patient then change his position after the needle is removed, 
the complication of surgical emphysema is very infrequently en- 
countered. A few words of advice as to the use of the compres- 
sion apparatus. The most vital part is the monometer. It is to 
the operator what the compass is to the mariner and a disregard 
for its danger signals will surely spell disaster. In addition to a 
sustained negative pressure with free oscillations, this the only 
condition under which the initial insufflation is warranted, there 
are other readings of great importance. For instance, fluctua- 
tions equidistant above and below zero indicate that the end of 
the needle is in the lung, or, the column of water is uninfluenced 
when the end of the needle is extra pleural, or is surrounded by 
dense adhesions or occluded by tissue or blood. A partial oc- 
clusion acts as a valve and the readings must be interpreted ac- 
cordingly. When the water rises slowly on the negative side of 
2The intrapulmonary, also described as ordinary atmospheric pressure is usually 6' m.m. 
higher than the intrapleural. This difference is designated the “negative” pressure. The 
admission of air into the pleural cavity equalizes this pressure so that it becomes equal to 
that in the pulmonary tissue. This difference, that is, the pressure in the lungs or or- 
dinary atmospheric and that in the pleural space is registered with the monometer the 
moment the needle enters the pleural space. CARE OF THE TUBERCULOUS—(SURGICAL) 
243 
the monometer and the pressure decreases slowly without any 
oscillations during ordinary respiratory movements, the needle is 
practically plugged. It should be removed and another needle 
introduced in the same tract. Failure to locate the free space is 
often due to coagulated blood and no attempt should be made to 
reintroduce the needle as long as there is oozing at the puncture. 
After some compression is produced, the dosage and the neces- 
sary length of intervals between refills can be roughly deter- 
mined by the monometric readings. Some idea of the elasticity 
of the mediastinum may also be obtained, but not until the pres- 
sure approaches zero or becomes positive. The monometer may 
confirm the diagnosis of spontaneous pneumothorax. 
As to the amount of air required for the initial and the sub- 
sequent insufflations a wide difference of opinion exists among 
various operators and whereas one operator limits his first inflow 
of air to 100 ccm another uses from 800 to 1000 and more. How- 
ever, practice has proven that it is not necessary to use large 
amounts—from 100 to 300 at most is usually sufficient for the 
beginning amount and after this from 300 to 400 may be injected 
every second or third day until a partial compression becomes 
established, after which the compression may be repeated once 
in four to five days until at the end of about six weeks it will be 
sufficiently collapsed, after which it is repeated about once a 
week to maintain the compression. As absorption of the re- 
tained air takes place more or less rapidly, more so at the be- 
ginning of the treatment and less so as time goes on, a refilling 
about once a month will usually be sufficient. If fluid should 
follow the injection of air or gas into the pleural cavity, the 
time for reinsuffiation may be postponed. In this manner the 
treatment may be carried along for months and years.—E. M. 
Complications incident to the production of (55) artificial 
pneumothorax. With the gradual perfection of the technic and 
a more careful selection of cases, accidents in the course of lung 
compression are gradually diminishing in number. Whatever 
is used, nitrogen gas or sterile atmospheric air, it must never be 
permitted to enter until the monometer establishes the connec- 
tion with the pleural cavity—by sustained negative pressure and 
free oscillations. Another important factor is asepsis. Local an- 
aesthesia of the entire needle tract should be insisted upon for 
the prevention of pleural shock. Excessive pressure within the 
pleural cavity should always be avoided and even positive pres- 244 
CLINICAL TUBERCULOSIS 
sure is not entirely necessary for the production of effective com- 
pression. An important exception should be made in cases of 
severe hemorrhage in which bleeding persists till a marked posi- 
tive pressure is established. Lung compression should never be 
employed in the presence of severe cardiac complications. The 
most frequent complication in the course of artificial pneumo- 
thorax is pleural effusion. It is variously ascribed to infection, 
to progressive irritability of the pleura due to trauma, to slow- 
ing of the lymph circulation in the compressed lung, to breaking 
of tubercles through the pleural surface, etc. It is estimated 
that this incident occurs in from fifteen to fifty per cent of cases. 
The exudate may remain serous, become mucupurulent or even 
pus, all of which adds to the gravity of the case and here a radi- 
cal surgical operation is frequently indicated. The most serious 
complication is gas or air embolism, the onset of which is usually 
sudden and the minifestations may be from temporary uncon- 
sciousness to convulsions, hemiplegia, to gradual recovery or to 
fatal coma in from fifteen minutes to two or three days. It is 
supposed, according to Saugmann, that the fatal termination re- 
sults from lodgment of air or gas in the coronary arteries or in 
the vessels of the brain. It is the opinion of many observers that 
this grave incident by a better technic and greater care can be 
avoided. 
In Saugmann’s experience between 1906 and 1910, 98 pa- 
tients, 2,000 punctures—1 death; between 1910 and 1912, 63 
patients, 1,200 punctures—1 death; between 1912 and 1914, 49 
patients, 2,000 punctures—no death. 
Forlanini—10,000 operations, gas embolism four times, two fa- 
tal. 1,058 cases treated by 22 American operators, the accident 
occurred three times in a group of 191 cases by three authors and 
in the remaining 876 cases by 19 operators, the accident did not 
occur in a single instance. Pleural reflex, pleural shock or 
eclampsia, as it is called by Forlanini, thrombi and other grave 
manifestations during or following the induction of artificial 
pneumothorax are all ascribed as of gas embolism. 
Immediate and ultimate result of lung compression. Almost 
immediately following the induction of a pneumothorax the 
cough is increased, the expectoration becoming more copious as 
a result of expulsion of the secretion from the lung and in cases 
where cavities have been compressed, enormous quanties of 
muco-purulent or purulent material have been expectorated. CARE OF THE TUBERCULOUS—(SURGICAL) 
245 
This, however, is soon followed by a diminution and nearly to- 
tal disappearance of all expectoration. With collapse the tem- 
perature frequently rises due to a flooding of the lymphatics with 
toxins of the diseased lung, but this soon ceases, as the compres- 
sion becomes more stable by a decline or disappearance of all 
fever, showing diminution or inhibition of absorption from the 
mixed as well as from the tuberculous infection. In a number 
of cases the heart’s action also becomes greatly increased, espe- 
cially on compression of the left lung, or distressing palpitation 
may follow if the heart is moved too quickly from its normal po- 
sition. Here even dire results may follow. Compression is sel- 
dom followed by cardiac hypertrophy. The pulse almost always 
becomes rapid, feeble, hardly palpable, but with amelioration of 
the other symptoms the pulse is usually again normal. Nervous- 
ness may supervene incident to the procedure, the patient be- 
coming pale, faint or showing an expression of fear. This, how- 
ever, is usually only transient, the composure returning very rap- 
idly. The injected gas or air in the pleural cavity may exert 
pressure upon the diaphragm, causing annoying gastric symp- 
toms and in some patients a most distressing hiccough has been 
observed. In most individuals there is a temporary and slight 
loss in weight which is very soon followed by a reaction of grad- 
ual and perceptible increase. 
The ultimate result of the induction of artificial pneumothorax 
after all is the bringing about of the formation of scar or con- 
nective tissue. This stands out distinctly in the healed or ar- 
rested cases and is the evidence of the efficacy of the treatment. 
Some patients almost from the very beginning of the compres- 
sion express a feeling of general well-being noticeable by a 
marked improvement in health. The question is often asked 
how long the treatment should be maintained or how long the 
lung should remain collapsed—long enough to give nature an 
opportunity to form a firm fibrosis in the diseased pulmonary tis- 
sue independent as to time that may be required. A lung should 
not be permitted to resume functioning until assured that it is 
entirely healed; to achieve this the time of compression may be 
continued from one-half to two years and longer. Even after 
that length of time of collapse the lung when released will grad- 
ually resume its function. The pneumothorax must be main- 
tained within certain limits of volume of compression so as not 
to interfere very materially with the free movements of excur- 246 
CLINICAL TUBERCULOSIS 
sion of the healthy lobe which during the collapse of its mate is 
compelled to do compensatory or vicarious work. In far ad- 
vanced or active and very chronic cases the compression if in- 
duced should always be maintained and the refillings at stated 
intervals should never be omitted. 
It may be of interest to note the results of lung compression as observed 
by both American and European operators. The final or ultimate result 
is very similar in both countries. The result of 1,108 cases of pulmonary- 
tuberculosis treated by 24 American operators corresponds very closely 
with the result of 224 cases treated by three of the leading European 
authors: American 21.7% of quiescent, arrested or cured cases as against 
25.9% European. American 29.2% of improved and palliative cases, 31.2% 
European. American 49.1% of failures to induce lung compression, 42.9% 
European unimproved or dead. 
Thoracotomy. Surgical operations other than pneumothorax 
for the treatment of pulmonary tuberculous disease (89). 
(a) Pneumonotomy. Incision and drainage of pulmonary cav- 
ities. This procedure, in isolated cases, dates back for centuries, 
but the real attempt at drainage by surgical means extends to 
the time of the introduction of tuberculin as a therapeutic rem- 
edy. It was considered an established fact that the administra- 
tion of tuberculin favored the production of a sequestrum about 
the walls of the tuberculous cavities which it was desired to elim- 
inate. As many cavities empty themselves through the bron- 
chial tubes without surgical interference the opening of cavities 
through the external thoracic wall has been little practice; be- 
sides, if an incision was made it usually left a pulmonary fistula 
which added greatly to the patient’s discomfort. 
(b) Pneumonectomy. The removal of a part of a lung or of a 
complete lobe. According to Murphy: “Pneumonectomy has 
been the triumph of surgical technic but clinical results have 
been extremely unsatisfactory and whilst the operation of re- 
moval of a complete lobe of lung has been successfully performed 
the number of deaths following pneumonectomy has been so 
large that the operation has practically been abandoned.” Most 
operators now agree that in the surgical procedure for the ob- 
literation of cavities by pneumonectomy the prognosis is ex- 
tremely grave and a combination of all methods of rib resection 
which follow collapse and compression of the lung and ultimate 
scarring of the cavities with pneumonectomy is the only advised 
surgical method. We observe that pneumonectomy for the com- 
pression of cavities frequently is not a practical procedure; be- CARE OF THE TUBERCULOUS—(SURGICAL) 
247 
sides grave danger accompanies the method; however, pneu- 
monectomy may be advisable if the cavities lie very superficially. 
The only procedures of real value are those which aim to put 
the diseased lung at rest; namely, pneumothorax and thoraco- 
plasty. 
(c) Pneumolysis. An extra-pleural packing operation for cav- 
ity compression suitable for unilateral, chronic tuberculous cavi- 
ties situated in the upper lobes, less applicable in lower lobe in- 
volvement. A subperiosteal resection of several ribs on the 
upper half of the thorax. The principle of the operation consists 
in an extra-pleural separation of the diseased portion of the lung 
by an artificially produced thorax window, removing from one 
or two ribs a piece about 6 cm in length and through this win- 
dow with the index finger carefully separating the parietal pleura 
and filling the so produced space with a sterile non-absorbable 
material. The only severe difficulty encountered is the separa- 
tion of the costal pleura, leaving the tissue wholly intact. Vari- 
ous substances have been used. Tuffier uses for extra-pleural 
packing or implantation sterile fat, Baer, paraffine prosthesis and 
Gwerder following the method of Baer observed that a hollow 
body is equally as efficient and uses a rubber ball or a rubber 
balloon with a tube attachment which allows of its inflation 
after it is put into place. This pneumatic plombing or packing 
is very simple, safe and non-irritating, adapts itself well to the 
irregular outline of the cavity and the pressure may at will be 
increased or decreased. If fat is used as a packing or plombage 
it may be used in the fresh state and in that event it may be 
taken from the patient or from a friend whose abdomen is well 
padded with fat. The fat so implanted is usually healed in about 
three weeks and beginning organization is already noticeable. 
Wilms is of the opinion that fat so implanted from one individual 
to another does not undergo changes. It may usually require 
from 300 to 450 grams of either fat or paraffine to completely fill 
a cavity. 
(d) Phrenicotomy. Artifical paralysis of the diaphragm in the 
treatment of pulmonary tuberculosis, Stroutz 1911, Sauerbruch 
1913. The lung is put to rest by placing the diaphragm in the 
position of extreme expiration. The treatment is proposed for 
severe one-sided chronic particularly cavernous lower lobe tuber- 
culosis by severing the phrenic nerve in order to put the diseased 
lobe to rest. In cutting the nerve, the diaphragm ascends to an 248 
CLINICAL TUBERCULOSIS 
expiratory position, the mobility of the lung diminishes, the 
lower lobe becomes compressed, lessening the danger of aspirat- 
ing tuberculous material into the remaining healthy lung tissue; 
this has been confirmed both clinically and roentgenologically. 
The operation is simple and is usually done under local anaes- 
thesia using a 1 % novocaine solution. 
(e) Thoracoplasty—partial and complete. Partial rib resection 
as practiced by Wilms and complete removal as advocated by 
Friederich, Marburg. A method for bringing about a lessening 
of the circumference of the chest and a lung contraction for the 
treatment of pulmonary disease, as recommended by Wilms, con- 
sists in the removal of pieces of rib from the posterior chest wall 
near the spine from 3 to 4 cm in length. A piece is taken out of 
every rib from the first to the eighth inclusive, some say to the 
10th, and eventually at a subsequent time the same operation is 
performed on the anterior chest wall and by this so performed 
operation the circumference of the chest can be lessened from 
6 to 8 or more cm or about three inches, permanently lessening 
the capacity, the elasticity and the excursion of the lung, bring- 
ing the diseased parts into close apposition, and favoring a heal- 
ing tendency. The thoracoplasty of Friederich consists in an 
operation for extensive resection of the ribs on the affected side 
from the second to the tenth inclusive in extensive one-sided 
tuberculous disease. The ribs may be removed near the medias- 
tinal fixation or from the posterior axillary line to near the ster- 
num. The patients selected should be between the ages of 15 to 
40, as beyond the latter age the resistance to overcome the shock 
of an ordeal of such proportions necessary is usually wanting. 
Extremely anemic individuals as well as those who are suffering 
from recent tuberculous involvement of other organs must be 
excluded. In cases of very active tuberculous disease running 
a rapid course in which there are dense pleural adhesions and 
which would not justify an attempted pneumothorax, extra- 
pleural thoracoplasty, either partial or complete becomes an 
operation of choice and cases favorably influenced by these 
operations show a collapse and obliteration of the cavities, sub- 
sidence of the fever, lessening of the sputum and general im- 
proved condition. These operations on the thorax should be 
done by removing the ribs either whole or in part subperiosteally 
and without injuring the parietal pleura. In some cases it may 
become necessary to combine thoracoplasty and phrenicotomy, CARE OF THE TUBERCULOUS—(SURGICAL) 
249 
especially in upper lobe tuberculous disease, so as to avoid the 
aspirating of tuberculous material into otherwise healthy tissue. 
Most surgical operations on the thorax, artifical pneumothorax, 
pneumonectomy, phrenicotomy, thoracoplasty all aim to immobil- 
ize the lung, to put it at rest, to keep it quiet and compressed 
for a sufficient length of time to bring about an arrest and heal- 
ing of the tuberculous process. Paradoxical as it may seem, an- 
other thoracic operation is advocated in pulmonary tuberculosis 
which aims at a decompression to give the lung more motility, 
more power to expand, if the disease is already established. This 
also favors an arrest or healing of the tuberculous process; if not 
already established, a freer lymph and blood flow inhibiting a 
beginning disease. This operation known as chondrotomy is 
applicable only if the involvement is in the apex of either upper 
lobe. 
(f) Chondrotomy. Freund’s operation, in apical tuberculous 
disease, consists in a resection of the cartilage of the first rib and 
widening of the aperature. He is of the opinion that in some 
cases of beginning tuberculosis the abnormally short first rib 
and early ossification of the cartilage bring about a shortening 
and a consequent stenosis of the upper aperature; this if it is 
not the direct cause of tuberculous disease, owing to loss of 
respiratory movements, furnishes in all probability a predispos- 
ing factor, and a separation of the cartilage and an enlargement 
of the upper aperature gives a better aeration and a more free 
lymph and blood circulation through the apices. This theory 
has many followers but also many opponents, the latter main- 
taining that ossification of the cartilage is not primary but a 
secondary condition, is really an attempt of nature in active 
tuberculous disease at lung immobilization and rest and that for 
this reason demobilization is contraindicated. However, there 
is no doubt that both Freund and his pupils, Hart, Harras and 
many other operators have proven the excellent result following 
the operation in selected cases. CHAPTER 21 
ASSOCIATED THERAPEUTIC MEASURES IN 
PULMONARY TUBERCULOSIS 
(A) CHEMOTHERAPY IN TUBERCULOSIS 
A therapeutic agent which, if incorporated into the body of the 
tuberculous individual, would have no deleterious effect or in- 
fluence upon the normal body cells or tissues would be per- 
fectly harmless but would have a definite and decided inhibitive 
and destructive influence on the tubercle, tuberculous tissue and 
the tubercle bacillus has been the wish, and its discovery the 
fond hope of the clinicians and the aim and the object of research 
of the laboratory diagnosticians. A remedy which, under most 
favorable conditions, could be brought into close contact in the 
human body with the living germ or virus, in short, a therapea 
magna sterilisans in the Ehrlich sense. Up to the present time 
we are not familiar with any such acknowledged or approved 
remedy, but that such a preparation may be within the near 
possibilities of experimental medicine can, judging from the in- 
defatigable work being done, be accepted. 
The use of chemical substances for the inhibition of bacillary 
growth within the human or animal body is not of recent intro- 
duction. Soon after the discovery of the tubercle bacillus as the 
etiological factor of the disease this was attempted, and we learn 
that as early as 1890 Robert Koch had shown that gold cyanide 
will inhibit bacillary growth in the experimental animal in a 
dilution of 1 to 2,000,000. Luton, a French dermatologist, in 
1894 first suggested the use of copper salt preparations as a 
therapeutic agent in the treatment of cutaneous tuberculosis. At 
the International Tuberculosis Congress in Rome in 1912 the use 
of copper salt solution as recommended by Prof. Finkler was 
much discussed. He and his co-workers tried experimentally the 
various salts of copper, the sulphate, chloride, and tartrate in 
definite strength solutions, but the best results were obtained 
from a complex copper preparation known as Leucetyle, a com- 
bination of copper, lecethin and cinnamic acid, and lecithin in 
250 ASSOCIATED THERAPEUTIC MEASURES 
251 
combination with iodo-metheline blue. Most of this work was 
done after Finkler’s death (89) by the Countess v. Linden at her 
laboratory. It was then suggested that the supposed favorable 
influence of these complex copper salts on the tuberculously 
infected experimental animal be tested on the human, and 
Meissen, a clinician, applied it in the treatment of pulmonary 
tuberculosis, and Strauss, dermatologist, in a number of tuber- 
culous skin lesions. At the laboratory of Prof. H. Gideon Wells 
of the University of Chicago, Dr. Lydia M. DeWitt and assist- 
ants have done a great amount of experimental work along these 
lines, using various chemicals and chemical combinations. The 
result of these carefully conducted experiments were not as hope- 
ful as we were lead to believe from the above mentioned earlier 
work. 
The chemicals generally used by most laboratory workers 
were besides the copper salts mentioned above, the acetates, 
oleates and to some extent colloidal copper. The introduction 
of drugs into the animal organism was done in all conceivable 
ways—by feeding, by intravenous, subcutaneous, intramuscular 
and intraperitoneal injections and injections into the anterior 
chamber of the eye. The results of all this experimental work 
on the previously infected animal were about the same, namely, 
that in no case was any positive inhibitive effect on the tuber- 
culous process noticeable. The observations with these various 
copper salts admit the following conclusions: if the entire body, 
the blood and fluids circulating throughout, could be made to 
carry at all times one part of copper to 100,000 parts of body 
weight, we might be able to inhibit the growth of the tubercle 
bacillus and perhaps eventually also to kill it; copper is of no 
particular value in the fight against tuberculosis, in fact, its use 
is unjustifiable, is even dangerous. 
Of added interest in Chemotherapy is the fact that many water 
soluble dyes possess the property of penetrating the tubercle 
bacillus in tuberculous-tissue. This had already been studied by 
Ehrlich and his co-workers at an early date, and vital stains or 
such dyes as can be introduced into the living animal without 
material injury to the tissues or cells are now extensively used 
for experimental purposes. Paul A. Lewis and Robert B. Krause 
reported their observation with trypan red to the effect that if 
this dye is injected into a living tuberculous animal it becomes 
concentrated in the necrotic portion of the tubercle. Other in- 252 
CLINICAL TUBERCULOSIS 
vestigators report similar properties of a number of dyes includ- 
ing trypan blue, isamine blue, pyrrhol blue, iodo-metheline blue ; 
many others have been used, including combinations of trypan 
red with iodoform and with Thymol, Eucalyptol, Guaiacol, Iodin, 
etc. 
According to DeWitt metheline blue is the most classic ex- 
ample of a vital stain or dye now in use in chemotherapy. The 
permeability of tissue cells to drugs and dyes has in recent years 
been extensively investigated and it was proven conclusively 
that in the tuberculous lesion there exists a special affinity or 
specific attraction for some of these drugs, an affinity inherent 
in the caseous portion of the tubercle; both trypan red and 
iodine, when injected into the tuberculous animal, are found 
localized in the necrotic portion of the tubercle, but so far as 
observed they have no favorable therapeutic action on the tuber- 
culous process. A combination of the salts of gold with can- 
tharadin as Aurocantan has given much promise in chemo- 
therapy. Cantharadin when administered causes a local reaction 
about the tubercle and other inflammatory foci, and this fact may 
be utilized in using cantharadin as a vehicle in carrying the gold 
into the tuberculous tissue. Both auric and aurous salts seem 
to exhibit a specific attraction for tuberculous tissue. The prop- 
erty of permeability of the tuberculous lesion by these chemicals 
is due to the fact that these tissues all behave in every respect like 
simple non-living colloids permitting crystallin bodies to diffuse 
readily but being little or not permeable to non-crystallizable or 
colloid substances, simply a process of osmosis or diffusion. 
Loeb first showed that a tuberculous lymph gland takes up 
relatively more iodine from the blood than any of the other or- 
gans but that the caseous material of the gland takes up many 
times as much as the remaining still normal gland tissue. 
Many chemical substances and various salts and combinations 
have been used and tried in experimental chemotherapy, the mer- 
curic and mercurous chloride, iodide, salicylate, succinamate, 
etc., arsenous and arsenic salts and many others, and all have 
been found worthless, unreliable and dangerous. 
Lydia M. DeWitt on “Copper in the treatment of tuber- 
culosis” makes a terse statement which seems to apply to nearly 
all the other chemical substances used. “Those therapeutic 
measures given just before or at the time of remission of the 
active tuberculous disease may be found a favorable time to be ASSOCIATED THERAPEUTIC MEASURES 
253 
regarded as an apparent improvement and may be even so 
heralded as a certain curative agent, whereas, if given just before 
or onset of a period of exacerbation these same measures may be 
considered as worthless or injurious.” 
Organic Acids in Chemotherapy 
Many diluted organic acids, lactic, phosphoric, malic, etc., dis- 
solve tubercle bacilli as is true in the preparation of the partial 
antigens according to Much, Deyche and Leschke.(190) In cul- 
ture media it has been proven that diluted lactic acid kills and 
dissolves tubercle bacilli and bacilli circulating in the blood or 
in recent tuberculous inflammatory areas can be affected by in- 
travenous injection of diluted lactic acid. It may be indicated in 
such cases as are usually early recognized by experts and which in 
general practice are usually referred to as neurasthenia, anemia, 
cardiac palpitation, gastric disturbances, dysmenorrhoea, rheuma- 
tism or to other prodromal signs. It may also be used in bronchial 
gland tuberculosis and in cases of mild and closed pulmonary 
disease, that is, while the disorder is still circumscribed. Phthisi- 
cal cases are not suitable because the diseased area cannot be in- 
fluenced by the blood current, and then again the lytic action 
may be so pronounced that the body can not cope with the 
effected bacteriolysis. It may be possible that the acid has bac- 
teriolytic action on the bacilli circulation in the blood current 
and also on the bacilli in the pulmonary tissue, which the blood 
stream may surround, and then again it may also be possible 
that the action of the diluted lactic acid causes a dissolution of 
some of the red blood corpuscles liberating the autoimmune 
bodies, on the theory advocated by Carl Spengler. In selecting 
cases, individualize, using a 1 % lactic acid solution injected once 
or twice weekly, finally once a month. In beginning cases it may 
give most promising results. 
Iodine in Chemotherapy 
When iodine in the form of the tincture or its salts is ad- 
ministered to the human body in whatsoever way it readily 
makes its presence known in the blood. Next to the blood 
the normal kidney is most permeable, containing as much 
iodine as the blood itself, and during active secretion even 
more. Iodine is very rapidly and quickly eliminated through 
the kidneys and its presence in the urine is demonstrable in a 
comparatively short time after its incorporation. The blood al- 
ways contains more iodine than any tissue or organ of the body, 254 
CLINICAL TUBERCULOSIS 
normal or abnormal.(85) The liver and spleen usually only con- 
tain about 1/3 as much, the lungs a little less; the lymph glands, 
however, take up more than either the liver, spleen or lungs; 
muscle tissue is usually not very permeable, usually containing 
only about 1/10 as much as the blood; however, necrotic tissue, 
even necrotic muscle tissue, is very permeable, containing as 
much iodine as the blood itself, and the same applies also to an 
inflammatory exudate. As stated above, this is due to the fact 
that colloid masses permit crystalloids to pass readily, but nearly 
completely inhibit the passage of colloids. Based upon these 
well known facts I began a number of years ago, in many forms 
of tuberculosis, the administration of tincture of iodine in enor- 
mously large doses, with most gratifying and encouraging re- 
sults. The human body is most tolerant to unlimited doses of 
the tincture and it can be given for months even years without 
the le&st disturbance. Iodine tolerance can not be satisfactorily 
tested on the experimental animal, but its long use now for many 
years has convinced me that the human body is tolerant to ex- 
cessively large doses. 
Practically some years ago, by a mere accident, I learned more of this 
tolerance. It came about in this way. I was consulted by a colleague 
concerning a woman who was operated on for gall stones and who about 
a week after the operation developed a severe cough which became so 
persistant and the expectoration so copious as to attract the attention of 
the attending physician, who upon examination of the sputum found it 
tubercle bacilli positive. My first thought on hearing about the case was 
that it was a miliary disease and I directed that she be given 20 drops of 
the tincture of iodine in milk three time a day. As months passed I was 
informed from time to time that she was steadily improving and was 
gaining in weight and as I now became more interested in the case, I 
desired a consultation with a view of making a physical examination. 
This proved that she had a right sided old tuberculous pleurisy. I now 
also learned that she had misunderstood the general directions and in 
place of taking the tincture of iodine 20 drops three times a day, had 
taken twenty drops every two hours, and appearing in such general good 
health, I directed that from then on she take twenty drops every hour, 
which she did, continuing this dosage for many months. Repeated 
sputum examinations were negative and most particularly a distinct gain 
in weight was noticeable. 
Many cases of tuberculous adenitis, bone and joint disease, 
psoas abscesses and chronic pulmonary tuberculosis have been 
on an iodine treatment persistently for months and years with 
most gratifying results. Iodine in the form of the tincture may 
safely be administered in extremely large doses and for very long ASSOCIATED THERAPEUTIC MEASURES 
255 
periods of time without anticipating any deleterious effects. 
Iodine is perfectly innocuous and non-irritating to the gastric 
mucosa if given in its proper vehicle, good wholesome milk. 
Further observations have convinced me that beneficial and last- 
ing results follow the ingestion of iodine only if large doses are 
given; small doses are not dependable. When iodine is admin- 
istered, its presence can readily be demonstrated in the various 
fluids of the body, both excretory and secretory, but within a 
comparatively short time nearly all, excepting perhaps a slight 
trace will have again disappeared from the body. Therefore, it 
should be given persistently, often repeated and in fairly large 
doses to keep the tissue saturated and to inhibit bacterial growth. 
For some time I have been administering the tincture in 10 to 30 
and more drops in milk at intervals of 4 or 5 hours or at break- 
fast, luncheon, dinner and at bed time. As iodine when admin- 
istered with milk is perfectly harmless and innocuous to the 
tissue and cells of the body, but is largely destructive and in- 
hibitive to all microorganisms, its use can not be followed by 
any deleterious results to the human economy. 
It has repeatedly been observed that if to a tuberculous individual 
intensive doses of tincture of iodine have been administered for some 
time, his tuberculin sensitiveness disappears, so far as it concerns a rise in 
temperature. This fact seems to depend upon the reduction or lessening 
of the temperature, producing tuberculotoxic substance in the body by 
virtue of the iodine ingestion.1 
(B) HELIOTHERAPY—SUNBATHS 
Light Treatment. (Sun Light, Arc Light, Quartz Lamp, X-Ray, 
Phototherapy, Radiotherapy, Roentgenotherapy, Etc.) 
Historical Note: Heliotherapy was well known to the ancient 
Greeks and its method of application in those times is well de- 
scribed in the works of Herodotus B. C. 430.(18) He mentions: 
“To bathe in the sun is necessary to increase and strengthen the 
muscles of people in need of such treatment. The direct rays of 
the sun are favorable in winter, spring and fall but not in sum- 
mer to weak and feeble persons.” Hippocrates, it is said, ex- 
posed his patients to the direct rays of the sun, and Celsus 
recommended sun baths as a potent remedy in epilepsy and in 
!In administering Tincture of Iodine the patient should always be under the care and 
supervision of the attending physician (87). Very exceptional patients are intolerant 
to the ingestion of Iodine. In such instances, the use of the drug must be discontinued, 
most patients, however, are tolerant to very large doses. Patients who exhibit much 
nervous disturbances, increased rapidity of the heart’s action or hyperthyroidism during 
the Iodine treatment are not suitable and the drug should be discontinued. 256 
CLINICAL TUBERCULOSIS 
disease of the abdominal organs. We observe that, in prehistoric 
times, prehistoric man directed his caves all towards the east or 
south, most presumably on hygienic principles. The sun was 
worshiped by the Egyptians in Rhea, the Sun God, by the 
Persians and Greeks in Helid and in Sol by the Latins. The use 
of sun baths was extensively practiced by the Greeks in their 
Heliosis or resting places about their homes, below the domes of 
the temples or in the sands. Excavations made in the old temple 
of Aesculapius in Epidaurus exhibit a long gallery with a south 
exposure connected with rooms or wards for the sick. In ancient 
Rome there was a Solarium in every home, and pictures from 
Pompeii show many examples of the inhabitants, who were wont 
to take their sun baths on the roofs of their homes or in terraced 
places. All Thermos were provided for sun baths. 
We find nothing more recorded about the sun as a health 
given agent from about the second century until the second half 
of the eighteenth, when Faure in 1774 reported to the Royal 
Academy of Medicine his observation on the “Use of heat from 
sunlight in the treatment of ulcers”; LePeyre and LeCounte, 
1776, increased the action of the sun by passing its rays through 
lenses, reporting the cure of ulcers and even of carcinoma; Bert- 
rand, 1799, presented a dessertation and essay before the Faculty 
of Medicine, Paris, on “The influence of the sun’s rays on dis- 
eased parts of the body.” Heliotherapy received its first definite 
recognition 100 years ago when Lobal in 1815 in the Journal f. 
pract. heilkunde stated that he recommends insolation in all 
cases of indisposition in which the vegetative system of the or- 
ganism has suffered, when the extremities are cold, for general 
weakness and in an inactivity of the lymphatic system; such 
treatment is indicated in gout, rheumatism, dropsy, diarrhoea, 
intestinal disturbances, imperfect functioning of the skin, in 
nervous disturbances, but is contraindicated in acute inflamma- 
tions, active lung affections, hemoptysis, congestions, etc. The 
French school at Lyons was the first to apply heliotherapy in the 
treatment of tuberculous arthritis, and Bonnet, 1845, in his 
treatise on the diseases of the articulations recommends insolation 
of the knee joint as a matter of choice. Lebert, 1849, “Practical 
treatise on scrofulous and tuberculous diseases,” advocates the 
use of heliotherapy in chronic joint disease. Turek, 1852, called 
attention to the efficacy of sun and light baths and gave specific 
directions for their use. ASSOCIATED THERAPEUTIC MEASURES 
257 
Bonnet’s idea was further advanced by Ollier and subsequently 
by Poncet applying heliotherapy in the treatment of tuberculous 
joint diseases and a pupil of the latter was induced to write a 
treatise on “Insolation in the treatment of articular tuberculosis,” 
reporting four cases which were very much improved by this 
method of treatment. Previous to 1911 Rollier knew nothing 
about the work done in heliotherapy by the pupils of the French 
school at Lyons and the work in heliotherapy was done and the 
results achieved by him independent and without any knowledge 
that such was ever attempted before. Rollier applied helio- 
therapy in the treatment of tuberculous disorders most exten- 
sively in every stage and in every form, but especially in bone, 
gland and joint disease for many years with most gratifying re- 
sults. To Rollier (assistant to Prof. Kocher), who (18) in 1903 
instituted the first establishment for the cure of surgical tuber- 
culosis by means of the sun’s rays at high altitude, (at Leysin in 
the Vandoises Alps, Switzerland, 4200 feet above sea level), 
much credit is due for bringing heliotherapy prominently before 
the medical profession as a most efficient measure in the treat- 
ment of tuberculosis, not only in surgical where it finds its great- 
est application but in all other various forms, if only diligently 
used. The demonstration in 1899 by Finsen of the effect of red 
rays upon variola and ultra violet rays upon lupus was an epoch 
making event in the application of the sun’s rays as therapeutic 
agent, and since that time much has been done in heliotherapy 
in giving a scientific explanation of the effect of the rays upon 
the organism. Much work along this line was done by Roux, 
Arloing, Winteritz, Panwitz, Schroetter and others and the work 
was all concentrated upon the penetrability of the solar or light 
rays into the human body and upon the possible effect this would 
have upon the pathogenic microorganisms. 
Heliotherapy in Tuberculosis 
In order to know what healing effect the application of the 
sun’s rays will have on the tuberculous process we must briefly 
consider, first, what particular rays possess a special inhibitive 
action on the tuberculous process, second, by what special 
method or technic can this object be accomplished, and third, 
what physiological manifestation does this curative process 
bring about. 
As to the varying intensity of these rays, we note that the 258 
CLINICAL TUBERCULOSIS 
difference in intensity of the ultra violet rays between a high 
and a low altitude is that it reaches its maximal in winter and 
becomes less as the warm season or summer approaches. 
Physical meaurements have proven that the ultra violet rays 
are the ones which in heliotherapy are the beneficial rays, and 
the question arises in which way and under what biologic con- 
ditions they become active and evidence their presence. It is 
known that pigmentation is brought about by these rays; we 
also know that pigmentation predisposes a healing tendency, and 
is an index to a prognosis; and it has also been proven that the 
appearance of pigmentation evidences the presence of ultra 
violet rays in white light. 
The Effect of Heliotherapy on the Human Body 
Following the use of the sun’s rays on the body, there is an 
increase in the number of erythrocytes, a decreased leucocytosis, 
an increase of the hemoglobin content, and with pigmentation 
the lymphocytes increase proportionately. This improvement is 
evidenced from the very beginning of the treatment. In closed 
tuberculosis the leucocyte count is below 10,000, but in open 
adenitis an increase is present, an increase of the polymorphonu- 
clears and a lessening of the lymphocytes. With healing a 
change in the curve is observed, the polynuclears decrease and 
the lymphocytic curve increases. This increase of the lymphocytes 
may be the result of active hyperemia due to the stimulating 
effect of the treatment. Insolation produces vasodilation of the 
blood vessels and through extensive hyperemia of the integu- 
ment a decongestion of the internal organs and increased textural 
changes in the derma are brought about, and an increase of body 
energy from the absorption of light in the presence of hemo- 
globin and increase of the ozydizing changes, favor an exchange 
of gases between the blood serum and the tissue cells. The 
peripheral blood by means of the activity of the short waved rays 
is altered, is energetized, giving up this energy to the inner tis- 
sues and the increased energy changes the oxy to methemo- 
globin. Light favors the free supply of oxygen to the needy 
tissue cells. It has also been shown that the ultra violet rays 
have a decided effect on respiration, by lessening the frequency 
of breathing for the time being, but increasing the fullness of the 
inspiratory phase. ASSOCIATED THERAPEUTIC MEASURES 
259 
The Effect of Insolation on Individual Organs and Tissues of the 
Body. 
Heart. The activity of heliotherapy upon the heart is mani- 
fested by a decongestion of the internal organs and a lessening 
of the blood pressure, most likely by the direct influence of the 
ultra-violet rays upon the nervous system. 
Blood Pressure. The lessening of the blood pressure is a re- 
sult of dilatation of the peripheral vessels by means of the direct 
influence of the rays upon the vaso-motor dilators. The rays are 
pain relieving and sedative in their action. 
Kidneys. The action of the rays upon kidney functioning is 
manifest by increased diuresis. 
Mind. The action of the ultra-violet rays upon the mind of 
the tuberculous is particularly noticeable and the mental effect 
is the hopeful spirit, the buoyancy, the increased activity and in- 
creased working capacity and above all an increased feeling of 
well being. 
Metabolism. Another effect of the ultra-violet rays is upon 
the ferment action accompanying metabolism, favoring dissocia- 
tion which increases the oxygen consumption with a conse- 
quential increase of nitrogenous waste. 
The Posological Consideration in Heliotherapy 
Here, as in all phthisotherapeutic measures, exact dosage is 
necessary. The indications for dosage vary very much, different 
clinicians recommending different amounts. Malgal does not 
exceed the time of heliotherapy to 20 minutes, whereas Rollier, 
on the other hand, extends its application to as much as eight 
hours. The beneficial influence of the sun’s rays on the body 
must be judged by the subjective sensations, pulse, temperature, 
blood pressure and pigmentation of the skin, the intensity of the 
latter being proportional to the favorableness of prognosis. The 
three important factors to observe and to consider are (1) the 
light of the sun as a whole, (2) the reaction of the various organs 
to heliotherapy and (3) the special reaction of the different dis- 
orders to the treatment. 
(A) As to light. The light of the sun is composed of heat, 
light and chemical rays, is subject to changes, as to locality, 
intensity, etc., depending upon whether the treatment is to be 
considered at the seashore, in the valleys or in a high altitude, 
hence a dosage in sun’s rays must be elaborated which is 
suitable to these various conditions. For instance, the treat- 260 
CLINICAL TUBERCULOSIS 
ment at the seashore must consider the variable climatic 
conditions. The direct insolation or exposure to the sun’s rays 
is lessened in intensity from the high to the low level and the 
direct opposite with diffuse day light. The direct rays traveling 
from above down do not lose in force proportionally as much as 
the indirect rays gain, and considering the reflection from the 
washed surfaces, the surrounding shores, the cloudy days and 
moist atmosphere, it becomes very evident that a constant dos- 
age must be desired and the technic understood. A cold sunbath 
below body temperature may act as a hypertonicum and may 
lead to very unfavorable results, while a warm sunbath above 
body temperature may result most favorably. 
(B) The reaction of the sun's rays on various organs. We find 
that the sun’s rays act locally in two ways, physiologically and 
therapeutically, namely, bacteriocidally, increasing phagocytosis, 
favoring fibrosis, producing scar tissue and relieving pain. A 
cutaneous erythema or what is known as dermatitis solare is to 
be especially guarded against, but pigmentation is desired. 
Favorable reactions, like a lessening of the amount of sputum or 
the return of a normal bowel movement after heliotherapy are 
the objects desired, and unfavorable reactions, like vomiting fol- 
lowing the application of the sun’s ray to the abdomen for the 
treatment of tuberculous peritonitis or enteritis show that the 
treatment is not suitable and may do much harm. A favorable 
reaction is evidenced by a feeling of well being with an increase 
of body weight; without these, the dosage is faulty. The observa- 
tion of the subjective sensibility is only of relative value, but the 
registration of the pulse, temperature and respiration is of un- 
usual importance. Generally after the bath there is a slow rise 
in all three, which after a while is again equalized. Continuing 
in the bath, both pulse and temperature remain usually below 
the initial bath, but the respirations remain as high as in the be- 
ginning, graduallv dropping to the level indicated before the 
bath. In the beginning of the treatment deviations from this 
rule may be present but they do not last. If they do not disappear 
the dosage is either not well selected or the individual possesses 
an intolerance to the sun treatment. Pulse frequency, respiration 
and temperature alone can not be considered; the question of the 
reaction immediately after the sun bath must be taken into 
account. 
The blood changes indicating a favorable influence in helio- ASSOCIATED THERAPEUTIC MEASURES 
261 
therapy are an increase in the number of erythrocytes and 
an accompanying increase of hemoglobin, a slight lessening of 
the white corpuscles with the presence of eosinophiles. An in- 
creased leucocytosis usually indicates either a retention of the 
tuberculosis toxins or a more rapidly progressing morbid process 
and if present is generally a sign of caution. The tuberculin 
test may be applied to give an indication as to the result of the 
treatment, the reaction being negative if the therapy is not well 
tolerated by the organism, becoming positive if conditions are 
more favorable. It must be borne in mind that heliotherapy 
when applied to pulmonary or peritoneal tuberculosis requires 
greater care and caution than when used in the treatment of 
lupus or certain tuberculids. 
(C) The special reaction of the different disorders to the treat- 
ment. The most favorable conditions for heliotherapy are bone, 
joint and skin tuberculosis, but with a careful technic good re- 
sults are also achieved in intestinal and urogenital tuberculosis 
in mediastinal gland and pulmonary disorder but they require 
greater caution and closer observation. In children, if the dis- 
ease of the tracheobronchial glands has extended beyond this 
region and has actively invaded pulmonary tissue, the use of the 
treatment by heliotherapy is contraindicated. It is also contra- 
indicated in hemorrhagic cases. 
Technic and Clinical Results 
(A) Exposure to the solar rays. In using the rays for healing 
or curative purposes it is necessary that we begin with a very 
light or but little exposure, gradually exposing the whole body 
as far as the head to the action of the rays. Beginning at the 
extremities, little by little, gradually extend the exposure to the 
abdomen and ultimately to the chest with a one to three minute 
exposure, and if no unfavorable indications arise, increase daily 
by three minutes; this is in internal disease. In external or local 
disorder the rise is more rapid to 5 minutes daily. The best 
results are attained by exposure to a temperature between 86 
and 104, and exposures above and below these points may be well 
tolerated by vigorous patients but must be applied a very limited 
time. The treatment must extend over long periods of time in 
some cases, as in gland tuberculosis, perhaps two or three 
months, while two or three years may be required in Pott’s dis- 
ease. The treatment must be continued until the symptoms have 262 
CLINICAL TUBERCULOSIS 
completely disappeared, otherwise a quick return of the disorder 
results. 
According to Kisch and Graetz, (212) bone and joint tubercu- 
losis with fistulae are most favorably influenced by heliotherapy, 
requiring on an average about one year’s treatment. Fistulae of 
the soft parts require about from 4 to 6 months. The cure of 
tuberculous fistulae under heliotherapy is not due to an encap- 
sulation of the mycotic or fungoid substance nor to a burying of 
the tuberculous disease but to a contraction of the tuberculous 
mass and the formation of new scar tissue. Hermann v. Schroet- 
ter, Vienna M. M. W. 1914 No. 21 says: “Insolation in combina- 
tion with fresh air treatment is the surest therapy in surgical 
tuberculosis and can never do any harm. Heliotherapy should 
find its greatest applicability and extensive use in childhood. By 
means of its early use to free the system from diseased influences, 
to bring about a healing of local disorder, insolation becomes a 
prophylactic measure for the future healthy growth and develop- 
ment of the child. The result in the main is dependent upon the 
unlimited duration of the treatment. The tendency towards 
tuberculosis and the limited capability to pigment formation 
stand in relation, possibly in combination, with changes in the 
internal secretions. The respiratory phase and character of 
breathing are stimulated by insolation. All are agreed that in- 
solation must be a very gradual process beginning by applying 
the rays to the lower extremities and gradually extending the 
treatment upwards, covering all of the body as far as the head. 
In all cases of arthritis, Pott’s disease, fixation and immobiliza- 
tion is essential and like all other means it is not a cure, it is only 
a most valuable aid in therapy.” 
(213) C. Arndt admits that Rollier’s excellent curative meas- 
ures can not always be attained, and that in the valleys the result 
of heliotherapy is not as favorable as it is at high altitude. Even 
in the treatment of tuberculosis at high altitudes the healing is 
slow, very slow, but nevertheless an attempt at heliotherapy 
should be made in the valleys and solariums and sun bath facili- 
ties should be established in connection with every tuberculosis 
sanatorium, and if the institution is not located in the mountains, 
results may be achieved by having recourse to the roentgen ray 
or the quartz lamp in lieu of heliotherapy in surgical tubercu- 
losis. In all cases that are favorable for the treatment and if it ASSOCIATED THERAPEUTIC MEASURES 
263 
can be extended over long periods much good may be accom- 
plished. 
R. Ridard, on the other hand (211), takes issue with the 
opinion of the enthusiast who maintains that all cases of local- 
ized bone, joint or gland tuberculosis are curable by means of 
heliotherapy and without surgical intervention. Without under- 
estimating the value of fresh air, baths and insolation in surgical 
tuberculosis, orthopedic treatment is most desirable, and no rule 
can therefore be laid down. The treatment by insolation must 
be adapted to the form of the disorder, the place or location, the 
time, the complications, the age and the social conditions of the 
patient, and it is now admitted that it is only a valuable adjunct 
in the treatment of surgical tuberculosis, exceeding by far medi- 
cinal therapy. The assumption that surgical tuberculosis is only 
a local affair and requires only local measures in its treatment is 
no longer tenable; on the contrary it is preeminently a general- 
ized disorder requiring in addition a dietetic, hygienic, and 
medicinal treatment, with rest and heliotherapy of the entire 
organism. 
In our country heliotherapy as a measure for inhibiting, arrest- 
ing or curing a tuberculous process has up to the present time 
not received the full attention it deserves. At the sanatoria situ- 
ated south west amongst the mountains the instituting of the 
solarium should be a regular program and this should be at- 
tempted even at the sanatoria situated in the low lands. At low 
altitude the sun treatment may not be quite equally as effective 
in a given time, but with prolongation of the time most efficient 
results may be achieved. That not sufficient interest is taken in 
heliotherapy in our country is quite evident when we note that 
amongst all the papers offered at the National Tuberculosis Asso- 
ciation at their annual meetings, beginning with the first meet- 
ing in 1905 and up to and including 1919, not a single one was 
ever presented on heliotherapy. It is equally of interest to note 
that at the meeting of the International Congress on Tubercu- 
losis held in Washington, D. C., in 1908, with the exception of a 
paper on heliotherapy read by Rollier of Leysin, not a single 
other paper on this important topic was offered. Of the value of 
this method of tuberculosis treatment there can be no doubt, and 
it behooves us as clinicians to take advantage of this form of 
medication and to recommend in our large country the establish- 
ing of solaria where many cases which are suitable for this CLINICAL TUBERCULOSIS 
264 
method of treatment can have their tuberculous processes ar- 
rested. 
In this country, the first systematic application of the sun’s 
rays with the open air treatment in surgical tuberculosis accord- 
ing to the method of Rollier was attempted in 1914 at the J. N. 
Adam Memorial Hospital (168), Perrysburg, N. Y., under the 
supervision of Dr. John H. Proyer. This treatment was found 
so successful there that since that time its use has been attempted 
at various sanatoria throughout the country. 
This Solarium in New York state is situated at a height of 
1650 feet above sea level, and the results of insolation at this 
Fig. 40. Schematic diagram of Insolation. Showing the progressive exposure of a 
patient to heliotherapy. (After A. Rollier.) (From reprint by Drs. Clarence L. Hyde and 
Horace La Grasso, Perrysburg, N. Y., 1917.) 
elevation are found to be nearly as efficient as that in higher 
altitudes. With but slight modification the technic used there is 
very similar to that applied at Leysin by Rollier. Usually 
the radiation is by direct exposure to the sun’s rays, that is dur- 
ing bright days; to continue the treatment, however, during the 
days when there is no sunshine, artificial ultra-violet rays are 
used by means of a mercury vapor lamp. As a general rule, no 
attempt at radiation is made until after the patient has been 
admitted at least three days, and no insolation is attempted dur- 
ing the hottest days in summer as it is found to be too depress- 
ing, too fatiguing during this period. The dosage of insolation 
must be a graduated and gradual one; it usually is given accord- 
ing to the following rules, beginning with a most limited bath 
the first day and adding each day a little more exposure. ASSOCIATED THERAPEUTIC MEASURES 
265 
First day : The patient is dressed in a fabric or flannel garment 
according to the season, and the head and eyes are protected, the 
former by a linen cap, the latter by means of colored glasses. 
The feet are exposed and bathed in the sun’s rays for five minutes 
three or four times at hour intervals. 
Second day: The feet are insolated ten minutes and the legs 
from ankles to knees five minutes three or four times at hour 
intervals. 
Third day: The feet are insolated for fifteen minutes, the legs 
from ankles to knees ten minutes, and the thighs five minutes 
three or four times at hour intervals. 
Fourth day: The insolation of the previously exposed parts 
is increased by five minutes and the abdomen is exposed five 
minutes three or four times at hour intervals. 
Fifth day: The insolation of the previously exposed parts is 
increased by five minutes and the chest is exposed five minutes 
three or four times at hour intervals. 
Sixth day: The patient is now turned on his abdomen if con- 
ditions are favorable, and the same course is prescribed as in the 
previous five days. 
It may be advisable to insolate the body both front and back 
the same day. Here then we may begin by bathing on the first 
day the anterior surface of the feet for five minutes and perhaps 
an hour afterward the posterior surface for five minutes, each 
twice a day at hour intervals. The second day expose both the 
anterior and posterior surfaces of the legs from the ankles to the 
knees for five minutes and the feet for ten minutes, and proceed 
similarly to exposing the body as given above. 
The insolation may be continued, as is outlined in the appended 
diagram, until the baths are given daily for three to six hours. 
The chart here given shows the insolation for ten days. If it is 
desired to continue the same plan for more days, say up to fifteen, 
then we continue as in the preceding plan, adding five minutes 
more to each part exposed, so that on the fifteenth day the feet 
would be exposed for seventy-five minutes, the ankles and knees 
to seventy, etc., and after this time begin the day with a complete 
body bath. 
Although heliotherapy is most serviceable in surgical tubercu- 
losis, tuberculosis of bone and joints, the beneficial influence of 
the sun bath, the ultra-violet rays, on all the other forms of tuber- 266 
CLINICAL TUBERCULOSIS 
culosis including pulmonary, if the process is not too active or 
rapid, must be admitted. 
(C) HYDROTHERAPY IN PULMONARY 
TUBERCULOSIS 
A healthy and vigorous individual with good physiologic power 
of heat production will find the cold morning bath a most whole- 
some and delightful measure (162). Such an individual on ris- 
ing in the morning will get into a tub of cold water, take what is 
known as a dip, or remain in it from one to five minutes, dry 
himself and with a coarse towel thoroughly rub the skin till it 
begins to glow; this is called the reaction. Upon being dried 
and dressed he experiences a fine feeling of skin warmth, a most 
pleasant sensation; the cheeks are pink, he looks and feels well, 
eats a hearty breakfast and begins his day’s work with vim. A 
sick and weakly person seeing this reaction in the healthy indi- 
vidual naturally becomes much impressed with the supposed 
value of the cold bath or spray. As a rule he does not seem to 
comprehend the difference in their physical make-up; in such an 
individual, try as he may, the cold bath is not followed by a 
vigorous skin reaction, but on the contrary, it has a most decided 
depressing effect, and whereas the vigorous person will look 
forward to his daily morning cold bath with a feeling of delight 
and enjoyment, the enfeebled and sickly soon begin to show dis- 
tinct signs of dislike for it, complains that the bath is followed by 
headache, shivers, after the bath, and the nose and lips look 
blue, complains of rheumatoid pains, shows a nervous fear with 
the approach of morning at the thought of the cold bath. An 
active pulmonary tuberculous individual is generally a weakly 
one, possesses no power of reaction and in place of being invig- 
orated by the bath becomes much depressed; hence the cold bath, 
plunge or shower should not be advised; on physiologic grounds 
alone the cold bath for the tuberculous is contraindicated. Being 
tucked up in a warm bed with sufficient blankets to maintain a 
uniform body heat, perhaps sleeping out-of-doors in the open, 
inhaling the cold air, all of this he greatly enjoys. Then, being 
in a warm bed, he is suddenly asked to leave his warm quarters 
to plunge or be plunged into a cold water bath. If there be much 
fever the cold bath may bring about a drop in the heat curve, but 
the depressing effect of the bath, the feeling of discomfort is very 
great. A daily sectional cool bath or sponge with the patient ASSOCIATED THERAPEUTIC MEASURES 
267 
remaining in bed, sponging first one limb, drying it and putting 
it under cover, then the other, next the abdomen, then the chest, 
the back, the arms and last the face, as usually done by a nurse 
or attendant, is a most desirable treatment, however, for the 
active tuberculous the daily warm or hot bath is the most 
effective hydrotherapy. Even for the tuberculous who is still 
strong the full or half bath in warm water is preferable to the 
cold, and the favorable influence of the cold bath on the fever 
curve can not be compared to that of the warm bath. We see 
that in the application of hydrotherapy individualization becomes 
a most important element. The variation of a few degrees of 
temperature in a bath may be sufficient to act as a stimulating 
tonic to the skin of a given individual whilst the same degree 
may become quite irritating to another. It is best always to give 
the bath in the morning at the time when the fever is absent or 
is at its lowest point. In febrile cases a warm bath given every 
third day will often tend to greatly reduce the temperature and 
in those suffering from night sweats a morning or evening bath 
or cold plunge followed by an alcohol rub will often inhibit 
these subjective symptoms. In the matter of giving baths, 
either cold or warm, the tuberculous patient’s comfort must 
always be considered and not the individual taste of the at- 
tendant or nurse or perhaps of the physician in charge in whom 
the cold bath may act as a vigorous stimulant; here as in the 
treatment of tuberculosis in general, good judgment must be 
used and common sense applied. The patient immediately after 
the bath should be put to bed and remain for some time so as to 
avoid what is known as shock. With increase of body energy 
the cold cloth application may be applied to the naked body from 
the shoulders down, the patient standing, the attendant rubbing 
the body vigorously through the wet sheet; this is then followed 
by a dry cloth application and very gentle rubbing, after which 
the patient is put back to bed to remain lying for about one 
hour. A warm foot bath on retiring often gives very prompt 
relief from headache, restlessness, insomnia, and sweaty and 
coldish feet. A short, slightly cold sitz bath with abdominal mas- 
sage during or before the bath often gives prompt relief for stub- 
born and chronic constipation. 
Hydriatic measures much in use at many tuberculosis sana- 
toria, particularly in Europe, are cold water dressings according 
to the directions of Winternitz. Clean, absorbent roller bandages 268 
CLINICAL TUBERCULOSIS 
of suitable width are wrung out of cold water and applied to 
the chest in the figure of 8 form. Beginning posteriorly at the 
right axilla the bandage is passed over the left shoulder back 
under the arm, to the opposite shoulder under the arm back to 
the starting point, a second layer is applied in a similar manner, 
then continue the bandage over the anterior and posterior chest 
down to the 8th rib in the axillary line. A dry roller bandage 
is now evenly covered over this, and all may then be covered by 
a tight fitting vest. 
Nervous individuals and those with a very sensitive skin 
usually complain much if cold water dressings are applied accord- 
ing to this method; here vigorous rubbing of the skin previous 
to the cold dressing will often obviate the discomfort. This form 
of bandaging is best applied just before retiring. It may, how- 
ever, also be applied during the day, in febrile cases once in three 
hours and in the afebrile once in six hours. It is advisable always 
to give the skin a thorough rub down before applying the dress- 
ing. The chief value of this cold bandage depends upon its 
beneficial influence on the respiratory organs. The cold applica- 
tion at once produces a general feeling of warmth and by means 
of the tight bandage the lungs are put to rest; the general feel- 
ing of comfort acting soporifically induces invigorating sleep, 
the cough generally subsides, chest and pleural pain abate, 
breathing becomes more free, expectoration easy, sputum less 
tenacious, more fluid, and general improvement of conditions are 
noticeable. Tuberculous individuals who are very anemic or 
undernourished and complain of a cold feeling after this method 
of hydrotherapy or perhaps manifest rheumatoid or arthritic 
pains are better treated by substituting warm water for the cold; 
in fact, in many sanatoria the use of the hot water figure 8 band-1 
age is altogether applied in lieu of the cold. Many patients can- 
not tolerate a cold dressing at all; besides, the hot bandage also 
has definite fever reducing tendencies and in patients in whom 
the cold pack is contraindicated the hot pack may be of decided 
value. Hydrotherapy is also contraindicated during the men- 
strual period. In general, however, it may be said that in the 
treatment of pulmonary tuberculosis, in patients showing much 
restlessness, nervousness, or much fever, the use of the figure 8 
bandage either cold or warm can not be too highly recommended. 
“For safety and comfort, then, for freedom from disagreeable 
symptoms that may or may not be harmful, for certain positive ASSOCIATED THERAPEUTIC MEASURES 
269 
benefits that cold baths usually fail to give, the hot morning bath 
is to be commended with great confidence as a daily resource 
and a daily joy. The cold bath is useful chiefly for those who 
least need the invigorating effects of any bath, that is, the well 
and husky people. The hot bath is most valuable for that great 
mass of our population (especially the tuberculous) who are be- 
low their physiologic par and who need every influence that can 
increase their strength and resisting power. Many of these half 
invalids and invalids by means of the cold bath are now with 
true heroism daily subjecting themselves to shivering discom- 
forts often lasting for hours and with no benefit—or worse than 
none—solely because of a false notion derived from the partial 
experiences of the strong. It is a shameful waste of courage and 
power in a good cause. The worst griefs in life are those that 
are preventable, and the cold bath martyrdom is uncalled for.” 
(Norman Bridge.) 
(D) PULMONARY GYMNASTICS 
(Pulmonary Massage) 
Their Use and Abuse. Their indications and contraindications 
(173). 
Throughout the whole field of conservative tuberculosis 
therapy individualization becomes the necessary watchword. No 
two cases can be treated exactly alike; this applies most par- 
ticularly in the recommended breathing exercises for tubercu- 
losis disease which are known by the simple term—pulmonary 
gymnastics. The indiscriminate use of these exercises is often 
followed by the most distressing consequences whilst with proper 
application in carefully selected cases adequately supervised, 
the method becomes a most valuable therapeutic measure; hence 
pulmonary gymnastics or carefully supervised breathing exer- 
cises may be very suitable measures if we are only particular in 
selecting proper cases. For these exercises cases may be con- 
sidered suitable in which the process becomes arrested, in which 
there are no active symptoms, beginning cases with little or no 
activity and a fairly good general condition. Schultzen considers 
the so-called curable cases, with little or no advanced involve- 
ment, no acute symptoms or complications, as the favorable cases, 
briefly, those cases with increased temperature, rapid pulse, acute 
pulmonary processes are not suitable for pulmonary gymnastics. 270 
CLINICAL TUBERCULOSIS 
In such cases it is better to keep the range of respiratory motion 
as small as possible so that there will be no disturbance of the 
inflamed pulmonary tissue. Two problems must be most care- 
fully considered in recommending these pulmonary exercises; (1) 
does deep breathing favor or hasten the process of arrest by its 
beneficial influence on the local and general condition and; (2) is 
deep breathing, if it produces no observable and favorable influ- 
ence on the patient, likely to produce harm? We are not all 
agreed as to its salutary tendency, for instance, Cornet, Lieber- 
meister and others express their opposition to the application 
of these exercises in pulmonary tuberculosis, as a result of per- 
sonal experience and upon theoretical grounds. According to 
these clinicians, there is great danger from aspiration pneu- 
monia, from interference with the formation of a zone of de- 
markation, a tendency towards hemorrhage, development of 
emphysema, a tearing apart of the delicate cicatritial tissue and 
conservative pleural adhesions, conditions, which are favorable 
to the growth of the tubercle bacillus and increase absorption of 
toxins, aspiration of bacillary sputum into the still healthy por- 
tions of the lungs, etc. This opposition is met by such clinical 
observers as Dettweiler, Turban, Fraenkel, Schultzen and many 
others, all of whom have had extensive personal experience; they 
all favor and employ under carefully guarded conditions pul- 
monary gymnastics. Dettweiler after giving explicit instruc- 
tions as to how deep breathing should be applied concludes by 
saying, “The habit will become a necessity and through its meas- 
ure the tendency to a troublesome and distressing cough will be 
blunted,” and Turban declares that “deep breathing continuously 
and methodically employed is most advantageous, especially with 
the habitually weak breather.” He further states that an extreme 
expansion of a tuberculous lung may result most seriously but 
that systematic deep breathing increases the ventilation and cir- 
culation of the lungs. 
Cornet and his school base their opposition to active lung 
excursion in manifest pulmonary tuberculosis upon the fact that 
in almost every other form of tuberculosis it becomes essential 
that the parts are put to rest to favor repair, and if this is true 
why should not this principle apply to pulmonary tuberculosis as 
well? So it does. We all, without exception, advocate that in 
active or progressive pulmonary tuberculous disease the more 
absolute this rest can be maintained, the greater the amount of ASSOCIATED THERAPEUTIC MEASURES 
271 
rest which can be put upon the pulmonary tissue the better the 
prognosis, the quicker the recovery; it is the same principle 
which we apply in all other forms of tuberculosis. After the 
process is healed, for instance, after the tuberculous disease in a 
joint no longer exists do we not all recommend and encourage 
that passive motion or massage be applied to the joint? Then why 
should we not advise passive motion, pulmonary massage (and 
that is all pulmonary gymnastics is) when the tuberculous pro- 
cess in the lungs has become arrested or perhaps healed? After 
a lung has been compressed for some time, either artifically or 
naturally, and the pulmonary lesion is supposed to have been 
healed, do we not recommend pulmonary gymnastics on similar 
grounds ? Schultzen, among others who have had extensive experi- 
ence in the therapy of pulmonary gymnastics, gives the following 
contra-indications to their use: (1) in the presence of fever; 
(2) great bodily weakness; (3) in acute inflammatory processes 
of the lungs; (4) in progressive softening and disintegration of 
pulmonary tissue; (5) in increasing extension of the tuberculous 
process usually accompanied by copious expectorations; (6) in 
the presence of old or perhaps newly formed large cavities; (7) 
in recent pleurisies or pleural effusions; (8) in recent hemor- 
rhages; (9) in pathological conditions of the blood; (10) in ad- 
vanced or ulcerative tuberculous laryngitis; (11) in accompany- 
ing intercurrent disease; (12) possible unexpected occurrences 
such as may be produced or excited by pulmonary gymnastics. 
HOW TO PRACTICE PULMONARY GYMNASTICS 
Breathing here should be done, as is now so generally taught 
in our schools, by inbreathing through the nose with the mouth 
closed and outbreathing through the mouth. Take a full, deep 
breath very slowly through the nose, the mouth being closed, 
the breath then being held for a few seconds after which the air 
is to be exhaled very slowly and fully through the mouth. The 
act of inspiration can be strengthened by gradually raising both 
arms to a horizontal position during inbreathing, letting them 
fall again in outbreathing. The expiratory phase can also be 
fortified by uttering a few short words at the end of expiration 
like one, two, three, etc. Usually in the beginning I direct that 
the patient take half a dozen exercises twice a day, the first thing 
in the morning on rising and just before retiring. In this way the 
individual generally becomes accustomed to these exercises so 272 
CLINICAL TUBERCULOSIS 
that gradually he increases the number of deep breathings to one 
exercise every three hours. A patient with an arrested tubercu- 
lous process should take at least six such breathing exercises each 
day, this to be maintained almost indefinitely. It becomes imper- 
ative to caution patients taking pulmonary gymnastics that the 
exercises must not be vigorous, hurried or forceful but that they 
must be fairly full but slow, very easy and quiet and that on 
full inspiration the breath must be held for a few seconds. These 
exercises may be supplemented by those which I have found most 
helpful in arrested cases, the patient taking a full breath and while 
outbreathing carrying the breath slowly along a certain key until 
all the air is expelled. Begin the exercises at first with a very low 
key, the next exercise a little higher note and so on until che voice 
is carried along on the highest possible note. These deep but 
steady breathing exercises should be taken while the patient is 
in the upright or standing position; however, for those who are 
not quite up to full standard, pulmonary gymnastics in the re- 
cumbent position may be advised and as the patient improves in 
general health, deep breathing and other exercises may be judi- 
ciously recommended such as singing, loud reading, loud speak- 
ing, etc., and in addition to these exercises of full, slow and deep 
breathing with a proportional resting pause, the cycles of breath- 
ing per minute become necessarily lessened in number, perhaps 
in some instances to nearly one-half giving the tuberculously 
diseased lung in that proportion a longer period of rest. 
“In advising pulmonary gymnastics it cannot be too strongly 
emphasized that in active tuberculous disease this procedure is 
proven to do much harm. During the active stage of the disease 
it is better to produce chest immobilization and not chest excur- 
sion, hence this method is advisable only if the tuberculous 
process is arrested or probably healed and we desire more pul- 
monary aeration and better blood and lymph flow. From clinical 
observations by most competent clinicians we can conclude that 
pulmonary gymnastics carefully applied and supervised both 
from experience and theory are shown to be useful in aiding, 
hastening and maintaining the arrest, and that there is no con- 
clusive evidence that any harm results from them. Furthermore 
the patients themselves express a sense of well-being from such 
breathing exercises, and besides, the mental effect can not be 
too highly appreciated.” (Dr. E. O. Otis, Boston 1906). CHAPTER 22 
PHYSIOTHERAPY, VOCATIONAL AND 
OCCUPATIONAL 
Rehabilitation—Reconstruction 
Historical Data. Hippocrates according to Lunton,(90) (145) 
wrote upon Airs, Waters, and Places; in the latter part of the 
18th Century hydrotherapy was fashionable. The history of work 
therapy is more obscure. Eva Charlotte Reed states that Galen 
says “employment is ‘Nature’s Physician.’ ” Occupational ther- 
apy was advocated in Pinel’s writings in 1791. He states that 
“Moderate employment and regular exercise cooperating with 
the energies of nature herself, restored him in a short time to the 
full enjoyment of his intellectual faculties.” The translator of 
Pinel’s Traite, Davis, makes reference to much earlier thera- 
peutic uses of occupation and diversion as follows: “At both 
extremities of ancient Egypt, a country that was at that time 
exceedingly populous and flourishing, were temples dedicated to 
Saturn, whither melancholies resorted in great numbers in quest 
of relief.” 
Whatever gifts of nature or productions of art were calculated 
to impress the imagination were there united to the solemnities 
of a splendid and imposing superstition. The most voluptuous 
productions of the painter and the statuary were exposed to pub- 
lic view. Groves and gardens surrounded those holy retreats 
and invited the distracted devotee to refreshing and salubrious 
exercise. Gaily decorated boats sometimes transported him to 
breathe amidst rural concerts the purer breezes of the Nile. In 
short, all his time was taken up by some pleasurable occupation 
rather than by a system of diversified amusements enhanced and 
sanctioned by superstition. 
Dunton (130) tells us that in 1798 Benjamin Rush, in a letter 
to the managers of the Pennsylvania Hospital, advocated work 
as a remedial measure. In 1822 Wyman, Superintendent of Mc- 
Lean Hospital, in his annual report, says that, “The amusements 
provided for patients, as draughts, chess, backgammon, nine pins, 
273 274 
CLINICAL TUBERCULOSIS 
swinging, sawing wood, gardening, reading, writing, music, etc., 
have a powerful effect in tranquilizing the mind.” 
In 1884 Kirkbride stated in an article on the management of 
hospitals for the insane, “Labor is one of our best remedies. It is 
useful in improving the health of the insane as in maintaining 
that of the sane.” During the past ten years an unusual interest 
in the subject of work therapy has developed, in large measure 
due to the publication of the book by Miss Susan E. Tracy in 
1910, entitled “Invalid Occupations.” Following the publication 
of this book it has since been recognized that occupation is one 
of the best of the means we have for aiding the sick. 
In the treatment of pulmonary tuberculosis, Physiotherapy, 
vocational and occupational, plays a most important role. The 
physical reconstruction of those incapacitated by pulmonary 
tuberculosis necessitates a long period of continued treatment 
consistent with the nature of the disability. This treatment may 
consist in light mental and manual labor, physiotherapy, thermo- 
electro, hydro and mechanic therapy, massage, calisthenics, gym- 
nastics, heliotherapy and psychotherapy and amusements in 
and out-of-doors, etc. 
Herman Brehmer of Gobersdorf, Germany, first systematically 
formulated the general therapy for the treatment of pulmonary 
tuberculosis. He began to do this about sixty years ago, and his 
methods still exist. He prescribed methodical walking and hill 
climbing exercises in order to strengthen the heart, the smallness 
and relative insufficiency of which were in his opinion the chief 
causes of pulmonary tuberculosis. These exercises were carried 
out during the day for hours at a time as much as possible in all 
kinds of weather. They consisted in going slowly up hill or 
gently ascending paths, in the frequent insertion of cautious, 
methodical deep breathing and in the avoiding of everything that 
would tend to tire the patient and of every excitement of the 
heart. 
Brehmer’s Sanatorium was built on the lowest spot of a moun- 
tain valley, so that all paths that led to it could be so made that 
there was a gentle down grade. 
Brehmer was a great disciplinarian and stated that only one 
patient among thirteen thousand suffered from over-exertion. 
This patient disobeyed the rules and over-exerted himself, a 
severe hemorrhage resulted, from which he died. Brehmer did PHYSIOTHERAPY, VOCATIONAL AND OCCUPATIONAL 
275 
not allow patients to do any work with arms and he did not allow 
them to walk when their temperature was elevated. 
Rest treatment is to be ascribed in large degree to Dettweiler. 
His views, however, were not always fully and correctly inter- 
preted. He was first a patient and later an assistant to Brehmer. 
At first he employed Brehmer’s methods entirely, and in 1873 
wrote as follows: “On discussing a broader, very important part 
of the rational therapy, I mean hill climbing, I must again refer 
to the circulatory and respiratory, respectively aspiratory anom- 
alies which are to he regarded the necessary presuppositions of 
subsequent phthisis. From this point of view it was a simple 
logical sequence to abandon the relaxing regimen of the older 
therapy, the fear of stimulating the blood vesseljs, etc., as harm- 
ful, and to make use of muscular work to increase the respiratory 
and circulatory energy.” 
In Dettweiler’s hands, however, some serious results occurred 
among his patients, and he modified his technic and intro- 
duced the reclining treatment. He emphasized most warmly 
permanent rest treatment in the open air, and warned against too 
much exercise of the heart and of the lungs. Because of these 
examples of harmful heart tiring through hill climbing, Dett- 
weiler’s rest treatment was carried out in reclining chairs. He 
built resting halls, open on one side, and placed in them com- 
fortable, adjustable chairs, where most of the patients without 
fever spent from seven to eleven hours daily. He also employed 
absolute rest to combat the fever of phthisis. 
Edward L. Trudeau of Saranac Lake, New York, may be men- 
tioned as the third great figure in the modern treatment of pul- 
monary tuberculosis. About the year 1882 he learned of the work 
of Brehmer and Dettweiler from articles that appeared in “The 
Practitioner,” an English Medical Journal. At first he tried to 
use Brehmer’s methods on his own person. He found, however, 
that vigorous exercise produced fever and caused a lighting up 
of his disease, while on the other hand, if he exercised mildly his 
disease remained quiescent. He soon became convinced that 
rest in the open air was a more important factor in the cure of 
pulmonary tuberculosis than exercise, and that exercise was to 
be employed not in all but only in certain cases. 
Inspired by the work of Brehmer and Dettweiler, Trudeau 
founded the Adirondack Cottage Sanatorium, in February, 1885. 
It was founded for the purpose of helping the sick, poor and per- 276 
CLINICAL TUBERCULOSIS 
sons with small means to regain their health. His sanatorium 
has always stood for a rational use of rest and exercise; he never 
allowed the patients any manual labor. Trudeau’s views on the 
subject of rest are fully described in his letter to Joseph H. 
Pratt, written in 1911. 
Lebert and Rhoden are for abundant bodily exercise at every 
season of the year, but warn against fatigue. In the last decade 
of the last century the re,st cure was employed in a most thor- 
ough manner in the People’s Sanatoria in Germany, so that it 
became known abroad as the German method. Only a few 
Phthisotherapeutists held strictly to the old regimen of Breh- 
mer: For example, Walther of Nordrach, and Chas. Page, who 
were strongly in favor of abundant bodily exercise; Liehe and 
H. Weber, who are not at all antagonists of the reclining method 
of treatment, consider an abundant amount of exercise indica- 
tive for a large number of patients. They are decidedly in- 
fluenced by Brehmer’s school. Liehe is opposed to Penzoldt, 
who believed that the sparing of the conserving methods is in- 
sufficient in sanatoria and who pleads for the most energetic con- 
serving of the strength of the patient on account of the short 
period of time of the institutional treatment and speaking warmly 
in favor of systematic exercise therapy. In the epoch in which 
the conserving or saving therapy was practiced in an exaggerated 
manner, there were always clinicians and phthisotherapeutists 
of repute who favored systematic exercise treatment on the 
ground of strict indications. Such clinicians were Cornet, Meis- 
sen, Frankel, Turban, Penzoldt, Trudeau, Vincent Bowditch, and 
E. R. Baldwin and others. 
Rational Physiotherapy 
Today it has become a principle of rational treatment to carry 
out sensible, methodical exercise treatment. We can also deter- 
mine the indications and forms of employment so that exaggera- 
tions toward the one or the other side can be avoided, taking for 
granted, of course, that the physician is able to judge of the lung 
condition. Physicians at times differ as to the amount of exer- 
cise considered proper for patients in tuberculosis sanatoria. 
The more radical have advocated laborious work, such as build- 
ing, masonry and ditch digging, while at the other extreme are 
those who are strong advocates of the rest treatment, with the 
addition of calisthenics and walking exercises. PHYSIOTHERAPY, VOCATIONAL AND OCCUPATIONAL 
277 
Recognizing physical exercise as a therapeutic measure 
patients at certain sanatoria are expected to perform a sufficient 
amount of work to insure physiological reaction on the part of 
the various tissues (skin, glands, muscles, etc.), which if left 
dormant for a considerable time would, through their failure to 
functionate, retard the patient’s recovery. 
Work assignment in a sanatorium should be a therapeutic 
measure and secondary to the medical care of the patients. Work 
assignment is an expedient used to divert the thoughts of the 
patient from his physical condition to other things. It may be 
expressed in the terms already mentioned, vocational therapy, 
graduate exercise, rehabilitation, occupational therapy, recon- 
struction, vocational education, vocational training, etc. 
a. Rehabilitation of the Handicapped. The Tuberculous Soldier 
While there is a direct relationship between occupational ther- 
apy and the war, many similar problems are also met with in civil 
life. We have industrial cripples from other causes, and these 
should be aided in becoming at least partially self-supporting, 
and should be taught some occupation which will help them to 
pass their leisure time pleasantly if not profitably. It is of in- 
terest to note that the great war has done much to emphasize the 
value of occupational therapy. 
In the first place the crippled have been taught methods by 
which their handicaps may be overcome or discounted, and 
secondly, occupational therapy has proved extremely valuable in 
the treatment of those functional disorders to which the name 
shell shock has been given. 
It became evident soon after the war began that the number 
of crippled returning to civil life would be so large, that the old 
plan of pensioning them would be impossible to carry out, espe- 
cially as the number of able bodied would be too few to support 
the tremendous financial load of taxation which would be neces- 
sary. The problem being an economic one attracted more im- 
mediate attention abroad than if it had been merely medical, and 
for this reason M. Herriott of Lyons, France, established two 
schools where the crippled were taught new trades or could learn 
to adapt themselves to former ones. The physical reconstruction 
of soldiers in this country, disabled by pulmonary tuberculosis 
during the great war, was a new problem. Occupational therapy 
and vocational training were recognized by the Federal Board 278 
CLINICAL TUBERCULOSIS 
(138) for Vocational Education as most valuable as an auxiliary 
means of treatment in tuberculosis. As applied to the treatment 
of soldiers in this country, it has proven an emphatic success, and 
especially so in a disciplinary and moral direction. Instruction 
has been provided in general subjects, commercial branches and 
light arts and crafts work, and, where possible, gardening and 
greenhouse work as well. It is designed that all training shall 
have a definite vocational bearing so that upon discharge, if the 
patient does not wish or is unable to undertake his former work, 
the experience which he has gained during his stay in the sana- 
torium may help him directly in earning his living. 
It mu(st be understood that there are many problems covering 
this subject yet to be solved, and it is hoped they may attract the 
attention of the research worker. There are many difficulties to 
be encountered concerning the emotional reaction of the patient. 
Men of the same mental caliber and from the same social level 
will differ in their adaptability to a given occupation one form 
of work appealing to one man and not to another. 
We have acquired increasing knowledge as to the value of 
work as a remedy and occupational therapy applied along the 
lines of reconstruction will give added value to this important 
subject. C. L. W. 
b. Reconstruction of the Tuberculous in Civil Life 
The most essential treatment of the tuberculous individual 
during and after sanatorium care is by regulated1 “rest and exer- 
cise.” (70) The principles of sanatorium treatment are so 
definitely standardized today as are those of surgery, but they 
are not nearly as familiar to the profession as is surgery. In 
every case of pulmonary tuberculosis, we must individualize in 
the application of these two most essential principles of rest 
and exercise. While one patient should not be permitted to 
raise his hand, where absolute rest is required, another may do a 
heavy day’s labor; between these extremes every case of tuber- 
!The tuberculous individual suffering from active disease is first put to rest in order 
to lessen the amount of tissue change, slow the pulse and reduce the temperature. This 
lessens the amount of autointoxication, autotherapy and autotuberculin absorption. If 
the process has been arrested and the patient’s condition has improved he may be allowed 
a little exercise just sufficient to keep his autotherapy within normal limits; if, however, he 
exceeds this and the exercise in whatever form it may be, is excessive then the autoabsorp- 
tion of tuberculin becomes too great, his therapy too high and the conditions are again 
bad. The active tuberculous individual at all times has sufficient tuberculin within his 
organism for normal medication and use, hence it must be our aim to keep his therapy 
within these limits so that the prescribed exercise pours just sufficent autotuberculin into 
the economy to act as a stimulant to the production of antigens and antibodies and the 
amount of labor demanded must be accurately graded for each individual case as best will 
bring about a rational autotherapy.—J. R. PHYSIOTHERAPY, VOCATIONAL AND OCCUPATIONAL 
279 
culosis can be placed. It becomes necessary to know how and 
when to direct, as fixed rules can not be applied. A good rule is 
not to put the arrested tuberculous at once to physically hard 
labor, but with returning good health heavier work may grad- 
ually be added, and it should be remembered that it matters very 
little whether this labor is performed in or out-of-doors so long 
as the vocation is healthful and not too strenuous. It is a very 
serious mistake to impress upon the tuberculous’ mind that on 
his return from the sanatorium where the disease has become ar- 
rested, he must follow a vocation different from the one he 
previously pursued. As the doctor must be guarded, must weigh 
carefully, in recommending a suitable sanatorium, in advising a 
change of climate, a sojourn in the mountains or at the sea-shore, 
so must he be equally guarded in recommending a certain voca- 
tion to follow for a livelihood. A returned tuberculous individual 
whose pulmonary process has become arrested will do best to 
follow the usual trade or calling which he followed for a liveli- 
hood before he entered the sanatorium, perhaps in a modified 
form, something light, but related to his previous training. For 
example, a machinist may learn to become a draftsman; a car- 
penter, an architect; a bookkeeper, a secretary; a doctor, a 
laboratory diagnostician, etc. Put the healed or arrested tuber- 
culous to work at a vocation or trade as near as possible to the 
one with which he is familiar. The learning of a new trade en- 
tails a hardship and is more of a handicap than an asset, and 
above all the patient will look with longing eyes to the work 
with which he is acquainted. After years of training along cer- 
tain lines, it is quite hard to take up new duties, especially so, if 
the family is dependent upon such an undertaking. Strictly 
regulate the hours of rest after work, regulate the hours of work, 
the individual’s living, sleeping, resting and eating conditions, 
and much can be accomplished. Entering into a new field is 
most difficult. It is better to become more efficient in the old 
and familiar one. 
Do not recommend that the tuberculous patient become a 
farmer, to raise cattle, sheep, horses, or poultry, to take up 
gardening or forestry, to become a traveling salesman, or become 
a timekeeper and to stay in the open in all kinds of weather. To 
follow any of these with success, to make a living, or perhaps 
take care of a family, requires work, and often times the hardest 
kind. It is hard because he is not sufficiently familiar with that 280 
CLINICAL TUBERCULOSIS 
kind of work, and as he had pictured these vocations as easy to 
learn, he becomes disheartened when he finds himself deceived. 
Reconstruction therapy then, for the arrested tuberculous in 
civil life should be supplied as near as possible to the individual’s 
interests, his likes, desires and aptitude and should be especially 
related to his former field of usefulness. Most tuberculous in- 
dividuals returning from the sanatorium with their pulmonary 
disorder arrested have families or dependents, and they are very 
anxious to again become efficient working units in the com- 
munity. The learning of a new trade, to master it so as to meet 
all competition, usually requires years of training, and can not 
be acquired in a short time; hence the suggestion that the healed 
tuberculous remain in the calling related to the one with which 
he is fully acquainted or follow the old vocation modified for 
easier labor, is the only good, rational and logical one. This is 
efficient reconstruction therapy. J. R. 
“Graduated Labor”—“Rest and Exercise” 
Paterson’s Method for Applying “Exercise and Rest” Treat- 
ment.(171) Paterson’s work was carried out systematically in 
the Brompton Hospital Sanatorium at Frimley, England, where 
patients were directly in his charge over a number of years, and 
it was largely through his work that “graduated labor” as an im- 
portant method of treatment gained more or less popularity in 
England and America. All patients were carefully selected and 
only fever-free patients and those free from other constitutional 
symptoms, and who had begun to show some signs of improve- 
ment were chosen. Several thousand selected cases were treated 
by this “graduated labor” method, and many of these patients 
had been able to perform five hours of hard labor each day with- 
out any apparent ill effect before leaving the sanatorium. It is 
shown that after returning to work, at the end of the first year 
but 62% were well and working, and this was lowered to 50% 
at the end of the second year. 
According to Paterson, the treatment by rest and exercise is a 
logical deduction from the theory of auto-inoculation,2 and auto- 
inoculation is descriptive of a process which consists in the in- 
2Auto-inoculation in every respect simulates tuberculin therapy. With little exercise, 
little tuberculin stimulation go hand in hand for the better, whereas with much exercise 
like much tuberculin, much damage, and even dangerous conditions may arise. Auto- 
inoculation is auto-tuberculinization. The judicious use is highly beneficial whilst the 
injudicious use is extremely dangerous.—J. R. PHYSIOTHERAPY, VOCATIONAL AND OCCUPATIONAL 
281 
troduction of bacterial products into the blood. As Wright 
states: “All active and passive movements which affect the focus 
of infection, and all vascular changes which activate the lymph 
stream in such a focus induce auto-inoculation by means of 
which the blood begins to provide for itself a protective mech- 
anism.” The process is one of immunization, and as a conse- 
quence, whenever bacterial products escape from the localized 
foci, intoxication phenomena and immunizing responses must 
necessarily supervene. 
Where the auto-inoculations continue and the immunization 
process is weak, death is inevitably the end. Where the defense 
is progressively equal to the attack, the assaults of the bacterial 
products are gradually worn down until the rising levels of re- 
sistance produce in the end complete immunity. 
Paterson calls attention to the fact that treatment by means 
of exercise is not of general application; it can only be used in 
the case of a patient who fulfills two rather onerous conditions. 
First he must be afebrile and free from all constitutional symp- 
toms ; and secondly he must have attained the position of an or- 
dinary person in the house by being able to remain up all day 
fully dressed, and to walk up and down stairs. 
The following classification of patients is made: 
1. Those who have been infected and have recovered without 
knowing of their infection. 
2. Those whose recovery is certain after rest and a holiday. 
3. Those who require additional help to that conferred by 
general hygiene. 
4. Those for whom no treatment will do any good. 
Therefore, there are only Classes 2 and 3 where treatment 
by the type under consideration is possible. These, again, are 
divided into febrile patients and patients free from fever. 
Paterson states that the control of excessive auto-inoculation 
by absolute rest is complimentary to its artificial inducement by 
exercise and must be instantly adopted upon the slightest return 
of fever. 
Fever means a temperature exceeding 99° F. in men and 99.6° 
F. in women, accompanied by constitutional symptoms, such as 
malaise, headache, and similar signs of hyper-intoxication. A 
temperature of 100° F. in a case where there are extreme signs 
in the lungs can be ignored, provided that there is absence of all 
constitutional disturbance. 282 
CLINICAL TUBERCULOSIS 
The immobilization of patients must be absolutely effective, 
and in addition to bed rest, patients are not allowed to move or 
to read; talking is forbidden, and steps are taken to repress any 
needless coughing, if necessary, by wearing a Burney Yeho’s in- 
haler. The use of the stethoscope is debarred, since it entails the 
taking of deep breaths. Visitors should be kept at a distance, 
and even the patient’s letters should be withheld if there is any 
probability of the intrusion of home worries. Six to ten days of 
such regime are in most cases sufficient to bring the patient’s 
temperature to normal. If the temperature remains normal, the 
patient is allowed to sit up in bed for half an hour, and the period 
is gradually extended until the patient is able to dress and remain 
up throughout the day. 
Should prolonged trial of immobilization fail to reduce the 
fever, more complete immobilization may be considered by the 
introduction of nitrogen gas or filtered air into the pleural cavity 
to neutralize the intrapleural negative pressure. 
Graduated exercise and systematic labor mark the second con- 
trol. Patients who have been immobilized, owing to the pres- 
ence of fever and constitutional symptoms, begin by walking 440 
yards a day. The temperature and constitutional symptoms form 
the guide throughout, and should there be no marked deviation, 
this exercise is continued for a week, and is then increased to 880 
yards per day. The third week two miles is prescribed, which is 
increased to four in the last week of the month, and the final 
walking stage is over six miles, and is attained automatically. 
Cavities involving four lobes with good muscular condition 
form no reason for the proscription of the quarter mile grade. 
Such a patient can be started on the four or six-mile grade, 
whereas the patient having little or no physical signs, but with 
poor physique, must be watched carefully. With the revival of 
no unfavorable symptoms, the grades of labor are entered upon 
successively. 
Grade I consists in carrying for a distance of 50 yards up a 
gradient of 1 inch, 1 to 7 baskets containing materials and aver- 
aging about 10 pounds in weight. The number of times daily 
should be adjusted to the distance of seven miles. 
Grade II is a slight extension of Grade I, 18 pounds of ma- 
terial are carried a longer distance in a larger basket; while the 
third grade allows of more arduous work, such as chopping fire 
wood, cutting grass, hoeing, etc. The fourth grade is shovel PHYSIOTHERAPY, VOCATIONAL AND OCCUPATIONAL 
283 
work, or its equivalent: mowing grass, sawing trees, etc. Two 
tons of earth lifted into a cart is the daily task in the beginning, 
gradually increasing to above twice that amount. In Grade V six 
tons a day is the prescribed amount, a larger shovel being used, 
while patients in the last grade are required to do five and a 
half hours of the heaviest type of work. 
The average time for the various grades is as follows: Grade 
I, one week; Grade II, one or two weeks; Grade III, one or two 
weeks; Grade IV, two weeks; Grade V, three weeks, and the 
patient is then permitted three weeks from his discharge, to work 
on the heaviest grade. 
Paterson calls attention to the fact that an important aspect 
of a system of sanatorium treatment is the demoralization of the 
sick, produced by the mental and physical lassitude of long 
periods of inactivity. Graduated labor from this point of view 
has a psychological and moral value impossible to over- 
emphasize. C. L. W. CHAPTER 23 
TUBERCULOSIS IN CHILDREN 
Tuberculosis of the Tracheo-Bronchial Lymph Nodes.(15) 
Here especially we must recognize the difference between 
being tuberculously infected and tuberculously diseased. The 
tracheo-bronchial lymph nodes being regional glands are usually 
secondarily infected after the primary infection, but tuberculous 
disease of these glands is primary tuberculosis.(183) 
In children tuberculosis is primarily localized in the bronchial 
glands, and the clinical picture of tuberculosis so often seen is 
that of an extension of the disease from these glands to other 
organs of the body, to the meninges, the lungs, the bones and 
joints, the kidneys, spleen, etc. After puberty, pulmonary tuber- 
culosis by far displaces all these various forms. 
In very early infant life the tuberculous process is usually 
rapid, the glands having not yet acquired the power of resistance 
to the disease and consequently rapid dissemination follows, the 
disease usually running a rapidly fatal course, but after infancy 
and from child life to puberty the tendency to a generalized dis- 
semination is lessened, the glands having acquired a greater 
degree of resistance, and now a localized gland tuberculosis, 
chiefly of the bronchial glands, is the clinical picture presented. 
However, at this period, intercurrent conditions may arise, such 
as injury and shock, measles, whooping cough, etc., which may 
again lower the resistance of these bronchial glands, and material 
being disseminated may again be followed by generalized lesions, 
miliary tuberculosis, meningeal, bone and joint disease, pulmo- 
nary tuberculosis, etc. 
Enlarged bronchial glands do not always lead to active disease, 
on the contrary in the greater number of instances the conditions 
terminate favorably, the glands undergoing calcification and be- 
coming encapsulated, but if the contents should undergo soften- 
ing, and the soft material enter the lymph channels or more par- 
ticularly the blood vessels, then this would be followed by 
speedy miliary disease. This latter may occur at any time during 
284 TUBERCULOSIS IN CHILDREN 
285 
infant and child life even into adolescence and up to old age. 
Tuberculosis in child life often manifests a great degree of 
latency, and frequently after a period of apparently perfect 
health, suddenly, as though out of a clear sky, an attack of tuber- 
culous meningitis may appear, after a very short and stormy 
course leading to speedy death from miliary tuberculosis. 
Clinical tuberculosis, as has been previously stated, may be 
divided into three stages. After infection has taken place, the 
regional glands become secondarily involved. This may be fol- 
lowed by primary tuberculosis of these glands, and the process 
may terminate here, or it may extend at any time to the second 
Fig. 41. The Lung (schematic) after Ghon. Autopsy No. 1006. Cause of death gener- 
alized Tuberculosis, male child, 3 years. Note the cavity in the apex of the upper left 
lobe surrounded by an adherent apical pleuritis, and pleuritis of the greater portion of the 
left pleura. The regional lymph nodes, the left broncho-pulmonary have undergone com- 
plete caseation and partial caseation of the tracheo-bronchial. 
stage by metastatic involvement of other organs or tissues, either 
hematogenous or lymphogenous, or it may manifest itself in 
years after as chronic pulmonary, the third or tertiary stage of 
tuberculosis. Tuberculosis in infants and children is usually 
primary or secondary, and only exceptionally tertiary. 
(A) The Primary Stage of Tuberculous Disease in Children. (77) 
Primary Tuberculosis. Clinical Manifestations 
as Seen in Infant Life. 
In children somewhat advanced in life definite symptoms are 
generally absent. In small children, however, the clinical pic- 
tures are those of fever, emaciation, anemia, etc. The fever may 
have the typical every day rise. Emaciation may come on sud- 
denly or be more or less protracted. Night sweats are more fre- 286 
CLINICAL TUBERCULOSIS 
quent in the elder than in the infant life. All these signs are 
very indefinite and although suspicious of tuberculosis, may 
have to be confirmed by the tuberculin test. 
Bronchial Gland Tuberculosis: Tuberculosis of the Tracheo- 
Bronchial Lymph Nodes. Glandulae Tracheo-Bronchialis. 
The lymph flow from the upper portion of the lungs is to the 
upper group the tracheo-bronchial glands, the middle and lower 
to the lower glands, and these glands communicate with the deep 
mediastinal and with the glands of the supraclavicular region 
about the bulbus vena jugularis, and not with the cervical glands, 
nor with the tonsillar lymph nodes; hence in speaking about 
gland tuberculosis only the tracheo-bronchial lymph nodes, and 
perhaps the deep-seated mediastinal, are considered, and not the 
palpable cervical glands. Bronchial or more correctly peri- 
bronchial gland tuberculosis is most frequently found in children, 
and only occasionally and exceptionally in adults. Primary 
gland tuberculosis is as infrequent in adults as is pulmonary 
tuberculosis in children. The cause of the disease in these or- 
gans is, like tuberculosis anywhere in the body, the tubercle 
bacillus, either the human or the bovine. In bronchial gland 
tuberculosis the human bacillus is most frequently the causative 
factor, while in tuberculosis of other regional glands the bovine 
bacillus may play the more important role. 
Infection with the human bacillus usually takes place after 
birth, exceptionally before; (see Chapter 3) and whereas a single 
mild infection may often give immunity against future infection, 
a massive or a frequently repeated small infection may be fol- 
lowed by early manifest disease and death. The period of infec- 
tion may be at any time after birth and up to about the sixth year 
and infection after that time is very infrequently followed by 
active disease. Tuberculosis may rightly be compared with lues, 
that is, after infection, a period of incubation follows, lasting a 
short time, then a more or less protracted primary manifestation 
of the disease occurs, and later secondary, and still later tertiary 
symptoms. In children the primary manifestation of the disease 
is usually at the cradle, that is, before the school age, the sec- 
ondary or metastatic form at the school age, and the tertiary, the 
pulmonary from after the school age or at the high school years, 
that is, at puberty and beyond. Nearly all pulmonary tuber- 
culosis and which is the tertiary form of the disease has been TUBERCULOSIS IN CHILDREN 
287 
preceded by the glandular or primary form. Bronchial gland 
tuberculosis is primary tuberculosis, may manifest itself at any 
time after infection, or it may become more or less subacute, and 
later in child life assume the chronic form. 
The anatomical seat of primary tuberculosis is usually in the 
regional glands or glands nearest to the first or primary infec- 
tion, and as in the human body, this primary infection is either 
subpleural or parenchymatous, that is, in the lungs, the glands 
nearest to the root of the lungs, the tracheo-bronchial, are sec- 
ondarily infected, and it is here that primary tuberculous disease 
manifests itself. Three groups of glands are generally involved, 
those along the trachea, those at the bifurcation, and those at the 
hilum, communicating with the deep mediastinal. The palpable 
cervical glands, if tuberculous, are not of this origin, but are due 
to infection from the mouth, teeth, tonsils, etc.; this enlargement 
may also be from various other microorganisms. 
Signs and Symptoms of Gland Tuberculosis 
The symptoms may be very characteristic in child life, or there 
may be absence of all objective signs, and again in many in- 
stances there are no definite signs, with perhaps the single sign 
of pain. Pain in the chest anteriorly, mainly to the right of the 
sternum and posterior interscapular backache, is much com- 
plained of. A painful cough with an expiratory stridor, how- 
ever, is usually present, due to the swollen glands pressing upon 
the bronchi, producing pressure symptoms and there may be a 
metallic cough and expiratory dyspnea, whooping cough-like 
symptoms supposed to be due to irritation of the branches of the 
vagus. This cough, hollow, barking, metallic, sounds like a 
whooping cough and is differentiated only by close study and 
long observation. In ordinary whooping cough there is usually 
an inspiratory dyspnea, with attacks of vomiting and cyanosis; 
in bronchial gland tuberculosis the attacks are generally accom- 
panied by an expiratory dyspnea. This piping and particularly 
high expiratory murmur is much increased after exertion or ex- 
citement. It is more protracted in the very young than in the 
elder children. Other signs occasionally observed are emacia- 
tion without any definite assignable cause, nutritional and gastric 
disturbance, discharges from ears, eczematous patches about the 
ears or multiple abscesses, slight fever at first, and broncho- 
pneumonic areas at the base of the lungs. In some instances the 288 
CLINICAL TUBERCULOSIS 
swollen bronchial glands may cause pain in swallowing, or there 
may be loss of voice from pressure upon the recurrent laryngeal 
nerve, and on examination of the trachea by means of the endo- 
scopic mirror, encroachment of the lumen and bulging of the 
tracheal wall may be revealed. Pressure upon blood vessels 
often gives distinctive signs. If the superior vena cava is com- 
pressed the vessels of the chest and neck become more full, the 
face becoming eventually edematous and cyanotic. If the veins 
of the lungs are compressed, a distinct tendency to nasal bleed- 
ing often results, and by the Valsalva method the veins of the 
neck over the affected side may become congested and pressure 
upon the arteria pulmonalis may produce a systolic murmur. In 
a healthy child, if on deep inspiration a Valsalva is practiced, the 
pupils become contracted, while in the diseased the pupils will 
become dilated, especially on the involved side. 
Pathologic-anatomically the right bronchus is most frequently 
compressed from enlarged and caseating glands, mainly about 
the bifurcation, and bending of the bronchus towards the upper 
lobe, the expiratory dyspnea, a harsh loud sound, expiration 
much prolonged, inspiration scarcely audible, accompanied by 
inspiratory contraction of the chest due to the pressure of en- 
larged glands upon the trachea, if continued for some time, and if 
accompanied by emphysema of the lung, the face becoming con- 
gested, the veins dilated, cyanosis, and in protracted cases club- 
bing of the fingers, all bespeak primary or bronchial gland tuber- 
culosis. Physical diagnosis is usually negative. In spite of the 
frequency of bronchial gland tuberculosis in the first and second 
and perhaps up to the fourth year of child life, these character- 
istic signs are but seldom observed, and endothoracic gland en- 
largement is during life infrequently diagnosed. 
Physical Examination and Diagnosis. As in the examination 
of the chest in pulmonary tuberculosis, so we apply the classic 
methods of physical examination by inspection, palpation, per- 
cussion, auscultation and roentgenology for the interpretation of 
the signs of bronchial gland disease. 
Inspection usually presents a frail child, chest somewhat con- 
tracted, Adam’s apple more or less prominent, and in many cases 
the pupil on the affected side is dilated due to pressure upon the 
sympatheticus by enlarged swollen glands; there may be un- 
ilateral sweating or flushing of the face; the temporal veins on 
the affected side are usually prominent and enlarged; the skin is TUBERCULOSIS IN CHILDREN 
289 
usually dry and covered with a downy growth of hair. 
Palpation. Interscapular backache is frequently complained 
of. If the physician places the tips of the fingers of one hand 
along the spine, and the other hand over the sternum and slight 
pressure is made from above down and again up, the child being 
placed sideways, standing before the physician; and if then 
close attention is paid to the child’s facial expression while this is 
being done, one will often observe that when certain points along 
the spine are touched, the child shows signs of flinching as if in 
pain. This technic was first described in detail by Petruschky 
under the term “spinalgia.” Pressing upon the thoracic spines 
from the second to the seventh, particularly on the third and 
fourth, will often cause pain. In palpating the upper intercostal 
spaces anterior, near the sternum, towards the right side pain is 
also often elicited if the glands are swollen. It is to be borne in 
mind as a differential diagnostic point that often in cardiac dis- 
ease, pain on pressure can frequently be elicited over the first to 
fourth dorsal spine and in stomach disorders from the fourth to 
the eighth. 
Percussion. Percussion anteriorly over the sternum is of little 
value, as an enlarged thymus or a deep and low lobe of the thy- 
roid may give a dull note and a dull note along the parasternal 
line right side between the second and third interspace is usually 
not due to enlarged glands, but to a retraction of the right lung 
border. Koranyi has pointed out that posteriorly in the normal 
condition, the percussion note may be dull and osteal over the 
spine to the fourth thoracic vertebrae, and pulmonary below that 
point, but that dulness to the fifth and sixth dorsal spine is al- 
ways pathological. This dulness may extend on both sides or to 
either side to the paravertebral line. With the dull note the 
resistance is also increased. 
Auscultation. Endothoracic gland enlargement can often be 
diagnosed by means of the stethoscope. If listening with the 
stethoscope along the spine of a normal child while breathing, 
beginning in the neck up over the fourth or fifth cervical verte- 
bra, we will note distinct bronchial breathing, and as we proceed 
downward the sound will continue, with perhaps a little less 
intensity but of the same quality until we pass the first thoracic 
spine, when it becomes fainter and is nearly lost at the second. 
If next we listen along the spinous processes of a child whose 
bronchial glands are enlarged, the tubular sound which we hear 290 
CLINICAL TUBERCULOSIS 
up in the neck will be carried downward, often as far as the sixth 
and seventh dorsal spines and beyond (Spino-trachael breathing). 
D’Espine has pointed out that if we listen with the stethoscope 
along the spine from above down and slightly to either side while 
the patient counts one, two, three in a whisper, the whispering 
voice in the presence of enlarged endothoracic glands can often 
be distinctly heard as far down as the seventh thoracic verte- 
brae. This bronchophonic voice is usually accompanied by a 
distinct echo, that is, as the patient counts one, two, three, an 
additional but slightly fainter three is heard. In normal children 
the whispering voice sounds are not heard or perhaps very faintly 
below the first or second dorsal. 
The humming sound occasionally heard when listening over 
the anterior chest along the clavicles and sternum while the head 
of the child is drawn upwards and backwards, and which is 
usually known as Smith’s sign, is not of much diagnostic value. 
This sound is very often heard in children up to the fourth and 
fifth year and occasionally beyond but is not common after the 
twelfth. It is supposed to be due to the pressure induced upon 
the innominate vein by the enlarged endothoracic glands while 
the child’s head is extended. 
O, de La Camp considers the physical possibility of diagnosing bronchial 
gland tuberculosis chiefly the tracheo-bronchial situated at the hilum. The 
symptoms are variable and are chiefly present in the pronounced cases 
although the principle symptoms of gland enlargement are usually always 
present. The characteristic dry, brassy cough, slightly husky voice, dif- 
ference in the .pupils, pain between the shoulder blades, spinalgia (Pet- 
ruschky) pain on pressure from the second to the seventh dorsal spine, 
and the passing of a sound into the oesophagus causing pain (Neisser), etc. 
Percussion over and near the sternum anteriorly and posteriorly in the 
paravertebral line to the right and left of the spine is of less value than 
percussion directly over the spinous processes as was first demonstrated by 
Koranyi, a relative dulness over the fifth and sixth dorsal spine by moder- 
ate percussion indicates gland enlargement. 
Tuberculosis of the endothoracic glands in a child is the first stage of 
the disease. Its early recognition and treatment is of the greatest moment 
and we are without doubt in a position early to recognize bronchial gland 
disease and by means of proper therapy at our command we can success- 
fully treat it. Tuberculin injections and radiographic examinations are 
only auxiliary methods in the hands of a capable and competent clin- 
ician. (89) 
Roentgenology. The roentgenology of tuberculosis in chil- 
dren. Peribronchial. Pulmonary. Miliary. Differentiation. 
(See Chapter 17.) TUBERCULOSIS IN CHILDREN 
291 
An X-ray plate is the objective representation of that which 
can be seen by the Roentgen ray. A radiographic examination 
is often of great aid, and may lead to an immediate diagnosis. 
It is especially valuable in children, where the clinical examina- 
tion is difficult and its findings often misleading. Technically, 
instantaneous exposures are essential on account of the rapid 
respiration and restlessness of children. 
Solitary or multiple (rarely more than four, usually all on one 
lobe) pea to bean sized, dense sharply circumscribed shadows, 
which lie free in an otherwise clear lung, may represent, in 
young children, a primary tuberculous focus (Ghon). If so, 
definite shadows of the enlarged, regional or corresponding peri- 
bronchial glands are usually present, and the v. Pirquet reaction 
is positive. An active, upper lobe, tuberculous process, asso- 
ciated with a positive tuberculin reaction, appears in children in 
two types of shadows. 
1. Fine, flaky or streak-like shadows in one or both upper 
lobes, which intensify the normal markings, are heavier near the 
hilum, and radiate outward, are suspicious for tuberculosis in 
young children. Peribronchial gland shadows are usually pres- 
ent. The radiating shadows may or may not extend to the peri- 
phery. Percussion and auscultation usually reveal only pro- 
longed and harsh expiration. A positive v. Pirquet in these 
cases makes the diagnosis probable. 
2. In the more advanced form, the shadows are not only more 
extensive, but the flakes are larger and denser. The streaks run 
into one another, and although appearing to coalesce, still show 
that they are individual shadows. There is frequently a high 
position of the diaphram on the affected side, with diminished 
respiratory movement. Clinically, there is dulness, harsh, often 
bronchial breathing, cough, and tubercle bacilli may be in the 
sputum. 
On plates this shadow is to be differentiated from that given 
by any chronic inflammatory process, such as asthma or chronic 
bronchitis. These latter shadows are evenly distributed over 
both lungs, and extend well toward the periphery. They are 
well defined and linear. Sometimes the markings on one side are 
a little heavier than on the other. 
In older children, with advanced tuberculosis, shadows are 
usually found in the upper lobe of one or both lungs. These 
shadows are cloudlike, composed of various sized, smaller or 292 
CLINICAL TUBERCULOSIS 
larger, individual shadows which have become confluent. These 
never become homogeneous in density, as found in pleuritis, 
lobar pneumonia, or exudate. Frequently there are present well 
defined clear areas, or a few small well defined shadows, the 
latter in the vicinity of the larger, of the confluent shadows. The 
lower parts of the lungs are usually exceptionally clear. 
In other cases a triangular shadow may occur in the middle 
part of either lung. The base of the triangle is toward the cen- 
tral shadow; the apex extends toward the periphery, diminishing 
in density as it extends outward. In rare instances the position 
of the triangle is reversed. One margin is often sharply defined 
along an interlobar septum, while the other, usually the upper, is 
irregular and not well defined. Again, both margins may be ill- 
defined. The rest of the lung is clear. Such a shadow speaks for 
lobar pneumonia, either early or after the crisis, but might be 
intrapulmonary tuberculosis. The latter is differentiated from 
pneumonia, in that it does not change, or but slowly, on repeated 
examination. If it is tuberculosis, several small, isolated, sharply 
circumscribed, dense shadows are scattered through the area in- 
volved. The corresponding glands in the hilum give heavy 
shadows. Upper lobes are often involved. In children with 
these findings there is persistent fever, cough and emaciation, 
with a positive tuberculin reaction. The shadows seen in sub- 
acute tuberculous processes in children may be general or local- 
ized. 
Sharply circumscribed shadows, usually small, but not all of 
even size, which lie free in the lung fields and are irregularly 
distributed over one or several lobes, speak for disseminated, 
caseated or calcified, tuberculous foci, in children with a positive 
tuberculin reaction similar shadows in the apex, which do not 
communicate with the hilum, speak for a healed apex tubercu- 
losis, in the presence of a positive tuberculin reaction. 
Diffuse cloudiness of the apex region, associated with a posi- 
tive tuberculin reaction, and with pronounced dulness without 
change in breath sounds, speaks for a healed tuberculous pleu- 
ritis. There may be a narrowing of the apex, or a shrinking of 
the whole side, due to the pleuritis, to the stenosis of a bronchus, 
or, more especially, to pressure from tuberculous bronchial 
glands. Diffuse cloudiness of the apices can also be caused by 
scoliosis, heavy muscles, struma, supra or infra clavicular glands 
or cervical rib, etc. TUBERCULOSIS IN CHILDREN 
293 
The general type of lung tuberculosis in children extends from 
the hilum toward the periphery. Primary involvement of the 
apex, either with clouding, or with more definite markings, is 
rare in children, almost never occurring before the sixth or 
seventh year. 
Roentgenologially, increased density in the region of the hilum, 
is of more significance in children than in adults. This appears, 
on X-ray plates, as rounded shadows, often as heavy as the heart 
shadow. These may be single or multiple, large or small, in 
masses or discrete. The margins are usually fairly smooth. 
They may be hazy and indistinct. Such shadows may be covered 
by the heart and not be visible, or only dimly made out. These 
shadows correspond to peritracheal and peribronchial lymph 
gland involvement, and if associated with a positive tuberculin 
reaction, speak for tuberculosis. 
Acute hematogenous, or miliary tuberculosis may be definitely 
diagnosed from X-ray plates. In children it appears in two 
types. 
First, that consisting of numerous, nearly equal sized shadows, 
(possibly larger in the upper lobes), evenly and symmetrically 
distributed over both lungs. These shadows are just visible in 
size and lie very close together simulating a cloudy veil which 
may even blur the central shadows. In the second type they are 
very similar, but larger and farther apart. 
Extra-pulmonary lesions, such as thickened pleura and hydro 
and pneumothorax are similar in children and adults. (See 
Chapter 17.) 
A tuberculous abscess is a dense, rounded sharply defined 
shadow, lying near the spine. Its level corresponds to the verte- 
bra affected, or depends upon how far down the cold abscess has 
descended. C. B. R. 
Tuberculin. For diagnostic purposes in suspected gland tuber- 
culosis, the use of tuberculin finds its greatest application. The 
use of tuberculin as a probationary and therapeutic remedy is 
fully described in Chapter 24, “Tuberculin and Its Uses.” 
(B) The Secondary Stage of Tuberculous Disease in Children. 
Secondary Tuberculosis. The Secondary Form of the Disease. 
Dissemination of tubercle bacilli through various channels, a 
metastatic form of the disease. In many there is no picture of 
activity. It does not appear in children infected in later life, that 294 
CLINICAL TUBERCULOSIS 
is in those infected after the sixth year and it is usually the 
cause of death of all those children infected in early life and who 
have not succumbed to the primary infection. 
Two forms are generally recognized: 
1. A very malignant form. This form of tuberculosis mani- 
fests itself either as an acute miliary tuberculosis or as a basal 
meningeal. This form is usually hematogenous, the tubercle 
bacilli gaining entrance directly into the blood stream from a 
caseating or degenerating gland. 
2. A more or less benign form, appearing usually somewhat 
later in infant or child life in the form of bone and joint tuber- 
culosis, chronic meningeal or spinal tuberculosis, etc. This form 
is most likely lymphogenous. Many bacilli after entering the 
lymph channels are held back by the nearest glands and only few 
gain access to the circulation. 
(1) a. Acute Miliary Tuberculosis in Children 
The most malignant form of the secondary stage is the acute 
miliary, a hematogenous infection. In children between two and 
five the meningeal form is the most fatal. If the brain is not 
Fig. 42. The Lung (schematic) after Ghon. (Posterior view.) Autopsy No._ 553. 
Cause of death tuberculous meningitis, male child, 5 months. Note the large cavity in the 
lower part of the left lower lobe surrounded by a tuberculous pleuritis. The regional 
lymph nodes the left broncho-pulmonary and the epi-bronchial have undergone total casea- 
tion, and partial caseation of the upper tracheo-bronchial and para-tracheal on both sides. 
Miliary tubercules in both lungs. The initial primary and older lesion was in lower 
portion of the left lower lobe. 
swamped with many bacilli then the symptoms of a generalized 
miliary form prevail. We notice here again a period of quies- 
cence, and from the spread of the bacilli until beginning of mani- 
fest disease about two weeks elapse usually without prodromal 
symptoms. These miliary symptoms last from one to three TUBERCULOSIS IN CHILDREN 
295 
weeks, seldom longer. An increasing bronchitis may reach a 
high stage with severe cyanosis, mind being somewhat impaired, 
with signs of meningeal disease. Glands may suppurate and per- 
foration into a bronchus or into the oesophagus may take place, 
usually toward the point of least resistance, or the contents of 
the glands may gain access into the lymph channels and in that 
way produce a secondary miliary tuberculosis. 
The affection may manifest itself at any age and at any time, 
usually under the form of an acute infection, beginning either 
suddenly or with pulmonary symptoms, loss of appetite, slight 
feverishness, indifference and drowsy condition of one or two 
weeks’ duration. This is quickly followed by a rise in temperature, 
an irregular pulse, negative lung findings, dyspnea, cyanosis, a dry 
hacky cough, with expiratory stridor, little or no expectoration, 
enlarged spleen, and a strong tendency to meningeal symptoms. 
The diagnosis often offers many difficulties and is largely de- 
pendent upon the tuberculin test, examination of the lumbar fluid, 
and the ophthalmoscopic examination (chorioidal tuberculosis). 
It may be difficult to differentiate from typhoid, although it 
usually is by the negative Widal, from lobar pneumonia, broncho- 
pneumonia and capillary bronchitis by the pulmonary findings, 
and even a localized bronchial gland tuberculosis may simulate 
the acute miliary form. The course is usually short, fast and 
very stormy, and exitus letalis from a few days to a few weeks. 
(1) b. Basal Meningeal Tuberculosis in Children. 
Tuberculous Meningitis. 
Acute basal tuberculosis in infancy is less infrequent than we 
are forced to believe. It may often accompany an existing otitis 
media or mastoiditis, or a previous cerebral tuberculosis. The 
infection is usually hematogenous from a caseating tracheo- 
bronchial gland, the bacilli being carried into the meshes of the 
arachnoid at the base of the brain. The diagnosis may often be 
made with great difficulty, owing to the symptoms simulating 
tetany. The diagnosis must be based on the clinical findings, 
these very often being meager. Lumbar puncture may be re- 
sorted to. The prognosis is grave. Therapeutic remedies are 
useless. Pain may be relieved by sodium bromide. Morphine is 
indicated in sufficient doses. 
(2) A more or less benign form. A lymphogenous infection. 
The second form of secondary tuberculous disease. A metastatic 296 
CLINICAL TUBERCULOSIS 
form of tuberculosis. This form of tuberculous disease so fre- 
quently seen in children during the school age is fully described 
in Chapter 30, “Tuberculosis of Bones and Joints,” 
(C) The Tertiary Stage of Tuberculous Disease in Children. 
Tertiary Tuberculosis. The Tertiary or Pulmonary 
Form of the Disease. 
This form of tuberculosis is the usual pulmonary form which 
we see so persistently throughout adult life but infrequently in 
children; however, in children, it usually runs a much faster 
course, and as it does not differ from the tertiary form of the 
disease in the adult or from pulmonary tuberculosis, as men- 
tioned in the text on pulmonary disease, the definitions given 
there are applicable to both and a review of Chapters 10 to 18 
inclusive is advised. 
Therapy. 
The Treatment of Tuberculosis of the Tracheo-bronchial 
Lymph Nodes. 
(1) Prophylaxis: To prevent infection of the child and to in- 
crease its resistance. 
It becomes the duty of the mother, if possible, to protect her 
child from infection, after infection it becomes her duty to pre- 
vent the child from becoming tuberculously diseased, that is, to 
increase its resistance and here good housing conditions, whole- 
some fresh air, out-of-door living, with frequent baths, good food, 
etc., are the necessary factors. The well known axiom of v. 
Behring, “Tuberculous disease in the adult is simply the last 
tune of that song which was first sung at the cradle,” brings pul- 
monary tuberculosis as observed in the adult back to childhood. 
With the introduction of Tuberculin as a specific diagnostic 
measure by v. Pirquet the early infection and subsequent tuber- 
culous disease was again definitely placed in childhood. All this 
only goes to prove that suitable therapeutic measures directed 
against the disease must begin in childhood. 
Tuberculosis is primarily a child disease, is preventable in 
childhood, is acquired in childhood, it should be treated in child- 
hood and can be cured in childhood. 
In children before the school age much out-of-door life is most 
essential and during the school age body development must keep 
pace with mental training. It may perhaps be better not to send TUBERCULOSIS IN CHILDREN 
297 
the tuberculous child to school or only for a few hours each day. 
The instructions at school should be followed by gymnastic exer- 
cises and with sufficient rest and sleep, good food, obedience to 
the rules of health, including hygiene of the mouth, etc. 
Primary tuberculous disease, peribronchial gland tuberculosis 
can with our present knowledge be definitely diagnosed and 
should receive our closest attention. If peribronchial gland 
tuberculosis is. the first manifestation of tuberculous disease fol- 
lowing the implantation of the tubercle bacillus into the human 
body, and this implantation is in early child life and that all the 
other forms of tuberculosis are only a sequel of this primary dis- 
order then does it not become our imperative duty to apply thera- 
peutic measures at a period when the disease may become 
promptly arrested and so guard against a more serious disturb- 
ance in later life, at puberty? We must endeavor by appropriate 
therapy to raise the child’s resistance to increase its immunity 
so that it may safely be carried beyond those years when new im- 
pulses contribute to a reactivation of a latent tuberculous process 
but now attacking a more vulnerable organ, the lungs. Only too 
frequently this early disturbance is treated very lightly and when 
the more grave symptoms begin to show, when resistance has 
been so much lowered then there is no longer an arrest of the 
tuberculous process possible. 
As soon as a diagnosis of bronchial gland tuberculosis has been 
definitely made, no matter how well the general condition of the 
child may appear it becomes the imperative duty of the physician 
to institute a proper therapy. It may be advisable if possible to 
have the child taken care of at a Preventorium away from the 
congested districts of a city—out in the open, in the country 
where under medical care and nurses supervision, and strict 
obedience to hygienic laws improvement in the child’s condition 
becomes readily noticeable. The child’s stay at a Preventorium 
must be long enough to assure complete arrest of the process 
after which a periodic examination should be made at least once 
every three months. This should be done for a period of years 
or until the child is safely carried beyond puberty. The same 
rules must apply if the child is taken care of at the home and 
here the physician must see that strict and general hygiene are 
instituted similar to institutional care. If all the children, who 
from the first to fifth or perhaps the sixth year, are victims of 
persistent and troublesome whooping cough like symptoms, and 298 
CLINICAL TUBERCULOSIS 
who most likely are suffering from peribronchial gland tuber- 
culosis, could be under close observation for many years to 
follow, we would have fewer cases of pulmonary tuberculosis in 
young adult or in later life. 
(2) Symptomatic Treatment. 
Besides living up to strictly hygienic rules much good may be 
accomplished in the care of the tuberculous child by proper 
medication. Symptomatic treatment, if necessary, should be 
applied as the occasion arises, our chief aim in using medica- 
ments must be to increase the child’s resistance and to raise its 
immunity. Children who do not eat well, appear anemic, per- 
haps cachectic, underfed or undernourished, the addition of some 
palatable preparation of iron to their daily diet may be advisable. 
The albuminate of iron and simple syrup in equal proportions 
make a most admirable combination. This may be given in one- 
half teaspoonful doses. Less palatable, perhaps more efficient, is 
the syrup of ferrous iodide and glycerin in equal parts, given 
in 10 to 30 drop doses three times a day. Although not an 
iron preparation but one which I have found most satisfactory 
especially to the very young is the preparation known as Lilly’s 
Coca Quinine. This I direct to be diluted equally with syrup 
of tolu to be given to a child say about three or four years of 
age one-half teaspoonful three or four times a day. A remedy 
which I find most dependable is the ordinary tincture of iodine 
U. S. P. Five to ten drops to be given in milk three or four 
times a day, giving it for months, perhaps years. A pleasant 
stomachic for children is: 
Tincture of Nux Vomica drops 16 ( 1.0 cc) 
Tincture of Cardamom Compound drachms two ( 8.0 cc) 
Simple Syrup sufficient to make two ounces (60.0 cc) 
Directions: Give one-half teaspoonful three times a day with meals, in 
water. 
To children with pronounced anemia from two to five drops 
of Fowler’s solution of arsenic may be given three times a 
day. Cathartics as a rule should not be given. Regulate the 
bowels by giving the child a suitable diet. A most reliable 
combination is any of the numerous cereals or breakfast foods 
now so much in use, with cream and sugar to which a heaping 
tablespoonful of bran has been added. Give freely of cooked 
and raw fruit and vegetables. Apples are most ideal if they are TUBERCULOSIS IN CHILDREN 
299 
washed and eaten skins and all. Same applies to pears and many- 
other fruit. Milk is the most ideal of all foods. It is best to give 
it raw and cold, cooking lessens its value, is less palatable, less 
nutritious. If the milk is from a reliable herd it will be perfectly 
safe to have the child drink it raw; however, it may be best to 
pasteurize it. If there should be the least doubt then by all 
means it must be cooked. Besides milk, good and wholesome 
bread and butter, crackers, potatoes, meats, ice cream, eggs, etc., 
should constitute the chief articles of diet for the tuberculous 
child. As to fats sufficient is secured in the form of butter in the 
ingested milk or cream, sufficient to supply the necessary cal- 
ories. Other animal or vegetable fats are unnecessary. Perhaps 
the addition of a teaspoonful of olive oil several times a day may 
be added to the daily regime but cod liver oil should be strictly 
tabooed; it was never intended for a child’s stomach. 
(3) The Tuberculin Therapy in Gland Tuberculosis— 
The Specific Therapy. 
To tuberculin must be assigned the most conspicuous place 
for the treatment of peribronchial gland tuberculosis. Ever since 
its use, it has been observed that its effect, particularly in gland- 
ular disease in children may often be called a specific, and palpa- 
ble cervical glands from bacillary infection by way of the mouth, 
teeth or tonsils have often been noticed to disappear as if by 
magic. Children as a rule are very tolerant to tuberculin even 
if it is given in fairly large doses. The belief entertained by 
some pediatricians that children do not tolerate tuberculin very 
well, not as well as adults, is founded upon error, on the contrary 
they tolerate it very well. The many excellent, even complete 
curative results which from time to time have been reported fol- 
lowing the use of tuberculin in the treatment of glandular tuber- 
culosis, even such as may be accompanied by much swelling and 
tumefaction, if not actual-breakdown of the gland with open 
sinus formation may in the main be due to the fact that in the so 
employed tuberculin a component is found just the suitable anti- 
gen for an arrest, inhibition, or perhaps practical cure of the 
tuberculous process in the gland in a given case, whereas if the 
same tuberculin is employed in another case it may be followed 
by only a negative result. The many favorable impressions, even 
in some cases of complete cure following the use of old tuber- 
culin in glandular tuberculosis, goes to prove that in the con- 300 
CLINICAL TUBERCULOSIS 
tained antigens necessary to bring about this change are constant 
substances, which are given out during the growth of the bacillus 
and are present in the protein element of the bacillus and not in 
the lipoid substance of the organism. This also readily explains 
why the use of tuberculin in pulmonary cases is not followed by 
any marked success, this is because these, the pulmonary cases, 
require an antigen which will inhibit, destroy or dissociate the 
bacillus, this tuberculin can not accomplish, such a body is not 
contained in tuberculin. These pulmonary cases are not con- 
cerned with any bacillary products but these products are of 
prime importance in the treatment of glandular cases. 
In administering tuberculin hypodermically for curative effect 
old tuberculin is generally understood and used, beginning 
with a most minute dose a 1/10 cc of the No. 5 Standard Dilu- 
tion, this equals one millimilligrams or 1/600,000 of a grain. The 
hypodermic injection should be repeated once in four days, in- 
creasing the dose by 1/10 cc with each subsequent medication. 
When the individuals “Tonic” dose has been reached the tuber- 
culin may be given once in seven days. This should be continued 
for some time, then given once in two weeks, then three weeks 
and ultimately once a month for almost indefinite time, for years. 
For full consideration of this important topic the reader is 
referred to Chapter 24 “Tuberculin.” Its therapeutic appli- 
cation. 
(B) The Treatment and Care of the Metastatic Form of Tuber- 
culosis in Children. The Secondary Form of Tuberculosis. 
The treatment of the malignant forms both miliary and men- 
ingeal has been given when considering these two types. The 
treatment of the benign form, bone and joint tuberculosis is 
usually a surgical one. This treatment is fully considered in 
Chapter 30—“Tuberculosis of Bones and Joints.” 
(C) The Treatment and Care of Pulmonary Tuberculosis in 
Children. The Tertiary Form of Tuberculosis. 
This does not differ from that of the adult. As pulmonary 
tuberculous disease in the child runs a course somewhat similar 
to that of the adult and as the treatment of adult tuberculosis is 
fully described in Chapter 19, “The Care of the Tuberculous— 
General and Medical” and as all that is stated there applies 
equally to the treatment of this disease in children the physician 
is referred to that chapter. TUBERCULOSIS IN CHILDREN 
301 
As the disease in early child life runs a more acute, perhaps a 
more rapid course, the child must be under constant observation 
and the instituted treatment be it dietetic, hygienic, medical, 
tuberculin or whatsoever must be more intensely and vigorously 
enforced. It is always advisable to place the child suffering from 
pulmonary tuberculosis under the care of a competent nurse or 
still better to be cared for at a Sanatorium where the treatment 
can be better supervised. 
Children suffering from tuberculosis of the genito-urinary tract, of the 
eye or mucous surfaces, of the peritoneum and the various other tissues 
and organs of the body should be treated according to the rules given in 
these respective chapters to which the reader is referred. 
The Groups of Glands. 
As tuberculosis of the lymph glands and glandular disease in 
general plays so important a role in child life (89), occasionally 
in adult life as well, it seems advisable that we study the various 
groups of glands and their lymph flow in relation to the lungs 
and the other organs of the body. 
We shall first consider the lymph supply to (a) the cervical, 
(b) to the tracheo-bronchial and then that to (c) the other intra- 
thoracic lymph nodes. 
(A) The lymph vessels of the tonsillar region supply the group 
of glands at the angle of the internal jugular and the anterior 
facial veins; the lymph flows from there to the middle group of 
the deep cervical, and terminates not by way of the thoracic duct 
but as cervical trunks directly into the veins, showing that the 
deep cervical glands empty into the venous system without any 
support from the supraclavicular lymph nodes, demonstrating 
positively that the latter, the supraclavicular glands, do not be- 
long to the regional glands of the pharynx and tonsils. There is 
no direct communication between the cervical and the supra- 
clavicular glands, however, by means of the numerous anasto- 
mosing vessels existing, communication may be established. It 
has never been indisputably demonstrated that the lymph flow 
from the cervical glands is towards the region of the apical pleura 
nor to the tracheo-bronchial lymph nodes. 
(B) The tracheo-bronchial glands are the regional and local 
glands of the pulmonary circuit. They form part of the great 
regional lymph apparatus of the lungs and all material, either 
infectious or noninfectious, which finds its way into these glands 
must come by way of the lungs. These lymph glands, the 302 
CLINICAL TUBERCULOSIS 
tracheobronchial, are divisible into two main groups, the pre- 
tracheal and the paratracheal. The first group, the pretracheal, 
also receives lymph from the mucous surface lining the anterior 
tracheal wall, and the flow may be from there to the laterally 
situated paratracheal glands, usually, however, to the supracla- 
vicular. The second group, the paratracheal, which is generally 
designated the tracheo-bronchial, lies in long chains in the fur- 
row between the trachea and the oesophagus. This group is again 
divided into two subgroups, one of which lies median to the arch 
of the aorta, the other lateral to the pulmonary artery, that is, 
between it and the hilum. The lymph vessels from all of this 
region converge towards the supraclavicular nodes and terminate 
either in one of the supraclavicular glands or more frequently 
direct into the vein at the lateral angle of the bulb of the jugu- 
laris. 
(C) The lymph glands of the lungs are in groups at the angles 
of the bronchial tree. The lymph flow is towards the hilum and 
it is gathered in the bronchial glands around and about the bifur- 
cation of the trachea. They are described as the right, left and 
inferior tracheo-bronchial, the inferior group receiving its supply 
from the middle and lower portions of both the right and left 
lung and the lateral groups, the right and left tracheo-bronchial 
glands, from the middle and upper portions of the lung, from 
the apices of the lungs the lymph flows from the periphery to- 
wards the hilum supplying the nearest lymph nodes. From the 
tracheo-bronchial glands on either side a few large trunks ex- 
tend laterally and upwards behind the large veins, to the angle 
between the subclavian and the jugular, or as may occur on the 
left side empty either into the veins or into the thoracic duct. 
The lymph vessels of the upper portion of the pleura extend 
back to the intercostal glands, those of-the lower and posterior 
flow towards the glands situated before the spinal column and 
behind the aorta, emptying into the thoracic duct, and those 
lymph vessels of the anterior pleura supply the group of glands 
situated along the internal mammary vein and the artery. 
Palpable Glands in Children. It is undoubtedly a sad mistake 
to diagnose all children in whom we find enlarged cervical glands 
as suffering from gland tuberculosis. When we speak of gland 
tuberculosis we generally allude to a disease of the endothoracic 
glands, to a primary tuberculous gland disease, and not simply 
to tuberculously infected glands. Cervical adenopathy, a few TUBERCULOSIS IN CHILDREN 
303 
enlarged glands in the axilla, or in the inguinal region are very 
common in children. Every physician knows the great fre- 
quency of gland enlargement following chicken pox, as a com- 
mon occurrence in the exanthemata, common in children suffer- 
ing from head lice, in eczematous patches about the ears, etc., 
in all of which the adenopathy may last for years. Cervical 
gland enlargement may follow infection from the mouth, teeth, 
tonsils, etc., but this infection is infrequently due to the tubercle 
bacillus. It is now generally recognized that about 65 per cent 
of all children at the school age are suffering from cervical gland 
enlargement, and this is caused from infection from various 
micro-organisms, but in only about 10 per cent is this infection 
due to the presence of the Koch’s bacillus. Because a child has 
enlarged glands, chiefly cervical, we have not the right to stig- 
matize it as tuberculous. Gland tuberculosis is the primary 
stage of the disease; it follows a secondary infection of the 
regional glands, after the primary infection, but it is not the in- 
fection itself. We only too often confuse being infected with 
being diseased. 
It may be of interest to observe at this point that full term infants very 
exceptionally have palpable axillary glands, and even seven months’ chil- 
dren are born without palpable axillary glands. The weight of the child 
has nothing to do with the presence of enlarged glands, and children 
nourished at the mother’s breast have on an average less palpable glands 
than those artificially fed. Children sufifering from chronic intestinal dis- 
turbances have many palpable groups of glands, and every chronic dis- 
turbance is accompanied by enlarged glands. In lues and sepsis we 
usually find a great many palpable glands, but comparatively few in 
tuberculosis. 
The Treatment of Tuberculous Adenitis. 
In the treatment of tuberculous adenitis there must be consid- 
ered: (1) The general constitutional and hygienic conditions; 
(2) The local treatment to glands and (3) locating and treating 
the primary point of infection. (193) (194) (195) (196) 
(1) The General Constitutional Condition of the patient must 
be determined and any change in mode of living and general 
hygienic conditions corrected, so as to increase the general body 
resistance to its maximum. This can only be accomplished by 
thoroughly examining the entire body and all its physiological 
functions and institute whatever therapeutic measures necessary 
to accomplish this end. In other words, the patient should be 
treated as if an active pulmonary lesion were present in order to 
secure the quickest and most satisfactory results. 304 
CLINICAL TUBERCULOSIS 
(2) The Local Treatment. All cases of tuberculous adenitis, 
whether cervical or located elsewhere, should receive a prompt 
and thorough course of radiotherapy, regardless of the stage at 
which they first come under observation. Over ninety per cent 
will subside and present a clinical cure under this treatment by 
converting the lymphoid and granulating tissue into fibrous 
tissue, occasionally calcification will result. Surgical treatment 
is never indicated until after a thorough course of roentgeno- 
therapy has been employed, then there will be only a very small 
percentage that will require surgical interference. In cases where 
the development is slow, running a painless course, and the 
glands are separated, a prompt result can be expected within 
three months, with a fair amount of radiation* once every three 
weeks. 
With the more malignant type of cases where the glands de- 
velop rather rapidly and tend to fuse into a large mass, which 
may show early signs of caseation and abscess formation, very 
heavy radiation is indicated, which should be limited only by the 
skin tolerance, in order to get as rapid regression as possible. 
They yield more slowly than the type first described and will 
require a longer period of treatment. Exposures are usually 
made every three weeks over a period of three or four months, 
and then continued at six week intervals for three or four months 
more. If caseation and abscess formation develop, it is well to 
aspirate as much as possible and in this way avoid free drainage, 
as it saves the patient much time and discomfort. Occasionally 
the skin will break down, so that free drainage is unavoidable, 
which will in no way interfere with the radiotherapy. 
(3) The primary point of invasion. This should be located if 
possible, and treated. The tonsils and naso-pharynx are fre- 
quently found to be sources of the primary lesions. The question 
of removal of the tonsils is the subject of much discussion at 
present. A general anaesthetic should be avoided whenever 
possible, as a slight diminution in the general body resistance 
may be the direct cause of a rapid extension of invasion to the 
lungs or the other parts of the body, so when tonsillectomy is 
decided upon, it should best be done under local anaesthesia. A 
safer procedure is to treat the tonsillar area and naso-pharynx 
by X-ray, the object being to retard lymphoid cell proliferation 
"It is inadvisable to attempt to describe X-ray dosage, as no uniform standard of 
measuring the amount of radiation given has been decided upon. The treatment should 
be put into the hands of a competent radiotherapeutist who will be able to judge the 
radiation necessary in each case. TUBERCULOSIS IN CHILDREN 
305 
and in this way produce a shrinking of the tonsil as well as all 
other lymphoid tissue with a diminution in size of the crypts and 
obliteration in some cases. 
Too much emphasis cannot be placed on roentgenotherapy of 
all peripheral tuberculosis, for over ninety per cent of all cases 
will yield to a properly administered course of treatment, and 
will save the patient the possible complications which accompany 
operative interference. The absence of a scar on the neck is also 
to be desired, especially by female patients. A. R. M. 
The following observations by competent pediatrists are most inter- 
esting. The Frequency of Tuberculosis in Children 
Death shows the highest point in the first year of infant life. Cornet 
reports from 10,000 living, who died from tuberculosis as follows: 
From 0 to end of 1st year—boys 23, girls 26 
From 1 to end of 2nd year—boys 21, girls 21 
From 2 to end of 3rd year—boys 12, girls 14 
From 3 to end of 5th year—boys 6.9, girls 8.0 
From 5 to end of 10th year—boys 4.5, girls 6.0 lowest point 
From 10 to end of 15th year—boys 4.9, girls 8.9 
Clinical observations are much more frequent in the middle years of 
child life when the secondary stage of the disease manifests itself in the 
form of gland, bone and joint disorder which usually do not cause death. 
From 0 to 1st year of life 15% show tuberculous lesions at autopsy. 
From 1 to 2nd year of life 40% show tuberculous lesions at autopsy. 
From 2 to 4th year of life 50% show tuberculous lesions at autopsy. 
From 4 to 6th year of life 56% show tuberculous lesions at autopsy. 
From 6 to 10th year of life 63% show tuberculous lesions at autopsy. 
From 10 to 14th year of life 70% show tuberculous lesions at autopsy. 
The tuberculin test applied (after Franz Hamburger) to children con- 
sidered perfectly healthy is as follows, v. Pirquet test: 
From 0 to 1st year the reaction was positive in 0 children. 
From 1 to 2nd year the reaction was positive in 9 children. 
From 2 to 3rd year the reaction was positive in 20 children. 
From 3 to 4th year the reaction was positive in 32 children. 
From 4 to 5th year the reaction was positive in 52 children. 
From 5 to 6th year the reaction was positive in 51 children. 
From 6 to 7th year the reaction was positive in 61 children. 
From 7 to 8th year the reaction was positive in 73 children. 
From 8 to 9th year the reaction was positive in 71 children. 
From 9 to 10th year the reaction was positive in 85 children. 
From 10 to 11th year the reaction was positive in 93 children. 
From 11 to 12th year the reaction was positive in 95 children. 
From 12 to 13th year the reaction was positive in 94 children. 
From 13 to 14th year the reaction was positive in 94 children, 
or approximately 0% in the first year, 9% in the second year and 94% in 
the 11th to 14 years. 306 
CLINICAL TUBERCULOSIS 
This was found to apply to the larger cities amongst the poorer popula- 
tion. The wealthier classes show relatively a slightly less infection and 
this is undoubtedly due to the fact that amongst the poorer classes we 
find more active or open cases of the disease and the children are found 
to live in closer contact with the tuberculous adult and in consequence 
thereof all such children become more readily infected. Hamburger con- 
cludes that tuberculosis in childhood is relatively a harmless disease and 
states that the prognosis becomes progressively better as the age of in- 
fection increases. Inactive or latent tuberculosis is most infrequent in 
infancy or in the first years of child life because nearly all succumb to 
this early infection and only in very exceptional cases can they overcome 
the infection. See Chapter 7—“The Course of the Tuberculous Disease.” 
The mortality is always great in early infant life, decreasing as years go 
by. Mortality 1st year 90% to 100%, 5th year 20% to 30%, 11th to 14th 
year 1 or 2%. Most individuals are infected in childhood chiefly through 
the inhalation route, and this leads to the formation of a primary focus 
in the lung giving a certain degree of relative immunity which lowers or 
weakens the activity of the bacillary bodies to reinfection. 
Mary Hamilton Williams’ observation on 3159 school children in 1910 
in Worcestershire 16.2% were found affected with pulmonary tuberculosis 
is worthy of note. 
Pulmonary tuberculosis ages 3 to 6—boys, 9.4%; girls, 10.4%. 
Pulmonary tuberculosis ages 12 to 14—boys, 11.5%; girls, 18.7%. 
She is of the opinion that as age progresses, more children suffer from 
tuberculous lesions although decreasing numbers die from the results. 
These findings do not agree with the above given or with our observa- 
tions. Pulmonary tuberculosis is very infrequent in the school days, or 
early child life; it only begins to make its presence definitely known as the 
child approaches puberty. In the early school days other forms of tuber- 
culosis are more frequently seen, pulmonary very seldom. 
Some interesting observations from the Stockholm Public Schools 
1908-1909. 
Out of a total of 25,600 school children, 15,219 between the ages of 8-15 
were examined. 
Pulmonary tuberculosis, 1.61% (of all children); boys, 1.72%; girls, 
1.50%. 
Suspicious of being pulmonary tuberculous, 2.21% (of all children); 
boys, 2.63%; girls, 1.80%. 
Pulmonary tuberculosis is less in the younger children between 8-9 
years 1.17%. 
Pulmonary tuberculosis is greater in the elder children between 14-15 
years 2.21 %. 
Swollen cervical glands in 65% of all children. 
Tuberculous glands in only about 10%. 
Bone and joint tuberculosis, 0.59%. 
About 1/5 of all children were emaciated and about 1/6 of all under- 
nourished. Vol. Ill, 559.(89) CHAPTER 24 
TUBERCULIN 
A PRODUCT OF THE BACILLARY GROWTH AND 
OF METABOLISM. 
Tuberculin is the product of disease producing bacteria, an 
heterogenous mixture of specific and non-specific substances de- 
rived from bacillary growth, bacillary bodies and from the cul- 
ture media upon which these bacteria are grown. It does not 
contain living germs,'is not a serum like diphtheria antitoxin, 
nor a lymph like the virus of vaccine. It is distinctly an isopathic 
remedy, one that may be used in the treatment of a disease by 
the disease’s own specific products. Its action can in no way be 
increased or modified by similar substances, there are no syner- 
gistic remedies known and if its use is at all proposed either 
diagnostically or therapeutically, a previous contact with this 
substance has always been anticipated. Tuberculin in itself is 
not a toxic remedy. It can be administered in large doses with- 
out producing any body disturbances. It, however, becomes 
highly toxic if given to individuals who have had a previous 
contact with this agent. (51) (52) 
From our present knowledge it is evident that not a single so- 
called tuberculin is of definite chemical composition, nor have we 
any tangible knowledge as to what the active therapeutic agent 
in this remedy may be. All the various bacilli of the acid fast 
group, human, bovine, avian, grass, smegma as well as those 
found in cold-blooded animals, like fish, turtle, etc., produce dur- 
ing the process of growth and multiplication a tuberculin-like 
substance, differing only in the amount of its active but still un- 
known specific body, and on which the value of the various 
tuberculins depends. They do not differ qualitatively but dis- 
tinctly quantitatively. All the tuberculins with which we are 
now familiar, and from whatever source derived, are mixtures of 
a specific, with more or less non-specific bodies, mostly albumin- 
ous substances, fatty bodies, salts, odoriferous principles, etc. 
Tuberculins from bouillon cultures, from albumin-free media, 
or more direct, from the bacillary bodies, a bacillary extract, all 
307 308 
CLINICAL TUBERCULOSIS 
are clinically and biologically alike. Up to the present we have 
not been able either by chemical or biologic methods to isolate 
or produce the active principle or clinical agent on which this 
specific effect depends. 
What Led to the Discovery of Tuberculin? 
After the discovery of the tubercle bacillus by Koch in 1882 
he continued his studies of the properties of this newly dis- 
covered bacillus as well as of tuberculous material, on experi- 
mental animals, arriving after careful and exact observation at 
certain definite conclusions which under the caption of “Prin- 
cipia” were promulgated as immutable, physiological and bio- 
chemical laws. He observed that (1) if healthy guinea pigs were 
injected, intracutaneously or subcutaneously with a pure culture 
of a bacillary growth, that at the point of inoculation nothing 
was noticeable for 10 to 14 days, that, however, after that time a 
nodule began to form at the point of introduction, which nodule 
soon showed signs of softening, breaking down and discharging 
pus and that the nearest lymph glands became enlarged. This 
so produced ulcer would not heal, but continued discharging pus 
during the remainder of the little animal’s life. (2) If, however, 
after a period of about six weeks, the same experimental animal 
was reinoculated with a like amount of the same material as the 
first, the effect upon the primary sore was quite pronounced, and 
the secondarily produced ulcer behaved very differently from the 
first. After the first inoculation nothing was observed for 14 
days; however, after the second inoculation, a sloughing ulcer 
began to form in a few days, healed very readily, and the neigh- 
boring gland did not become enlarged. 
This second sore, healing quickly, showed a great difference in 
the tissue reaction in the animal previously inoculated. It also 
demonstrated that the first inoculation overcame the effect of 
the second and as the primary infection, now showing a healing 
tendency, a tendency which was never observed without giving 
a second inoculation, the second infection definitely showed a 
distinct effect upon the first. (3) Next, he observed that if 
dead bacilli were injected into healthy animals, no disturbance 
was brought about, and at the point of injection only a local sup- 
puration was noticeable, which soon healed, causing no further 
tissue destruction. (4) If, however, dead bacilli were injected 
into a guinea pig previously inoculated with live virus the effect TUBERCULIN 
309 
would be quite different; following the injection the animal 
usually died in from 6 to 48 hours. His further observations were 
that if only small doses are used, this would cause much destruc- 
tion of tissue and death, whereas most minute doses caused 
neither death nor destruction of tissue, and that if infinitesimal 
doses were given at intervals of two days, much improvement in 
the primary ulcer followed. This primary ulcer which under 
ordinary conditions never healed now showed a distinctly healing 
tendency, the regional or secondarily involved lymph glands be- 
came reduced, the animal showed much improvement, and the 
disease became seemingly arrested. This proved definitely 
that dead tubercle bacilli, if injected into a healthy guinea pig 
were non-toxic, that the injection only resulted in the formation 
of an abscess which soon healed, but that they were highly toxic 
to previously infected animals, producing death if given in fairly 
large doses, and apparently curative if given in very minute 
doses. (5) Owing to the fact that when he injected dead 
tubercle bacilli into animals, no absorption of the bacilli took 
place, but that they were expelled with the abscess material, 
he separated by means of filtration the dead bacilli from the 
fluid media, and he then noticed that if this so obtained filtrate 
was used, the results were identical in action with that of the 
dead bacilli, but without the production of suppuration. This 
bacillary filtrate since that time, that is, since 1890, when Koch 
conducted these experiments is known as “tuberculin.” This is 
now prepared as a commercial product, is an artificial tuber- 
culin, and in short is designated “tuberculin” in contradistinction 
to the product given off by the bacillus while passing through 
the human or animal body, which is known as the natural 
tuberculin. It is estimated that the artificially prepared tuber- 
culin, as it is now offered as a remedial agent, contains about 
one per cent of an active, not yet isolated nor identified protein 
principle. 
The Tuberculin Reaction. 
The newly established fact, that this filtrate, the media in 
which the bacillary bodies grew, proved .to be non-toxic if in- 
jected into healthy guinea pigs, but highly toxic to inoculated 
animals if given in larger doses and seemingly curative if given 
in very minute doses, now received the most intensive study and 
consideration. After closely observing the effect of this new 310 
CLINICAL TUBERCULOSIS 
remedy on a large number of experimental animals, Koch began 
experimenting on himself by injecting into his body 0.25 cc of 
this filtrate, and he became more than surprised with its effect. 
He observed on himself a rise in temperature, a rapidity of the 
pulse, a reaction at the point of injection, much malaise, loss of 
appetite, headache, etc., in short for a time he considered himself 
made fatally toxic. Nothing like this had ever been observed in 
man before. 
From our present knowledge concerning the almost general 
tuberculous infection in the human family, we would anticipate 
such a reaction in the tuberculously infected, but in his time 
nothing was known concerning the ubiquity of tuberculosis, and 
he was at a loss either to understand or to explain the reaction, 
but long before his death he was made acquainted with all the 
newer problems involved in tuberculosis, and the tuberculin reac- 
tion as first observed on himself was then perfectly clear to him. 
Explanation of the Tuberculin Reactions. 
The so-called tuberculin reaction as we observe it today is 
usually three-fold: (1) A reaction at the point of application, 
identified by more or less redness or hyperemia; this is desig- 
nated the local reaction. (2) The application of the tuberculin 
may be followed by symptoms of malaise, headache and other 
constitutional disturbances; this is known as the constitutional, 
systemic or general reaction, and (3) more or less hyperemia and 
turgescence about the various tuberculous foci in the body. This 
is usually described as the focal reaction. That this latter does 
take place can readily be demonstrated in lupus, where after a 
tuberculin application a hyperemic area or a reddened line is 
frequently observed surrounding the lupoid structure. 
There are various views entertained concerning these reactions. 
(1) Koch’s View or Explanation. Tubercle bacilli when grow- 
ing in the tissue produce a substance or substances which kill 
protoplasm, the death of which brings about tissue necrosis; this 
necrosis checks the growth of the bacilli in consequence of which 
many die. If now tuberculin is administered, it will favor the 
production of large necrotic areas, and this causes many more 
bacilli to die, and if now these tuberculin injections are fre- 
quently repeated, more and more bacilli will be destroyed until 
ultimately all are killed, when the process becomes healed and 
the reaction ceases. TUBERCULIN 
311 
(2) The Wolff-Eisner Theory (28). When tubercle bacilli are 
deposited in the tissues of the human body and begin to show 
activity, that is, growth and multiplication, antagonistic forces 
are inaugurated. These forces are of two kinds, one of which 
is to destroy the bacilli, the other to neutralize the toxic products 
given off in this destruction. The first kind or class of antago- 
nistic substances are known as amboceptors or lysins, bacterio- 
lysins, the functions of which are to break down and digest the 
bacilli, converting them into simpler as well as into complex and 
toxic bodies; the function of the second class of substances is to 
neutralize these complex poisonous bodies, and these in general, 
are spoken of as antibodies. Lysins or amboceptors not only 
destroy tubercle bacilli, but tuberculin, the toxic product of bacil- 
lary growth, as well. Tuberculin is non-toxic to healthy indi- 
viduals, even if given in large doses, but it is highly toxic to most 
tuberculously infected and many diseased individuals, and in 
such persons the injected or applied tuberculin is seized by the 
lysins or amboceptors present in the organism, the result of 
which is the conversion of the injected tuberculin into a tuber- 
culo-lysin, which is now highly toxic. This lysinized tuberculin 
causes a reaction at the point of application, at the site of in- 
jection, circulating through the system producing a general or 
systemic reaction, and acting as a toxic irritant on the tubercu- 
lous centers, a focal reaction. If this lysinized tuberculin is now 
completely neutralized by the second substance, the antibodies, 
then no reaction follows. 
(3) Ponndorf’s Law (100). Ponndorf, sanitary physician at 
the Variola Institute at Weimar, reports most interesting experi- 
mentations. His observations relating to immunity in smallpox 
vaccination established certain notable facts, namely, that as the 
skin and mucous membrane of every person offer most suitable 
protection to the body against mechanical insults of all kinds, 
examples of which are daily observed by the external influences 
of heat and cold, so they offer also a protection to the organism 
after infection from various microorganisms and their products; 
further that the elaborated specific toxins, the result of bacterial 
infection and subsequent growth and development are taken up 
by the epithelial layers of both the skin and mucous membrane, 
and there with more or less rapidity reduced, changed or disso- 
ciated into simpler and less toxic substances, and that a subse- 
quent infection or contact with the same microorganisms or their 312 
CLINICAL TUBERCULOSIS 
toxins will produce, with the chemically changed contents or 
modified toxins of these cells, new combinations, which manifest 
themselves in the production of an inflammatory reaction at the 
site of application and by a generalized systemic disturbance. 
He then made analogous observations on the skin and mucous 
membrane of tuberculous individuals. After infection with the 
tubercle bacillus there will be found, at all times, deposited in the 
epithelial cells of the skin and mucous membranes modified, 
changed or dissociated natural tuberculin, and the great bio- 
chemical affinity existing between this modified tuberculin in 
these cells and the now added artificial tuberculin brings about a 
chemical reaction. This view seems most plausible. It is well 
known that the bacilli and toxin free organism does not react 
to tuberculin, this because when artificial tuberculin is applied 
to the skin of an individual who has never been infected, it does 
not find modified or changed, systematically produced tuberculin 
with which to enter into chemical union, hence no reaction. On 
the other hand, the toxically tuberculous individual also does not 
react to this applied tuberculin because the tuberculin present 
in the epithelial cells of the skin in such persons is unchanged, 
not modified, and being identical with the artificially produced 
product, no biochemical change can take place within these cells. 
The Various Kinds of Tuberculins. 
Up to the present time there are offered to the medical pro- 
fession in round numbers about 100 different tuberculins. This 
in itself speaks for the great uncertainty and diversified compo- 
sition of this preparation. The therapeutic value and cutaneous 
reaction of all depend upon a supposed biochemical toxic sub- 
stance present in each in varying amounts. The following in the 
order given are the best known tuberculins now in use: 
(1) Old tuberculin O. T. Koch’s old tuberculin, the original 
tuberculin of 1890, also known as extract tuberculin. Prepara- 
tion: A pure live virulent culture of the tubercle bacillus of 
human origin in a 5% glycerine nutrient broth is incubated for 
5 or 6 weeks, after which it is sterilized for one-half hour, evapo- 
rated at 70° C to one-tenth its volume, filtered and 0.5 of pure 
phenol added. Tuberculin so prepared contains from 40 to 50% 
glycerine, 10% peptone or albuminose, toxic substances, the de- 
rivative of the bacillary growth, and bacillary extract derived 
from the process of heating and evaporation. TUBERCULIN 
313 
(2) Deny’s boullion filtrate. B. F. This preparation is very 
similar to the former, the old tuberculin, differing only in that in 
preparing it no heat is employed, hence it contains less bacillary 
extract. 
(3) Tuberculin. B. O. T. Nathan Raw and Carl Spengler 
suggested a tuberculin after the manner of the O. T. preparation, 
inoculating the culture media, the broth, with a virulent strain of 
the bovine bacillus. It is in every other particular identical with 
the original old tuberculin. 
(4) New tuberculin. T. R.=tuberculin residue, 1897. Endo- 
plasm turberculin. Koch’s reasoning led him to the conclusion 
that in the use of old tuberculin the object is the obtaining of an 
immunity against a tuberculin toxicity and not a true immunity 
against the bacterium, hence, his aim was to produce a product 
which would give to the organism when applied a bacterial as 
against a toxic immunity. With this object in mind he offered 
in 1897 a new tuberculin now generally known as T. R. This is 
prepared as follows: Dried, virulent tubercle bacilli of the 
human kind are thoroughly triturated and ground with distilled 
water then centrifugalized and the supernatent watery fluid re- 
jected. The residue remaining in the centrifuging tube is dried, 
again triturated, ground with distilled water and centrifuged, the 
process being continued until all of the bacillary mass has been 
taken up by the water, 20% of glycerin is then added to the 
impalpably powdered bacilli held in suspension by the distilled 
water. This preparation is of such standard strength that each 
cc=2 milligrams of solid substance or 0.002. 
(5) Bacillen emulsion. B. E. A combined tuberculin, both 
endoplasm and bacillary extract, 1901. After four years’ use of 
new tuberculin, a second preparation of tuberculin, known as 
second new tuberculin was advanced by Koch. This is now 
known as bacillary emulsion or simply B. E., a combination of 
endotoxin and exotoxin. It is supposed to bring about when 
applied both a bacillary and a toxic immunity. 
It is prepared by suspending 0.5 gram of the impalpably pow- 
dered tubercle bacilli in 100 cc of equal parts of glycerine and 
distilled water. This is then repeatedly shaken until an emulsion 
is effected. Each cc=5 milligrams or 0.005. It is not a bacillary 
emulsion but simply a bacillary suspension of bacilli in an impal- 
pable powder in a suitable vehicle. 
(6) Polyvalent tuberculin. A polyvalent T. B. emulsion. Poly- 314 
CLINICAL TUBERCULOSIS 
valent autotuberculin. A combination of 8 different strains of 
various virulence, like an autogenous vaccine. It fell quickly 
into disuse and at the present time is but little employed. 
(7) Tuberculin Beraneck, T. B. K., an extract and endoplasm 
tuberculin. This tuberculin is a mixture of a culture of the 
human kind, free from all tubercle bacilli, evaporated at low 
temperature in vacuum to a syrupy consistency, and a bacillary 
extract obtained by treating bacillary bodies with a 1 % solution 
of orthophosphoric acid, without evaporation. This tuberculin 
presents a bacillary protein in the form of a phosphoric acid 
albumin combination. The culture media used is free from pep- 
tone and albuminous substances, furnishing a tuberculin free 
from non-specific proteins. 
(8) Spengler’s I. K. (Immune Koerper.) Immune bodies. The 
value of this preparation is based upon the supposed facts dem- 
onstrated by Carl Spengler, namely, that in the red blood cor- 
puscles, the erythrocytes, of every infected human being, pre- 
cipitins, tuberculo-precipitins are present which in a dilution of 
1-10,000 can be recognized. Specific tuberculin treatment will 
increase these bodies (1-1,000,000 and more). The amount of 
these precipitin bodies in the human organism is variable; they 
are naturally increased with the increase of resistance to infec- 
tion. 
(9) Albumose-free tuberculin T. A. F., a tuberculin produced 
or prepared by cultivating tubercle bacilli on a media free from 
' foreign albumin. The non-specific albumin content of the ordi- 
nary or old tuberculin and to which action many of the undesir- 
able reactions have been attributed is thereby wholly eliminated. 
(10) Endotoxin. Tuberculinum Purum. Gabrilowitch. Of- 
fered under the name of Tuberculinum Purum, this tuberculin is 
supposed to be free from all foreign proteins. It is prepared 
by the use of chemical reagents like alcohol, ether, chloroform, 
xylol and by precipitation, washing, decantation, centrifugaliza- 
tion, etc., from albumose—free tuberculin. 
(11) Partialantigens or Partigens. Much, Deyche, Leschke. 
These co-workers have demonstrated that the tubercle bacillus 
by means of diluted organic acids, lactic, malic, phosphuric, etc., 
can be dissociated or separated into its component parts and that 
these separated parts consist of a free fatty acid, a lipoid sub- 
stance, a toxic principle, a neutral fat, a protein product, various 
salts, etc. Their extensive research has proven that the antibodies TUBERCULIN 
315 
produced in the tuberculous individual are not of a simple nature 
but that different defense agencies are produced, differing from 
those following the injection of pure tuberculin, from those fol- 
lowing the incorporation of the neutral fat, the fatty acid or the 
other toxic components of the bacillus. They have demon- 
strated that by means of the complement fixation test and by 
testing the hypersensitiveness with these separate components, 
it is possible in every case of tuberculosis to show which partial- 
antigens are present and which are not present and it is only 
necessary to ascertain in each case which are present in or absent 
from the organism and then to supply such as are needed to 
effect a favorable result, that each component part when injected 
into an animal or the human body is capable of producing dis- 
tinct, definite and specific antibodies in the organism so injected, 
that these bodies or antigens are specific for each individual 
antibody and that the tuberculously infected person with a pul- 
monary lesion is in dire need of these antigens to produce in the 
infected organism the necessary antibodies to cope with the 
invasion. If all are absent, the combined partialantigens must 
be employed to bring about the necessary antibodies.1 
(12) Friedmann’s (89) Prophylactic and Curative Vaccine, 
(so-called) or the Friedmann Remedy. This dates back to 1902 
and 1903 when he experimented with a bacillus passed through a 
turtle (161). These organisms are supposedly avirulent; live, 
natural bodies. If they are human bacilli attentuated by repeated 
passage through cold blooded animals, like a turtle, or if they are 
really cold blooded animal bacilli, has not been determined sat- 
isfactorily. Nothing definite is known, it is still in the experi- 
mental stage and while it finds some friends it has also found 
many who are not friendly, however, from the literature, we have 
learned that what can be achieved with this remedy can be se- 
xThe tubercle bacillus is dissociated under the influence of lactic acid 
into a soluble (L) and into an insoluble (R) Antigen. The reaction of the 
soluble (L) is dependent upon the toxin hypersensitiveness and the in- 
soluble or (R) upon immune body sensitization. According to Much, 
the soluble portion (L) of the bacillus is very fatal to guinea pigs, not so 
the insoluble (R) or residual portion. The soluble (L) portion is a 
pure tuberculin. The insoluble (R) portion is further devisible into 
products designated respectively A. F. & N. With R or the products 
of R, the body’s immunization activities can be increased and the toxin 
hypersensitiveness decreased. A specific odoriferous body has also been 
isolated. 316 
CLINICAL TUBERCULOSIS 
cured with the products of the ordinary tubercle bacillus. In 1913 
the Friedmann Remedy was first heralded as a tuberculosis cure 
since which time and up to the present it has been extensively 
used by many clinicians of repute, still we have no proof of its 
special curative properties. 
(13) The Serum Therapy. (1) Maragliano’s Serum. An attempt 
at a cure or arrest of the tuberculous process by means of passive 
immunization, by serum therapy. Maragliano maintains that 
it is made possible by means of serum injections to produce spe- 
cific antibodies and also to immunize the organism against tuber- 
culosis. Horses or cattle are treated first with avirulent and then 
later with moderately virulent tubercle bacilli. After a prolonged 
treatment a serum is secured similar to the method in use for 
preparing diphtheria antitoxin. 
(2) Marmoreck’s Serum. A serum similar to the above but 
with slight modification, which has had a fairly good run of suc- 
cess. It has been proven that in a measure it is possible by pas- 
sive immunization to inhibit the tuberculous process. 
The use of Tuberculin—(a) therapeutically; (b) diagnostically. 
Indications and Contra-indications. (72) (75) (76) (79). 
(A) Therapeutic Indications 
In the use of tuberculin for therapeutic purposes, the object 
desired is to bring about a destruction, if possible, of the 
tubercle bacillus, to inhibit its growth, to stop the toxin forma- 
tion,—in short to bring about bacteriolysis. 
Tuberculin, like all other therapeutic agents, has its limita- 
tions and can be used in some cases for good, in others, and this 
by far the greater member, for bad; hence, it more often has no 
place in the treatment of tuberculosis. If the human organism is 
supplied with more than sufficient tuberculin from within, that 
is, produced within the body, then it is absolutely useless and 
even harmful to supply more from without; this means that each 
case must be carefully studied before we give tuberculin. The 
therapeutic use of tuberculin is usually indicated in two classes 
of cases: 
1. In the Presence of Localized Colonies. Here the lesion is 
generally not active, and there is little or no extension of the 
process, hence little or no production of tuberculin within the 
body. As a consequence there is no absorption of toxin, no toxin 
in the circulating blood and no body changes. This we find TUBERCULIN 
317 
usually in tuberculosis of the glands, in bone and joint disease 
and in lupus. With such lesions the process generally does not 
heal because body changes have not taken place, no bacteriolysis 
being present, or if present, insufficient in amount to check the 
slow extension of the process. In such cases the use of tuber- 
culin is indicated to excite the production of lysins. 
2. In Generalized Tuberculosis. If autotuberculin absorption 
is taking place, tuberculin is contraindicated and must not be 
used because there is already too much tuberculin from within 
in the body. This is usually in cases having night sweats, high 
temperature and rapid pulse, where with rest and quiet a lessen- 
ing of tuberculin absorption may be brought about to control an 
autotuberculin absorption. 
In beginning cases, old tuberculin may be used successfully if 
not accompanied by much fever. Bacillen Emulsion is generally 
indicated in second and third stage cases; hence, tuberculin may 
be used in the beginning or in progressive cases if we always 
carefully bear in mind what we desire to accomplish. 
When, How and How Long Should Tuberculin Be Administered? 
Different views are entertained by various therapeutists as to 
the length of time that a tuberculin medication is to be con- 
tinued.2 There exists also a difference of opinion as to the re- 
action; should tuberculin be given with (52) the aim of produc- 
ing a slight reaction or should we always stay within the limits, 
strictly avoiding a reaction. 
Petruschky begins with small minute doses, gradually increas- 
ing until fairly large doses are given. This he continues for a 
period of three months, after which for a like period no tuber- 
culin is administered. Then, in a similar manner, tuberculin in 
fairly large doses is again given for three months and discon- 
tinued for three months and so on for a period of two years. 
Sahli begins with minute doses, the initial dose being 1/100 
mg., gradually increasing the dose till large doses are given, 
avoiding at all times a local reaction and a rise in temperature; 
however, should there be a rise in temperature during the treat- 
ment, the dose must be lessened by one-half the dose which pro- 
duced the disturbance. The treatment may then be continued in 
2A person who is hypersensitive to tuberculin if treated with fairly large doses may have 
such a severe reaction as to result in most dire consequences. An active and hypersensi- 
tive tuberculous individual if given a 1/20 millimilligram or less of tuberculin, may show 
within six to twenty-four hours a distinct systematic disturbance, malaise, rapidity of the 
heart’s action, depression of spirits, rapid respiration with increased expectoration, in fact 
a sudden and severe aggravation of all symptoms. 318 
CLINICAL TUBERCULOSIS 
this manner for a period of months and even years or the treat- 
ment may be discontinued for some time and then again resumed. 
Lowenstein, among others, entertains opposite views. He ad- 
vocates the giving of tuberculin to a point of producing a re- 
action. We do not yet know if the giving of tuberculin which is 
followed by a reaction is favorable to connective tissue forma- 
tion, as is so vigorously maintained by some, or if it favors the 
propagation and extension of the tuberculous process, as is the 
opinion of others; however, it is a much safer and wiser plan to 
stay within the limits of a reaction, to avoid reactions; large 
doses are dangerous whereas small doses are often very bene- 
ficial. 
There may be a pseudo lessening of the temperature curve 
following the use of fairly large doses of tuberculin, but a pulse 
frequency, loss in weight, dyspnoea and nausea give evidence of 
the liberation of large amounts of endotoxins from bacteriolysis, 
all indicative of overstimulation. 
As a therapeutic remedy for the treatment of tuberculosis, 
tuberculin can not be considered a specific. It is no more a 
specific remedy than are the other agencies in use. The dietetic- 
hygienic, the fresh air and all other remedies at our command 
are just as specific as any in aiming to bring about active im- 
munization. 
In the treatment of tuberculous disease, when the process is 
still localized, the method as first suggested by Wright finds 
its best application. Here the object is to produce a mild 
immunization without tolerance. By this, the Wright method, 
tuberculin is first given in minute doses every 4th or 6th day, 
the dose being gradually increased until a dosage is reached at 
which the individual expresses a feeling of well being, after 
which this same dose is maintained for some time. This is the 
patient’s proper dose, “the tonic dose.” In generalized tuber- 
culosis, however, the method of Koch is the one usually em- 
ployed. This is giving tuberculin with tolerance; by this method 
tuberculin is administered progressively until enormous amounts 
are given even up to the point of giving pure tuberculin. At the 
present time most therapeutists are giving tuberculin in all and 
every form of tuberculous disease according to the former, the 
Wright method, selecting the “Tonic dose” which may be given 
for long periods, almost indefinitely, for months and even years. 
In administering tuberculin we must bear in mind that the ob- TUBERCULIN 
319 
ject sought is the bringing about of a toxic immunity, an im- 
munity against the patient’s produced body tuberculin but not 
against his tuberculosis, because we do not make him tuber- 
culosis immune. 
If, in cases of generalized tuberculosis, tuberculin is used at 
all, it should be given in the interim between the exacerbations 
and remissions. If at all it is then most effective and if bene- 
ficial, is followed by an immunizing response, a feeling of well 
being. The infected individual as well as the actively diseased 
is generally very sensitive to tuberculin, is tuberculin sensitized; 
this must always be borne in mind when using this agent. 
In the use of tuberculin for therapeutic purposes all forms 
have been tried from old tuberculin down to the newer sera. 
When given as a curative remedy, tuberculin as an initial dose is 
usually applied in the most minute dilution. The introduction of 
tuberculin into medicine was hailed as a remedy of great prom- 
ise ; it was thought that at last a remedy had been discovered 
which would cure tuberculosis. The fiasco following its induc- 
tion as a therapeutic agency is still fresh in the memory of many, 
but gradually after a better understanding concerning the action 
and possibilities of this valuable drug, it found its proper level, 
and at the present time it is chiefly used in therapy, as an addi- 
tional measure for the control of this disease, mainly as a help as 
a tonic or stimulant in the treatment. 
Tuberculin in itself never has, never can and never will cure a 
case of tuberculosis, but it is a most valuable adjunct in the fight, 
if aligned with fresh air, good food and out-of-door life, etc. In 
specially selected cases its use is undoubtedly indicated. The be- 
ginning dose must always be a small one and the dosage must 
be most accurate. The method of administering is with the 
hypodermic needle. Whereas tuberculin for diagnostic purposes 
is given cutaneously, percutaneously and intracutaneously, for 
therapy it should be given subcutaneously, under, and not into 
the skin.3 
The Methods of Administration 
After having selected a case of pulmonary tuberculosis for 
treatment, or for that matter any form of the disorder, we usually 
to active tuberculous individuals tuberculin is given subcutaneously in 
fairly large doses to test the patient’s tolerance, his sensitiveness. This should not be 
construed as giving tuberculin diagnostically. In such instances the diagnosis has been 
definitely made, no need of tuberculin to aid us . in the diagnosis. Here the test is only 
given with the object of testing the patient’s tolerance to tuberculin, his immunizing 
activities. 320 
CLINICAL TUBERCULOSIS 
begin by giving a very small quantity, say 1/20, 1/10, 1/2 or 
perhaps in exceptional cases 1 millimilligram as a first or initial 
injection. The treatment is repeated at first every 4th day, giv- 
ing 2/10, then 3/10 then 4/10 millimilligrams and so on, always 
with gradually increasing dosage. After 14 or 16 injections have 
been given, the remedy should be administered every 7 days, and 
after continuing the treatment for some time the interval be- 
tween injections may be lengthened, giving a treatment once in 
2 or perhaps 3 weeks, or the treatment may be entirely sus- 
pended for a while, say for a month or two when a similar pro- 
gressive course may be given. If during the treatment, say after 
a dozen or more doses have been administered, a reaction should 
follow the last injection, then it is usually customary to drop 
back to half the dosage which caused the reaction and give that 
amount at the next treatment, then gradually increasing the 
dosage until fairly large doses are given, watching the effect 
after each treatment. Always remembering that the use of 
tuberculin for therapeutic purposes is directly in opposition to 
the activity of the disorder, that if the disease is pursuing a very 
slow, a more or less protracted course with little or no fever, 
pulse not very rapid and showing a tendency to fibroid tissue 
change, the therapeutic use of tuberculin may be of great value; 
if, however, the tuberculous process is very active or exacerba- 
tions and remissions follow each other in rapid succession or if 
the disease shows a very stormy tendency, the tuberculin must 
not be used—is strictly contraindicated. 
Tuberculin in the treatment of pulmonary tuberculosis has not always 
fulfilled all the anticipated requirements of a therapeutic remedy. We 
must remember that the tuberculously infected and the diseased indi- 
vidual suffering from an active, chronic disorder is very frequently not 
in need of any more antigens because his own body supplies him with 
a* amount sufficient over and above all requirements of his body in the 
l>' t. Here the body is not in need of more corpuscles, possessing pro- 
le " splitting properties, but it requires above all such agencies as will 
produce lipolysis, and the stimulus or antigens necessary for that is not 
contained in the tuberculin, either old or new; hence, the great failure of 
a tuberculin impression being followed by very favorable results. 
We recognize usually three phases of tuberculin administra- 
tion: (1) the tolerant; (2) the stimulating and (3) the toxic or 
exciting. In mild cases, a slightly positive tuberculin reaction is 
a favorable sign. If the reaction during the process of the dis- 
ease becomes negative, this also is a favorable indication; how- TUBERCULIN 
321 
ever, in progressive cases a negative reaction presages an ap- 
proach of death. A tuberculin reaction indicates that the re- 
acting individual is either already clinically tuberculous, that is, 
diseased, or that a previous infection has immunized him, and 
although a reaction is present he is clinically healthy. 
Occasionally while using tuberculin therapeutically, even in 
very minute doses, the injection may be followed by a very 
severe reaction, and we must not at once conclude that the sub- 
ject is hypersensitive. In the use of tuberculin as is now in 
vogue, six separate dilutions of this powerful drug are by com- 
mon usage recommended, each one ten times stronger than the 
one next in order, and it is more than evident that in the use of 
such a potent remedy if we should give to a suspected person 
one milligram tuberculin equal to 1/60 grain for diagnostic pur- 
poses and then a moment after, using the same hypodermic 
syringe, give to another patient one-tenth of a millimilligram 
equal to 1/600,000 of a grain that untoward effects may manifest 
themselves; hence, a separate syringe should be used for each 
separate dilution. 
Begin the Treatment with Very Minute Doses 
The question has often been asked why we begin with such 
minute, infinitesimal doses in order to safely influence the tuber- 
culous person. I cannot do better than to direct your attention 
to a graphic picture which I have so often used to explain this 
phenomenon: 
Qj, 
& 
a 
37. 
& 
Fig. 43. Illustrating the degree of tuberculin tolerance between four infected individuals 
when compared with the non-infected. 322 
CLINICAL TUBERCULOSIS 
Let the lines, A, B, C, D and E represent five patients, and let 
A represent a person who has never been infected with the virus, 
while B, C, D and E represent tuberculously infected individuals. 
A, never having been infected is tolerant to enormously large 
doses, is not sensitized and will tolerate from one to ten centi- 
meters or more of any of the solutions in our series, but not so 
B, C, D or E, who have been infected, and having been infected, 
they are more or less sensitized, but we do not know up to which 
point or to what dosage. We know A’s tolerance, but we have 
up to the present time no positive knowledge about the tuber- 
culin tolerance of either B, C, D or E, the infected persons. Let us 
assume then that B’s tolerance ceases at X, and if by any sure 
means we could ascertain that, we could begin our tuberculin 
medication a little short of that point and gradually encroach on 
sensitiveness, but we have no absolute way of knowing this in ad- 
vance, and for that reason we must begin at the extreme end and 
give the most minute quantity, and slowly and gradually ad- 
vance the dose. C’s tolerance is at Y, and D’s at Z, and the same 
applies as in B’s case. E is also tuberculously infected, but is so 
much sensitized that he will not tolerate the most minute quan- 
tity of our dilution of 1-1,000,000, and we can encroach on his 
sensitized state only by repeated minute injections and that at 
long intervals; it is for this reason that in all the four given cases 
of infected persons the initial therapeutic dose should be in- 
finitesimally small so as to ascertain the individual’s tolerance; 
when once that has been established correspondingly larger doses 
may be given.4 
Tuberculin is a most valuable and reliable therapeutic agent 
for the treatment of tuberculosis if properly administered. Its 
use must cover a long period of observation. It is not a cure, 
does not bring about true immunization, but does produce stim- 
ulating activities in the organism. It is simply a most valuable 
adjunct in our armamentarium. In giving tuberculin to an in- 
dividual, we first must be sure that he or she is really tuber- 
culous. The statement has been made by some therapeutists 
that those patients usually do best, are more readily healed, un- 
der tuberculin medication in whom the tubercle bacillus can not 
be demonstrated, that is in the closed and not in the open cases, 
4During the course of tuberculin therapy, the cutaneous reaction often becomes negative. 
This then is an indication that the tubercu'ous process is becoming arrested. With a 
reactivation of the process, however, the skin reaction may again become positive, hence 
during specific treatment the dermal reaction may become alternately positive and nega- 
tive or vice versa. TUBERCULIN 
323 
but here the question arises whether they actually had tubercu- 
losis, and even with physical signs present it may still leave a 
doubt. 
Various Other Therapeutic Methods for Administering Tuberculin 
The giving of Tuberculin therapeutically by means of the hypodermic 
syringe (subcutaneously) is not the only method of tuberculin medica- 
tion. There are many other serviceable methods now in vogue, some of 
which may be equal or even superior to a subcutaneous injection. The 
Mantoux or intradermal method, so successfully used in the application 
of tuberculin for diagnostic purposes, may also be applied to the prin- 
ciple of treatment. Produce a Mantoux upon the cleansed cutaneous 
surface of the upper arm of the tuberculous individual using Yio cc 
No. 5 Standard Solution and carefully note the result of this first applica- 
tion. If a slightly hyperemic area is noticeable then in seven days from 
the time this first intracutaneous injection was given, a similar amount or 
Yio cc No. 5 should again be given. Should the second cutaneous medica- 
tion prove similar to the first then in seven days give another Yio cc, No. 5. 
This dosage of Yio cc No. 5 may be repeated a number of times and be 
continued until no inflammatory area is noticeable at the point of appli- 
cation when with the next medication we use 0.1 cc, No. 4 and proceed 
as with No. 5. By this method the tuberculous individual often becomes 
rapidly tolerant to fairly large doses of tuberculin, expressing a feeling 
of well being, not so quickly acquired by the ordinary subcutaneous 
injection method. This treatment may be maintained for some time 
and after an interval or period of rest a second similar course may be 
given. It is not necessary to continue with the treatment until large 
doses are given. I have never given a dose higher than Yio cc, No. 3. 
The same rule applies here as in all other methods of tuberculin medi- 
cation, that is, if during the course of treatment the intracutaneous injec- 
tion is followed by much inflammation, perhaps also systematic disturb- 
ances then it is advisable to discontinue the method altogether for some 
time or drop back to a lower dilution. This method of tuberculin medica- 
tion has proven most satisfactorily in treating tuberculous disease of the 
eye, skin, cervical glands, joints, etc. 
Within current years the use of tuberculin for therapeutic purposes by 
the Ponndorf Method of Cutaneous Vaccination (83) has found much 
favor, and judging from the available literature, the results appear most 
promising, the method most rational, even to a point of supplementing 
all the other methods of treatment. The upper arm of the tuberculous 
individual is thoroughly cleansed, sponged with alcohol, then scarified 
with an ordinary v. Pirquet scarifier or preferably a hypodermic needle 
with not too sharp a cutting edge. Make upon this so prepared surface 
of the skin from 10 to 20 or more linear scarifications about 2 (5 cm) 
inches in length (parallel lines) and about Yio (2 mm) inch apart. Do 
not scarify deep nor draw blood, just sufficient to denude the surface of 
the skin and upon this so prepared area place a drop of O. T. or B. C., or 
T. R., or any form of pure tuberculin and with the middle finger of the 
right hand, well protected with a sterile rubber finger cot, rub the tuber- 324 
CLINICAL TUBERCULOSIS 
culin well into the abraded surface. A glass rod with a rounded end or a 
small test tube will answer the purpose just as well. Now cover this 
tuberculinized surface with waxed paper securely held in place by a few 
strips of adhesive plaster allowing it to remain for 24 hours. A word of 
precaution. It is well known that very sensitive individuals will react 
to most minute quantities of tuberculin, hence a cutaneous vaccination 
using pure tuberculin may be followed by most distressing consequences. 
In order to avoid such unpleasant occurrences, it is best first to test the 
individual’s tuberculin susceptibility; this can readily be accomplished 
by making a v. Pirquet or a Mantoux before beginning the tuberculin 
therapy by the vaccination method. If the probationary test is very 
positive, then the cutaneous medication must be given very cautiously, 
probably making only a few scarifications and using only a minute quan- 
tity of tuberculin, or better, postpone the treatment for a month how- 
ever, if the probationary test is found fairly positive then in about one 
wreek after, the vaccination may be made. These vaccinations should be 
repeated but once in 21 days or even at longer intervals and usually not 
more than 10 such scarifications are necessary. The results obtained by 
this method of treatment are often more than phenomenal. 
Another method of tuberculin medication should here be mentioned. 
One first suggested by Petruschky, namely a 1% tuberculin, glycerin 
solution. A drop of this mixture is placed upon the previously cleansed 
skin of the arm, back, or chest, is well rubbed in and no covering applied. 
A drop may be so applied every other day for an indefinite period. I have 
seen most satisfactory results follow this form of medication when ap- 
plied to small children suffering from tuberculous peritonitis, in tubercu- 
lous skin lesions, in tuberculosis of the cervical gland and for the after 
treatment'in surgical tuberculosis. 
(B) Contraindications in the Use of Tuberculin 
Much harm can be done if tuberculin is used in cases in which 
it is strictly contraindicated. Tuberculin should never be used 
if in a tuberculous individual the fever is very high, showing 
toxin absorption, nor if the tuberculous process is massive, show- 
ing great pulmonary involvement, or in suspected mixed infec- 
tion. It should not be used if both lungs are the seat of much 
disease, if the disease is pursuing a rapid course, the pulse very 
rapid, nor in hemorrhagic cases. In diabetes and nephritis, if 
complicating pulmonary tuberculosis, the use of tuberculin is al- 
ways contraindicated. In tuberculous subjects suffering from an 
accompanying neurasthenia, epilepsy or cirrhosis of the liver, 
tuberculin must not be used. It is very dangerous to use tuber- 
culin if measles, influenza or pneumonia preceded the active 
tuberculous process. In diffuse tuberculosis without expectora- 
tion, tuberculin as a therapeutic measure must not be employed, 
and tuberculosis and cardiac complications are always signs for TUBERCULIN 
325 
inhibition; hence, in all the above enumerated conditions it is 
advisable not to use tuberculin; it is strictly contraindicated. 
Tuberculin for Diagnostic Purposes 
Although tuberculin as a therapeutic agent for the treatment 
of tuberculosis has its sharply defined limitations, in its use as a 
diagnostic or probationary remedy it finds its widest application. 
The characteristic value of tuberculin as a specific remedy de- 
pends upon the reaction produced on the cutaneous or mucous 
surfaces of the tuberculously infected. As previously stated (see 
page 311, this chapter) this reaction results from the presence of 
modified natural tuberculin in the epithelial cells of the skin, 
which, having great affinity for the added tuberculin, by bio- 
chemical changes produces a hyperemic area at the point of 
application; hence, in order to bring about a reaction, modified, 
natural (or artificial) tuberculin must be in the individual on 
whom the test is applied; the person must have come in con- 
tact with the virus, or its toxins at some previous time. 
In a person who has at no time come in contact with the 
tubercle bacillus or its products no reaction5 will follow even if 
very large doses of tuberculin are given, showing that it has 
toxic properties only in the infected organism and that it is 
perfectly non-toxic in the non-infected. It is in this respect that 
it possesses specific actions and it is in this sense understood 
when we refer to tuberculin as a specific remedy. 
Various kinds and different quantities of tuberculin are used 
for diagnostic purpose, some using tuberculin in its purity, others 
using it in the different dilutions. 
The Various Tuberculin Tests 
Four approved tests are now in general use. 
1. The Ophthalmic or conjunctival test. The application of 
tuberculin as a diagnostic measure to mucous surfaces is usually 
in the diluted form, and the mucous membranes of the nose, 
ear and vagina have all been used, but that of the eye alone has 
been found convenient. This is now generally known as the 
Calmette test. By means of this method, also known as the 
5In order to produce a tuberculin, reaction in the organism, the foci of infection must 
be so situated that the products of metabolism of the invading bacilli have entered the 
circulation, producing what is now generally known as a positive reaction. This condi- 
tion is in pulmonary tuberculosis almost always fulfilled, but not always so in the other 
tuberculous disorders. If there is no destruction nor products of bacillary disintegration 
and growth to enter the circulation, then there is no tuberculin reaction. The small 
amount of tuberculin applied favors encapsulation of the glands, arrest of the necrotic 
process, healing, and under strictly hygienic and dietetic treatment, improved and an 
increase in body weight. CLINICAL TUBERCULOSIS 
326 
Wolff-Eisner, a drop of diluted tuberculin 1-100 is instilled onto 
the conjunctiva of one eye, the other being used as a control. In 
a few days the treated eye will be quite hyperemic, swollen and 
irritated, while the untreated eye remains normal. This is known 
as the Calmette reaction. Clinically a positive conjunctival re- 
action points with great probability to an active tuberculous 
process, however, as a sure diagnostic sign it must not be con- 
sidered. This method is now somewhat in disfavor and is but 
little employed; in fact the mucous surfaces are very little used 
when compared with applications of tuberculin to the cutaneous 
surface. 
The application of tuberculin to the derma for diagnostic pur- 
poses is known as (1) the Moro, the percutaneous test; (2) the 
v. Pirquet, the cutaneous test; and (3) the Mantoux, the intra- 
cutaneous test. 
2. The Moro or the percutaneous test. A 50% ointment pre- 
pared by mixing intimately equal parts of lanolin and tuberculin 
O. T., is applied to a previously prepared surface of the skin. 
An area about 5 cm in diameter over the chest, abdomen or 
upper arm is thoroughly cleansed with soap and water, then with 
alcohol, and when dry the Moro ointment about the size of a 
split pea is rubbed well into this prepared surface and covered 
with waxed paper for 24 hours. A reaction, said to be positive, 
is followed within 24 to 48 hours by a reddened area slightly 
elevated, throughout which many or few more or less raised 
papules are noticeable. The reaction usually lasts a few days, 
gradually fading away and leaving a slightly pigmented spot. 
For me the Moro test is the one of choice in all small children 
up to about the fourth year. 
The tuberculin reaction in infants and small children is of 
great clinical importance. A positive reaction in a child does not 
tell us if the case is active, but in a child up to the second year 
the reaction generally indicates an active tuberculous process, 
because in children at that age the disease is always active. 
3. The v. Pirquet or the cutaneous test. This test is usually 
applied by making three slight scarifications on the upper or fore- 
arm, the cutaneous surface having been first thoroughly cleansed. 
A specially devised scarifier is generally used, but any instru- 
ment with not too sharp a cutting edge may be substituted. The 
scarifications should be made just sufficient to produce a slightly 
hyperemic point, just sufficient to denude the skin, just below TUBERCULIN 
327 
the horny layer. Three scarifications are made in a row usually 
from 2.5 to 3 cm apart and to two of these, generally the outer, 
the first and third, a minute quantity of pure tuberculin is ap- 
plied, the central scarified point being used as a control. This is 
now covered with waxed paper for 24 hours. In a positive v. 
Pirquet, an hyperemic zone 1 cm or more is usually'noticeable 
at the points of application, the control showing little or no in- 
flammation. As occasionally may happen when the scarifications 
are made too deep, the tuberculin applied areas as well as the 
control may show hyperemic areas of about equal size, which is 
due simply to the irritation to the skin, and must not be con- 
strued as a positive test. In such an event, a second test must 
be made at an interval of about a week. 
A positive v. Pirquet usually shows a hyperemic area about 
the size of a dime, the control being negligible. The v. Pirquet 
test is applicable in children from the 4th year up to the 12th, and 
perhaps to puberty but not beyond. The v. Pirquet in young 
children may be positive in only about 45% of cases to a first 
application and 65% to a second, while the next, the Mantoux, 
is positive in nearly 80% to a first test. 
4. The Mantoux, the intracutaneous or intradermal test. Is 
also described as the Esherich or Romer. This test is generally 
made by injecting into and not under the skin a definite quantity 
of tuberculin in salt solution. The amount for an initial dose is 
generally a milligram, 0.001. Many diagnosticians give as an 
initial dose, l/10th of a milligram and if no reaction is noticeable 
in 3 days, 1/2 milligram; if again there is no reaction, a full 
milligram, continuing as high as 10 milligrams; if still there is no 
reaction, the individual is pronounced non-tuberculous. Most 
adults react to a dose of 1 milligram, 0.001, a second injection is 
usually not necessary, should, however, no reaction follow this 
dosage, then the use of 2 or more milligrams is justifiable. If the 
tuberculin has been well deposited into the epithelial cells of the 
skin, generally in the tuberculously infected individual, a re- 
action will be recognizable which is distinct and specific. Usually 
within 12 to 48 hours, occasionally as late as 72, at the point of 
application a reddened area from 1.5 to 3 or more cm will be 
observed, and the area is generally surrounded by a distinct halo 
of lessened hyperemia in size from 5 to 8 or more cm. To the 
palpating finger the perception of a distinct induration under the 
skin often referred to as a “button” is imparted. The reaction 328 
CLINICAL TUBERCULOSIS 
usually begins about six hours after the injection reaching its 
greatest intensity after the second day. The induration may 
last a few days or evidence may still be noticeable in a few weeks. 
Usually, with a very positive Mantoux there is great hyperemia 
at the point of application, the temperature rises and the pulse is 
quickened somewhat, the patient complaining of malaise, want 
of appetite, perhaps a slight headache, all of which are recognized 
as more or less systemic disturbances, the accompanying cough 
giving evidence of the focal reaction. It goes without saying that 
the skin should be cleansed before giving an intracutaneous in- 
jection—alcohol usually sufficing. A typical Mantoux should be 
given, as has been so aptly stated by Carl Spengler, in a centrifu- 
gal manner, the skin being slightly raised and pitted, giving it the 
appearance of being blanched; and the injected tuberculin should 
lie about the point of the needle so that the point lies in the cen- 
ter of the produced wheal. The giving of tuberculin by mouth 
for diagnostic purposes should here be incidentally mentioned. 
Give old tuberculin in pill form in 0.05 gram dose if not systemic 
reaction is noticeable, then, after three days, give 2 or 3 pills 
of the same strength, and if no reaction follows this dosage, an 
intradermal injection should be given. By this method the pre- 
viously prepared organism responds much more readily to the 
tuberculin if given intracutaneously. 
The Negative Tuberculin Reaction 
The tuberculin reaction is negative in three classes of cases, 
first, in individuals who never came in contact with the virus 
and consequently have no defense agencies or antibodies in their 
blood plasma, second, in those who at some time in their lives 
have come in contact with the virus, and either not sufficient 
time has elapsed since the infection for the body to produce 
antibodies, or for some reason the body is not putting up a 
defense, perhaps possesses a definite immunity and is wholly 
indifferent to the invaders. Again, the reaction is negative in 
cases of active and advanced disease, much cachaxia, in such, 
the defense powers have long been exhausted, the test applied 
too late, long after the body was capable of enlisting the defend- 
ing forces against the invaders. In such individuals the artificial 
tuberculin used for the test and the natural tuberculin in the 
body are alike, hence no reaction. In the first two instances the 
test was applied too early and in the last too late to be of diag- TUBERCULIN 
329 
nostic importance. It is only when the body shows that it is 
disturbed by the invaders, is trying to throw off the infection, 
when the infection has aroused the body’s defense powers in 
either a limited or in an extensive degree, that the test becomes 
positive. Of greatest importance is the negative reaction, be- 
cause this may eliminate tuberculous disease, with the exceptions 
already mentioned above. 
To this may be added a fourth. It is a well known fact that in 
the exanthemata the tuberculin test is generally negative. A 
child just beginning to show prodormal symptoms of measles, or 
even before, if tuberculin is given intracutaneously a negative re- 
action will follow, this, then, may be utilized as a positive measle 
test. 
In this connection it may become necessary to call attention 
to the following questions often referred to: 
What is meant by a distinctly positive tuberculin reaction? 
The tuberculin test is positive6 whenever the defense agencies 
or antibodies are freely present in the economy (a good prog- 
nosis). These antibodies are most abundant in the first years of 
infection, after an attack of recurring tuberculosis and after a re- 
infection, either from without or from within. A positive re- 
action does not state what stage is present, whether a beginning 
stage or a remission. If clinical symptoms point to a tuber- 
culous process, a positive tuberculin reaction, simply confirms 
this suspicion. In infants the tuberculous process is less latent; 
hence, here a positive reaction usually indicates a tuberculous 
disease. 
What does a mildly positive reaction indicate? It indicates 
that there has been a previous infection but that the antibody 
content of the organism is not very extensive (a less favorable 
prognosis). This is frequently found in healed processes; it may 
yThe Nature of Resistance to Tuberculosis (164) 
(1) Reaction occurs only when anatomic tubercle is present in the body; 
(2) The reaction begins. to manifest itself with the establishment of the tubercle; 
(3) Up to a certain point, as the tuberculous involvement or disease progresses, the 
intensity of the reaction increases; 
(4) As the tuberculous disease heals or retrogresses, the intensity of the reaction 
lessens; 
(5) As tubercles probably are never completely eradicated from the body, the power 
to react is probably never completely lost. Hnce the following corollary: 
(1) The presence of the tubercle endows the body with power to greatly resist increased 
numbers of newly added bacilli. 
C2i) This increased resistance to reinfection manifests itself with the establishment of 
the primary focus. 
(3) Up to a certain point, resistance is proportionate to the extent and severity of the 
initial disease. 
(4) With the healing of the diseased foci, resistance diminishes. 
(5) If tuberculous disease remains, the increased power to resist is probably never 
lost entirely and does not drop to the level before first infection. (Allen K. Krause.) 330 
CLINICAL TUBERCULOSIS 
also indicate an old progressive condition (tuberculous). Tu- 
berculin in adults frequently gives but a mild reaction. The re- 
action following a previous subcutaneous tuberculin injection 
(secondary reaction) is of this order. No reaction, no sensitive- 
ness in miliary tuberculosis or in measles, croupous pneumonia 
as concomitant disorders, in tuberculous meningitis nor in cases 
incorporated with large doses of tuberculin. Most tuberculous 
individuals to whom tuberculin is administered in the usual way 
never react to the dosage; some only react when fairly large 
doses have been given. 
In giving tuberculin diagnostically and that applies to its use 
for therapy as well, the patient must be under the constant ob- 
servation of the physician. Tuberculin to be used intelligently 
must be diluted with the greatest accuracy and I will next de- 
scribe in detail this method of dilution. 
Tuberculin Dilutions 
The necessary apparatus for preparing the proper dilutions of 
tuberculin are few; one-half dozen 10 cc bottles, a graduated 10 
cc cylinder, a pipette or medicine dropper, a quantity of a normal 
salt solution to which of 1% of phenol has been added and a 
small amount, say 1 cc of pure tuberculin. 
In using the word tuberculin, O. T. or old tuberculin, the orig- 
inal tuberculin is generally understood, but any of the other 
kind may be used. After the vials which are intended to receive 
the different dilutions have been thoroughly cleansed, rinsed 
with distilled water and dried, we will be ready to proceed, grant- 
ing that the pipette, the graduated cylinder and the other neces- 
sary apparatus are also perfectly clean. Place into the 10 cc 
graduated cylinder 1 cc of tuberculin and add to it 9 cc of the 
phenolized salt solution and after all is well mixed pour it into 
one of the clean bottles at hand and label it No. 0. This is a 
10% tuberculin dilution, it is a stock solution and is seldom used 
for either diagnostic or therapeutic purposes. Next pour 1 cc 
of No. 0 into the 10 cc graduated cylinder and dilute it with 9 
cc of phenolized salt solution, place it into a clean bottle and 
label it No. 1. This is a 1% solution, the dilution most fre- 
quently used for diagnostic purposes. Now take 1 cc of No. 1, 
dilute with 9 cc of salt solution and label it No. 2; this is a 
1/10 of 1% solution. 1 cc of No. 2 and 9 cc of phenolized salt 
solution makes No. 3, a 1/100 of 1% solution. Again 1 cc of TUBERCULIN 
331 
No. 3 and 9 cc of salt solution makes a 1/1000 of 1%, or No. 4, 
and 1 cc No. 4 with 9 cc of salt solution is known as No. 5, equal- 
ing a 1/10,000 of 1% solution. No. 5 usually furnishes the initial 
doses when tuberculin is given therapeutically. A 1/10 cc of 
this solution No. 5 equals 1/100,000 of 1%, being the first dose. 
Occasionally it is advisable to begin with still smaller doses, 
when 1/20 of a cc is given as the beginning dose. In labeling 
the bottles from 0 to 5, no special reason can be given for this 
designation; a 1 to 6 labeling may be just as proper, it is only 
that originally I began making dilutions from 0 to 5 and this I 
have ever since maintained. 
Fig. 44. Tuberculin Dilutions. Standard Scale, 
As to dosage, begin by giving 1 / 10th cc of No. 5 and observe 
whether there is any reaction, always remembering that ex- 
tremely hypersensitive individuals may react to a most minute 
dose; if there is no reaction, in about 4 days, give 2/10 of No. 5, 
always watching; after 4 days more give 3/10, 4 days more 4/10, 
and so on until 9/10 cc of No. 5 have been given. Now with the 
10th treatment we do not give a full cc of No. 5, but 1/10 cc 
of the next dilution, No. 4; this is because 1/10 of No. 4 equals 
a full cc of No. 5; by giving the former we simply lessen the 
amount of fluid to be injected. We now continue in a similar 
manner with the solution No. 4 as we did with No. 5, perhaps 
giving the injection less often, say once in 5 or 7 days until the 
9th dose of No. 4 has been given, when with the next dose we 
give 1/10 cc of No. 3 in place of a full cc of No. 4. We con- 
tinue with No. 3 in like manner and by this progressively in- 
creasing dosage it is often possible to reach a dosage of pure tu- 
berculin in full cc of No. 0. This, however, is not advisable. If 
the patient is tolerant to a dosage when No. 2 is reached, it is 
good practice to discontinue all further treatment for a few 
months and then repeat the medication. 332 
CLINICAL TUBERCULOSIS 
In giving tuberculin therapeutically, we aim to be within the 
limits of a reaction, within tolerance, for diagnostic purposes, 
however, our purpose is to bring about a reaction. If during the 
course of tuberculin therapy the patient is doing well, the pulse 
rate somewhat reduced, temperature within the normal for a tu- 
berculous individual, and he expresses a feeling of well-being, 
then the dosage at the time this is observed may be maintained, 
giving this same dose once or twice a month, or perhaps only 
monthly. This then is the individual’s tonic dose. 
It must become apparent to anyone administering tuberculin 
that after giving the drug for a comparatively short time after 
this method, enormously large doses may be given. As the 
amounts increase in 10s in each dilution and as each is 10 times 
stronger than the next lower (higher number), when No. 2 is 
reached, we are giving 1000 times the dosage, when compared 
with the initial dose. In using tuberculin dilutions according to 
the plan advocated by Prof. Beraneck, the dilutions rise in po- 
tencies of 2 instead of 10; hence, the treatment may be carried 
on over much longer periods and more gradually. The accom- 
panying table is self-explanatory: 
Decreasing Scale 
H = T.B.K. (BeraneckTuberculin) 
G = T.B.K./2 Beraneck T. Dilution 
F = T.B.K./4 Beraneck T. Dilution 
E = T.B.K./8 Beraneck T. Dilution 
D = T.B.K./16 Beraneck T.Dilution 
C = T.B.K./32 Beraneck T. Dilution 
B = T.B.K./64 Beraneck T. Dilution 
A/1 = T.B.K./128 Beraneck T. Dilution 
A/2 = T.B.K./256 Beraneck T. Dilution 
A/4 = T.B.K./512 Beraneck T. Dilution 
A/8 — T.B.K./1024 Beraneck T. Dilution 
A/16 = T.B.K./2048 Beraneck T. Dilution 
A/32 = T.B.K./4096 Beraneck T.Dilution 
A/64 — T.B.K./8192 Beraneck T.Dilution 
A/128 - T.B.K./16384 Beraneck T. Dilution 
A/2S6 = T.B.K./32768 Beraneck T.Dilution 
A/512 = T.B.K./65536 Beraneck T.Dilution 
A/1024 = T.B.K./131072 Beraneck T.Dilution 
A/2048 = T.B.K./262144 Beraneck T.Dilution 
A/4096 = T.B.K./524288 Beraneck T.Dilution 
etc. if desired 
Beraneck Scale 
Increasing Scale 
A/16384 Beraneck T. Dilution 
A/8192 Beraneck T. Dilution 
A/4096 Beraneck T. Dilution 
A/2048 Beraneck T. Dilution 
A/1024 Beraneck T. Dilution 
A/S12 Beraneck T. Dilution 
A/2S6 Beraneck T. Dilution 
A/128 Beraneck T. Dilution 
A/64 Beraneck T. Dilution 
A/32 Beraneck T. Dilution 
A/16 Beraneck T. Dilution 
A/8 Beraneck T.Dilution 
A/4 Beraneck T. Dilution 
A/2 Beraneck T. Dilution 
A Beraneck T. Dilution 
B Beraneck T. Dilution 
C Beraneck T. Dilution 
D Beraneck T. Dilution 
E Beraneck T. Dilution 
F Beraneck T. Dilution 
G Beraneck T. Dilution 
H (Tuberculin Beraneck) 
A Y-2, syringeful of any dilution equals in amount a whole 
syringeful of the next, in the decreasing scale. In using Bera- 
neck’s tuberculin, each cc is again divided into 1/5 cc (or 1/10 
if desired), giving 5 doses before giving the next higher solu- 
tion. TUBERCULIN 
333 
The approximate value of Beraneck’s tuberculin B. T. K. and 
the various dilutions is expressed in cc, grams, grains and frac- 
tions thereof, as follows: 
H = B.T.K. 1 cc = 1 grm. = 15 grs. (approximately) 
G = B.T.K./2 1/2 cc = 1/2 grm. = 8 grs. (approximately) 
F = B.T.K./4 1/4 cc = 1/4 grm. = 4 grs. (approximately) 
E = B.T.K./8 1/8 cc = 1/8 grm. = 2 grs. (approximately) 
D — B.T.K./16 1/16 cc = 1/16 grm. = 1 gr. (approximately) 
C = B.T.K./32 1/32 cc = 1/32 grm. = 1/2 gr. (approximately) 
B = B.T.K./64 1/64 cc = 1/64 grm. = 1/4 gr. (approximately) 
A — B.T.K./128 1/128 cc = 1/128 grm. = 1/8 gr. (approximately) 
A/2 — B.T.K./256 1/256 cc = 1/256 grm. = 1/16 gr. (approximately) 
A/4 = B.T.K./512 1/512 cc = 1/512 grm. = 1/32 gr. (approximately) 
A/8 — B.T.K./1024 1/1024 cc = 1/1024 grm. = 1/64 gr. (approximately) 
A/16 ~ B.T.K./2048 1/2048 cc = 1/2048 grm. = 1/128 gr. (approximately) 
A/32 — B.T.K./4096 1/4096 cc = 1/4096 grm. = 1/256 gr. (approximately) 
A/64 — B.T.K./8192 1/8192 cc = 1/8192 grm. = 1/512 gr. (approximately) 
A/128 = B.T.K./16384 1/16384 cc = 1/16384 grm. = 1/1024 gr. (approximately) 
A/256 = B.T.K./32768 1/32768 cc = 1/32768 grm. = 1/2048 gr. (approximately) 
A/512 = B.T.K./65536 1/65536 cc = 1/65536 grm. = 1/4096 gr. (approximately) 
A/1024 = B.T.K./131072 1/131072 cc = 1/131072 grm. = 1/8192 gr. (approximately) 
A 12048 = B.T.K./262144 1/262144 cc = 1/262144 grm. = 1/16384 gr. (approximately) 
A/4096 B.T.K./524288 1/524288 cc = 1/524288 grm. = 1/32768 gr. (approximately) 
Ad infinitum. 
In administering tuberculin therapeutically the standard dilu- 
tions mentioned should be given in gradually increasing dosage. 
This increase must be a steady one so as to avoid any untoward 
disturbances such as are occasionally observed in the treatment. 
Tuberculin, being a remedy of great potency, may produce very 
alarming symptoms in an individual who is not tolerant to the 
drug. In using the ordinary or standard dilutions now in gen- 
eral use, only too frequently very large, even enormous amounts 
are given after comparatively few injections. If in a given case 
we begin the treatment, as is usual, with a very minute dose, say 
1/10 cc of No. 5, which is equal to l/10th of a millimilligram, 
and then writh each succeeding dose we gradually increase this 
amount, we will, when given the 19th injection, have adminis- 
tered a dosage equal to 100 times that of the initial dose; hence, 
the intervals of dosage must now be lengthened and the results 
carefully observed. Note the rapid increase: 
The Standard Tuberculin Dosage 
The 1st injection of No. 5 or 1/10 cc = 0.000.000.1 = 1/10 mmg. 
The 2nd injection of No. S or 2/10 cc = 0.000.000.2 = 2/10 mmg. 
The 3rd injection of No. 5 or 3/10 cc — 0.000.000.3 = 3/10 mmg. 
The 4th injection of No. 5 or 4/10 cc = 0.000.000.4 = 4/10 mmg. 
The 5th injection of No. 5 or 5/10 cc = 0.000.000.5 = 5/10 mmg. 
The 6th injection of No. 5 or 6/10 cc = 0.000.000.6 = 6/10 mmg. 
The 7th injection of No. 5 or 7/10 cc = 0.000.000.7 = 7/10 mmg. 
The 8th injection of No. 5 or 8/10 cc = 0.000.000.8 = 8/10 mmg. 
The 9th injection of No. 5 or 9/10 cc = 0.000.000.9 — 9/10 mmg. 
The 10th injection of No. 5 or 10/10 cc = 0.000.001.0 = 1 mmg. but 
one cc of No. 5=1/10 cc of No. 4, and so instead of giving a 
full cc of No. 5 we give only a 1/10 of a cc of No. 4 as its 
equivalent and then we proceed as before. 334 
CLINICAL TUBERCULOSIS 
The 10th injection is from No. 4 (1/10 cc) =0.000.001; this 
equals in amount 10 times the quantity given with the first in- 
jection. 
The 11th injection is 2/10 cc from No. 4 = 0.000.002. This, 
however, does not equal 11 times the initial dosage but 20 times 
that amount. 
Next, the 12th injection from No. 4 = 3/10 cc = 0.000.003 — 
30 times and not 12 times the initial dosage, and 
the 13th injection from No. 4 — 4/10 cc = 0.000.004 = 40 times (the initial dose) 
the 14th injection from No. 4 = 5/10 cc = 0.000.005 = 50 times (the initial dose) 
the 15th injection from No. 4 = 6/10 cc = 0.000.006 = 60 times (the initial dose) 
the 16th injection from No. 4 rr 7/10 cc = 0.000.007 — 70 times (the initial dose) 
the 17th injection from No. 4 — 8/10 cc = 0.000.008 = 80 times (the initial dose) 
the 18th injection from No. 4 ~ 9/10 cc = 0.000.009 = 90 times (the initial dose) 
the 19th injection from No. 4 = 10/10 cc = 0.000.010 ”100 times (the initial dose) 
but 10/10 cc (or 1 cc) from No. 4=1/10 cc from No. 3, and if we 
proceed as before, then the 28th injection would be 10/10 of No. 
3 or 1/10 of No. 2. This amount would equal 1000 times the first 
or initial injection. The 37th6 injection would be 10/10 of No. 2 
or 1/10 of No. 1, and this amount would equal 10,000 times the 
first dose. The 46th injection would equal 100,000 times the 
initial dose and 1/10 cc the 55th injection 1,000,000 times the 
initial dose or pure tuberculin. 
For table of Standard Tuberculin Dilutions, see Page 542. 
6Note: The students’ attentions are specifically directed to these figures. They are 
intended to illustrate here simply the rapid rise in the tuberculin dosage and not intended 
for actual use or medication. Such enormous doses never have and never can be given; 
this would be a dangerous and an irrational and impossible therapy. CHAPTER 25 
TUBERCULOSIS AND PLEURISY 
Tuberculous Pleurisy. Pleuritis Tuberculosa. Idiopathic 
Pleurisy. Pleuritis Idiopathica 
General Consideration. (47) If a tuberculous pleurisy mani- 
fests itself without accompanying inflammatory conditions then 
only the formation of tubercules is present. This is often ob- 
served in generalized miliary disease as an accompanying miliary 
tuberculosis of the pleura. An idiopathic tuberculous pleurisy 
in the course of chronic pulmonary disorder is the most frequent 
phenomenon. In this two forms are recognized—a dry or sicca 
and a moist or humida. (a) The dry form favors the apices, the 
paravertebral areas and at the bases the lateral regions (bor- 
ders). This may be either circumscribed or cover quite exten- 
sive areas. In this the exudate is generally fibrinous and may be 
reabsorbed or as most frequently happens, connective tissue scar 
formation takes place, producing adhesions of the two pleural 
surfaces, or if much thickening results, may undergo calcifica- 
tion or extensive adhesions between which more or less fluid may 
be sacculated, (b) In the other, the moist, the fluid may be 
either serous, sero-fibrinous, purulent or hemorrhagic. The ser- 
ous fluid in the pleural cavity is usually the result of an inflamma- 
tory process of toxic origin and not due to the presence of the 
tubercle bacillus. In the sero-fibrinous form fibrinous flakes, yel- 
lowish in color, are mixed with the serum, and in this fluid tu- 
bercle bacilli are usually demonstrable. The quantity of serous 
or sero-fibrinous fluid may vary from one hundred to many thou- 
sand cc; in fact, the fluid in the pleural cavity may be sufficient 
in amount to compress the lung completely, dislocate the heart, 
liver spleen and diaphragm, more or less adhesions between 
the lungs and other viscera take place and if the fluid is 
incompletely absorbed, new tissue develops consisting of con- 
nective tissue and blood vessels, the inevitable consequence 
resulting in a pleural thickening of 1 to 2 cm. A purulent tuber- 
culous pleurisy, a tuberculous empyema, results either from the 
335 336 
CLINICAL TUBERCULOSIS 
presence of the tubercle bacillus or from pus germs in the pleural 
cavity, however, it frequently happens that the pus is sterile, 
that is, free from all foreign organisms. In such instances the 
presence of the pus is usually the result of a chemical toxin. 
The Frequency of Tuberculous Pleurisy. A great diversity of 
opinion exists among the various authors as to the frequency of 
a tuberculous pleurisy. Many good observers maintain that per- 
haps only about 10% of all pleurisies are tuberculous, while, on 
the other hand, equally good clinicians state that nearly all are, 
and Landouzy among others opines that at least 98% are tuber- 
culous, whereas Osier has made the terse expression, “that the 
more I see of pleurisy the more I become convinced that 
they are all tuberculous.” However, that may be, close observa- 
tion has undoubtedly proven that idiopathic pleurisies, in more 
than 95% as a rule, are followed by active tuberculous disease 
within the first five years. Tuberculous pleurisy it may be stated, 
is always or perhaps most frequently secondary to a pulmonary 
tuberculous disease. It must be admitted that pleurisy may 
accompany tuberculosis of the bronchial glands, Pott’s disease, 
a tuberculous peritonitis, may even be hematogenous, etc., and a 
possibility of a primary tuberculous pleurisy may be anticipated 
from penetrating thoracic wounds, carrying infection directly 
into the pleural cavity. In all those cases in which an apparent 
idiopathic pleurisy existed previously to a pulmonary tubercu- 
losis, the lung disease was either latent or it was not earlier 
recognized. Men are more prone to a tuberculous pleurisy than 
are women in the proportion of 2 to 1, and seasons also play a 
very important role, there being more in the midwinter months 
and less in the fall. 
Symptoms. In miliary tuberculosis of the pleura the clinical 
symptoms are negative so long as a plastic inflammation or a 
serous exudate is absent. An apical pleurisy is usually a pleur- 
itis sicca. A dry pleurisy shows the characteristic symptoms of 
localized pain on pressure and a dry cough and the pain is in- 
creased on breathing in consequence of which the excursion of 
the chest is limited: The patient endeavors to suppress the 
cough and at the same time makes inward pressure over the 
involved pleura, or he lies on the afflicted side. In simple idio- 
pathic pleurisy with little pulmonary activity, fever is usually 
absent or else very slight, and a dry pleurisy if accompanied by 
much pain for some time is usually quickly followed by the TUBERCULOSIS AND PLEURISY 
337 
exudative or moist form; hence the course of the process may 
vary, may remain of the dry, or be followed by the moist variety, 
or the pleura may remain thickened without any adhesions, or 
both surfaces of the pleura become adherent. The most frequent 
seat of a pleuritic inflammation, the seat of predilection is in the 
axilla. 
The course of the disease. This varies greatly. In the dry 
form it may remain stationary for years, or retrograde, leaving 
only a slightly thickened pleura, or the visceral and parietal 
pleura may become adherent, or it may eventually assume the 
exudative form. The exudative form usually begins with a pain 
or stitch in the side, which is very much aggravated by coughing, 
sneezing, and breathing and as the amount of fluid increases in 
the pleural cavity, separating the two surfaces of the inflamed 
pleura, the pain subsides (indux and redux) but the dyspnea 
now generally increases, the severity of the shortness of breath 
depending upon the rapidity with which the fluid accumulates 
and upon the quantity of fluid in the pleural cavity. If, on the 
other hand, the fluid accumulates slowly dyspnea may be en- 
tirely absent even with large amounts of exudate. Pleurisy may 
not be suspected until a physical examination reveals the true 
nature of the disorder—the patient complaining only of a tired 
feeling, loss of appetite, and some gastro-intestinal distress. This 
usually in the subacute form of the disease. 
Physical Examination 
Inspection. On inspection we observe a lessened or impaired 
motion on the affected side, and owing to the pain on respiration 
the patient usually lies on this side to suppress as much as 
possible the movements of the chest. The intercostal spaces 
suffer very little change and although it is frequently stated that 
with a large exudate in the pleural cavity the intercostal spaces 
bulge, I have never observed it. 
Palpation. On palpation we observe an absence of vocal 
fremitus and a sense of fulness or inelasticity is imparted to the 
palpating finger; the intercostal muscles feel spastic. 
Percussion. The note is flat immediately over the fluid, dull 
above and becoming more or less resonant and tympanitic as we 
proceed upward, depending upon the amount of fluid in the 
pleural cavity. The percussion sounds change but little with the 
changed position of the patient, this is because the fluid is 338 
CLINICAL TUBERCULOSIS 
not free to move about in the chest cavity but is held in position 
by the inflamed and adherent pleural surfaces about the fluid; 
however, if the patient remains for some time in the changed 
position the fluid will be found to have changed also. The fluid 
in moist pleuritis is usually at a higher level in the axilla and 
lower toward the spine as well as toward th,e sternum. This 
was early pointed out by Damoiseau, Ellis, Garland, and others. 
Auscultation. In pleurisy it is most distinct and definite. In 
recent pleurisies and while the pleura is still thin, the sound con- 
duction is very clear but this changes gradually as the pleura be- 
comes thickened from fibrinous deposit, and from the increase of 
the exudate, and while vesicular sounds are not audible over the 
pleural fluid, bronchial sounds become most distinct and the 
whispering voice is that of whispering bronochophomy. In this 
respect it may simulate pneumonia very much, from which, how- 
ever, it can readily be differentiated by the absence of the tactile 
fremitus. The compressed lung above the fluid also gives bron- 
chial breathing, increase in the vocal fremitus whilst towards 
the apices increased vesicular sounds may be heard, and often a 
high and tympanitic note may be elicited on percussion and over 
the upper portions of the exudate and where the fluid layers are 
thin the egophonic voice may be heard. If the exudate is profuse 
the heart may be found dislocated or crowded toward the 
healthy side, the diaphragm is usually lowered and in right sided 
pleurisies the liver as well. 
Diagnosis. An early diagnosis is of the greatest importance in 
pleurisy although in only too many instances the first symptom 
which alarms the patient is the difficulty in breathing for which 
he consults the physician when the chest is already found greatly 
filled with fluid. Pleurisy, both the dry and the moist form, is 
usually of tuberculous origin, secondary to a tuberculous process 
in some part of the organism. It is a well known fact that micro- 
organisms other than the tubercle bacillus may cause a pleuritis, 
however, this is infrequent. A latent tuberculous process in a 
lung may show activity many years after a pleurisy, it is for this 
reason the imperative duty of the physician who is taking care 
of a case of pleuritis to inform the patient that this disorder may 
sooner or later be followed by active pulmonary tuberculosis, 
the same applies to pneumonia and to the so-called walking 
typhoid cases as well. The subjective symptoms usually ob- 
served are pain in the chest, stitch in the lung, sideache, TUBERCULOSIS AND PLEURISY 
339 
pressure symptoms and neuralgia-like apical pain. Tuberculous 
patients who are free from pain generally have an intact pleura. 
In the dry form of pleuritis a friction murmur simulating the 
creaking of leather is audible and frequently palpable as well. 
These pleural friction sounds are in general audible during the 
whole inspiratory phase and sometimes during the expiratory 
and subcrepitant rales are audible at the apices, usually at the 
end of the inspiratory act, if the bronchi are free and the air 
currents can reach the bronchiols and alveoli. Friction sounds 
are nearer to the ear more superficial than murmurs produced in 
the lungs proper. 
Differential Diagnosis. Fine crackling sounds heard over the 
lungs at their borders or in the axillary lines from the 5th to the 
8th rib may be either of pleural origin or are due to atelectatic 
or emphysematous changes in the lung proper. These latter are 
differentiated from pleural sounds which are heard through the 
whole of the inspiratory and part of the expiratory phase, by 
being heard with the height of inspiration only, they are produced 
in the pulmonary parenchyma. Harsh, interrupted or systolic 
breathing may be confused with dry pleurisy, but the pulsating 
or cardiac rhythm gives the differentiation. With pleural ad- 
hesions the friction sounds cease. Apical pleuritis is often very 
difficult to recognize. Friction sounds are usually absent and 
an early obliteration of the costal pleura the rule. Muscle sounds 
may simulate pleurisy and pain may be entirely absent or very 
slight, not especially noticeable by the patient when changes on 
the chest are observed, such as a slight prominence of the clavicle 
or the suprascapular fossa, or posterior muscle spasm or slight 
shoulder pain, perhaps a definite pulmonary involvement show- 
ing that an apical pleurisy may be suspected. In pleurisy with 
effusion the diagnosis as a rule is much easier, although cases are 
not infrequently encountered in which the diagnosis offers many 
difficulties. In moist pleurisy the fluid may appear either very 
slowly or the pleural cavity be filled with a fibrinous exudate in 
a very short time. It may be accompanied by a sharp lancinating 
stitch in the side as is usually observed in the acute form or it 
may be wholly unknown to the patient, as in the subacute form, 
where often the pleural cavity is found nearly filled with an 
exudate and the one symptom of shortness of breath on exertion 
leads to an examination. 
A paravertebral dulness, Grocco’s sign (1902) also called 340 
CLINICAL TUBERCULOSIS 
Rauchfuss’ sign (1904) demonstrable along the spine on (89) the 
healthy side if the pleural cavity of the opposite side contains 
much fluid. This dulness is present if the exudate reaches the 
height of the 8th dorsal vertebra. With lessening of the fluid 
the dulness disappears. This dulness is in the form of a triangle 
with the apex along the spine indicating the height of the fluid, 
the broad end of this triangle corresponding to the upper sur- 
face of the diaphragm. The cause of this triangular dulness 
accompanying an exudative pleurisy is the change in the per- 
cussion note along the spine from the normal. The fluid is 
present only on one side of the spine—none on the other. In per- 
cussing the thoracic vertebrae from above down, that is, from the 
first to the tenth, the note normally is usually loud and some- 
what resonant but osteal above and below these points. This is 
due to the adjacent air containing lung structure on both sides 
of the spine. If fluid is on one side in the pleural cavity the note 
changes and as the exudate compresses the lungs, the note be- 
comes gradually more flat as the fluid increases and we reach a 
lower level, the dulness extending more and more to the oppo- 
site or healthy side—the dulness along the fluid entirely over- 
shadowing that of the normal side. That this paravertebral dul- 
ness is not due to any mediastinal displacement has been corro- 
borated by numerous roentgen examinations. If rapid absorp- 
tion of the exudate takes place, Grocco’s sign is absent. In 
croupous pneumonia, although the lung is consolidated, the signs 
of paravertebral dulness are absent on the opposite side perhaps 
due to the conduction which is good in pneumonia and poor in 
pleuritis. 
The differentiation between lobar pneumonia and pleurisy. 
In both the note is dull or flat on percussion but in the 
former the vocal fremitus is increased while it is diminished or 
absent in the latter, moreover in pneumonia the onset is 
sudden, usually with a chill and high fever, soon followed by 
rusty sputa; in both there is pain, but the most distinct single 
diagnostic point is the whispering voice which is heard over both 
the consolidated area and over the pleural exudate but over the 
latter only while the pleura is still free from fibrinous deposit; 
bronchial breathing is also heard over both but somewhat more 
intensely and nearer in pneumonia than in pleurisy, but there is a 
great difference as to fremitus which is very pronounced in 
pneumonia and absent in pleurisy. If the fluid has persisted for TUBERCULOSIS AND PLEURISY 
341 
some time and the surfaces of the pleurae become thickened, 
both the whispering voice and bronchial breathing disappear and 
an entire absence of all sounds is noticeable. Baccelli’s sign 
that the whispering voice is distinctly transmitted through 
serous fluid and not through purulent is not dependable. This 
also depends upon whether the pleura is thin or thickened from 
fibrinous exudate. 
Exploratory Puncture and Paracentesis. The time has long 
since passed when a positive diagnosis of pleurisy with effusion 
was made immediately after the fluid was withdrawn. It is 
perhaps permissible, nay advisable in doubtful cases, to make an 
exploratory puncture and withdraw a few cc of fluid to confirm 
the diagnosis. The question has often been asked when is it 
advisable to withdraw the fluid from the pleural cavity? The 
general rule is that if the patient is in great distress, is extremely 
dyspneic and the fluid fills the greater portion of the pleural 
cavity, sufficient fluid should be withdrawn to make the patient 
comfortable. If, however, the patient is quite comfortable and 
is neither dyspneic nor distressed, it is best to leave matter to 
nature. We notice that frequently after a certain amount'of 
fluid has accumulated the effusion becomes limited, after which 
reabsorption often begins. Again, in other instances, although 
the accumulated fluid is great the patient is not at all distressed, 
absorption does not take place at once and perhaps only after a 
long period does a gradual lessening of the fluid become notice- 
able. It has been observed that only large pleural exudates exert 
a beneficial influence on the tuberculous process in the lung and 
that a small amount or very little fluid is detrimental. A tuber- 
culous pleuritis in the course of pulmonary tuberculous disease 
often exerts a very beneficial influence on the diseased process 
both in advanced and in beginning cases, all of which goes to 
show that we must consider well when to puncture or whether to 
withdraw fluid at all. 
Where to Puncture. Best in the 7th intercostal space posterior 
axillary line, in the 8th or 9th intercostal space midscapular line 
or in the midaxillary line in the 6th interspace. Here the aver- 
age diameter of the adult chest wall, at these points is about 4 
cm. These punctures should always be made close to the upper 
border of the rib so as to avoid the important intercostal vessels 
and nerves. 
Prognosis. The miliary form is very grave. The dry form 342 
CLINICAL TUBERCULOSIS 
gives a more favorable prognosis. Here usually adhesions be- 
tween the two surfaces of the pleura take place. In the sero- 
fibrinous form the prognosis is equally good. Pleuritis, in every 
case of pulmonary tuberculosis, if fairly large, exerts a favorable 
influence on the tuberculous process if the pleurisy is on the 
same side1 as is the pulmonary disorder. By compression of the 
lung structure and pulmonary rest, it presents a tendency to heal 
the tuberculosis; in fact, the favorable influence exerted on the 
tuberculous process by the fluid in the thoracic cavity as early 
observed by the profession led to the artificial induction of lung 
compression by means of nitrogen gas or filtered air and it is 
for this reason that the fluid if not troublesome, if not accom- 
panied by much fever, no less in weight nor profuse perspira- 
tion or complications, should remain until gradually absorbed. 
The fluid in the pleural cavity may for some time remain serous 
or more often sero-fibrinous or it may assume gradually a muco- 
purulent character, and when conditions become much more 
grave, an empyema may develop which if evidenced by constitu- 
tional disturbances indicates operative interference. 
Medical Treatment of Pleurisy. Pleuritis, as stated, may be 
ushered in abruptly, very acutely, or it may not be known to the 
patient until shortness of breath compels consulting a physician, 
when the nature of the disorder is recognized. In this latter form 
usually little medication is indicated but in the acute form 
remedies for the relief of symptoms are sought early. The most 
distressing symptom is the pain or stitch in the side. The 
patient should rest and sleep lying on the affected side—absolute 
rest. He must be made comfortable, the distress and nervous- 
ness relieved, and for this purpose the use of opium in any form 
or one of its many derivatives is indicated and morphia sulphate 
is usually resorted to, being given hypodermically in *4 to 
grain doses. In cases in which the symptoms are less acute, the 
use of local remedies applied directly to the chest over the seat 
of pain are very efficient, and here the use of mustard is most 
desirable, preparing a slight mustard draught or a plaster con- 
sisting of one tablespoonful of ground or powdered mustard 
mixed with four or five tablespoonfuls of flour made into a paste 
with some warm water and of sufficient consistency to allow it to 
'Many internists maintain that in the majority of instances the tuberculous process 
usually manifests itself on the same side as the pleural involvement, that is, on the side 
of the pleurisy. If in latent tuberculous disease where it often follows the pleurisy in 
years after, then usually the active process in the lung is found on the opposite side of the 
old pleuritis. However, if the pulmonary process is active at the time when pleurisy is a 
concomitant disturbance then it is generally on the same side as the pulmonary disorder. TUBERCULOSIS AND PLEURISY 
343 
be spread evenly upon a clean piece of cloth to cover a surface 
of about 6 by 6 inches or larger if desired. A plaster so prepared 
should remain firmly applied to the chest for about twenty min- 
utes after it begins to smart, then removed, the skin dried and 
covered with a layer of olive oil and a bandage applied. The 
use of a tablespoonful of pure and finely ground mustard well 
mixed in a quart of hot water, a towel wrung out of this warm 
solution and at once applied to the affected side often gives 
prompt relief. A topical remedy of great value is the use of 
ordinary tincture of iodine U. S. P., painted over a large area 
on the affected side; allow it to dry and cover lightly with a 
cloth but do not apply a bandage. Both the use of mustard or 
the tincture of iodine or any other counterirritant must not be 
used too frequently, say not oftener than once in two or three 
days, because if used too freely the skin over the affected area 
will become blistered, adding more to the discomfort. If the 
skin is normal or has not been irritated too much by the applica- 
tion of local remedies, the use of adhesive straps is a most de- 
sirable procedure, these to be applied in strips of about two 
inches in width extending from the middle of the sternum to the 
middle of the spine and from a point above the fluid down to and 
below the costal arch and ribs. With the use of adhesive plaster 
we aim to immobilize the ribs and prevent the intercostal muscle 
from contracting during the respiratory act. Such adhesive 
strips must be applied after the patient expels as much air as 
possible and then holds the breath. To promote absorption of 
the exudate many remedies have been recommended, particularly 
such as possess more or less diuretic action. Potassium citrate 
in 10 grain doses, sweet spirits of nitre in 10 or 15 minum doses, 
potassium acetate in 5 to 10 grain doses may be combined or 
given separately in water three times a day. Infusion of digitalis 
in y-2. to one tablespoonful doses three times a day or Diuertin in 
5 grain tablets. In general to favor absorption the iodides are 
much in vogue and the syrup of hydriodic acid in teaspoonful 
doses every four hours, the use of iodide of potassium in 5 to 
10 grain doses or the equivalent in sodium or ammonium iodide 
every four hours dissolved in water or the use of the tincture of 
iodine U. S. P. in 10 minum doses given in milk every three or 
four hours are found most reliable. Next to the above the sali- 
cylates are much in use. The sodium or ammonium salicylates 
in 5 to 10 grain doses every three hours. If there is pain and 344 
CLINICAL TUBERCULOSIS 
restlessness, Dover’s Powder in 10 grain doses at bed time will 
be found very advantageous, codeine in small doses or some of 
the synthetic drugs like veronal, (barbital) trional or sulphonal 
in 5 grain tablets are also useful. 
Surgical Treatment of Pleurisy 
The pleural exudate may be removed by forcing air into the 
pleural cavity and thereby crowding the fluid out, the contained 
air displacing the exudate. Results have been found most grati- 
fying. The technic is quite simple. A hollow needle is passed 
between the ribs, 10th intercostal space, into the pleural cavity, 
and a second needle or better a trocar is now passed into the 
8th or 9th intercostal space above connecting the latter with an 
apparatus by means of which nitrogen gas or filtered air may be 
forced into the pleural cavity, the pleural fluid being expelled 
from the lower opening or needle. Before inserting the second 
needle or the trocar allow as much fluid to flow from the first 
puncture as will flow out spontaneously, after which use of the 
air pressure should be made. In most instances nearly all the 
fluid may in this manner be removed without sudden disturbance 
of the heart, the inserted air under pressure taking the place of 
the withdrawn fluid. This also will prevent pleural adhesions or 
thickening, and the amount of air allowed to enter should equal 
about the fluid'expelled or withdrawn. Restlessness, cough, 
dyspnea or pain are usually negative. It very much shortens the 
course of the disease. It is best to connect such an apparatus 
with a monometer so as to control the amount of air which is to 
be passed into the chest cavity. Early removal of the fluid fol- 
lowed by the entrance of air or nitrogen is advocated by many, 
the exudate being usually sero-fibrinous its early removal pre- 
venting pleural thickening or adhesions. 
Empyema, Rib resection, etc. Scapular line 8 to 10 interspace, 
posterior axillary line 8th, axillary line 7th or 8th and anterior 
axillary line 6th and 7th. In empyema the pus may escape in 
small amounts at a time through the lungs and be expectorated 
—the process in months may eventually heal out spontaneously. 
See Chapter 20—“Surgical Treatment of Tuberculosis.” 
Autoserotherapy. In a number of cases of pleurisy with effu- 
sion after the withdrawal of a syringeful of the serous fluid 
from the pleural cavity and immediately injecting it subcutane- 
ously, the fluid in the chest cavity begins rapidly to diminish, to TUBERCULOSIS AND PLEURISY 
345 
be absorbed; in other cases again no result follows this treat- 
ment. If the case is favorable a rapid increase in the urinary 
flow is observed; the tuberculous process, however, is not in- 
fluenced thereby. 
Diaphragmatic Pleurisy. Sacculated Pleurisy. Here the diag- 
nosis. often presents many difficulties. The following signs are 
characteristic of this form of pleurisy, (1) A vertical prolonga- 
tion from the outer margin of the sternum meeting horizontally 
along the tenth rib gives at this point a painful spot on pressure, 
next, the respiratory reflex; quick contraction of the rectus ab- 
dominus muscle at the point of attachment on deep inspiration, 
sometimes a reflex of all the abdominal muscles; (2) Sacculated 
mediastinal pleurisy may simulate mediastinal tumors or en- 
larged glands, the characteristic sudden onset and the presence 
of fever differentiating; (3) Interlobar Saccular pleurisy. Here 
the diagnosis is often most difficult and a thorough knowledge 
of the topography of the interlobar fissures is necessary. The 
accumulated fluid most frequently follows the interlobar septa. 
Often during life this condition is not recognized when at 
autopsy a large quantity of pus is found walled off between the 
lobes of the lungs. If the fluid in amount exceeds 500 cc 
then the first evidence of disorder generally shows itself on the 
anterior chest in the anterior axillary line; it is here that the 
fluid is in closest contact with the parietal pleura, making it 
easily accessible for exploratory puncture. There may be much 
pain and pulmonary gangrene may accompany the picture. In- 
terlobar pleurisy may be either dry or moist but in the by far the 
greater number of instances it is a purulent affair, an interlobar 
empyema or lung abscess. 
Summary and Conclusions 
(1) In pleuritis sicca of the apices, immobilization of the arm 
on the affected side may give quick relief from pain. A tuber- 
culous-pleurisy often exerts a most favorable influence on the 
underlying cause of the disorder and this not only in cases of 
advanced tuberculosis but in beginning or first stage cases as 
well. This can not be attributed to a mere mechanical influence; 
there must be a chemical momentum present. 
(2) The muscle pain, spasm or rigidity is diagnostic of apical 
pleurisy. The trapezeus, pectoralis major, the supra and infra 
spinatae, even the brachial plexus is sensitive to pressure, and 346 
CLINICAL TUBERCULOSIS 
Sternberg’s symptom complex similar to Pottenger’s is not re- 
flex as stated but most probably due directly to the inflammatory 
process in the nerves about the shoulders. 
(3) In 90% to 95% of all idiopathic pleurisies in the adult the 
tuberculous nature is positive and a pleurisy is more or less 
grave if after withdrawal of the fluid it reappears or accumulates 
quickly, if there be but little fibrin in the fluid and if it shows a 
strong tendency to remain localized. Concerning the prognosis 
as to the future condition, it may be stated that pleuritis is a 
most favorable manifestation of a tuberculous process. In latent 
cases generally the process will manifest itself, that is after the 
pleurisy, on the side opposite, or the side free from pleuritis. In 
pulmonary tuberculosis of the bases, accompanied by a dia- 
phragmatic pleurisy, the symptoms may simulate a gastric ulcer, 
such as pains in the stomach, eructation of gases, vomiting, etc. 
(4) Remember that pleuritis in an adult is always a very 
serious question, being generally secondary to a tuberculous 
process, whereas in the child2 it is of far less import. It indicates 
either an already existing active tuberculous disorder or a latent 
condition; hence every patient suffering from an attack of 
pleurisy when the physical findings in the chest do not give 
evidence of active pulmonary disease should be treated as a 
latent tuberculous individual, be under constant observation, 
always remembering that very frequently in later years and after 
the pleurisy has subsided for some time that the lung findings 
may become positive. 
2Altliough pleuritis is frequent in child life, still in the majority of cases the process is 
arrested, heals out completely, leaving very little if any evidence of the original _disorder. 
In children in but a small minority is pleurisy followed by serious tuberculous disease. CHAPTER 26 
TUBERCULOSIS AND PREGNANCY 
General Consideration. The two most dangerous conditions 
to which women of childbearing age (15 to 45) are commonly 
exposed are tuberculosis and pregnancy. The mortality statistics 
from the area of registration, comprising 67.1 per cent of the total 
population of the United States, shows that 29,200 women be- 
tween ages of 15 and 45 died in 1915 from the various forms of 
tuberculosis; 10,134 died from childbirth of which 4,173 were 
from puerperal sepsis; 5,766 from the various circulatory dis- 
turbances ; 6,458 from all kinds of digestive disturbances; 5,549 
from pneumonia, all types; 5,424 from cancer and other malig- 
nant tumors; while for these ages syphilis is given as cause of 
death 647 times and gonorrhoea 174 times. 
Tuberculosis is largely a preventable disease, and most of the 
deaths from puerperal sepsis and other obstetrical accidents are 
unnecessary and also preventable. 
The campaign of education on the cause and spread of tuber- 
culosis has resulted in a steadily declining death rate from this 
disease. The dangers of maternity are, on the other hand, calmly 
ignored by both physician and layman with the assumption that 
this appalling, mortality is the sacrifice which women must lay 
on the altar of motherhood. The death rate from maternity is 
just as high, if not higher, today than three score and ten years 
ago when anesthetics were little used and antisepsis unknown. 
Pregnancy with tuberculosis (65) is a most unfortunate and 
very fatal combination. The cases of tuberculosis with preg- 
nancy are so widely scattered that it has been impossible for any 
one observer to study and report a series large enough to warrant 
definite conclusions. Nevertheless, the precentages of the vari- 
ous writers, who have reported small series of cases, correspond 
so closely that for the present they may be accepted as typical. 
1. Amenorrhoea and Sterility in Tuberculous Women. (181) 
Tuberculosis is one of the recognized causes of constitutional 
amenorrhoea. In a series of 214 tuberculous women in which 
Norris made a careful study of the menstrual changes, complete 
347 348 
CLINICAL TUBERCULOSIS 
amenorrhoea was present in five per cent and scanty or scanty 
and irregular flow, in an additional fifty-three per cent.(137) 
There may be a scanty menstruation or even a complete cessa- 
tion in the early stages of tuberculosis. In advanced cases men- 
struation and probably ovulation are often suppressed. There is 
an old superstition among the laity that amenorrhoea is the 
cause of consumption and varied attempts are made to induce 
menstruation in these cases. It is now recognized by the profes- 
sion, however, that the amenorrhoea is a result of the secondary 
anemia, and, therefore, one of the body’s conservative measures. 
With the arrest of the tuberculous condition and an improve- 
ment in the general health of the patient, there is a return of the 
menstrual function. 
Amenorrhoea is not as suggestive a sign of pregnancy in the 
tuberculous as in the normal woman; nor is the presence of 
amenorrhoea without pregnancy a proof of sterility, since ovula- 
tion may occur without menstruation. Fortunately, however, 
tuberculosis, particularly in advanced cachectic cases, may be a 
cause of sterility. 
Women with tuberculosis of the uterus or tubes are usually 
sterile. Tubal tuberculosis may become latent or even disappear. 
Carstens,(112) in a recent paper, claims that if nature can remove 
the myriads of tubercles in the peritoneum, in whatever part they 
may be, nature will also remove the few that can be found in the 
tubes, and urges that the latter need not be removed on that 
account. He reports subsequent pregnancy in two patients whom 
he had operated for tuberculous peritonitis with tubal involve- 
ment. Most of the cases of severe tubal tuberculosis, however, 
result in a permanent closure of the tubes and sterility. 
2. Incidence of Tuberculosis Among Pregnant Women. Preg- 
nancy demands an unusual amount of work from the various 
organs of the body. The relation of pregnancy to the incidence 
of tuberculosis is debatable, yet it is undoubtedly responsible 
for the active symptoms of phthisis in a considerable number of 
patients. Some of these might have shown evidence of the dis- 
ease without the test of pregnancy, while others would never 
have developed an active process. 
In a recent review of 300 cases together with a review of the 
literature, Douglass and Harris report as follows: (69) 
“In the analysis of the histories of a series of tuberculous 
women admitted to the Ohio State Sanatorium from December, TUBERCULOSIS AND PREGNANCY 
349 
1909, to April, 1917, inclusive, it is apparent that in a large num- 
ber of cases we are dealing with an exacerbation of a latest or 
quiescent tuberculosis, rather than an initial lesion, and that, in 
married women, pregnancy is one of the leading factors in light- 
ing up this inactive process.” 
“Under the term ‘pregnancy’ we have included the period from 
conception to the end of the puerperium. To determine its im- 
portance as an etiological factor, 392 married tuberculous women 
were considered, 92 of whom gave no history of pregnancy, leav- 
ing 300 cases in the series on which to base our observations. 
In 88 of these cases, or 29 per cent, pregnancy was the leading 
factor to which the onset of tuberculosis was attributed. In 24 
additional cases, or 8 per cent, pregnancy was a presumptive 
factor, making a total of 37 per cent.” 
These figures correspond closely to others found in the litera- 
ture. The variations, to a considerable extent, are due to differ- 
ences in methods of making comparisons and tabulations. The 
following figures are from different reviews. Trembley of Sara- 
nac,(179) in a series of 240 cases, had 151, or 63 per cent, who 
said the tuberculosis originated or, at least, was first discovered 
after the birth of a child. Turban of Schauta’s clinic, reports 
that 29 per cent of the tuberculous women, observed by him, 
gave a positive history of the disease originating or becoming 
definitely recognizable during pregnancy or the puerperium. In 
a series of 337 tuberculous women reported by P. Jacob and 
Pannwitz, 25 per cent traced the origin or aggravation of the 
disease to pregnancy. Scarborough reports 94, or 47 per cent, 
of 200 married women admitted to the Iowa State Sanatorium in 
whom the symptoms of active tuberculosis appeared after child- 
birth. The combined statistics of Funk, Jacob, and Pannwitz, 
and a number of other observers with a total of over 1000 cases 
show that 39 per cent believe their infections originated during 
pregnancy or the puerperium. In view of these reports, it is 
certain that pregnancy plays an important role in the develop- 
ment of active tuberculosis in women. It must be considered 
one of the important predisposing causes. 
3. Effect of Tuberculosis on Pregnancy. There is little indi- 
cation that spontaneous abortion is any more common in tuber- 
culous women than among others, yet occasionally, tuberculosis 
is recorded as the cause of the abortion. Any chronic infection 
may act as a predisposing cause of abortion, but, unfortunately, 350 
CLINICAL TUBERCULOSIS 
only the more severe or hopeless cases of tuberculosis show any 
considerable tendency to sterility or, in case of pregnancy, to 
abortion. 
Polak and Matthews (181) in their reviews state: “The effect 
of tuberculosis on the course of pregnancy is practically nil.” 
They quote Emil Sergent as stating that tuberculous women 
seldom become pregnant, but that if pregnancy does occur, abor- 
tion is rare even in the advanced cases with cavity formation. 
Lobenstine considers it reasonable to believe that abortion is 
more common in the tuberculous than in the non-tuberculous 
woman due to the cough, haemoptysis, fever, and the possible 
tuberculous involvement of the placenta or decidua. It is ap- 
parent, however, that mild cases will usually go to term. 
4. Effect of Pregnancy on Tuberculosis. Tuberculosis may 
have little effect on pregnancy, but the converse is unfortunately 
not true. It has already been stated that about 39 per cent of 
the married tuberculous women believe their active tuberculosis 
began during or subsequent to a pregnancy. This, undoubtedly, 
means that pregnancy caused a lighting up of latent and perhaps 
old lesions in these women. 
In cases of known tuberculosis, there may be an increase in 
the amount of gastric disturbances during the first trimester, 
anl abortion may result. During the second trimester, a con- 
siderable percentage of the patients show a definite improvement 
due to the increased metabolism, and they may continue to term 
without any particular difficulty. During the last three months, 
however, many of the patients lose ground with an alarming 
rapidity and may die at any stage of labor or the puerperium. 
For the advanced cases with an exhaustive cough, haemoptysis, 
and fever, the prognosis is invariably bad. Death may occur at 
any time during pregnancy, labor, or the puerperium. Most of 
the advanced cases will have died within a month after delivery. 
Existing tuberculosis is usually aggravated by pregnancy. 
Lobenstine,(184) in the Bulletin of the Lying-In Hospital of 
New York, states that 38 per cent of their cases were seriously 
affected by parturition. Lebert believes that 75 per cent of tuber- 
culous women are badly influenced by pregnancy and the puer- 
perium; Diebel, 64 per cent; v. Rosthorn, 70 per cent; v. Bar- 
deleben (180) wrote, from the communications of fourteen phy- 
sicians, that 71 per cent of tuberculous women grew worse from 
parturition, and that 47 per cent of the active cases proved fatal TUBERCULOSIS AND PREGNANCY 
351 
(Lobenstine). Norris and Landis report that in their experience 
“about 20 per cent of mild, quiescent, pulmonary tuberculosis 
and 70 per cent of more advanced cases exhibit exacerbations 
during pregnancy or the puerperium.” 
It is self-evident that if the tuberculous woman becomes preg- 
nant or the pregnant woman shows signs of tuberculosis, she 
should have the most careful attention during the entire par- 
turient period, from the beginning of pregnancy to the end of 
the puerperium. Careful sanatorium care during this period will 
lessen the dangers to some extent, but the end results are still 
unsatisfactory. McSweeny and Wang (102) report 18 child- 
births at Sea View Hospital, one patient having a second child 
three years after the first. Ten stated that the onset of their 
clinical tuberculosis occurred before pregnancy; of these, after 
labor, four died, three seemed improved, and three seemed unim- 
proved. Three stated that the onset of their clinical tuberculosis 
occurred at about the time they became pregnant; of these, after 
labor, one died and two seemed improved. Five stated that the 
onset of their clinical tuberculosis occurred after they became 
pregnant; of these, after labor, four seemed improved and one 
seemed unimproved. The woman with the second pregnancy 
retrograded during pregnancy and after labor; she was a patient 
in the hospital when the report was made. In their summary, 
these authors report that during pregnancy, as near as could be 
ascertained, ten (55.5%) seemed to retrograde, five (27.7%) to 
improve, and three (16.6%) were apparently unchanged. After 
labor, of the moderately advanced cases, seven were improved; 
of the far advanced, five (45.5%) died, one (9%) improved, and 
five (45.5%) retrograded. This series while small is valuable 
owing to the careful treatment afforded. 
Polak and Matthews have summarized the effects of preg- 
nancy on tuberculosis as follows: 
“Practically all observers agree that labor and the puerperium 
are the periods of the greatest danger to the woman. During 
labor, sudden death may occur from cardiac failure, pulmonary 
oedema, or pulmonary hemorrhage. During the puerperium, 
the tuberculosis may become fulminating and cause death in a 
surprisingly short time. Schlimpert, with his great experience 
in dissection, asserts that the greatest number of deaths from 
tuberculosis during pregnancy occur during childbed. Acci- 
dents during the puerperium are liable to occur in all types of 352 
CLINICAL TUBERCULOSIS 
tuberculosis with active lesions and sometimes of only mod- 
erate severity. In other words the puerperium is a period of 
‘watchful expectancy,’ for one can hardly expect to prognosti- 
cate correctly in any case, latent or active, where the uncertainty 
of the reaction is so great.” 
Bacon (134) estimates that from 1 to 1.5 per cent of all preg- 
nant women have tuberculosis to such a degree that it can be 
detected if careful examination is made. He quotes Freund as 
finding 12 cases in 1000 pregnant women examined. Using 
Bacon’s estimate of from 24,000 to 36,000 tuberculous women 
confined in the United States each year, we would judge from 
the few carefully observed and reported cases that several thou- 
sand of these women will die within a month after delivery. Yet 
the ordinary tables of vital statistics do not show pregnancy as a 
contributory cause of death. Until such times as it is so re- 
corded we can have no definite knowledge as to the real mor- 
tality resulting from the strain of pregnancy, labor, and the 
puerperium. 
It is generally believed, and quite properly so, that by careful 
medical attention, with thorough use of absolute rest, feeding, 
and fresh air, ease of mind, and obedience, many more pregnant 
tuberculous women would be brought safely through pregnancy 
and the puerperium with an eventual hope of cure. Bacon advo- 
cates this management before and after labor, with a free use of 
oxygen during labor. Only careful records over a period of 
years will show to what extent this management is valuable. It 
is estimated by Bacon that under present conditions 33 per cent 
of tuberculous women who become pregnant die in less than a 
year after delivery. 
5. Effects of Maternal Tuberculosis on the Fetus. Tuber- 
culosis (although extremely infrequent) may be transmitted 
directly from the mother to the fetus in utero. This is particu- 
larly true in cases of miliary and laryngeal tuberculosis. The 
tubercle bacillus has never been found in spermatozoon, but 
Norris believes one may become attached to the spermatozoon 
and with it reach the ovum1. This, however, while possible from 
the theoretical standpoint, is most improbable. See Chapter 3, 
The Genitogenetic Route of Infection. 
To quote further from Polak and Matthews: “Hauser, in 1898, 
Ordinarily the child in utero will not become tuberculously infected; this can only 
take place if the mother is toxic tuberculous. TUBERCULOSIS AND PREGNANCY 
353 
found in the literature reports of 18 cases of congenital tubercu- 
losis. Martha Wollstein, in 1905, reported a case of ‘proved con- 
genital tuberculosis.’ Novak and Ranzal claim that in 70 per 
cent of the cases of positive tuberculosis in the mother or in the 
fetus, the placentae contain tubercle bacilli. Schmorl and Giepel 
assert that in 45 per cent of known tuberculous women the pla- 
centae contain tubercule bacilli. Charles Norris states that from 
a summary of 67 cases of maternal tuberculosis gathered from 
the literature, 30 per cent presented positive evidence of tubercle 
bacilli (see Chapter 3) in the placenta. In a personal communi- 
cation, Norris says that he has found 20 per cent of the placentae 
of positively tuberculous women to contain tubercle bacilli, and 
furthermore he believes that it is possible for tubercle bacilli to 
be transmitted through a normal placenta.” These observations 
are very important, if true. Placentae of tuberculous women 
should be examined microscopically and treated with antiformin 
and the results tabulated with a brief of the patient’s history. 
The whole problem of management may hinge on the accuracy 
of these observations. 
The child of a tuberculous mother inherits a tissue weakness 
and may not have an equal chance with that of the healthy 
mother. Any chronic disease lowers the mother’s vitality and 
may be expected to interfere to some extent with a healthy 
development of the fetus. Again, the mother cannot safely 
nurse these children, and, in most cases, a wet-nurse not being 
available, they must be raised on a bottle, generally under the 
same roof or in the same room with a tuberculous mother. Under 
past and present conditions most of these children will certainly 
develop some type of tuberculosis. The mortality has been 
extremely high during the first twelve months. The late Dr. 
Jacobi (133) estimated that 70 per cent succumb during the first 
year; Weinberg, 67.9 per cent; Zirkel, 58 per cent; Pankow and 
Kupferle, 54.5 per cent. Miller and (91) Woodruff working in 
New York examined 150 children, born of tuberculous parents, 
and found that 51 per cent were definitely tuberculous, 20 per 
cent were doubtful, and only 20 per cent showed no signs of 
tuberculosis. Similar results are reported from Boston by Floyd 
and Bowditch, who found tuberculosis of the lungs in 36 per 
cent and infection elsewhere in 30 per cent, or a total of 66 per 
cent of the children of tuberculous parents with tuberculosis in 
some form. These results, however, only apply to children who 354 
CLINICAL TUBERCULOSIS 
have remained with their parents. To date there are no statistics 
showing the degree to which the children may be saved by im- 
mediate removal from infected parents. 
6. Nursing and Tuberculosis. It is generally recognized that 
it is dangerous for the tuberculous mother to nurse her child. 
Although it is very desirable for the weak infant of such a 
mother to have the benefit of mother’s milk during the first 
weeks of life, the dangers from nursing, both from the considera- 
tion of the mother and child, are such that it would seem wiser, 
in most cases, to depend entirely on artificial feeding, if milk 
from a healthy mother cannot be obtained. This is especially so 
in the interest of the mother and less that of the child. 
For the mother, the puerperium is the period of greatest dan- 
ger, as at that time particularly, she needs all of her reserve to 
combat the infection. The quantity and quality of her milk is 
often impaired. Rarely, the breast may be infected with tuber- 
culosis, but this can only be determined by careful microscopic 
examination of the breast contents. The child usually contracts 
tuberculosis from the sputum coughed out by the mother while 
nursing. This danger may be lessened by careful cleansing of 
the nipples and having the mother wear a gauze mask. 
7. Birth Control Among the Tuberculous. Marriage of all 
persons with active tuberculosis should be prevented. Tubercu- 
losis is second only to gonorrhoea and syphilis as a contraindica- 
tion to marriage. After the “cure” has endured for a period of 
two or more years, a man may marry with little danger to him- 
self, his wife, or offspring. But, in view of the great tendency 
for lighting up of tuberculosis during pregnancy, it is more diffi- 
cult to determine when the woman may safely marry. Matri- 
mony may interfere with the cure, and pregnancy may soon lead 
to a fatal termination. 
Prevention of pregnancy in the tuberculous is easily advised, 
but very rarely accomplished. Except in extreme cases it is 
almost useless to urge abstinence; however, until such times as 
the woman has gone without any symptoms for a number of 
years every effort should be made to prevent pregnancy. In the 
few cases where the abdomen may be opened for other condi- 
tions sterilization may, at times, be advisable. The advisability 
of opening an abdomen for this alone is questionable, and the 
resection of the tubes per vaginum is usually difficult in the nulli- 
para. The so-called operations for temporary sterilization of TUBERCULOSIS AND PREGNANCY 
355 
women are, in most cases, temporary only in theory. 
8. Prophylaxis of Tuberculosis in Pregnancy. There is abund- 
ant evidence that pregnancy plays an important part in the light- 
ing up of old tuberculous lesions, and it is probable that during 
pregnancy a woman is more prone to reinfection. Regardless of 
the debatable question of new or old lesions the danger is real 
and becomes one more strong argument for carefully supervised 
care of every woman during the entire period of pregnancy, 
labor, and the puerperium. 
Woman has always paid a fearful price for the old and false 
belief that childbirth, being a normal function, needs no particu- 
lar consideration. While under the care of capable obstetricians 
serious complications are not common, very few women have 
perfectly normal, physiological pregnancies or labors. Scientific 
prenatal care, with skilled supervision during labor and the 
puerperium, will not only increase the number of normal cases, 
but will also greatly lessen the present high mortality and mor- 
bidity. 
Tuberculosis is not one of the chief causes of this appalling 
maternal mortality and morbidity, but with a general improve- 
ment in the care of women who are becoming mothers, fewer 
women will die from tuberculosis. Both the public and the pro- 
fession must be educated; hospital facilities must be provided; 
the district or home nursing organizations must be enlarged 
until they may provide nursing care at a reasonable rate for all 
women who are to become mothers. These organizations should 
receive city, county, or state assistance. So far as possible, all 
tuberculous women should be taken to the hospital or sana- 
torium for delivery. When beds are scarce, any woman whose 
condition is good may be taken home in an ambulance at any 
time after delivery and be cared for by the visiting nurses. 
9. Treatment of Tuberculosis With Pregnancy. The treat- 
ment of tuberculosis complicated by pregnancy will be much the 
same as when not so complicated. Owing to the dual nature of 
the condition, however, the obstetrician should always work with 
the internist. 
The tuberculous women, due to her diseased condition, may 
have an unusual amount of gastric disturbance during the first 
trimester. It is essential that this be quickly controlled or the 
resulting loss of strength will greatly lessen the possibility of an 
ultimate recovery from the tuberculous disorder. 356 
CLINICAL TUBERCULOSIS 
There is undoubtedly a disturbed metabolism with every 
pregnancy, and the development of symptoms depends, appar- 
ently upon the metabolic reaction of the patient and the presence 
of one or more conditions as possible causes of the nausea and 
vomiting of pregnancy. The following plan of treatment has 
given much relief to patients suffering from the gastric disturb- 
ances of pregnancy; with slight modifications of diet it may be 
used for the tuberculous, pregnant women. 
1. A carefully taken history will usually reveal any previous 
gastro-intestinal disturbance, nervous disorder, or other physical 
condition which makes the patient more susceptible to the meta- 
bolic disturbances of pregnancy. 
A physical examination may reveal any source of local irrita- 
tion or infection. Remove any source of infection found in the 
teeth or in the tonsils. Dental work must not be neglected dur- 
ing pregnancy. Try to correct any uterine displacement. Treat 
acute cervicitis when present. Any of these may tend to in- 
crease the nausea and vomiting of pregnancy, but should be 
regarded as predisposing rather than causative factors. 
2. Keep the patient in bed until the nausea and vomiting is 
controlled. With the non-tuberculous it may be sufficient to 
keep the patient in bed for a few hours after breakfast, but the 
tuberculous need complete rest in bed. 
3. Give an antacid, dry type of diet, such as is used in the 
nervous type of vomiting among the non-pregnant. Solid food 
may be retained when liquids are vomited. Allow no liquid 
within the hour before meals or the first one and one-half hours 
after. The patient may have enough cream or milk to moisten 
cereals but should have no other liquid. Bulgarian milk may be 
well borne when sweet milk is not. For the non-tuberculous 
woman, this'diet is high in carbohydrates and low in fat and 
proteins. But so long as the diet is of the solid type, the per- 
centages of carbohydrates, fats, and proteins may be varied to 
meet the requirements of the individual patient. 
4. Alkalinize the system by the use of alkaline water or 
sodium bicarbonate. From twenty to sixty grains of sodium 
bicarbonate, t. i. d. in a full glass of water taken midway be- 
tween meals and at bedtime may be needed for several days. 
After the urine becomes alkaline, the dose is reduced to ten 
grains and continued, t. i. d. If, on subsequent tests, the urine is 
found strongly acid, the dose of sodium bicarbonate is again TUBERCULOSIS AND PREGNANCY 
357 
increased. The alkaline treatment is continued throughout preg- 
nancy. 
5. Stomach lavage is needed at times. The simplest method 
is that of having the patient drink several glasses of tepid water, 
each containing one-third teaspoonful of baking soda. This, when 
vomited, washes the stomach effectively and causes less irrita- 
tion than the tube. The tube should be used when stomach tests 
are indicated. 
6. Bromides are of value in the cases not controlled by the 
dry diet and alkaline treatment. Ten or fifteen grains may be 
given in a little water, thirty minutes to one hour before the 
taking of food. The effervescent triple bromide is perhaps best 
borne by the stomach. Cerium oxalate, two grains every half 
hour for three doses, is at times useful in cases of simple nausea, 
but of no value in the more severe. The use of cocaine is not 
favored, even though good results have been reported. 
7. Corpus luteum extract is administered hypodermatically 
when the history suggests ovarian insufficiency and when there 
has been one or more miscarriages. It is claimed that both 
thyroid and corpus luteum extracts increase metabolism, so 
there might be some benefit from giving it to the tuberculous, 
pregnant woman. 
8. It is believed that prompt management of cases with 
nausea and vomiting of pregnancy will prevent their reaching 
the so-called pernicious stage. Patients with the severer forms 
of vomiting require a special nurse or better be in a sanatorium 
as it is extremely difficult to secure absolute rest and quiet in 
the home. If seen before the stage of marked dehydration and 
severe acidosis, stop all food and liquid by mouth and given glu- 
cose solution of from 2 to 5 per cent per rectum. Two hundred 
fifty cc of the glucose solution containing from thirty to sixty 
grains each of sodium bromide and sodium bicarbonate may be 
given every four or six hours as a retention enema, which given 
with a small tube, is usually easier on the patient than the drip 
method. It may be advisable to elevate the foot of the bed. As 
the nervousness is controlled reduce the bromides to thirty 
grains. After twenty-four or thirty-six hours of this treatment, 
if the nausea is relieved, the patient may have small amounts of 
fluid and, later, solid food by mouth. 
9. The severe cases seen after marked dehydration is present 
should have 800 to 1000 cc, N/NaCl solution under the breasts. 358 
CLINICAL TUBERCULOSIS 
When possible, it is advisable to give these patients an 18 or 20 
per cent glucose solution intravenously according to the technic 
of Woodyatt, Wilder and Sansum.(119) 
10. Constipation is a common complaint and may be an im- 
portant factor in causing some of the nausea and vomiting. 
Various plans of treatment have been tried, but at present milk 
of magnesia and liquid petrolatum are the two forms of medica- 
tion most commonly employed. With the alkaline treatment, 
many patients make a complete recovery from constipation. 
Fresh air, rest, properly balanced diet, happy family associa- 
tions, freedorii from household cares, etc., so necessary to. every 
pregnant woman, are even more important to the pregnant 
tuberculous. It is always better that she have the advantages 
of sanatorium treatment. A child in utero develops, parasite 
like, by taking from the food and oxygen of the mother and, 
like parasites, it also takes to the last, regardless of the strength 
of the mother, and, in cases of disturbed nutrition, the mother 
suffers out of all proportion to any effect shown by the fetus. 
Toxins in the maternal blood will certainly affect the fetus, the 
degree depending upon the nature of the toxins and the age of 
the fetus. With proper care during pregnancy, the children of 
tuberculous mothers will, as a rule, be born healthy. Preg- 
nancy is a very serious complication of tuberculosis, and regard- 
less of the treatment, frequently prevents a permanent cure. 
10. Treatment of Pregnancy With Tuberculosis.2 In the 
past, there has been a general sentiment that in case a preg- 
nant woman has an active tuberculosis, she should be aborted 
“Therapeutic abortion had reached such proportions in Amsterdam and the Netherlands 
that Tussenbrock (89) engaged in a most critical study in order to ascertain what influence 
pulmonary tuberculosis had on the mortality of pregnant women. Here at the onset two 
most important but very difficult questions arose. First, how great quantitatively is the 
loss in women as a result of pregnancy complicated with tuberculosis? This first question 
may be answered in three parts, (1) In Amsterdam, the tuberculosis mortality in women 
during the puerperium, that is, during the first six months after child birth, is very high, 
but in the following six months is most perceptibly low, so that the average mortality rate 
for the year does not exceed that of the non-pregnant tuberculous women. (2) In the 
mortality curve for women after puberty, there is an absence of the sharp lowering 
which would show a greater mortality in relation to pregnancy and tuberculosis as a 
cause. (3) In Amsterdam there is only a relatively less frequent mortality amongst 
the married; this in part must be attributed to other causes than to the process of 
child bearing. The second question is: have we any correct methods or definite signs 
by which we may differentiate the pregnant woman who has tuberculosis, but who goes 
through the puerperium unharmed, from the woman who does not tolerate her pergnancy 
well and goes all to pieces? This question is still more difficult to answer. Some -tuber- 
culous women undoubtedly do not do well under the combined strain of pregnancy and 
tuberculosis, while other women are not influenced for the worse while pregnant. There 
probably exists a group of tuberculous women who tolerate pregnancy very poorly; it is 
however, difficult to ascertain which class that is, nor do we know what form of tubercu- 
losis so frequently shows a tendency to influence the pregnancy so disasterously. The 
prevailing opinion, in the Netherlands, that the tuberculosis mortality is greatly increased 
by pregnancy and the puerperium can not, judging from these observations, be substantiated, 
and the general belief of an Abortus Provocatus in pregnancy, if accompanied by active 
pulmonary tuberculous disease, can not be approved. Catharina van Tussenbrock. Amster- 
dam. Arch. f. Gynack. 1913.—J. R. TUBERCULOSIS AND PREGNANCY 
359 
if seen during the first three months. The results of inter- 
ference after the first trimester are so poor that most observers 
are agreed that if the diagnosis is made after the fourth 
month she should be carried to term. According to Bacon, 
the collected results of therapeutic abortion are not favorable, 
and he does not believe abortion justifiable in over 10 per 
cent of the pregnant tuberculous women. Veit (182) found that 
there was no improvement following abortion, in 43 per cent of 
the cases collected by him. Trembley, at Saranac Lake, with 
patients under most favorable conditions, has not seen enough 
improvement after abortion to warrant the establishment of a 
general rule. v. Bardeleben states that 50 per cent of his cases 
died after the pregnancy had been terminated by therapeutic 
abortion. It is impossible to estimate the percentage of aborted 
women who would have died had the pregnancy continued. A 
study of the literature leads to the suspicion that the end results 
would be about the same without abortion if the patients could 
have adequate care during the entire period of pregnancy, labor, 
and the puerperium. All cases of therapeutic abortion should be 
reportable to the health department, and the end results carefully 
tabulated for future guidance. 
Dr. Bacon says of therapeutic abortion (59) : 
“It certainly should not be the general rule, because of several 
reasons. One is this: the results of abortion are not very good. 
There are two indications—prophylactic and vital—for abortion 
to prevent further trouble, and save the woman’s life. The vital 
indication is worthless. If the woman is in such condition that 
she is pretty sure to die if she goes on with the pregnancy, she 
will be pretty sure to die after abortion is induced, so that it is 
not really a reasonable indication. Possibly we want to save hei 
to her family a little longer, but most authorities agree that 
women go down pretty nearly as fast after the operation as with- 
out it.” 
“The prophylactic indication is the prevention of further in- 
crease of trouble in a woman that has a good hope of success 
in her fight with tuberculosis. Before deciding on this indica- 
tion, it is necessary to answer the questions: How can the 
pregnancy be managed? Can the patient be treated in her 
home or in a sanatorium properly? If she is sent to a sana- 
torium to be cared for in an ideal way during her pregnancy, 
and the labor conducted in a proper way, the child taken from 360 
CLINICAL TUBERCULOSIS 
her and properly cared for, if that can be done, I believe it is 
very much better than induction of abortion. I should say that 
it is very seldom that induction of abortion is indicated. I 
think it will grow less and less as we can improve our manage- 
ment.” 
The tendency to abort all proven active cases of tuberculosis, 
when possible, during the first three months of pregnancy is 
largely the result of the old belief that the child was usually 
tuberculous. Should not the present knowledge that the child, 
when removed from direct exposure following birth, will be 
healthy, as a rule, lead to a greater consideration of the child? 
EDUCATE THE PEOPLE TO THE DANGER OF PREG- 
NANCY IN THE TUBERCULOUS. PREVENT THE MAR- 
RIAGE OF THE PEOPLE WITH ACTIVE TUBER- 
CULOUS LESIONS. LESSEN THE DANGERS OF 
LIGHTING UP OLD LESIONS DURING PREGNANCY 
BY SCIENTIFIC PRENATAL CARE. LIMIT THE 
THERAPEUTIC ABORTION TO THE COMPLICATED 
CASE WHERE THE CHANCES OF A HEALTHY CHILD 
ARE PRACTICALLY NIL AND THE PREGNANCY 
MAKES THE PROGNOSIS HOPELESS FOR THE 
WOMAN. REQUIRE THAT ABORTED CASES BE FOL- 
LOWED UP AND THE END RESULTS REPORTED FOR 
FUTURE GUIDANCE. 
In the few cases where early termination of pregnancy is 
believed advisable after unbiased consultation of experienced 
observers, the method of emptying the uterus should be left to 
the judgment of the operator. If the case is seen within the 
first two months, the cervix may be dilated with the Hegar dila- 
tors and the ovum removed with the placenta or curette forceps. 
After the first two months, the vaginal hysterotomy is perhaps 
the best procedure. Frankenthal believes in the slow dilatation 
of the cervix with tents. Other methods, as the use of a 
catheter or pack, are less satisfactory and perhaps more dan- 
gerous. When possible these operations should be accom- 
plished with local anesthesia. Both ether and chloroform are 
believed to be dangerous to the tuberculous. 
Radical operations to insure permanent sterility have been 
advocated, but are not favored as they jvill increase the imme- 
diate mortality. The legality of such a procedure may also be TUBERCULOSIS AND PREGNANCY 
361 
questioned in the absence of local pathology justifying the 
removal or mutilation of the organs of generation. 
The various writers on tuberculosis and pregnancy are appar- 
ently agreed that, unless terminated within the first three 
months, the pregnancy should be carried to viability or term. 
Some would induce premature labor on the ground that the 
mother’s chances are bettered. This would hardly seem justifi- 
able as it lessens the chances of the child without materially 
improving the prognosis for the mother. It is believed that 
mo,st women should be carried to term and the labor made as 
easy as possible with the use of analgesics and usually low 
forceps for all women with normal conditions of the perineum. 
The expulsive contractions of the second stage may be re- 
sponsible for grave circulatory disturbances. Pituitrin should 
not be used as a substitute for forceps in these cases. 
Hypodermic medication with heroin, morphin, or morphin and 
scopolamin may be used to control a painful first stage, and the 
use of nitrous oxid-oxygen analgesia for delivery. A gauze filter 
may be placed in the inhaler so as to prevent contamination of 
the tubes and gas bags. The inhaler should always be carefully 
cleansed with soap and water and sterilized with alcohol or lysol 
solution. It is advisable to wash the tube and bags with running 
hot water. C. H. D. CHAPTER 27 
TUBERCULOSIS AND PULMONARY HEMORRHAGE 
Hemorrhage in Tuberculosis. Pulmonary Hemorrhage. Bleed- 
ing from the Lungs. Symptoms of Pulmonary Hemorrhage. 
Methods for Treating and Controlling Hemorrhages. 
General Consideration. If an individual who for some time 
has been the victim of a troublesome cough, in a fit of coughing 
brings up a mouthful of blood that in all probability came from 
the lungs, and if at the same time he is suffering from active 
pulmonary disease, then the hemorrhage was positively pulmon- 
ary. Most all pulmonary hemorrhages are of a tuberculous 
nature. In about 20% of all cases it is an initial symptom but in 
the greater number (80%) it is a terminal event. In old chronic 
cases of pulmonary tuberculosis a little pulmonary oozing, a 
small hemoptysis is of very slight importance and does not call 
for immediate treatment. This slight hemorrhage is simply the 
expression of a favorably prognostic sign showing that the tuber- 
culous process is favoring a contraction. 
A pulmonary hemorrhage usually comes on suddenly without 
any previous symptoms or warnings; however, occasionally 
patients complain for days of premonitory signs of a dull heavy 
feeling, pressure like symptoms. This is particularly mentioned 
by those who have had repeated hemoptysis. Meteorological con- 
ditions seem to influence pulmonary hemorrhage. Pulmonary 
hemorrhages are more frequent on days of greater humidity than 
on the dry. There seems to be some connection between pul- 
monary hemorrhage and moist days, as if moisture in the air 
would play an important role; air pressure and the air currents 
also are accessory factors. The bleeding is less frequent with 
the north and east winds and more so when the winds are from 
the south and west, perhaps because the south and west winds 
carry more moisture. It is twice as frequent in men as in 
women. Hemorrhage appears more frequently as a recurring 
attack while in a high altitude and is much less frequent in the 
moderately high or in the low lands. A pulmonary hemorrhage 
362 TUBERCULOSIS AND PULMONARY HEMORRHAGE 
363 
means at least a teaspoonful of blood—a little blood streaked 
sputum should not be considered as a hemorrhage. In consider- 
ing pulmonary hemorrhages we must be sure that the blood was 
coughed up, not vomited, that it did not come from the stomach, 
from an oesophageal varix nor from the mouth or the posterior 
nares. 
The Treatment of Pulmonary Hemorrhage 
(a) Mechanical; (b) Medicinal 
Any treatment, either mechanical, medicinal or otherwise, has 
for its prime object the bringing about of an increase in the 
coagulability of the blood. 
(a) By mechanical methods. The coagulability of the blood 
may be increased and the intrathoracic pressure decreased by 
the old method of applying a ligature very tightly about one or 
both lower extremities, usually around the middle of the thigh, 
allowing the constriction to remain from a half to three-quarters 
of an hour, after which the binder must be slowly and gradually 
loosened. This by slowing the return circulation of blood to the 
chest cavity, produces venous stasis with increased carboniza- 
tion of the blood, increased viscosity and consequently increased 
coagulability. Another very simple and efficient method for con- 
trolling pulmonary hemorrhage is by means of adhesive straps 
applied firmly about that half of the chest cavity from which the 
hemoptysis is supposed to come in the manner so much in use 
in pleurisy and intercostal neuralgia. 
(b) By medicinal means. The coagulability of the blood may 
be brought about by remedies which will first increase the fib- 
rinogen content of the blood and secondly by such medicaments 
as will tend to increase the rapidity of the blood’s coagulability, 
or both. The fibrinogen may be greatly increased by injecting 
subcutaneously from 10 to 20 cc of some body foreign albumen, 
for which purpose horse serum is now most suitable, as well as 
available. This injection is followed by an increase of the fibrin 
ferment, globulin, and the fibrinogen coagulability is increased 
10 fold within 24 hours, remaining at that point 5 to 8 days and 
then again gradually returning to normal. In place of horse 
serum a sterilized gelatin solution may be employed; from 30 to 
60 cc of a 2 per cent solution may be given subcutaneously and 
like all solutions intended for subcutaneous medication must be 
prepared with all aseptic precautions. This gelatin solution has 
a decided advantage over horse serum in not producing an 364 
CLINICAL TUBERCULOSIS 
anaphylactic reaction which must always be considered when 
using the latter. 
To increase the rapidity of the blood’s coagulability remedies 
are used which will produce, either local or general, a change in 
the condition of the blood in the sense of bringing about a dilu- 
tion so that the blood vessels absorb more lymph fluid making 
the blood more hydrolytic. Experience has demonstrated that 
such blood possesses much greater and quicker properties to 
coagulate and R. van den Velden has shown that nothing favors 
this more than an intravenous injection of about 5 cc of a 10 per 
cent sterile salt solution. By this method the increased coagu- 
lability reaches its maximum in about 20 minutes, dropping again 
back to normal in about one hour when the injection may be 
repeated. To avoid these oft-repeated intravenous injections 
which to some patients may be very irritating, a subcutaneous 
one may be given, using from 100 to 200 cc of a 2 per cent 
sterile salt solution by the slow or drop method. Pulmonary 
hemorrhage may also be controlled by remedies which will bring 
about a change in the size of the lumen of the bleeding vessel. 
To bring about this change only one remedy is known in medi- 
cine and that is Adrenalin, but this remedy will also raise the 
blood pressure, which in consequence thereof may be followed by 
still more serious difficulties, as a thrombus may be loosened and 
in this may become the source of a renewed hemorrhage. This 
remedy in about one or two milligram doses may be given either 
by mouth or may be subcutaneously administered. 
A remedy used to lessen the quantity of blood flowing from 
a bleeding vessel in a given time is Amyl Nitrite, but it is un- 
reliable and not suitable because its therapeutic effect is of too 
short a duration. Two other remedies which are of very much 
importance in the treatment of pulmonary hemorrhage are tinc- 
ture digitalis and tincture aconite root, depending upon each 
individual case as to which one is to be given. In the presence of 
cardiac weakness and low blood pressure, feeble, hardly palpable 
pulse, and repeated small hemorrhages pointing to a passive con- 
gestion, give tincture digitalis, but if the pulse is full and bound- 
ing, much elevation of temperature, much excitement, slightly 
high blood pressure and much bleeding as is most frequent in 
pulmonary hemorrhages, then use tincture aconite. Of other 
remedies of undoubted service in pulmonary hemorrhage are 
potassium bromide in 20 to 30 grain doses every three hours, TUBERCULOSIS AND PULMONARY HEMORRHAGE 
365 
dissolved in cold water and calcium chloride or lactate in 5 
grain doses every three hours. Remedies like acidum tanni- 
cum, acidum gallicum, plumbum aceticum, ferri chlorida hydra- 
tis canadensis and the newer ones like Stypticine, Styptol, etc., 
should be discarded. Fluid Extract Ergot is of no value in 
pulmonary hemorrhages; it is positively contraindicated, for 
in order to produce the necessary contractions of a blood vessel 
to check the hemorrhage it would be necessary to give it in 
enormously large, in toxic, doses. 
In recent years the use of substances derived from tissues and 
organs of animals, chiefly colloidal in character, has found great 
therapeutic favor in the treatment of pulmonary hemorrhage, in 
some quarters. Organotherapy or opotherapy as it is known 
(from opos. juice) is applied today in the sense of supplying ani- 
mal derivatives to a diseased human organism with the desire to 
give either to such a diseased body something in which it usually 
is deficient, a condition which is chiefly manifested in body weak- 
ness, that is something to give strength, or to lessen the amount 
of labor required in the human economy by supplying the neces- 
sary protein already prepared and requiring simply absorption 
by the body tissues without any elaboration. It is also given 
with a view of stimulating the secretory functions in a diseased 
body, as they are usually in abeyance. 
For the treatment of pulmonary hemorrhage, Opotherapy Pul- 
monalae, or ingestion of dried, sterile, powdered lung extract has 
not been proven to be of any service, but Opotherapy Hepatica 
has been found to be of undoubted value. Gilbert and Carnot 
have found the giving of the dried, powdered, sterilized liver ex- 
tract to be a sovereign remedy in controlling pulmonary hem- 
orrhage. The Extractum Hepatica is given in pill form of about 
5 grains each, giving from 5 to 8 pills daily. These investigators 
recommend the giving of calcium chloride with extract of opium, 
simultaneously administered, but find that all other remedies are 
of very little avail when compared to liver extract. Trousseau 
recommends the use of powdered ipecac root in doses sufficient 
to produce nausea should Extractum Hepatica not prove prompt- 
ly efficacious. In place of ipecac root the isolated alkaloid 
Emetin offered in ampules in proper dosage is now used by 
many clinicians. Rest has tested the action of the extract pre- 
pared from the posterior lobe of the pituitary body in 12 cases of 
most profuse pulmonary hemorrhage which were not influenced 366 
CLINICAL TUBERCULOSIS 
by the ordinary methods of medication, with the most gratifying 
results; in most all cases the hemorrhage stopped quickly and 
promptly. 
In repeated and profuse hemorrhages occurring at longer or 
shorter intervals in which the usual medicinal treatment is of no 
avail, the establishing of an artificial pneumothorax may be most 
desirable. By proper compression of the lungs, bringing the 
cavity walls into closer apposition, the vessels from which these 
repeated hemorrhages occur are closed, and a permanent arrest 
of~the hemorrhage may confidently be expected if the pneu- 
mothorax is maintained for a sufficient length of time. 
Prophylaxis 
At the present time with our ever-increasing exactness, our 
knowledge of the use of medicines, of the etiology and causative 
factors of most diseases, with a closer observation and surveil- 
lance of patients at sanatoria as well as the ambulatory cases, we 
are in a position in many instances positively to anticipate a 
pulmonary hemorrhage and in many such cases are able by 
proper means and methods to avert it. In an active tuberculous 
subject a sudden rise in blood pressure may be the forerunner of 
a pulmonary hemorrhage. This rising phase of hypertension may 
gradually lead to hemoptysis or it may continue for weeks before 
the actual hemorrhage occurs, and in many tuberculous individ- 
uals with a tendency to bleeding this hypertension will be found 
constant with a gradual increase in tension up to the moment of 
the hemoptysis; hence, frequent blood pressure observations may 
point out the prophylactic treatment necessary in many cases of 
threatened hemorrhage, as the blood pressure in the tuberculous 
is usually very low, any tendency to a gradual increase of 
the tension without a corresponding improvement in the patient’s 
condition should always be received with much scepticism and 
immediate rest instituted. 
Another method intended as a protective measure applied to 
patients that have had a previous pulmonary hemorrhage is by 
administering autogenous vaccines. Judging from the literature 
on this point, the use of these vaccines of1 mixed infection is a 
favorable factor in preventing hemoptysis in proportion of 1 to 
3. The theory that the administration of autogenous vaccines to 
the tuberculous subject may inhibit further hemorrhages is based 
on the fact that the vaccines of mixed infection stimulate the 
antibody productions, preventing further action of the invading TUBERCULOSIS AND PULMONARY HEMORRHAGE 
367 
organisms upon the weakened, damaged and constantly de- 
stroyed lung tissue, protecting and strengthening the structure 
of the lung surrounding the blood vessel, thereby preventing fur- 
ther bleeding. 
Practical Rules for Controlling Pulmonary Hemorrhage 
In a given case of pulmonary hemorrhage the following general 
directions will be found both serviceable and practical. 
Put the patient at once into a comfortable bed with the head 
and shoulders slightly elevated. Instruct the attendant or nurse 
that the sufferer must not be moved or turned until all signs of 
hemorrhage have been for some days arrested. Exclude all idle 
gossipers and visitors from the room. Keep the room well ven- 
tilated, somewhat darkened. As soon as the patient is in a com- 
fortable position administer a teaspoonful of sodium chloride or 
salt dissolved in a glass of cold water; it is at this point that the 
inhalation of Nitrite of Amyl may be of service. Apply an ice bag 
over the heart and give by mouth oft-repeated small pieces of ice, 
which the patient should chew, swallowing the still undissolved 
particles. As it is also very necessary to limit the intake of 
liquids, especially water, in order to lessen the amount of fluid in 
the pulmonary circuit as well as to maintain a comparatively low 
blood pressure, the giving of ice in this manner will serve a 
double purpose. 
To quiet the nervous fears and to slow the rapid action of the 
heart, a hypodermic injection of morphine Y\ grain, and Mso atro- 
pine, should be given. At this time no attempt should be made 
by the attending physician at a thorough examination of the 
chest; light palpation as well as auscultation may be allowable, 
but percussion must be strictly withheld; a closer examination is 
permissible only after a few days. All drinks and foods must be 
given cold; solid foods are prohibited. Warm drinks and all 
stimulating beverages are strictly interdicted. The following 
prescriptions should be given alternately in cold water every 1 y2 
to 2 hours: 
Prescription No. 1. 
Take: Tincture Aconite root, M. xxiv (1.5 cc) 
Tincture Opii Deodorated, drachms two (8.0 cc) 
Antipyrene, drachms two (8.0 gms.) 
Syr. Orange Flowers, ounce one (30. cc) 
Aqua Cinnamon, sufficient to make three ounces.. (q.s.ad. 90.0 cc) 
Directions: One teaspoonful in little cold water once in 3 or 4 
hours. 368 
CLINICAL TUBERCULOSIS 
Prescription No. 2. 
Take: Sodium Bromide, drachms six (24.0 gms.) 
Calcium Chloride or Lactate, drachms two ( 8.0 gms.) 
Syrup of Licorice root, ounce one (30.0 cc) 
Aqua Peppermint, sufficient to make three ounces (q.s.ad. 90.0 cc) 
Directions: One teaspoonful in a mouthful water once in 3 or 4 
hours. 
These two prescriptions (No. 1 and 2) should be given alternately 
once every one and one-half to two hours. Here in the second 
prescription licorice syrup is added in order to differentiate the two 
solutions. 
This at least in a measure will check the immediately dan- 
gerous hemorrhage. Should the hemorrhage still continue in spite 
of all, the intravenous injection of 5 cc of a 10 per cent solution of 
salt should be given or 100 or 200 cc of a 2 per cent salt solution 
subcutaneously administered, or a pint or more of Normal Salt 
solution may be given by rectum (retention enema) according.to 
the usually employed drop method. Ligatures applied to the ex- 
tremities should be used earlier. Injections of horse serum 10 
to 20 cc or gelatin 30 to 60 cc of a 2 per cent solution may be 
resorted to if the case is not benefited by the simpler methods, 
leaving the use of the other recommended remedies as well as 
artificial pneumothorax to the discretion of the physician in at- 
tendance. CHAPTER 28 
TUBERCULOUS LARYNGITIS 
Tuberculosis of the Larynx. Laryngeal Tuberculosis. Laryn- 
gitis Tuberculosa. Laryngeal Phthisis. Throat Consumption. 
General Consideration. By way of introduction to the subject 
of laryngeal tuberculosis, and in order to indicate its relationship 
especially to pulmonary tuberculosis, it will be well at the outset 
to make certain statements of facts: Laryngeal tuberculosis, of 
itself, is an exceedingly serious disease; it does not exist unasso- 
ciated with pulmonary tuberculosis for more than a short time, 
if it exists independently at all; laryngeal tuberculosis is a very 
common complication of the pulmonary form, and affects pro- 
foundly and unfavorably the prognosis of that disease. It is 
prone to produce very severe pain, and by reason of this pain, 
induced by swallowing, breaks down one of the most important 
bulwarks of resistance to both the pulmonic and the laryngeal 
disease, namely, the taking in of nutriment. (27) (6). 
Etiology. In approaching more closely the subject of (57) laryn- 
geal tuberculosis, let us attempt to understand the anatomic and 
physiologic facts underlying the production of tuberculosis in 
the larynx. In probably much more than ninety per cent of the 
cases of tuberculosis of the upper air passages, the disease im- 
plants itself, not in the mouth, nose, pharynx, or trachea, but in 
the larynx. What is the explanation of this fact, that out of the 
perhaps fourteen or fifteen inches of distance between the lungs 
and the outer air, this little space of two inches, or less, should 
suffer so vast a preponderance of vulnerability to the tubercle 
bacillus? The larynx constitutes for the purpose of this subject 
simply a peculiar anatomic and physiologic section in the pas- 
sages through which all air and secretion must pass between the 
outer air and the lungs. But that statement applies as well to 
the trachea, below, and to the pharynx, the mouth, and the nose 
above, all of which spaces are several times more roomy than is 
the larynx. If we are to find the explanation for the extraordi- 
nary susceptibility of the larynx to tuberculosis, compared to the 
369 370 
CLINICAL TUBERCULOSIS 
other upper air spaces, we evidently must examine the peculiar- 
ities of the larynx itself. 
Two anatomic facts are significant. The larynx is not only 
extremely irregular in its anatomical conformation, but it is also 
exceedingly narrow. In passing through this narrow, irregular 
laryngeal space, it is easy for the air, dust, or secretion, whether 
moving upwards or downwards, to impinge on the epiglottis, 
Fig. 45. The normal larynx. Act of phonation (viewed from above) 
1. Vocal cord (true cord). 
2. Ventricular band (false cord). 
3. Epiglottis. 
4. Glosso-epiglottic ligament. 
5. Cushion of the epiglottis. 
6. Ventricle of the larynx (Mor- 
gagni). 
7. Ary-epiglottic fold. 
8. The cartilage of Wrisberg. 
9. Rings of the trachea. 
10. Inter-arytenoid fold (commis- 
sure). 
11. Posterior pharyngeal wall. 
12. The cartilage of Santorini. 
13. Pyriform, or pyramidal sinus. 
14. Bulbus portion of the aryteno- 
epiglottidean fold. 
the false cords, the true cords or to lodge in the sinus of Mor- 
gagni or the subglottic space. 
Not only is the larynx narrow and irregular, but it is one of the 
two or three most active- organs in the body. It moves quickly 
and intensively in talking, both with respect to the inner (in- 
trinsic) and the outer (extrinsic) musculature. In this move- 
ment of talking not only is the mucous membrane, especially in 
the arytenoid region, involved, but the vocal cords themselves 
are brought repeatedly into contact, especially if conditions of TUBERCULOUS LARYNGITIS 
371 
inflammation be present. The larynx also moves in coughing. 
In this process, the patient inhales deeply, the vocal cords close 
tightly together, the musculature of the chest wall contracts on 
the air in the lungs, thus producing air tension against the closed 
vocal cords, the cords open, and the air is projected violently 
upwards. 
Fig. 46. Sagittal section of the upper air passages. 
A. and P. Seifert, Berlin 
(From wax model, E. L. Kenyon collection) 
1. Frontal sinus. 
2. Sphenoidal sinus. 
3. Lower turbinate body. 
4. Orifice of Eustachian tube. 
5. Hard palate; superior maxillary 
bone. 
6. Soft palate. 
7. Epiglottis. 
8. Tongue; note the intimate mus- 
cular relationship between the 
larynx and base of the tongue. 
9. False vocal cord. 
10. Vocal cord. 
11. Lower maxilla. 
12. Base of sphenoid. 
13. Body of spinal vertebra. 
14. Brain. 
There is also movement of the larynx in swallowing-. Talking 
and coughing effect especially the arytenoid and vocal cord re- 372 
CLINICAL TUBERCULOSIS 
gions. Swallowing affects especially the upper aperture of the 
larynx, and the epiglottis. In swallowing, the bolus of food is 
received on the upper surface of the tongue and the tongue 
forces it backwards to the pharyngeal wall; the soft palate raises, 
the entire larynx is strongly elevated against the epiglottis, the 
epiglottis against the hyoid bone and base of the tongue. The 
base of the tongue moves backward and downward, and meets 
strongly the upmoving larynx, while the bolus is grasped by the 
oesophageal peristalsis. Thus we have a picture of the under- 
Fig. 47. Interior surface of left side of larynx 
(From wax model, E. L. Kenyon collection) 
1. Trachea, showing cartilaginous 
rings. 
2. Junction of trachea and larynx. 
3. Subglottic space of larynx. 
4. Left vocal cord, as if in the act 
of phonation. 
5. Sinus of Margagni. 
6. Left false vocal cord. 
7. Epiglottis. 
8. Thyroid cartilage. 
9. Cricoid cartilage. 
lying anatomical and physiological conditions which constitute 
the foundation for the lodgment of the tubercle bacillus in the 
larynx. TUBERCULOUS LARYNGITIS 
373 
It becomes necessary to show what factors encourage the 
lodgment of the tubercule bacillus. The bacillus gains access to 
the laryngeal structures either (1) by penetrating the superficial 
layers of the mucous membrane; (2) by way of the blood; or (3) 
by way of the lymphatics. While either of the two last sources 
of infection are certainly possible and, theoretically, may occur, it 
is believed that the larynx is almost always infected by pene- 
tration of the mucous membrane from the lumen of the larynx. 
One sometimes has the opportunity of witnessing in the pul- 
monary patient the invasion of a wound in the mouth, as after 
tooth extraction, by the tubercle bacillus.1 
Long ago Wm. E. Casselberry pointed out how inflammatory 
infiltration tended to encourage minute cracks in the laryngeal 
mucous membrane, especially where the arytenoid mucous mem- 
brane joins the posterior wall, and he also pointed out how the 
movements of the arytenoid in talking encouraged these abra- 
sions. 
Chronic laryngitis (non-tuberculous) has been mentioned by 
some authors as an important preliminary preparation for the 
local lodgment of the tubercle bacillus. That simple chronic 
laryngitis is extremely important in this connection does not 
seem to be clear. However, in so far as pharyngeal abnormali- 
ties, for example, pharyngitis, nasal accessory sinus disease, or 
other nasal abnormalities, constitute factors underlying a chronic 
laryngitis in a patient, the eradication of such abnormalities is to 
be given consideration. Another possible etiological factor lies 
in the lingual tonsil. If large, it undoubtedly may be responsi- 
ble for irritation in the larynx from mechanical causes, as it lies 
right above the epiglottis, on the base of the tongue. If in such 
a location it contained actual infection, the products of that infec- 
tion would certainly tend to get into the larynx. 
A most striking picture of resistance of the mucous membrane of the larynx to the 
tubercle bacillus is witnessed in a large percentage of patients with pulmonary tuber- 
culosis. For months the surface may be continuously bathed with infectious secretion 
from the lungs without local implantation of the disease. Finally, however, if the pul- 
monic disease becomes progressively more and more serious, the larynx, in the course 
of the downward progress of the patient's resistance, usually succumbs. 
Since invasion of the laryngeal mucous membrane occurs under such varying pulmonic 
conditions, relatively accidental factors may often determine the invading process. These 
factors concern both constitutional and local resistance. Constitutional resistance 
diminishes as the pulmonic disease progresses. So also does local resistance, until in the 
final stages of pulmonary tuberculosis, the larynx becomes involved in nearly all cases 
(probably more than 75%). When the constitutional resistance is relatively high, as in 
the early stages of a slowly progressing pulmonary tuberculosis, the larynx should not 
become involved, unless through diminished local resistance. In an organ so narrow, 
so irregular, and so movable as the larynx, which is continuously exposed to tuberculous 
infection, it is evidently of the greatest importance that the elasticity of the mucous 
membrane should not be impaired. 
lSee Chapter XXXIII—“Tuberculosis of the Eye and the Mucous Surfaces”—See Foot- 
note on page 448.—J. R. 374 
CLINICAL TUBERCULOSIS 
It is common for the pulmonary patient to locate the source of 
his cough in the vicinity of the larynx which signifies that the 
secretion is being driven upwards until it meets with laryngeal 
obstruction and there it sticks, irritates, and produces a cough. 
Oedematous infiltration is one of the consequences; impaired 
elasticity is another, impairment of the epithelial resistance of 
the mucous membrane, and even cracking of the surface, are then 
easy possibilities. The tubercle bacillus already present in the 
larynx, is, through the agency of cough and other laryngeal move- 
ment factors, presumably churned into a more or less pre-injured 
mucous membrane. 
Primary Tuberculosis of the Larynx (163). Very much has 
been said in support and denial of the proposition that laryngeal 
tuberculosis may precede tuberculosis of the lungs. No theo- 
retic reason exists which excludes the possibility of primary 
laryngeal tuberculosis, but this is probably a rare occurrence. 
Sir St. Clair Thompson believes that tuberculosis of the larynx 
can be primary, and cites one observed case in which the laryn- 
geal disease preceded any sign elswhere for three full years. 
The great difficulty is in proving the priority of the laryngeal 
invasion. When laryngeal tuberculosis is discovered as the first 
evidence of tuberculous disease in the body, the diagnosis of pul- 
monary disease practically always follows. Usually, if a laryn- 
geal tuberculosis exists as a supposedly primary disease an old 
latent tuberculous focus in the lung has probably pre-existed for 
some time; however, laryngeal tuberculosis may be primary and 
failure to prove pulmonary tuberculosis at the time is not suf- 
ficient reason for denying the truth of the laryngeal diagnosis. 
Course of the Disease. This varies with the clinical picture, 
i. e., whether the pulmonary or the laryngeal disorder predomi- 
nates. Most frequently the laryngeal disease follows late to the 
pulmonary form and usually shortly before the end. As stated, 
in most instances pulmonary tuberculosis is the chief difficulty, 
laryngeal generally secondary, and only exceptionally does the 
laryngeal disease play the leading part. 
Physical Manifestations of Laryngeal Tuberculosis. Visual 
study of the larynx is technically difficult, and, relatively to our 
study of the skin, the mouth or nasal organs, necessarily in- 
accurate. Not only is the organ small, fixedly distant from the 
eye, and imperfectly lighted, but it must usually be studied as 
depicted in a small throat mirror image and always from one TUBERCULOUS LARYNGITIS 
375 
point of vantage only. This is without consideration of the addi- 
tional difficulties resulting from sensitiveness, and consequent 
hindering movements, of the patient. If the study of this organ 
could be carried out with the accuracy with which dermato- 
logical lesions may always be studied, the earlier manifestations 
of any laryngeal disease could be as well defined as are those of 
the skin. 
The earliest manifestations of laryngeal tuberculosis are, for 
the above reasons, not even yet accurately defined and their rec- 
ognition is dependent upon long and extensive laryngeal experi- 
ence. They resolve themselves into (A) general paleness of the 
mucous membrane; (B) localized discoloration and infiltration; 
(C) localized ulceration. 
(A) The paleness of the mucous membrane reflects the general 
anemia of the patient and is to be expected in this disease. It is, 
however, offset many times by actual hyperemia, and especially 
by a peculiar dusky redness, dependent, for example, upon per- 
sistent breathing of cold air in winter, a simple laryngitis, or, the 
rarely excellent general condition of the patient. 
(B) Localized discoloration and infiltration gains its signifi- 
cance largely by its isolation and posterior location. The favor- 
ite sites are posterior, often at the junction of one vocal cord with 
its arytenoid, or in the posterior commissure at the side of the 
arytenoid, or on the laryngeal surface of the epiglottis. They are 
small, usually dusky red, and but little elevated and their signifi- 
cance is enhanced by their slowness of growth and great persist- 
ence. 
(C) Ulceration may inaugurate the tuberculous process. The 
locations are apt to correspond with those just mentioned for 
localized infiltrations. The ulcers when first seen may be very 
small, shallow, irregular, and covered by a thin greyish-white 
secretion. General paleness of the mucous membrane always 
adds to the diagnostic significance of any lesion. 
When such beginning lesions progress and especially if others 
be added, the picture of the larynx may attain striking variety 
and irregularity of disease manifestation. Understandable de- 
scription is beyond possibility. The lesions considered sepa- 
rately resolve themselves into (1) infiltration; (2) tumor-like 
masses; (3) ulceration; (4) miliary protuberances. Eventually 
in essentially all progressive cases ulceration sooner or later su- 376 
CLINICAL TUBERCULOSIS 
pervenes, but its advent may be relatively delayed. Any lesion 
may undergo ulceration. 
(1) Infiltration. Infiltration may involve one, or later, both 
vocal cords. The cords then appear rough and irregularly en- 
larged. Between the arytenoids (the posterior commissure), in- 
Fig. 48. Tuberculous Laryngitis. Swelling of the Arytenoid. 
E. Fletcher Ingals Collection, Rush Medical College 
filtration (thickening) may occur, even in pulmonary tubercu- 
losis, without local tuberculous significance, resulting apparently 
from excessive coughing and irritation. The same may be said 
of bilateral enlargement of the aryteno-epiglottic folds. If the 
latter enlargement be asymmetrical, and if the typical pear shape 
Fig. 49. Tuberculous Laryngitis. Large Granulation Tumor of the Left Vocal Cord with 
Congestion of the Epiglottis 
E. Fletcher Ingals Collection, Rush Medical College 
be present, even when bilateral, the picture becomes almost 
pathognomonic. The epiglottis is also commonly subject to in- 
filtration and this may be marked. 
(2) Tumor Formation. Tumor-like bodies are common espe- 
cially in the later manifestations, but may also begin the local TUBERCULOUS LARYNGITIS 
377 
disease. They may have smooth surfaces, appear compact and 
solid, or they may be irregular, soft, pale, and fungous, or papil- 
lomatous. These bodies may be surrounded by ulcerated sur- 
faces, or themselves be ulcerated. They may be small, or they 
may almost occlude the lumen of the larynx. The site of growth 
is most often posterior, especially about the arytenoids and pos- 
terior commissure. As the disease progresses, increasing ulcera- 
tion complicates and adds irregularity to the picture. 
(3) Ulceration. The marked tendency to ulceration is the 
most serious aspect of laryngeal tuberculosis. It often consti- 
tutes the very first indication of the disease, it becomes more 
serious as the disease progresses, and is the chief cause for 
the characteristic pain of the laryngeal sufferer. The ulceration, 
Fig. 50. Tuberculous Laryngitis. Superficial Ulceration. Fungous Granulation of 
Posterior Commissure 
E. Fletcher Ingals Collection, Rush Medical College 
when typically manifested, is shallow, with irregular “worm 
eaten” edges, irregular floor, and thin greyish-white secretion. 
A tendency to breaking down into ulceration in spots is charac- 
teristic, small ulcers existing between islets of intact mucous 
membrane. At times, especially on the posterior wall, the peri- 
chondrium and the cartilage itself is invaded with this spotted 
ulceration. The cartilage may be invaded by the tuberculous 
disease without ulceration, and this is likely to be accompanied 
by much infiltration. 
The epiglottis is frequently ulcerated both superficially in the 
mucous membrane, and deeply in the cartilage, and any portion, 
or all, of the organ may thus become destroyed. The surface of 
one, or both, vocal cords may be more or less extensively ulcer- 
ated, and, often, the irregularity of the destructive effects pro- 
duces a typical saw-edged appearance of the cord. Infiltration, 378 
CLINICAL TUBERCULOSIS 
different types of tumor formation and ulceration, may be pres- 
ent all in the same patient, and as has been said, the infiltrated 
and tumor areas may themselves be ulcerated. 
(4) Miliary Form. Another manner of typical appearance is 
also sometimes presented by the presence of scattered small mil- 
let seed sized rounded, greyish, or yellowish, elevations of dis- 
ease in the mucous membrane. Such deposits of miliary tuber- 
cles may also be seen in generalized miliary tuberculosis. 
Pathology. The microscopic pathology is not essentially dif- 
ferent from that of tuberculosis in other parts of the body. See 
Chapter 8, page 56 “Histology and Pathology.” 
Symptoms. Cough, irritation, impairment of the voice, local- 
ized pain, difficulty of swallowing, and, rarely, dyspnea due to 
laryngeal stenosis, are the localized symptoms of the disease. 
In any manner of laryngeal inflammation the most evident 
symptom is a local irritation that produces cough. Since, how- 
ever, cough, due to the lung disease is present, the local lesion 
may go unrealized by the patient, and especially the physician, 
until it produces other and more distinctly localizing symptoms, 
particularly hoarseness and laryngeal pain; and such delay in 
recognition is not uncommonly fatal to the patient. This fact 
emphasizes the importance of systematic laryngeal examination 
in all cases of pulmonary tuberculosis. On the other hand, if the 
primary symptoms referable to the larynx are those produced by 
laryngeal tuberculosis, the beginning localizing symptoms may 
be irritation with cough, or hoarseness alone, or both combined. 
Laryngeal tuberculosis may be present for some time without 
pain. When pain does occur, it is the most distressing symptom 
of the condition and may be of any degree and so excruciating 
does the pain often become on swallowing, that the patient would 
actually rather starve than go through the act of taking nourish- 
ment. Under such circumstances, the patient is steadily directed 
towards his final end as he is no longer willing to take the nour- 
ishment upon which his resistance to the disease depends. 
In certain conditions, even in the absence of ulceration, move- 
ment that involves laryngeal infiltrations, especially in the region 
of the arytenoids may result in a moderate degree of pain. But 
the more serious degrees of pain are dependent upon sensitive 
ulcerative surfaces, with their nerve endings, exposed to rubbing 
and to pressure. In ulcerative lesions of the lower part of the TUBERCULOUS LARYNGITIS 
379 
larynx, especially the vocal cords, the pain is likely to be absent, 
or moderate in degree. Coughing and talking may then be mod- 
erately painful. Rubbing together of ulcerated false cords on 
coughing and talking produces pain. Ulcers about the aryte- 
noids are painful, especially because of movement. This is true 
in all the upper part of the larynx. In proportion as the ulcer 
approaches the upper opening of the organ, and particularly if it 
involves the epiglottis, the resulting pain, especially from swal- 
lowing, is the most severe produced by this disease. Its inten- 
sity is often comparable with that caused by the passing of a cal- 
culus through the ureter. 
The general symptoms of laryngeal tuberculosis are usually 
obscured by the accompanying symptoms of pulmonary disorder. 
If the latter disease has not yet actively developed, slight in- 
crease of temperature and pulse rate, with a certain degree of 
general weakness are likely to be present. When the disease is 
limited to a small area, however, and not acute, no general symp- 
toms are to be expected from the laryngeal disease alone. 
Diagnosis—Differential Diagnosis.(153)—The presence of pul- 
monary tuberculosis, if known, serves to direct the suspicions 
of the laryngologist towards laryngeal tuberculosis. But when 
pulmonary tuberculosis is not known to be present, and not at 
the time discoverable, the diagnostician is, nevertheless, by no 
means warrranted in excluding from his consideration local tu- 
berculous disease. In either case he will find it necessary from 
a differential standpoint to consider especially chronic simple 
laryngitis, syphilis, lupus, and, rarely, carcinoma. In certain 
cases two, or even three of these diseases, including tuberculosis, 
may be present in the same larynx. The history often serves to 
shape the conclusion and general tests, as that with tuberculin, 
or the Wassermann reaction may be very important. The study 
of general symptoms, or of local symptoms elsewhere in the 
body, may be the factor that settles the doubt. Our view of the 
diseased larynx, as has been said, is always relatively hampered. 
The time when the diagnosis is of greatest importance is at the 
inception of the disease when the diagnosis is hardest to make. 
A study of the disease as to its manner of progress, or as to its 
response to treatment, may also be necessary before a clear diag- 
nosis is possible to be made. 380 
CLINICAL TUBERCULOSIS 
The distinctive features between Tuberculous Laryngitis, Chronic Sim- 
ple Laryngitis, Syphilitic Laryngitis, Carcinoma of the Larynx and Lupus 
of the Larynx may be seen in the following tables: 
A. TUBERCULOUS LARYN- 
GITIS 
B. CHRONIC SIMPLE LARYN- 
GITIS 
Usually young individuals. 
Age of Patient 
Not important as to age. 
(Catarrhal Laryngitis) 
Are usually present; slight, or severe; 
depend on condition of lungs. 
General Symptoms 
Are usually absent; possibly those of ac- 
companying bronchitis, or pharyngitis. 
Onset and Early Manifestations 
The mucous membrane apt to be gener- 
ally pale; lesion small, localized, mono- 
lateral ; posterior part of larynx; elevation, 
or ulceration; voice hoarse, weak or 
normal; slower progress than syphilis. 
A generalized hyperemia, is likely to be 
bilateral. Not ulcerated ; hoarseness; mod- 
erate swelling. 
Wassermann is usually negative. Tuber- 
culin may be positive. Tubercle bacillus 
when present, may have come from pul- 
monary and not from laryngeal sputum. 
General Tests 
Wassermann and Tuberculin tests usually 
negative; tubercle bacilli absent. 
Pain or Ulceration 
Is due chiefly to ulceration; depends on 
location of ulcer; most severe when pos- 
terior and high. 
Is rare; ulceration is absent. 
More rapid than carcinoma; less rapid 
than syphilis; lesions tend to become multi- 
ple, with multiple areas of ulceration. Ste- 
nosis of larynx rare. 
Lesions 
Rarely produces irregular localized infil- 
tration ; usually a generalized moderate 
swelling. 
Treatment 
The effect of antisyphilitic is negative. 
Treatment: General systemic and local as 
given in the text, chiefly paliative to relieve 
pain. 
Difficult of cure., Paliative and local. 
Not affected by antisyphilitic treatment. 
C. SYPHILITIC LARYNGITIS 
D. CARCINOMA OF THE 
LARYNX 
Not important, but most often young; 
may be child. 
Age of Patient 
Over thirty. 
Signs of disease elsewhere in body; lym- 
phatic glands enlarged; history of genital 
infection and progress (if obtainable). 
General Symptoms 
At first absent; later, loss of weight, 
weakness, and cachexia. 
Onset and Early Manifestations 
Depends on whether early or late lesion. 
If tertiary, localized elevation of mucous 
membrane; may be anterior; often rapid 
growth and quick ulceration; voice may be 
hoarse. 
Localized elevation of mucous membrane, 
gradually growing into actual tumor; 
growth slower than tuberculosis, or syph- 
ilis. 
Tests 
Wassermann test positive; tuberculin test 
usually negative; tubercle bacilli absent. 
Tuberculin and Wassermann negative. 
Tubercle,bacillus absent. 
Tertiary ulcer is typically deep, with ele- 
vated border, and sharp cut edges; rapid 
development. 
Ulceration 
Relatively late in developing; apt to be 
shallow and without much secretion; char- 
acteristic odor. 
Less characteristic than in tuberculosis, 
but may be severe and constant. 
Pain 
Varies, but may be severe when ulcer- 
ated, a relatively late symptom. 
Lesions 
Gummatous swellings that develop rapid- 
ly, and quickly, ulcerate deeply. 
Lesion develops usually as a defined tu- 
mor mass, infiltrating deeply and eventually 
closing larynx. 
Quickly improves under antisyphilitic 
treatment. 
Treatment 
Antisyphilitic treatment produces no ef- 
fect unless to reduce the pain temporarily. 
Operative, if life saving. Paliative to re- 
lieve pain and suffering. TUBERCULOUS LARYNGITIS 
381 
Age of Patient 
Young usually; may be a child. 
General Symptoms 
Practically absent. 
Onset and Early Manifestations 
Very slow and insidious. Usually free 
margin of epiglottis is first attackedmono 
lateral; extends downward; anemia not 
characteristic. 
Tests 
Wassermann usually negative; tuberculin 
test usually positive; tubercle bacillus ab- 
sent ; Lupus of face may be present. 
E. LUPUS OF THE LARYNX 
Pain 
Usually absent; if present slight. 
Lesions 
Smooth, hard, small nodules; these tend 
to soften and ulcerate; dry ulcer base; 
leave scar tissue and distortion; slow prog- 
ress. 
Treatment 
Antisyphilitic and general anti-tubercu- 
losis treatment is without effect. Local 
treatment. 
Undoubtedly the present widespread interest in the early 
treatment of pulmonary tuberculosis has not only reduced 
the number of cases of laryngeal tuberculosis, but has also 
served to arrest much incipient laryngeal disease. Formerly 
laryngologists offered little prognostic hope in the disease. In 
1919, Sir St. Clair Thompson (58) of London presented to the 
American Laryngological Association an important personal 
study of 883 pulmonary patients at a tuberculosis sanatorium. 
Of these, 687 were pulmonary, non-laryngeal, and 196 also lar- 
yngeal. The condition of these patients was investigated after 
they had been discharged from the sanatorium for from three to 
seven years. Of the non-laryngeal cases, 39.7 per cent had died 
at the end of this period, and of the laryngeal cases 68.9 per cent 
had died. Sir St. Clair writes: “Amongst all the fairly early 
cases of pulmonary tuberculosis admitted to a sanatorium, the 
expectation is that 60 per cent will be alive in 3 to 7 years. But 
of similar sanatorium patients with the larynx diseased only, 30 
per cent will be alive at the end of that period.” While this re- 
port must not be accepted definitely for all cases as to percent- 
ages, it undoubtedly shows clearly the serious prognostic gravity 
of the laryngeal complication of pulmonary tuberculosis; it also 
shows clearly that the disease is often recoverable. The serious- 
ness of the prognosis in the individual case is dependent upon the 
progress and activity of the pulmonary disease, as well as of the 
laryngeal, and upon the promptness and efficiency of the treat- 
ment for both. 
Treatment: (A) Prophylactic.(176) With respect to get- 
ting important results in laryngeal tuberculosis serious difficul- 
ties present themselves. But difficulties present themselves in 
pulmonary tuberculosis as well. Until the internist and laryn- 
gologist learn to co-operate more fully many more patients will 
die of laryngeal complication of tuberculosis than need to. The 
larynx should undergo frequent and systematic inspection in ev- 
Prognosis 382 
CLINICAL TUBERCULOSIS 
ery pulmonary patient. The conception that local measures (in 
combination with general measures) are capable of producing no 
better laryngeal results than can be secured by general measures 
alone is definitely and seriously false. 
Moreover, the laryngeal point of view is important even to the 
internist. For, as movement tends to encourage the lodgment of 
the tubercle bacilli in the larynx, so discouragement of move- 
ment tends to prevent such lodgment. This fact places control 
of coughing, talking, and swallowing definitely in the category of 
prophylactic measures having reference to laryngeal tubercu- 
losis. Excessive coughing demands sedatives, and such meas- 
ures of control as deep measured breathing to allay irritation. 
Coughing also demands study of nasal, post-nasal, and pharyn- 
geal conditions, in order, through local treatment, to eradicate 
catarrhal, cough-producing inflammations. Talking is subject to 
the control of the pulmonary patient and should be considerately 
discouraged by the physician. Even swallowing may be miti- 
gated in a measure as to its movement effects by careful chew- 
ing and swallowing of food, and by discouraging eating merely 
for pleasure and not for nutrition. 
Another manner of pharyngeal prophylaxis should be in the 
mind of the general physician, and should inspire of itself exam- 
ination of the upper air passages; that is, the possibility that 
chronic lingual or faucial tonsillitis, rhinitis, nasal sinusitis, phar- 
yngitis, may, by encouragement of simple chronic laryngitis, be 
also encouraging laryngeal tuberculosis. The neck in pulmonary 
patients, on similar grounds, should not be coddled, but ration- 
ally protected from exposure to the cold; excessive dust in the 
air should be guarded against. Smoking tends to produce dry- 
ness of the laryngeal and pharyngeal mucous membrane, and 
thus to encourage sticking of laryngeal secretion, with conse- 
quent cough, and is, therefore, from a laryngeal point of view, to 
be completely interdicted in all pulmonary patients, with or 
without laryngeal tuberculosis. 
(B) General and local measures. The general measures of 
treatment of laryngeal tuberculosis are those also of pulmonary 
tuberculosis. Tuberculin2 has been much employed, but has 
2Specific therapy in laryngeal tuberculosis. The use of tuberculin. As pulmonary tuber- 
culous disease generally causes the main disturbance and laryngeal tuberculosis is most 
frequently. only secondary, tuberculin may be most advantageously used if the indica- 
tions for its use are advised in the treatment of the ordinary pulmonary disorder. Should, 
the treatment with tuberculin be here contraindicatea, that is when the laryngeal 
disease is the more disturbing factor, then it has no place as a therapeutic remedy,—J. R, TUBERCULOUS LARYNGITIS 
383 
failed the medical profession of the essential value in laryngeal 
tuberculosis. 
When one approaches consideration of local treatment he is at 
once up against another real difficulty. This haS two phases. 
All local laryngeal treatment is difficult and requires much skill. 
In some patients anatomical conformations, especially with ref- 
erence to the epiglottis, render both observation and manipula- 
tion of instruments unusually difficult; while in certain patients, 
the extreme sensibility of the throat to the employment of in- 
struments may render local treatment so difficult and so trying 
to the patient as to practically prevent more than the minimum 
of such treatment. 
Again reverting to prophylaxis, it is to be realized that what- 
ever tends to encourage fluidity of the secretions that must pass 
outwards through the larynx is desirable. The tuberculous pa- 
tient whose throat readily admits of the effective employment of 
instrumentation, the use of simple alkaline sprays to the larynx 
by the patient himself, is to be encouraged, whether the patient 
has or has not developed local laryngeal disease. Another meas- 
ure that should tend to liquify secretion is the employment of 
oily, non-irritating sprays that stimulate the secretory glands of 
the mucous membrane and the use of oil inhalations could be 
readily arranged as a routine treatment for all pulmonary pa- 
tients. Menthol, oil of cloves, of wintergreen, or phenol, in li- 
quid petrolatum, are examples of suitable drugs for such a pur- 
pose. 
When tuberculosis has definitely made its appearance in the 
larynx, and there exists hope of its arrest, talking should cease 
completely, at least until the disease has come under control. 
The matter of local infection is extremely serious, and absti- 
nence from talking is one of the most important measures. If 
recovery is beyond hope, or when recovery has practically been 
secured, the amount of talking may be regulated in accordance 
with local sites and manifestations of the disease and other indi- 
vidual considerations. Whispering is much less harmful than 
loud talking, and may be permitted when loud talking should be 
forbidden. 
Coming to the subject of local medical or surgical treatment, 
we are confronted with two more or less definite attitudes on the 
part of the laryngologists. Speaking briefly, one group says, use 
as little local treatment as you have to, inhibit talking, strengthen 384 
CLINICAL TUBERCULOSIS 
general measures so far as possible, and then when local treat- 
ment is definitely demanded, use it with emphasis. The second 
group says, watch the larynx closely, inhibit talking, employ 
local antiseptics and caustics intelligently and persistently, as the 
conditions warrant. There is room for argument on both sides. 
Persistent use of chemical antiseptics and caustics in incipient, 
localized cases are often curative, after general measures have 
proven their ineffectiveness. This is a matter of repeated expe- 
rience. To argue that the general measures should first be per- 
mitted to prove their ineffectiveness before taking up local treat- 
ment, is to argue in favor of taking chances, owing to the prog- 
ress of the local and general disease, that local treatment may 
be instituted too late. On the other hand, to argue that, when- 
ever local measures are employed, to make them emphatic and at 
once destructive of the local lesion, may be to argue correctly. 
The two classes of treatment most discussed are, on the one 
hand, antiseptics and caustics with, or without, curettement, and, 
on the other, the electric cautery, or operation. Undoubtedly 
both classes of methods are capable, when expertly employed, of 
producing destruction of the local lesion. The actual cautery, 
since the application is difficult and must be applied with pre- 
cision, and is not without danger, demands the greater expert- 
ness. Any application to be destructive of disease must be ex- 
actly applied. Chemical agents of moderate, but increasing 
strengths, may, in certain lesions, be equally effective, but re- 
quire more time. Their advantage is that, either due to the ana- 
tomical difficulties presented by the individual patient or to 
movement, or to relative inexpertness on the part of the operator, 
no great harm results if the application is caused to extend be- 
yond the area intended to be reached. The antiseptics that may 
be employed include silver nitrate, argyrol, zinc chlorid, lactic 
acid, formalin, iodine, and balsam of Peru. Formaline has been 
f”iid to be especially effective in strengths of from 1 per cent to 
U t'er cent. Variation of the drug employed in the same pa- 
tient seems at times to be essential. 
The electric cautery is efficient in the destruction of ulcers, 
infiltrations, and tumor masses. Sprays are of general inhibitive 
antiseptic value, but are not curative of the tuberculous lesions, 
as such. Much the same may be said of the laryngeal syringe 
and of powders. The latter, owing to their effect in increasing 
the dryness and stickiness of the secretions, should not be used. TUBERCULOUS LARYNGITIS 
385 
A recent author advocates the passage of a rather large cotton 
swab saturated with a solution of menthol in olive oil between 
the vocal cords. The resulting irritation to the larynx due to 
the presence of the foreign body, causes the vocal cords to con- 
tract on the swab and squeeze the antisepticized oil out over the 
larynx. This would also serve for prophylaxis, or inhibitive 
antisepsis, rather than to destroy existing local tuberculous 
disease. 
Direct and suspension laryngoscopy have afforded the laryn- 
gologist a new measure of surgical approach to the larynx that 
is being employed for larger surgical procedures, as the ampu- 
tation of tumor masses, the amputation of epiglottis (132), 
curettement and the electric cautery. Local anaesthesia is usu- 
ally possible. Careful consideration of the general condition of 
the patient, in conjunction with the urgency of the operative 
measures to be employed, are requisite in determining the safety 
of such measures of treatment. 
It is many years since Enos, a general practitioner in Brook- 
lyn, studied a case of laryngeal tuberculosis in which the epiglot- 
tis had been entirely destroyed and in whom swallowing had not 
been interfered with. Lorenzo B. Lockard, of Denver (116), 
has since devoted much practical study to amputation, in whole 
or in part, of the epiglottis for tuberculosis. His studies indi- 
cate that even infiltrations not uncommonly penetrate into the 
perichondrium and even into the cartilage. Such lesions are 
curable only by removal or deep destruction. At first, the opera- 
tion of epiglottidectomy was performed solely for the pain, and 
such pain is thereby commonly completely eliminated. More 
recently the operation has been extended to include relatively 
incipient epiglottic cases, is undertaken to arrest and cure the 
local disease, and has won a recognized place in surgery iti 
laryngeal tuberculosis. The operation is performed by direct 
laryngoscopic methods, either by biting off the organ with fdr- 
cepts, or, preferably, by removal with the cold wire snare. 
For actual laryngeal occlusion, tracheotomy sometimes be- 
comes necessary. But even under relatively favorable general 
conditions, the operation has had fatal results in a large percent- 
age of cases, and should always be considered as serious. Helio- 
therapy has proven to be of value (121), but does not in any 
sense replace other local measures of treatment. The light may 
be applied from the dermatological surface of the larynx or with 386 
CLINICAL TUBERCULOSIS 
the aid of a throat mirror by actual reflection into the interior of 
the organ. Higher mountain altitudes are considered to have 
especial value by observers of experience, but many pulmonary 
patients find any but low, or moderate altitudes dangerous. 
To relieve pain in the larynx, and especially pain on swallow- 
ing, is to encourage recovery of both the general and local dis- 
ease. Of available drugs orthoform, either in powder, or emul- 
sion (Wolff Freudentahl) (53) has produced the best results. 
Anesthesin and cocaine (in mild spray, or powder) also have 
their place. Cocaine is too poisonous for extended use. Pro- 
paesin is well spoken of. If orthoform is well placed, especially 
when applied in emulsion by syringe, the effects are marked and 
prolonged for hours and the drug is not toxic. If needed, it 
may be repeated before each meal. 
The method of nerve blocking of the larynx first advocated 
by Hoffmann has won a permanent place in the treatment of 
local laryngeal pain. It consists in the injection of the internal 
branch of the superior laryngeal nerve with 65 to 80 per cent 
alcohol. The procedure does not paralyze, and offers no contra- 
indications. The superior laryngeal nerve is the nerve of sensa- 
tion of the laryngeal mucous membrane, the epiglottis, and a 
part of the base of the tongue. It is easily approachable. It 
passes into the larynx through the thyro-hyoid membrane, far to 
the outside, somewhat under the anterior border of the sterno- 
cleido-mastoid muscle. The nerve is not deeply seated, espe- 
cially in the emaciated tuberculous patient, and may be even less 
than one-quarter inch from the surface of the skin. The technic 
of injection described is that followed by Robert McD. Lukens 
(177). Position of patient: Sitting, head natural position, or 
supine on a pillow, head to one side. The greater cornu of hyoid 
and superior cornu of thyroid cartilage are located with the left 
forefinger. Needle (strong and blunt) enters about one inch 
anterior to directing finger, and one-quarter inch above that of 
the thyroid cartilage; it is pushed backward and inward, the 
point being raised from time to time, to locate its position by the 
directing finger tip of the left hand. If patient feels pain directed 
to the ear of the corresponding side he is previously directed to 
raise a hand. At that moment a drop or two is injected. If 
cough results the fluid has entered the larynx; the needle is then 
withdrawn a little and a few more drops injected; if cough 
does not ensue, Yz to 1 cc is injected, while moving the tip of TUBERCULOUS LARYNGITIS 
387 
the needle around a little, in order to surround the nerve. Other 
ways of approaching the nerve are also employed. 
One, or both, sides may be injected at one sitting. The injec- 
tion may be repeated at intervals of three to five days. Relief 
from a single injection varies from a few hours to a month or 
more. If successful the cessation of pain is completed. Unfor- 
tunately, no way exists by which the operator may be certain 
that the nerve has been exactly entered, and, therefore, a large 
proportion of failures must be expected. E. L. K. CHAPTER 29 
TUBERCULOUS PERITONITIS 
Peritonitis Tuberculosa. Miliary Tuberculous Enteritis. Tu- 
berculosis of the Peritoneum. Tabes Mesenterica. 
Tuberculosis of the Abdomen, Etc. 
Primary and Secondary 
General Consideration. Etiology. (47) (a) Primary tubercu- 
losis of the peritoneum in the adult is extremely infrequent; it is, 
however, more so in child life. It is usually always secondary, 
although cases have been observed without any evidence of tuber- 
culosis of other organs or tissues, but such cases are doubtful 
because the real primary focus either near or remote may have 
been entirely overlooked, and may have been only pinhead in 
size and have wholly escaped detection. 
(b) Secondary tuberculous peritonitis, that is secondary to 
tuberculosis of other organs of the body, is the general rule. 
It usually follows in the wake of tuberculosis of the lungs and 
pleura, intestinal tuberculosis, tuberculosis of the abdominal 
glands, the retroperitoneal and mesenteric, tuberculosis of the 
genital organs, in acute miliary tuberculosis and in the late form 
of chronic pulmonary disease. In the female a close relationship 
has frequently been observed between tuberculosis of the peri- 
toneum and that of the genital organs. Tuberculous peritonitis 
may be primary to a genital tuberculosis—the genital tubercu- 
losis being secondary to a peritoneal or extra genital. Tuber- 
culous peritonitis and tuberculosis of the genital organs may 
exist at the same time—both may be hematogenous from one 
and the same focus. A tuberculous peritonitis is most likely 
never secondary to a previous genital tuberculosis, although 
many good observers maintain that genital tuberculosis fre- 
quently leads, in about one-third of the cases, to a diffuse tuber- 
culous peritonitis and that very rarely the reverse is observed, 
namely, that a tuberculous peritonitis is followed by a genital 
tuberculosis. Tuberculous peritonitis is generally a disease of 
388 TUBERCULOUS PERITONITIS 
389 
young or middle life—it is very rarely encountered after the 
fourth decade. 
Clinical Forms (89). Tuberculous peritonitis is usually ob- 
served in one of two forms, (1) the acute and (2) the chronic, 
and the acute permits of a further division into an acute miliary 
and an acute circumscribed, (a) The acute miliary or generalized 
form, a hematogenous infection which is usually of short dura- 
tion—generally both surfaces of the peritoneum are involved, 
many miliary and submiliary gray nodules as a rule are present, 
extending over both surfaces of the liver and spleen, and owing 
to the short duration of the disease but little exudate is present, 
and if so, it is either serofibrinous, bloody or pus. (b) Acute 
circumscribed tuberculous peritonitis. The disease is limited or 
localized to areas with little tubercle formation but much 
fibrinous adhesions. 
(2) Chronic diffuse tuberculous peritonitis. A slow progres- 
sive form which may manifest itself as either a dry or moist, sicca 
or humida variety. In the dry variety owing to a fibrinous more 
or less plastic exudate, the abdominal organs become matted or 
glued together, adhesion between the various abdominal organs 
takes place, and the omentum becomes contracted and is rolled 
up as a palpable mass in the upper abdomen. This is the peri- 
tonitis tuberculosa adhesiva of the older writers. The exudative 
or moist variety, the peritonitis tuberculosa humida, is charac- 
terized by the presence in the abdomen of fluid which may be 
serous or serofibrinous, purulent or bloody. Adhesions between 
the intestines and the abdominal viscera are usually present. 
Many tuberculous nodules are found on both walls of the peri- 
toneum. As a rule they seldom calcify or caseate and not in- 
frequently such tuberculous nodules are found on the peritoneum 
surrounded by a hemorrhagic area, or as happens in older cases, 
the nodules are encircled by much dark pigmentation derived 
from the blood. The amount of fluid present may vary from a 
few cc to that of many litres and it may be either free in the 
abdominal cavity or found localized, that is, sacculated. If the 
peritonitis is the result of tuberculous enteritis, acute septic 
peritonitis results. Usually in the abdominal exudate the 
tubercle bacillus may be found. 
Symptoms of Tuberculous Peritonitis. They are present 
according to the nature of the inflammatory process. Symptoms 
of (1) acute, and (2) chronic peritonitis, (a) Acute miliary 390 
CLINICAL TUBERCULOSIS 
form. Owing to the extremely rapid progress of the disease the 
symptoms are quite variable—all followed by a swift over- 
whelming of the organism and early exitus. (b) Acute cir- 
cumbscribed or localized form is usually accompanied by fever 
and pressure pains, diarrhoea or constipation, friction sounds, 
marasmus, etc. (2) Chronic form, dry or moist. Symptoms of 
pain in the abdomen, loss of appetite, a feeling of weakness is 
present with a fulness in the abdomen, alternating pain from the 
spine to the abdomen, a bloated feeling, nausea, occasionally vom- 
iting, a body loss and an abdominal gain, particularly noticeable 
by the patient. Meteorism due to the lessening of the natural 
parastalsis, eructation of gases, vomiting, etc. If vomiting is 
accompanied by a fecal odor, much distension of the abdomen, 
colicky pain and constipation, ileus may be suspected due to 
intestinal paralysis or obstructions from inflammatory contrac- 
tions. Much gas or exudate in the abdomen may lead to 
dyspneic symptoms. Fever may be present or absent, the pulse 
and respiration both rapid and occasionally there is a more or 
less pronounced jaundice present and the bowel movements are 
colorless. This is especially so in children with diarrhoea. The 
disease may be slow and insidious in its course with constant 
remissions and exacerbations. The appearance of the abdomen 
may differ greatly according as the dry or moist variety pre- 
dominates. If the exudate is absorbed, thickened bands of the 
peritoneum are palpable and, on the other hand, if there is free 
fluid in the abdomen by percussion and change of position, it 
may be outlined and the amount of fluid approximately ascer- 
tained and if the amount is large and it is withdrawn or aspirated, 
the nodular or tumor-like masses in the abdomen become pal- 
pable. In cases in which the mesentary is contracted, a high 
tympanitic note is frequently elicited over the right abdomen, 
due to gaseous distension of the small intestine, while over the 
left the note is dull and flat. Death is due usually to asthenia 
or suffocation. Spontaneous cures have been observed and 
arrest of the tuberculous process is not infrequent. The dura- 
tion of the disease is variable. In about 50 per cent the disorder 
lasts from one to six months, in 25 per cent from six months to 
one year and in the remaining 25 per cent from one to five years, 
and not considering complications which may arise, such as 
ileus or perforation or perhaps the acute miliary form, the dis- 
ease runs a more or less protracted course. In a child a tuber- TUBERCULOUS PERITONITIS 
391 
culous peritonitis may also be either acute or chronic. In about 
one-third of the cases the disease is of the acute form and in 
the beginning it may be most difficult to differentiate it from 
appendix disease, typhoid, etc. Ascites in children generally 
indicates tuberculosis of the peritoneum and here again by ex- 
clusion we must differentiate from cirrhosis of the liver, late 
hereditary syphilis, obstruction of the hepatic vein and chronic 
inflammation of the peritoneum, pleura and pericardium. Tuber- 
culous peritonitis may be accompanied by pleurisy and in the 
chronically protracted cases, more or less inflammation of many 
serous cavities, known as polyseristis, polyseritis, polyorrhomen- 
itis, Morbus Bambergeri, etc., may be present. This is probably 
due to the disposition, which means a difference in the nutritious 
soil, a difference in the virulence or perhaps a difference between 
the disorder produced by the tubercle bacillus and that of the 
toxins. A gastro-intestinal disturbance followed by frequent 
and repeated colicky attacks extending over prolonged periods, 
loss of appetite, constipation and emaciation, distension of the 
abdomen and meteorism, face pale, slight temperature, abdominal 
pain, especially if the abdomen becomes tense, point to tuber- 
culous peritonitis. 
Diagnosis (Differential). The diagnosis is not always easy. 
It may present many difficulties and may simulate many non- 
tuberculous disorders. Peritoneal friction sounds if heard near 
the region of the heart may be mistaken for pericardial mur- 
murs. Exudative tuberculous peritonitis may be confused with 
cirrhosis of the liver, thrombus of the portal vein, carcinoma and 
sarcoma, ovarian cysts, ascites from unknown causes or follow- 
ing chronic heart and kidney disease and with chronic non- 
tuberculous peritonitis. The chronic course of the disorder, the 
pain, the changing fever, the exudate, the gradual emaciation 
and diarrhoea point to tuberculous peritonitis, particularly if 
taken in connection with tuberculosis of other organs. Three 
facts, an abdominal tumor, ascites and emaciation with anemia 
indicate tabes mesenterica. During the menstrual period the 
fever usually rises. In alcoholic subjects tuberculous peritonitis 
and cirrhosis of the liver may exist at the same time, because 
alcoholism favors both. In many instances the diagnosis is 
dependent upon either an exploratory puncture or laparotomy. 
In the non-exudative or dry form if an exploratory laparotomy is 
contraindicated, the diagnostic use of tuberculin may be resorted 392 
CLINICAL TUBERCULOSIS 
to. Usually with the intradermal use of tuberculin in one or 
two milligram doses in a case of suspected tuberculous peritonitis, 
increased abdominal pain following the injection strongly 
points to abdominal tuberculosis. Tuberculous peritonitis may 
escape notice entirely until complications reveal the true and 
serious nature of the disorder. In children chronic peritonitis 
is generally tuberculous, and only occasionally due to injury or 
to extension from a non-tuberculous focus. A high fever at 
the onset would suggest a pneumococcal rather than a tuber- 
culous peritonitis—hence a severe generalized peritonitis with- 
out any definite cause, great and rapid distension of the ab- 
domen, pain and tenderness, high fever and diarrhoea, is usually 
pneumococcic, while a round, tense distended and shining ab- 
domen with full veins, fluid in the flanks, resonance or tympany 
about a protruding umbilicus, pain, tenderness and fever is 
usually tuberculous. 
Prognosis.(20) In pronounced phthisis a tuberculous peritonitis 
is always unfavorable, exitus letalis in 96 per cent. Cases of 
peritonitis due to an intestinal ulcerative process with pus and 
pouring of the contents into the abdominal cavity are usually 
fatal. The dry form of the disease gives generally a better prog- 
nosis. Tuberculous peritonitis complicated by cirrhosis of the 
liver is early fatal due to the want of resistance from the gen- 
eralized tuberculous condition. In about 15 per cent of tuber- 
culous peritonitis, cirrhosis of the liver is found as an accompany- 
ing disorder, and in other cases of cirrhosis of the liver, fre- 
quently towards the terminal stage, a tuberculous peritonitis is 
noticeable. The longest duration of the disease is five years. 
Spontaneous cures are rare and the remissions frequent. Alco- 
holism is a frequent etiological factor with a grave prognosis. 
Ascites with pronounced tuberculosis elsewhere, constant 
diarrhoea, extreme emaciation, cutaneous hemorrhages, also 
presages a grave prognosis. In mixed infection the outlook is 
always bad. Relapses after latency or an apparent cure are fre- 
quent and are less common in children than in women with tu- 
berculous salpingitis. In general the prognosis is better in 
children than in adults, better if the ascites is serofibrinous in 
form. If other organs are involved or if the onset of the dis- 
ease is very acute the prognosis is less favorable; the dry form 
better and ulceration with pus very grave. Primary intestinal 
tuberculosis in early child life is less frequent than the path- TUBERCULOUS PERITONITIS 
393 
ologic respiratory tuberculosis as a primary disorder, but as to 
prognosis is just as unfavorable. 
Therapy—Surgical and Medical 
Surgical Treatment. When to treat surgically? In every 
active, in the so-called hopeless cases. The usual surgical pro- 
cedure is by laparotomy opening of the abdomen, removal of 
the fluid and incidentally of the appendix or a diseased ovary. 
Laparotomy is performed with the purpose of bringing about 
a reactive hyperemia and to stimulate the bactericidal action of 
a 10 per cent tincture of iodine freely applied to the abdominal 
cavity seems to be sufficient. Many surgeons apply iodoform to 
the peritoneum and the abdominal organs after the fluid has 
been withdrawn and before the abdomen is closed. The use of 
a 10 per cent Tincture of Iodine freely applied to the abdominal 
viscera and about the wound is often followed by most gratify- 
ing results, or aspirating, by means of a trocar and canula, the 
free fluid—this followed by washing of the inner abdomen with 
a sterile physiological salt solution after which about 100 cc of 
a 20 per cent iodoform emulsion are injected. In peritonitis tu- 
berculosa sicca the instituting of an artificial ascites by means 
of injecting about 30 grams of glycerine into the peritoneal 
cavity has met with most favorable results. The injections must 
be repeated at long intervals. The use of hydrogen peroxide, 
a 50 per cent solution, flushing of the abdominal cavity and in- 
testines followed by a physiological salt solution is highly rec- 
ommended and good results have followed the injection of pure 
and filtered oxygen into the abdominal cavity in amounts a trifle 
less than the amount of fluid withdrawn. Laparotomy is always 
indicated when the exudate is profuse and there is much dys- 
pnea, when the exudate is caseous or purulent, when the lumen 
of the ileum has become contracted from inflammatory causes 
or when a tumor of the generative organs accompanies the tu- 
berculous process. It is not advisable to operate too early if a 
healing of the tuberculous process is desired, corresponding in 
this particular with pleurisy with effusion of which it is the 
analogue where if the fluid is removed too early reaccumulation 
rapidly takes place. Therapeutically laparotomy will always 
give the best results if applied in conjunction with general 
treatment. 
Medical Treatment. When to treat the peritonitis medically? 394 
CLINICAL TUBERCULOSIS 
In the less acute cases, first and foremost, as in tuberculous dis- 
eases of other organs, institute the dietetic-hygienic treatment in 
combination with a tuberculin therapy. The tuberculin as well 
as the dietetic-hygienic treatment should be resorted to after 
an laparotomy. In all cases of tuberculous peritonitis, post- 
operative or otherwise, the use of old tuberculin in very small 
doses is always indicated and as a beginning amount give one 
millimilligram dose and so on every third or fourth day, increas- 
ing the dosage gradually until milligram doses are administered 
or till a marked improvement is noticeable, when a tonic dose 
may be given once in two or three weeks and maintained almost 
indefinitely. Warm applications to the abdomen either in the 
form of hot compresses or warm alcohol on a soft cloth are in- 
dicated and often give temporary relief. Remedies which favor 
resorption of the fluid are always desired and the anointing of 
the abdomen once a day with mercurial ointment using from 
y2 to 1 drachm or applying and rubbing gently over the abdomen 
from y2 to 1 tablespoonful of green soap. As a most satisfactory 
topical application I have found the use of tincture of iodine 
painting over the abdomen, repeating it once every three or four 
days. Camphor in the form of the camphorated oil or spirits of 
camphor slightly heated and applied is much in use. All diges- 
tive disturbances should be met as they arise, constipation by 
an appropriate anticonstipation diet and enemas, and diarrhoea 
by a suitable diet and remedies to check the excessive bowel 
movements. The most distressing symptom usually complained 
of is the constant feeling of fulness in the bowel, the distension 
with gases, meteorism. If there is absence of diarrhoea small oft 
repeated doses of calomel, say 1/10 gr. every hour for y2 dozen 
doses, are indicated. High colonic flushing with chamomile in- 
fusion is a valuable remedy. Salol in 5 to 10 grain doses every 
three hours, and for pain and distress in the abdomen 15 to 20 
drops of Chloranodyne given in a little water or still better in a 
y2 teacupful of an infusion of anis, fennel or caraway seed. For 
pain morphine is always indicated either by mouth or preferably 
hypodermically and alcohol and opium as a topical application. 
The use of spirits of caraway or the essence of anis or fennel 
seed may be used. The internal use of the tincture of iodine 
in milk I have found to be a most dependable drug promising 
good and lasting results, when given in 20 drop doses three 
or four times a day. It has been proven that the individual suf- TUBERCULOUS PERITONITIS 
395 
fering from tuberculous peritonitis is often very greatly bene- 
fited by a residence at the seashore, most likely due to the 
minute quantities of iodine contained in the air. The arsenical 
preparations and the various iron tonics are always admissible. 
Drugs like guaiacol and creosote although formerly much in 
use and which may have proven meritorious in the hands of 
some are now obsolete. 
Tuberculous peritonitis as the immediate cause of death is 
extremely rare, some intercurrent disorder usually ending the 
scene. The expectant and the operative treatment show about 
the same mortality. Usually surgical interference is indicated 
when the course is rapid and progressive as in asthenia, cardiac 
weakness and hectic fever, and if the conservative treatment has 
been without favorable results, otherwise, it should be the rule 
in all cases of exudative tuberculous peritonitis as long as the 
symptoms are those of a plain serous fluid even if there be much 
ascites to treat such cases for long periods of time simply con- 
servatively. It is immaterial whether the tuberculous peritonitis 
is simply of the serofibrinous variety or whether it is also accom- 
panied by ascites, though perhaps the latter is more quickly and 
more promptly influenced by the treatment. In the treatment of 
tuberculous peritonitis, whether surgical or medical, the object 
is to bring about a process of healing by inducing hyperemia 
and favoring transudation and adhesions. CHAPTER 30 
TUBERCULOSIS OF BONES AND JOINTS 
General Consideration. Tuberculosis of the bones and joints 
is a metastatic infection from a focus elsewhere in the individual, 
is always secondary, except for purely suppositious cases in 
which the track of tuberculosis may be a stab wound or other 
artificial means. Ordinarily it is an hematogenous infection. 
Little masses of tuberculous material from caseating glands or 
from other sources get into the blood current and are carried 
along until they find a favorable resting place. This place may 
be in normal tissue, or it may be, and is more likely to be, in 
tissue which has been bruised or injured just enough to cause a 
small local hemorrhage or stasis, as in the cancellous portion of 
the bone. Here the tubercle bacilli become arrested and begin 
to form typical lesions which can be seen as very small grayish 
spots in the cancellous bone. As these spots increase in size 
and number the centers become necrotic and caseous, and the 
bacilli escape and set up new foci in the surrounding bone. (36) 
(49). 
The most frequent site is in the epiphyses, near the joints but 
not actually in the joints; and, if treatment be successful, the 
disease may be arrested or cured without any invasion of the 
joints themselves. This result, however, is very rare, and in 
most cases the joint is sooner or later involved, with more or 
less destruction of the articular surfaces. The diaphysis, or 
shaft, of the bone is almost never invaded. Between the 
epiphysis (where the blood stream is more active and where the 
growing of the bone is largely accomplished) and the diaphysis 
exists a dense, and strong cartilaginous epiphyseal plate which 
is not readily penetrated by epiphyseal disease. This forms a 
barrier to the extension of the disease in that direction, so it is 
easier for tuberculous material to find its way into the joint. 
In exceptional instances, however, primary joint tuberculosis has 
been observed, where the synovial membrane was first infected, 
but these are exceptions. 
The subject of tuberculosis of the joints is of great importance 
396 TUBERCULOSIS OF BONES AND JOINTS 
397 
for several reasons'; it is a very common disease; it is a very 
chronic disease; and it is a very disabling disease. The economic 
loss, in time and money, is enormous. The pain, suffering and 
disability to the individual patients are distressing. 
Joint tuberculosis is primarily a disease of children. More 
than 85 per cent of all the cases occur in children from two to 
Diaphysis of 
Femur 
Metaphysis of 
Femur 
Epiphyseal Line 
Joint Surface 
showing marked 
erosion and 
destruction 
Epiphysis of Tibia 
Epiphysis of Head 
of Fibula 
Epiphyseal Line 
Diaphysis of 
Fibula 
Fig. 51. Tuberculosis of the knee joint. Anterio posterior view 
(Girl 8 years old. Duration of disease 2 years) 
(From The Children’s Memorial Hospital—H. J. Ullmann, Roentgenologist) 
ten years of age, and more than 50 per cent in children from 
two to five years. In about 40 per cent of all cases the disease 
occurs in the spine, in about 30 per cent in the hip, and in 20 
per cent in the knee. 
Symptomatology and Diagnosis of Bone and Joint Tuberculosis. 
The general symptoms of bone and joint tuberculosis are 
those of a slowly developing inflammation. The incidence is 
always slow, and this is one of the most important points in 
differentiation. In very small children the trouble may begin in 398 
CLINICAL TUBERCULOSIS 
the small joints of the hand or foot, but it is usually seen in the 
spine, knee, or hip. Ordinarily in the larger joints of the body, 
the first symptom that one can distinguish objectively is limita- 
tion of motion. For example, a child has a tuberculous in- 
flammation near the hip joint; the first thing that nature does is 
to try to limit motion in the joint; consequently as the child 
walks he cannot move his hip joint as freely as the other one, 
and the result is that he limps a little. Where tuberculosis of 
Diaphysis 
of Femur 
Patella 
Epiphyseal Line 
Epiphysis 
(condyle) 
Joint line 
obliterated 
(On account of 
its irregularity 
due to disease) 
Epiphyseal Line 
Epiphysis of 
Fibula. Seen 
Epiphysis of 
Tibia 
(Tuberosity) 
Early center of 
ossification of 
beak of 
Tibial Tubercle 
( Attachment of 
Ligamentum 
Patella) 
indistinctly 
through shaft 
of Tibia 
Fig. 52. Knee Joint Tuberculosis. Same case as Fig. 51. Lateral view 
the larger joints is accompanied by a limp, this is the first 
noticeable subjective and objective symptom. A little stiffness 
comes first, and the first thing the parent notices is this little 
limp, hyperextension of the hip joint being the first thing that 
is lost. The first objective sign that a skilled person can notice 
is a restriction of the mobility of the joint and the first that lay 
people notice is a limp due to the restriction of mobility. Simi- 
larly in cases of tuberculosis of the spine, the first thing that is 
noticed is that the spine is held stiffly. When the child bends TUBERCULOSIS OF BONES AND JOINTS 
399 
over to pick up an object from the floor he does not bend his 
back and curve it forward in a typical case of Pott’s disease but 
he walks up to the object and bends his knees without bending 
his back. This is due to the fact that nature is trying to hold 
the spine still. If the child attempts to bend the spine forward 
it makes pressure upon the bodies of the diseased vertebrae, 
which causes pain, and it instinctively protects itself against the 
possibility of pain by holding the back stiff. These symptoms of 
joint tuberculosis are very often misunderstood, and the diag- 
nosis is often incorrectly made. Persistent limitation is the 
commonest of all the signs in joint diseases. 
Disease of the spine is by far the most important, and we see 
the largest number of cases of spinal tuberculosis in the clin- 
ics. There are a great many more joints in the spine than 
there are in the knee and the hip. The spine is linked together 
with the seven cervical, the twelve dorsal and five lumbar artic- 
ulations as possible sites for the disease. The first thing no- 
ticed about the child is that he holds his back stiffly, that he does 
not bend it freely. It is rare for a child with an oncoming tuber- 
culosis of the spine to complain of any pain in the back. They 
do not feel pain consciously. They know there is something 
wrong with the back if they are old enough to reason at all, 
but they do not feel much actual pain. The mother is very apt 
to believe that because the child holds his back stiffly there is 
not anything the matter with it; that there must be some other 
site in the body for whatever trouble the child may have. The 
first thing the physician, however, observes is a characteristic 
rigidity of the spine that makes him suspect tuberculosis. Sup- 
pose it is a very early case and the child does not hold his back 
so very stiffly, but there is some limitation of motion. If the 
child be old enough and we ask him to bend forward, to bend 
either side, to bend backward, observing the child while going 
through these motions, we can usually see there is an area of 
rigidity in the back. A more accurate way of testing spinal 
rigidity is to have the child lie face down on a table; then as he 
lies comfortably face down, pick him up by the two ankles and 
curve his spine backwards, hyperextend it. With his body lying 
flat on the table, his hips and legs being curved upwards, nat- 
urally the back itself begins to bend. In the case of very early 
Pott’s disease of the spine we notice at once that above and 
below the region where we think there is disease the spine bends 400 
CLINICAL TUBERCULOSIS 
perfectly freely, but at the site where the trouble exists there 
will be an area involving three or four or perhaps five vertebrae 
that does not bend. There is as yet no kyphosis, no knuckle or 
gibbus in the spine, and all you can find is a little rigid area in 
an otherwise normal spine. 
Other symptoms which come on usually a little later are night 
cries. Almost all children with joint tuberculosis, whether it be 
in the spine, hip or knee, will have what are called night cries. 
The child goes to sleep, and as he is going to sleep, nature is 
exercising some control over that diseased joint, is causing a 
reflex spasm that holds the joint more or less stiff. As the 
child lapses into a deep, profound slumber, the muscles relax a 
little bit, and the child perhaps rolls or turns in bed, the joint 
is moved or twisted a little bit and instantly reflex action takes 
place. The muscles jerk and hold the hip or spine stiff again, 
and the child is awakened subconsciously with a cry. He gives 
a loud, shrill cry, but he does not know that he has done so and 
is asleep again immediately. It is a typical tuberculous night 
cry. It is a fairly constant symptom in joint tuberculosis. 
Symptoms of Reflex Pain. The next symptom observed is a 
reflex pain. In children, particularly, pain is never complained 
of in the place where the joint lesion exists. As a rule if a child 
has tuberculosis of the spine he never complains of pain in his 
back. This, however, does not hold good in adult tuberculosis of 
the spine because adults do have pain at the site of disease. This 
reflex pain is in the direction of the distribution of some of the 
nerves which supply this region. For example, in a mid-dorsal 
case of spinal tuberculosis, the intercostal nerves which come 
down from that region supply the upper part of the belly, and 
the child has bellyache. He has no disturbance of digestion, 
his bowels are regular; he has no flatus, no colic, none of the 
things that ordinarily produce bellyache in children, but he does 
have pain in his abdomen. It does not come on with any 
reference to his meals, and the pain is ordinarily thought to be 
due to indigestion or colic. In a case of stomach-ache in a child 
do not be contented by simply looking at the child’s belly, or 
perhaps examining the appendix region, but turn him around 
and look at the spine and you may find a sharp enough kyphosis 
or knuckle to be readily seen. 
If the trouble be higher up in the spine the pain will be 
noticed there and one may think of heart disease, lung tuber- TUBERCULOSIS OF BONES AND JOINTS 
401 
culosis or something else as the cause. If they be lower in the 
lumbar region, pains shooting around, down the front of the 
pelvis and sometimes down the thigh will be experienced. We 
see in cases of hip joint tuberculosis that the patient never com- 
plains of pain in the hip but always in the knee, and on the 
inner and front side of the knee, never on the outer. 
In spinal tuberculosis, the next sign that soon follows is a 
prominence of the spinous processes of the vertebrae at the 
site of the disease. The reason that these spinous processes 
become prominent is because the bodies of the vertebrae are 
eaten away, the vertebral bodies collapse and the spinous proc- 
esses in the back form a sharp bend. 
When the disease has eaten away a portion of one or two of 
these vertebral bodies and it is usually a single one that is 
attacked first, the spine begins to tip forward and a sharp lit- 
tle knuckle appears in the back. It is always a sharp knuckle, 
never a rounded kyphosis and this is one of the points in dif- 
ferential diagnosis. 
There are many cases of curvature of the spine or scoliosis 
in which there is a backward as well as a sidewise curvature, 
and we must ascertain if it is tuberculosis or not. A pretty 
clear history from the parents or friends that originally the 
tuberculous knuckle started as a little, sharp protrusion is char- 
acteristic. If a sharp kyphosis develops in a child’s back without 
a history of fracture of the spine, which is the only other thing 
that is at all common in children, you can be reasonably sure 
that you have tuberculosis of the spine. In addition you will find 
that the muscles up and down the back within four or five 
inches of this area are stiff, spastic; that is, they have a reflex 
spasm which is holding the spine stiff; this is very constant, 
and this little spasm of muscles sometimes precedes any of the 
other symptoms. Therefore, a stiffness of the spine in a local- 
ized area, with a little projection, in the absence of the history 
of sufficient traumatism to cause a fracture is diagnostic of 
Pott’s disease. 
Differential Diagnosis. There are other conditions that may 
produce kyphosis in a child’s back. Scoliosis does not produce 
a sharp, but a rounded knuckle which may simulate an old 
Pott’s disease, because the longer the case progresses, the more 
vertebrae are attacked, and the more rounded the kyphosis gets. 402 
CLINICAL TUBERCULOSIS 
Fracture of the spine is the only thing that we practically ever 
see. A definite syphilis of the spine, although extremely rare, a 
gumma, may cause a condition macroscopically very much like 
a Pott’s disease. Here other signs of syphilis, and a Wasser- 
mann or spinal fluid Wassermann may help in the diagnosis. 
New growths, sarcomas, etc., may start with a fairly sharp 
knuckle, but almost always involving at least two vertebrae in 
the beginning. Hypernephroma has at times caused a necrosis 
of the spine, but the hyperhephromas, by the time they make 
a kyphosis, have such a large tumor in the belly that one does 
not think of Pott’s disease in that connection. Those are the 
only other things that make a very sharp irregularity in the 
child’s back. 
As a broad general rule we may say that if a child has a 
sharp knuckle in the back, with a little stiffness of the spine, 
and perhaps a little referred pain, it is almost sure to be a case 
of Pott’s disease. 
Complications. The chief complication to be dreaded in 
tuberculous joint disease is the formation of tuberculous 
abscesses commonly called “cold” abscesses. These can some- 
times be prevented by early and careful treatment, but occa- 
sionally occur in spite of every effort. They are perfectly harm- 
less unless they become so large as to interfere with the wearing 
of proper apparatus or unless they become contaminated 
with other kinds of bacteria. The reason they are so dangerous 
is because physicians are apt to open and drain them under the 
mistaken impression that the contents of the abscess may be 
doing harm to the patient. In some instances the abscesses 
open themselves. Now, when a cold abscess is opened, it 
almost immediately becomes infected with the ordinary pus-pro- 
ducing micrococci, usually the staphylococci, in spite of the 
most careful methods of dressing, and in a few days this infec- 
tion travels up along the walls of the cavity and into every nook 
and cranny. This, in the case of the large psoas abscesses, 
means that a very considerable area within the body is now 
infected with active pyogenic cocci instead of being merely a 
reservoir for broken-down tuberculous material. The patient 
quickly responds to this infection, and develops fever, exhaus- 
tion and loss of weight, in addition to more rapid destruction 
of the joint and the neighboring tissues. It is, therefore, of TUBERCULOSIS OF BONES AND JOINTS 
403 
great importance to prevent the opening of such an abscess 
whenever possible. It may sometimes be clone by repeated 
aspiration of the contents, through a needle or small trocar, 
with perhaps the injection of iodine or a mixture of camphor 
and phenol. The method advised by Cheyne, open incision, 
evacuation, and suture in layers, is usually followed by failure, 
since the abscess, after refilling, almost always opens spon- 
taneously through the site of the incision. 
Another complication of tuberculous joint disease is the de- 
velopment of tuberculous meningitis, which is invariably fatal. 
It is, of course, possible that the meningitis may develop from 
the original focus of infection, but there is some evidence 
against this theory. 
A complication often seen in spinal tuberculosis is paralysis, 
due to the pressure upon the spinal cord of a cold abscess or of 
the products of inflammation of the membranes which cover 
the cord. The paralysis is almost always spastic in type, and 
occurs, usually, only in the dorsal and cervical cases. It comes 
on gradually, with weakness of the legs and increasing diffi- 
culty in walking until finally the patient becomes entirely unable 
to walk. It can be cured in all but a few cases by prolonged 
rest in bed, with fixation of the spine by apparatus or operation. 
Treatment of Bone and Joint Tuberculosis. (Conservative 
and Operative.) (A) Conservative Treatment. The local treat- 
ment is of the greatest importance. It takes at least two years 
for a tuberculous hip or knee-joint to get well, and at least five 
years for a tuberculosis of the spine, under conservative treat- 
ment, and it may take two or three times as long when the 
patient’s resistance is poor. The time may be shortened ma- 
terially by operation in those cases which are suitable for oper- 
ation. 
It is a well-established fact that tuberculous joints will get 
well if they are kept still for a long enough time. This means 
that some form of apparatus must be applied which will hold 
the joint in a fixed position so that it cannot move. Thg more 
perfectly it can be immobilized, the sooner it will get well. 
(1) The Treatment of Spinal Tuberculosis. This differs some- 
what from the treatment of the other tuberculous joints. In 
children if we hold the spine still long enough the tuberculous 
process will disappear and this is true in practically every case. CLINICAL TUBERCULOSIS 
404 
In acute and painful disease of the spine, the best method for 
rest is by absolute recumbency in bed, upon a “Bradford frame” 
made of gas pipe and covered with tightly stretched cloth. The 
frame is a few inches longer than the child, and two inches nar- 
rower than the width of the shoulders, and webbing straps are 
passed diagonally over the shoulder on one side and under the 
axilla on the other side, and buckled beneath the frame, so as 
to hold the thorax firmly to the frame. A folded towel is 
passed around the pelvis and pinned under the frame. This 
holds the spine almost immovable, and, in the case of Pott’s 
disease, requires thick pads on either side of the kyphosis (or 
hump) to prevent the skin from becoming excoriated by pres- 
sure. The routine that is necessary in practically all these 
cases of Pott’s disease is to lay the child on a frame and fasten 
it down so that it cannot get away. Every morning the child 
is carefully rolled over and the spine washed off with alcohol 
and ordinary talcum powder put on the back. This is a daily 
routine so long as they are in recumbency. Sometimes they are 
kept on such a frame for two or three or more years or until 
they become perfectly well. 
The further treatment is very simple, only to keep the spine 
still long enough. Ordinarily it takes four to five years for a 
tuberculous focus in the spine to get well. If after four or five 
years the child has no muscle spasm in the back, there is no 
sign of a tuberculous abscess, there is no paralysis, there is no 
referred pain, then the child may be well. We then place the 
child in an apparatus, in a brace or a cast. If the disease be 
above the mid-dorsal region this will not be sufficient unless it 
includes the head. The head, chin, occiput have to be sup- 
ported if the disease be above the sixth or seventh dorsal ver- 
tebra. We let the child up in this brace, increasing the time it 
can be upright until it is upright practically all day, and then 
we begin to take off the brace for a little while every day, and 
if then the child has no return of symptoms for six months or 
a year we consider it is well and we then let the child go with- 
out any support. Suppose, on the other hand that we have 
treated the child as long as it can be treated in bed; is it right 
to get it up in an apparatus any sooner? It probably in a good 
many cases can be gotten up sooner than two or three or four 
years if the mechanical principles can be carried out; if we can TUBERCULOSIS OF BONES AND JOINTS 
405 
make forward pressure on the knuckle and have enough lever- 
age above to push back on the child’s chest and pelvis, we can 
accomplish a good deal. It becomes then simply a plain ques- 
tion of mechanics. If the disease is high up, there is not a 
brace that has ever been made that will prevent a deformity. 
Tell the parents that no brace will prevent the deformity from 
increasing; that no cast will do so; that if the child is going to 
be upright it will have more deformity, also tell the parents 
perfectly frankly the exact proposition; that if they do not want 
the child to have a hump it must stay in bed two or three years 
on a frame. On the other hand, if they do not mind a hump, 
the child may be up and about in a brace. 
The general condition also has to be attended to. The child 
should live an outdoor life, and if possible, be rolled over so 
that the sun’s rays will shine on the back every day. (See 
Chapter XXI, B.—Heliotherapy.) 
(2) Hip and Knee Joint Tuberculosis. Cases of hip or knee 
joint disease are treated in the same way during the acute stage, 
with the addition of Buck’s extension by weight and pulley to 
correct whatever flexion deformity may be present. After a few 
months of bed treatment, it is advisable in most cases to get 
the patient up in some form of immobilization apparatus, be- 
cause the difficulty and expense of prolonged bed-treatment are 
almost prohibitive in the majority of cases. Many ingenious 
and efficient braces have been designed, the most useful being 
the Taylor brace for spinal disease, the modified long Thomas- 
Phelps traction splint for the hip cases and the Thomas knee- 
splint for the tuberculous knees. In some clinics, plaster of 
Paris is used for almost all cases. 
Most American surgeons believe that tuberculous hip joints 
and knee joints should be protected from weight-bearing, to 
prevent destruction of the joint-surfaces, but there is consider- 
able evidence that such joints are not apt to be very useful 
functionally, and that perhaps a speedy ankylosis is, after all, 
the quickest and best result to be obtained. The general rule 
should be that in children every effort should be made to obtain 
a useful, movable joint in hip and knee. If the disease goes on 
to suppuration, and becomes secondarily infected* with pus 
germs, it may be necessary to produce a rapid ankylosis in order 
to avoid the consequences of prolonged septic exhaustion. 406 
CLINICAL TUBERCULOSIS 
(B) Operative Treatment. There is a procedure that will 
hasten recovery, and that is an operative stiffening- of the spine, 
making the spine its own brace. In 1912 Albee and Hibbs 
(178), wrote about their experience of ankylosing the spine. 
Albee’s (36) idea was to split the spinous processes with a 
chisel, turning half to the side so as to make a V-shaped groove 
along the diseased area of the spine, two or three vertebra 
above and two or three below. Into that cleft which was 
made, a narrow strip of bone taken from the tibia with a chisel 
or a motor saw was sewed in place with kangaroo tendon or 
chromic catgut, keeping the child recumbent until body anky- 
losis took place. This is an extremely useful operation but it 
should not be done in the presence of sepsis; it should not be 
done if there is a discharging sinus, because after the operation 
infection may occur and the bone graft will be lost. I am pre- 
pared at the present time to recommend this operation for any 
case over seven or eight years of age, with the understanding 
that children will have to be treated by a brace or by recum- 
bency for at least two years afterwards, because the ankylosis 
which forms does not consist of very rigid bone, and in young 
children the bone may bend so that the deformity will increase 
unless carefully protected. We must not allow parents to think 
that the Albee operation will cure the case radically without any 
further treatment. Until children are twelve or fourteen years 
of age the bones have to be supported or the deformity will 
get worse. 
The Hibbs operation consists in paring off the periosteum 
from the spinous processes and the laminae, and the articular 
facets and laying strips of bone which are cut from the laminae 
themselves alongside of the spine, and nipping off the spinous 
processes with a bone cutting forceps so that each spinous 
process will lie down on the one below it, making a very com- 
plete and solid ankylosis of the spine by this method of fusion. 
In very young children who need the support of a bony anky- 
losis a Hibbs operation is advisable in preference to the Albee 
method. 
Tuberculosis of the Spine in Adults. In adults who have had 
for a long time a pain in the back at a definite site, always sus- 
pect something organic. Do not think it is a neurosis or hys- 
teria. Many cases are treated for neuroses, hysteria and men- TUBERCULOSIS OF BONES AND JOINTS 
407 
tal conditions who have perfectly typical Pott’s disease. Re- 
member, adults do not have pain about the belly, girdle pains, 
to the same extent that children have; they have a pain at the 
site of the trouble, that it is a constant, severe pain; that they 
do not get kyphosis early because the vertebrae are hard and 
solid; children get kyphosis early; adults late. The X-ray 
plate is not helpful in bone and joint tuberculosis until actual 
bony, destruction has taken place, although it sometimes shows 
fairly definite bone atrophy. Adults may go for years without 
a perceptible knuckle or before perceptible X-ray findings are 
discovered, although a definite tuberculous spondylitis may 
have existed during all of this time. The first thing known about 
an adult spinal tuberculosis is sometimes a rapidly oncoming- 
paralysis, a spastic paraplegia. 
Adults may also show an early abscess, a psoas abscess, 
which is the last thing that the average practitioner thinks 
about in a case of back pain. If a man has had pain in his back 
for a good while and you think he may have tuberculosis of 
the spine, do not neglect to feel of his abdomen. If a patient 
has any kind of symptoms, do not hesitate to have him remove 
his clothes. Many mistakes are made in perfectly simple cases 
by modesty on the part of the doctors or the patients them- 
selves in removing the clothes for the purpose of examination. 
In adults, tuberculosis of the spine demands a different kind 
of treatment from that in children and tuberculosis of the hips 
and of the knees also demands a different treatment. By chil- 
dren we mean cases under twelve or fourteen years of age, by 
adults everything beyond that. Children will get well with 
protection of the joints for a sufficient length of time, but 
adults with joint tuberculosis, whether it is in the hip, spine 
or knee, will not get well by either protection or conservative 
treatment. A man with Pott’s disease or with knee or hip 
joint tuberculosis will not get well by holding him in a brace 
even if for many years. Joint tuberculosis in adults does not 
tend to get well without operation. 
In adults with Pott’s disease we ankylose the spine by the 
method of Albee as soon as we can. In adults with hip joint 408 
CLINICAL TUBERCULOSIS 
tuberculosis we also operate as soon as we can. Here we do 
what is known as an arthrodesis which means a stiffening of 
the joint. For example, we find tuberculosis in the hip joint; 
we cut down on the joint, resect the trochanter temporarily 
because that is the easiest way of getting into the joint and 
with a chisel we scoop out the acetabulum; with the same 
chisel square off the head of the femur; put these two together 
and place the patient in a plaster cast. In ten or twelve weeks 
he will have a good ankylosis of his hip joint. In this way he 
will get well with a stiff hip, able to do his work, in nine or 
twelve months; whereas if we did not fasten up the hip joint, 
at the end of five, ten or fifteen years he would be still under 
treatment. In the same way we excise the knee joint for 
tuberculosis and cure in a few months cases that have been 
treated with casts and braces for five or ten years. I have 
seen many people with knee-joint tuberculosis who have been 
treated conservatively for from ten to seventeen years by 
competent orthopedic surgeons, and who were no more nearly 
well after this prolonged treatment than when the treatment 
was begun. I have never seen an adult with a proven tuber- 
culous knee get well without operation. Where we do a rapid, 
conservative arthrodesis, excision of the joint, taking away only 
a thin strip from the head of the tibia and the femur, putting the 
bones together and applying a cast, in a few months the indi- 
vidual gets a good stiff knee joint. There is a difference between 
the forms of treatment in children and in adults. As a rule be 
as conservative as you can, and as long as you can in the treat- 
ment of children; in the adults be as radical as you can, as soon 
as you can. We see people going about year after year with 
painful swollen tuberculous joints and spines, and comparatively 
soon after operations we see them well, the joints solid, free from 
any manifestations of tuberculosis and the patients able to go 
about and earn their living. Remember to suspect tuberculous 
joint disease in children whenever they have limitation of joint 
motion without any apparent sign, and also remember further 
that the way to get well is to make the joint stiff as soon as pos- 
sible whether this be done by artificial apparatus or by operation. 
Tuberculin. The question of tuberculin treatment is one of 
great importance. An experience extending over many years TUBERCULOSIS OF BONES AND JOINTS 
409 
has verified the facts that cases which get minute doses of tuber- 
culin do better than those which do not, and so it should be a 
routine in the treatment of bone and joint disease. Tuberculin 
should be administered hypodermatically (to small children it 
may be given by inunction according to the method of Pet- 
ruschky) beginning with most minute doses according to the 
direction given in Chapter XXIV, “Tuberculin—its therapeutic 
indications.”—E. W. R. CHAPTER 31 
TUBERCULOSIS OF THE GENITO-URINARY ORGANS 
General Consideration. Tuberculosis involving the genito- 
urinary tract in its early stages begins in either the urinary 
organs or the genital organs. Later in the course of the disease, 
or sometimes when the patient presents himself for examination, 
one finds that both of these tracts are involved, hence the use of 
the phrase—genito-urinary tuberculosis. In the cases in which 
the tuberculous lesion is located in only one or the other tract, 
it would be better to speak of it as genital tuberculosis or 
urinary tuberculosis. With this object in view the subject will 
be considered under these two headings. 
(A) Tuberculosis of the Urinary Tract 
Tuberculosis of the urinary tract, according to present day 
conception, always begins in the kidney, that is, the tuberculous 
process is usually primary in the kidney as regards the urinary 
tract. The exception to this are the cases in which late in the 
course of the disease the tuberculosis reaches the other kidney 
via the ureter. 
(1) Tuberculosis of the Kidney 
Frequency. Renal tuberculosis was formerly considered a rare 
lesion of the kidney. With the improvements in modern diag- 
nostic methods, the cases are more and more accurately diag- 
nosed, so that there is an apparent increase in this disease. 
Kapsammer, (185) who examined and reported 20,770 autopsies, 
was able to find renal tuberculosis present in about 1 per cent. 
Wildbolz (96) states that in 2,345 autopsies reported from the 
Pathological Institute at Berne, renal tuberculosis was found in 
5.3 per cent, and in this same series evidence of pulmonary 
tuberculosis was found in 20.7 per cent. 
Age. Renal tuberculosis is essentially a disease of adult life, 
the largest number of cases occurring between the ages of 20 and 
40. Cases occurring in children and young adults are not un- 
common, and doubtless many escape recognition. 
Sex. Renal tuberculosis occurs with about equal frequency 
in both sexes. Statistics vary on this point, however, and these 
410 TUBERCULOSIS OF GENITO—URINARY ORGANS 
411 
differences may be due to the diversity of the material of the 
various investigators. More women are operated upon than men 
but more men come to autopsy than women, so the disparity 
may be due in part to these facts. 
Side Involved. Statistics show that the right kidney is more 
often the seat of tuberculosis than is the left, which is probably 
due to the increased mobility of the right kidney. In Kiister’s 
(148) statistics there were 189 cases of right-sided tuberculosis 
as compared with 163 cases of left-sided. 
Predisposing Factors—(a) Traumatism. It is questionable 
whether traumatism in the strict sense of the word is a predis- 
posing factor in the production of renal tuberculosis. Because 
of its depth it is difficult to see how a patient could sustain a 
trauma that would predispose to the localization of tubercle 
bacilli without producing gross kidney disturbance. 
(b) Stone. The influence of stone in the production of renal 
tuberculosis does not seem to be very great. Primary stone and 
tuberculosis is a rare combination, but secondary stone is occa- 
sionally found in a tuberculous kidney. That the relationship 
existing betwe'en the two cannot be very great is evidenced by 
the fact that tuberculosis rarely develops in a patient who has 
previously been operated upon for renal stone. 
(c) Pyelitis. It is believed that chronic pyelitis may be a pre- 
disposing factor, but this is probably not true, as many patients 
who are diagnosed as cases of pyelitis are in reality cases of 
renal tuberculosis which are not recognized at the time. 
Pathogenesis. The present view regarding the origin of 
urinary tuberculosis is that the condition is primary in the kid- 
ney and that the process extends from the kidney down the ureter 
to the bladder, so that bladder tuberculosis, therefore, is sec- 
ondary to kidney tuberculosis. Kidney tuberculosis is, of course, 
secondary to a primary focus elsewhere in the body, such as 
Ivmph glands, lungs, bones, joints, * tendons, or synovial 
membrane. 
The theories regarding the origin of renal tuberculosis are 
generally considered under (a) hematogenous, (b) lymphogen- 
ous, and (c) urogenous. 
(a) Hematogenous. The present day views are almost unani- 
mous in holding that renal tuberculosis is a blood-borne disease, 
that is, that the tubercle bacilli are carried to and deposited in 
the kidney by the blood stream. 412 
CLINICAL TUBERCULOSIS 
(b) Lymphogenous. Various lympathic theories have been 
advanced. (See Chapter III.) 
(c) Urogenous. That tubercle bacilli may be promulgated up 
the ureter by the urinary current is possible. Cases of secondary 
tuberculosis of the bladder with ulceration, great frequency of 
urination, associated with straining and increase in intravesical 
pressure, are frequent. It has been shown that bladder urine 
backs up into the ureter, so that it is easy to see that urine from 
the bladder could travel up the ureter of the healthy kidney and 
carry with it tubercle bacilli, if the ureteral orifice is ulcerated or 
rigid and gaping. 
Symptoms—(a) Kidney. Tenderness to Pressure. This may be 
variable and may be demonstrated by ordinary palpation or by 
deep pressure with the thumb placed in the angle made by the 
last rib and the deep lumbar muscles. 
Great care, however, must be used in evaluating this symptom, 
as there is the possibility of this tenderness being manifested on 
the side of the healthy kidney, when it may be due to an enlarge- 
ment or compensatory hypertrophy of the normal kidney. 
(b) Colic. Renal colic associated with or as a symptom of re- 
nal tuberculosis is sometimes due to the presence of calculi. In 
the largest percentage of cases there are really incrustations of 
necrotic tissue in the tuberculous cavities. In other instances, one 
may find incrustations of tuberculous ulcerations in the pelvis. 
(c) Bladder Symptoms—Frequency of Urination. Frequency 
of urination may be the first symptom observed and one of its 
characteristics is its nocturnal occurrence, which may necessi- 
tate arising once or twice each night, or the patient may be dis- 
turbed as often as every fifteen to thirty minutes. Frequency is 
sometimes associated with great urgency, so that the patient is 
obliged to respond at once or the act becomes involuntary. As 
a rule, the onset of this symptom is gradual and progressive. 
(d) Pain. As a result of the tuberculous involvement of the 
bladder, the bladder mucosa becomes sensitive so that the act of 
micturition is painful. The pain usually radiates along the 
urethra, but may be localized in the bladder. 
(e) Pyuria. Pus in the urine is a more or less constant symp- 
tom. The amount of pus may vary from one examination to the 
other, so that a specimen examined one day may show a great 
deal, and a second specimen examined the next day may be 
relatively free from pus. TUBERCULOSIS OF GENITO—URINARY ORGANS 
413 
(f) Hematuria. This is not always present, especially early 
in the disease, although tuberculosis is one of the most frequent 
causes of hematuria. The blood may be microscopic in amount, 
or it may be so great as to overshadow and obscure all the other 
symptoms of renal tuberculosis. The hematuria may be so pro- 
fuse and continuous that the life of the patient is endangered, 
and knowledge of the fact that the hemorrhage was due to tu- 
berculosis is first obtained when the kidney is removed. Termi- 
Fig. S3. Tuberculosis of the Kidney Showing Early Lesion in One Papilla—(a) with 
Extension of the Process to the Mucosa of the Pelvis 
nal hematuria with the passage of small blood-stained shreds of 
pus is seen more frequently than is profuse hematuria, and it oc- 
curs generally at the end of urination and is associated with a 
great deal of pain. 
Pathology. Renal tuberculosis occurs in one of two forms, 
either as an acute miliary tuberculosis or as the so-called chronic 
renal tuberculosis. The acute miliary tuberculosis is a part of a 
generalized miliary tuberculosis in which the process is demon- 414 
CLINICAL TUBERCULOSIS 
strated throughout the entire body, and as such possesses no 
surgical possibilities and does not fall within the scope of this 
chapter. 
Chronic renal tuberculosis may be more or less arbitrarily 
classified as follows: 
1. The large cheesy, cavernous type. 
2. Tuberculous ulceration of one or more renal papillae. 
3. Chronic, discrete nodular type. 
4. Fibroid type. 
In addition, there has been described a so-called miliary tuber- 
culosis of the kidney proper, a so-called acute miliary renal 
tuberculosis, but it does not represent, as a rule, the early stage 
of a so-called chronic renal tuberculosis. 
Not infrequently more than one of these forms may be seen in 
the same kidney. In other words, these various types are not 
always as sharply defined as may appear from this classification 
Much speculation has been put forth regarding the part of the 
kidney in which the tuberculous process begins. Among the 
early cases operated upon, the most advanced lesion found has 
been in one of the renal papillae, either alone or with an involve- 
ment of adjacent calices. It was formerly believed that papillary 
tuberculosis was a special form of renal tuberculosis, but since 
cases began to come to early operation, those in which the 
papillae seem to be the first site of involvement have been 
noticed more and more. This, of course, is the result of early 
diagnosis. It is believed by many that all cases of renal tubercu- 
losis begin as tuberculosis of the papillae. 
In the early cases, the kidney appears to be normal upon in- 
spection. The cut surface shows changes in one or more papil- 
lae and the papillae corresponding to them may show the 
presence of tubercles, and at times, small areas of caseation may 
be seen. In the more advanced cases, the surface of the kidney 
shows the presence of tubercles, which may be arranged in 
groups. There may be more than one group and, as a rule, nor- 
mal appearing kidney tissue can be found between the groups of 
tubercles, which often project above the surface of the kidnev 
and are visible to the naked eye. The organ may or may not be 
slightly enlarged. Tubercles that may have the appearance of 
infarcts and areas of caseation may be seen on cut section. 
Between the areas of caseation may be seen large cavities with TUBERCULOSIS OF GENITO—URINARY ORGANS 
415 
thick walls which are often more or less irregular in outline. 
The walls are covered with thick, caseating masses, and the 
cavities are sometimes lined with thick, mucous granulation 
tissue. In the caseous tissue surrounding the cavities, tubercles 
may be found. Most of these cavities communicate with the 
renal pelvis. 
As the cavities increase in size, they enlarge toward the cor- 
tex of the kidney, the cortex becomes extremely thin and the 
Fig. 54. Tuberculosis of the Kidney Advanced. (Phthisis of the Kidney.) 
Extensive Involvement of Both Upper and Lower Poles, Showing Large 
Thick Walled Cavities—a, in Lower Pole 
cavities protrude above the surface of the kidney, so that the 
kidney surface becomes irregular, the kidney increases in size 
and loses its characteristic shape. Because of the loss of kidney 
tissue, it assumes a pale color. At this stage, tubercles are 
infrequently seen on the surface, being limited to the parts of 
the parenchyma that have not as yet undergone extensive 
change. < # *l 
Further increase in size is dependent in part on the condition 416 
CLINICAL TUBERCULOSIS 
of the ureter. If the kidney becomes strictured so as to inter- 
fere with drainage of the urine and pus, the kidney may reach an 
enormous size, resulting in the production of a so-called tuber- 
culous hydronephrosis. If the ureter remains patent, so the 
drainage is not interfered with, the kidney may undergo loss of 
parenchyma due to destruction by the tuberculous process, and 
it becomes very small, at times weighing not over 30 to 60 grams. 
The coverings of the kidney are sooner or later involved in 
the pathologic process. The fibrous capsule becomes thickened 
and adherent to the cortex as well as to the fatty capsule, and 
the changes in the coverings of the kidney may not advance 
beyond this point. At times, |however, the kidney is surrounded 
by thick, dense, fibrous tissue of almost cartilaginous hardness, 
due to the fusion of the fibrous and fatty capsules. This process 
of sclerosis often takes place at the expense of the fatty capsule 
and the fat remaining is often very fibrous. This thick, fibrous 
perinephritis is not typical of tuberculosis, as it is also seen in 
other chronic renal infections. 
Suppuration outside of the kidney may occur with the produc- 
tion of a tuberculous perinephritic abscess. This, however, is 
rare. The renal pelvis, as a rule, is involved early in the course 
of renal tuberculosis, and the earliest lesions are found in the 
region of its papillae. Tubercles are seen beneath the mucous 
membrane and tend to remain localized; later the process spreads 
over the entire pelvic mucosa. The tubercles undergo caseous 
degeneration with resulting ulcer formation and the pelvis un- 
dergoes dilation due to obstruction in the ureter, which rarely 
escapes infection, and, as a rule, is involved early. Miliary tuber- 
cles may be seen in the mucosa, arranged in small groups be- 
tween which normal mucosa is seen. These ultimately undergo 
caseation and form ulcers. The walls of the ureter show thick- 
ening and the ureter becomes firm and rigid. There are times 
when the kidney has a normal appearance. Stricture formation 
in the ureter is not uncommon. In rare instances, the entire 
lumen is dilated, resulting in the production of a closed tuber- 
culosis pyonephrosis, which has been termed auto-nephrectomy. 
In such cases the products of infection do not reach the bladder 
and the patient passes clear urine. 
The bladder may remain free from involvement for a long 
time and the earliest bladder changes are those seen around the 
ureter of the affected side. The ureter shows hyperemia and is TUBERCULOSIS OF GENITO—URINARY ORGANS 
417 
surrounded by tubercles which are undergoing caseation and 
ulceration. The process extends from the ureter, and, in cases 
seen early, tuberculous ulcerations are seen in the corresponding 
half of the bladder. Later, the entire bladder shows the pres- 
ence of tuberculous ulceration. Normal mucosa may be seen 
between these areas and the process is not limited to the mucosa, 
but involves the submucosa and muscularis, as a result of which 
the bladder undergoes secondary contraction and has limited 
capacity. The ureter on the corresponding side often is retracted 
and becomes dilated. This condition has been termed “golf 
hole ureter.” 
General Symptoms. Early in the course of the disease there 
may be no symptoms. As the disease progresses, general symp- 
tomatic manifestations present themselves. The patient com- 
plains of loss of appetite, he is below par, his strength is not up 
to the average, and a certain amount of anemia develops. A slight 
rise in temperature may be noted, which later becomes almost 
constant, doubtless due to the presence of a mixed infection. 
It is only late in the course of the disease that marked, general 
symptomatic manifestations are present. The diagnosis of tuber- 
culosis is occasionally disputed because of the general well-being 
and general appearance of the patient. The general condition of 
the patient is not always an index of the amount or extent of the 
tuberculous process in the kidney, because patients with well- 
developed or advanced renal tuberculosis often have no evidence 
as regards their general condition. 
Diagnosis, (a) General. Perhaps a large number of cases of 
renal tuberculosis are not recognized, or the possibility of renal 
tuberculosis is not being thought of. A persistent pyuria should 
always arouse suspicion of a possible tuberculosis, which may 
often be strengthened by the presence of tuberculosis in other 
parts of the body. Scars in the neck indicate tuberculosis of 
the lymph nodes. A history of long suppuration involving the 
bones, evidence of joint and tendon tuberculosis, and the pres- 
ence of tuberculosis of the lung are facts that should not be 
overlooked. In males, the evidence of a nodule in the prostate, 
the testicle, or epididymis is very valuable confirmatory evidence. 
In women, involvement of the tubes and ovaries is rare, whereas 
in men involvement of the genitals is common. 
Palpation may not give any additional information except for 
tenderness over the bladder, and if bladder tenderness is asso- 418 
CLINICAL TUBERCULOSIS 
dated with a history of painful distention and exquisite sensi- 
tiveness to instrumentation, much valuable information is 
obtained. 
(b) Urinalysis. Albuminuria is a constant finding. It has 
been said that renal tuberculosis does not exist without the 
finding of albumin in the urine and that its absence almost ex- 
cludes the possibility. 
A persistent pyuria that does not yield to the usual treatment 
within a reasonable time should always call for special methods 
of examination in order to exclude the possibility of tuberculosis. 
The pyuria is often small in amount and not much significance 
may be attached to its presence and hence early recognition of 
the cases fails. Large amounts of pus are always found late in 
the course of the disease. The urine may be free from pus in 
cases of so-called closed pyonephrosis. 
(c) Tubercle Bacilli in Urine. While many of the symptoms 
enumerated above may suggest the possibility of renal tubercu- 
losis and a presumptive diagnosis be made, the final diagnosis 
can only be made upon the demonstration of tubercle bacilli in 
the urine1. It was formerly taught that tubercle bacilli were 
difficult to demonstrate in the urine, but this old dogma has been 
disproven. (See Chapter XXXVIII—“The Urine in Tuberculo- 
sis.”) It has been variously estimated that in cases of renal tu- 
berculosis, the bacilli can be demonstrated in upwards of 90 per 
cent of the cases in direct smear. Undoubtedly, tubercle bacilli 
can be found much more readily in cases in which the bladder 
has become involved, that is, late in the course of the disease. 
Great care must be exercised in examining for the Koch’s 
bacillus, to exclude contamination by the smegma bacillus. This 
is of prime importance. A large percentage of errors can be 
eliminated if one thoroughly prepares the patient, and then care- 
fully obtains a catheterized specimen from the bladder, or better 
still examines a specimen obtained by ureteral catheterization 
in which event the danger of contamination by smegma bacillus 
hardly enters into consideration. See page 510. 
1The demonstration of the Koch’s bacillus in the urine is not indisputable evidence of 
genito-urinary tuberculosis. A bacillemia due to the tubercle bacillus may result in kidney 
permeability—this without any kidney lesions, simply the effect of the produced toxins 
circulating in the blood serum when the bacilli may pass through the kidney structures. 
Permeability to albumin in the supposedly normal kidney is shown in those cases des- 
ignated by clinicians as pretuberculous albuminuria (see chapter XI) in which the 
albumin content of the urine increases with the increase of the tuberculous activity in 
some near or remote part of the organism and tubercle bacilli themselves may pass 
through a weakened and irritable kidney tissue incident to the toxins and contaminate 
the urine.—J. R. TUBERCULOSIS OF GENITO—URINARY ORGANS 
419 
(d) Animal Inoculation. Guinea pig inoculation with urine 
of a patient suspected of having urinary tuberculosis is of value 
in confirming the clinical diagnosis. The objection to this meth- 
od, however, is the fact that it takes so long before the tubercu- 
losis develops in the guinea pig. 
Various methods of guinea pig inoculation have been recom- 
mended. The intraperitoneal injections have the advantage in 
that the pigs develop tuberculosis early, but have the disadvan- 
tage that very frequently the pigs die because of a mixed infec- 
tion, and when this occurs in cases in which the urine is obtained 
by ureteral catheterization, it means another ureteral catheteri- 
zation. 
Intrahepatic and intrasplenic injections have been advised. In 
order to shorten the period of incubation in the pig, the prelim- 
inary treatment of the pig by x-ray has been suggested. Crush- 
ing the inguinal glands and injecting the sediment directly into 
them has become the method of choice. Ebright has suggested 
sensitizing the pigs by the previous administration of large doses 
of tuberculin. 
(e) Diagnostic Injections of Tuberculin. The injection of old 
tuberculin for diagnostic purposes may not offer much in the 
way of an aid in the diagnosis of tuberculosis in the genito- 
urinary tract. It has been claimed that after a preliminary 
injection of tuberculin, tubercle bacilli can be found in the urine 
much more easily and much more frequently, and often in cases 
in which persistent search has failed to find them. Focal reac- 
tions at the site of the disease are supposed to occur after injec- 
tions of tuberculin. It is questionable, however, whether one 
would be willing to remove a kidney because of the production 
of pain in the region of the kidney following tuberculin injections. 
Special Methods of Diagnosis. (1) Cystoscopy and Ureteral 
Catheterization. Cystoscopic examination is the one single 
method that gives us the most important information, though in 
early cases it may be negative. In cases in which tuberculosis 
of the kidney is suspected and in which the patient has been 
repeatedly cystoscoped with negative findings, one may finally 
be rewarded by the finding of changes around one ureteral ori- 
fice. The early changes are hyperemia and tubercles, and later 
areas of ulceration. 
Ureteral catheterization enables us to determine the origin of 
the disease, whether right or left side, as well as to establish the 420 
CLINICAL TUBERCULOSIS 
origin of the tubercle bacilli. Furthermore, by means of this 
method the presence of a second kidney and whether or not it is 
involved in the tuberculous process may be determined. 
Since these group of cases have been more intensively studied 
by this method of examination, the percentage of cases showing 
bilateral tuberculosis has increased. It was formerly taught that 
all cases of renal tuberculosis were unilateral early in the course 
of the disease. Recent statistics, however, show that from 10 to 
15 per cent of the cases of so-called early tuberculosis of the 
kidney are bilateral. 
Cystoscopic examination in early cases is simple and easy. 
Later, it is difficult because of the exquisitely painful condition 
of the bladder, when an anesthetic must be resorted to. 
In advanced cases, the entire bladder mucosa is red, there are 
many areas of ulceration, shreds of mucous are seen adherent 
to the bladder wall and the ureteral orifice is dilated. When the 
areas of involvement are small, normal mucosa can be seen be- 
tween the groups of tubercles and ulcerations. 
(2) X-Rays. Routine examination of all patients suspected of 
having renal tuberculosis has shown that many of these patients 
show definite roentgen ray evidence. Areas of calcification are 
seen in the kidney region, and in cases of so-called “putty kid- 
neys,” the entire kidney outline can be seen. While the x-ray 
gives corroborative evidence, it should not supplant cystoscopy 
and ureteral catheterization, because the presence of calcification 
on one side does not necessarily mean that the tuberculosis may 
not be bilateral and that there may not be an involvement of the 
other side. 
(3) Functional Kidney Tests. Various functional tests have 
been advocated from time to time. The phenolsulphonaphtha- 
lein test is perhaps the one most relied upon today. A study of 
the function of the kidney which is to remain is important from 
the standpoint of first, demonstrating the presence of the kidney; 
second, of attempting to establish the functional capacity of this 
kidney—whether or not it will be able to carry on the work of 
the two kidneys, and third, whether or not infection is present. 
(4) Chromoscopy. Injection of indigo-carmin, first advocated 
by Felker and Joseph, is used by some to determine the func- 
tional capacity of the two kidneys, and in this way it obviates, in 
a certain number of instances, the necessity of ureteral catheteri- 
zation. After a solution of indigo-carmin has been injected TUBERCULOSIS OF GENITO—URINARY ORGANS 
421 
intramuscularly, it is eliminated by the kidneys. The diseased 
kidney eliminates the dye slower than does the well side, because 
it does not possess the power to eliminate as much dye as the 
well kidney, hence the urine from this kidney is pale blue, 
whereas the urine from the well side is dark blue. (See Chapter 
XXI.—A—Chemotherapy.) This test is of value not only in the 
study of the functions but as an aid in finding the ureters. 
Differential Diagnosis. Differential diagnosis may be consid- 
ered under two headings (a) differentiation from other lesions of 
the kidney and (b) differentiation from other lesions of the 
abdomen. 
(1) Lesions of the kidney other than tuberculosis. The 
lesions of the kidney that most frequently come under con- 
sideration are (a) stone, (b) tumor, and (c) pyelitis. In the 
largest number of cases, (a) stone can be excluded with good 
roentgen ray technic and with careful reading of the plates. It 
must not be forgotten, however, that there are a certain number 
of stones that cannot be demonstrated by means of roentgen 
ray. At times, areas of calcification in a tuberculous kidney call 
for differentiation from stone, and it must not be forgotten that 
in rare instances stone and tuberculosis may occur in the same 
kidney. While the clinical symptoms of (b) tumor and renal 
tuberculosis are not very often confused, a differentiation may 
occasionally be called for, which can be done by means of pyelo- 
grams. The routine use of pyelograms in renal tuberculosis, 
however, is not a desirable procedure and should not be used, 
(c) pyelitis. Many cases of pyelitis are in reality cases of 
renal tuberculosis. If pelvic lavage is instituted in the treat- 
ment of pyelitis and the desired result is not obtained within a 
reasonable time, careful search for tubercle bacilli and guinea 
pig inoculations should be made. 
(2) Lesions of Other Abdominal Viscera—(1) Gall Stones. 
Patients with right renal tuberculosis are often mistaken for 
cases of gall-stone disease. The history of severe abdominal 
colic, radiating to the shoulder blade, and the presence of dyspep- 
tic symptoms, coupled with the absence of urinary symptoms 
should lead us to suspect gall-bladder disease rather than renal 
tuberculosis, in which case bladder symptoms, albumin and pus 
in the urine are such constant findings. 
(2) Appendicitis. The most frequent mistake made is diag- 
nosing cases of renal tuberculosis as cases of chronic appendi- 422 
CLINICAL TUBERCULOSIS 
citis, as a result of which a perfectly harmless appendix is re- 
moved and the patient fails to obtain relief from his symptoms. 
In cases of chronic appendicitis, one should be able to elicit a 
history of repeated attacks'of acute appendicitis—a history which 
is classic. Sudden onset of pain, reflex nausea and vomiting1, 
and temperature is a symptom-complex that is not common in 
renal tuberculosis. The presence of pus or bacteria in the urine 
and the long duration of the patient’s symptoms argue rather for 
renal tuberculosis and against the so-called chronic appendicitis. 
(3) Pelvic Disease in Women. Next to appendicitis, the most 
frequent source of error is made in favor of pelvic lesions in 
women. Right sided tubal disease and right sided disease of the 
ovary are the conditions most frequently diagnosed, and because 
of the simplicity of vaginal examination and the finding of slight 
disease of these organs the patients are erroneously operated 
upon. When the pelvic findings are small or insignificant and 
there is pus in the urine and a history of long-continued bladder 
distress, these patients should be subjected to careful, pains- 
taking urologic examination before they are operated upon for 
tubal or ovarian disease. 
The Course of Renal Tuberculosis. Renal tuberculosis gen- 
erally pursues a very chronic course. Not infrequently patients 
give a history of onset dating back eight or ten years. On the 
other hand, the course is rather rapid in some cases, in certain 
ones of which the tuberculous process extends rapidly through 
the entire genito-urinary tract. 
The duration of life after the diagnosis has been made has 
been variously estimated. There are cases known to be alive 
ten or fifteen years after the diagnosis of renal tuberculosis was 
established. Kornfeld (188) found 15 out of 200 cases that lived 
longer than six years. 
Prognosis. In renal tuberculosis as regards the infection in 
one kidney the prognosis is good. It must, however, be guarded 
because of the possibility of the tuberculous lesions being pres- 
ent in other parts of the urinary tract. Many women who have 
been operated upon have subsequently become pregnant and 
the one kidney may carry the patients through pregnancy with- 
out any difficulty. 
Causes of Death. The more frequent causes of death are renal 
insufficiency and cachexia associated with myocarditis and mye- 
loid degeneration. Tuberculosis outside of the genito-urinary TUBERCULOSIS OF GENITO—URINARY ORGANS 
423 
tract is often the primary cause of the deposit of these tubercles. 
A patient with tuberculosis of the genito-urinary tract is apt to 
be particularly susceptible to tuberculous meningitis. 
It has been agreed that spontaneous cure does not take place, 
though cases of auto-nephrectomy, as mentioned above, are 
sometimes cited as examples of spontaneous cure. 
Treatment. The treatment is prophylactic, hygienic, and 
dietetic. The same rules regarding the management of tuber- 
culosis in other parts of the body apply to the management of 
cases of bladder and kidney tuberculosis. Included in the pro- 
phylactic treatment is the avoidance of infection in the urinary 
organs which might prepare the soil for invasion by tubercle 
bacilli. In this category should be placed the treatment of 
urethral strictures, so as to insure free drainage, and the preven- 
tion of gonococcus infections. 
Tuberculin. There are no proven cases of cured tuberculosis 
of the kidney per se that have been treated by tuberculin, but as 
an adjunct to the surgical treatment it is a most desirable rem- 
edy, hence it should always be used after surgical treatment. 
Surgical Treatment. Once the diagnosis of renal tuberculosis 
has been made the question of surgical removal of the kidney is 
under discussion, and nephrectomy is the only operation that 
should ever be contemplated. Unless there is distinct contra- 
indication, such as an active and well-advanced tuberculosis of 
the bones or lungs, the presence of a severe nephritis in the 
opposite kidney, a tuberculous kidney should be removed as soon 
as the diagnosis-is definitely established. Among the common 
causes of death following nephrectomy for renal tuberculosis one 
may mention hemorrhage, pneumonia, myocarditis and menin- 
gitis. 
Results of Operation. In early cases, the results of the opera- 
tion is a very rapid amelioration of symptoms. The results to 
be obtained are in direct ratio to the duration of the condition, 
that is, if the patient has had bladder symptoms for two years, 
it will take about two years after operation for these symptoms 
to disappear. In other words, cases that are recognized and 
operated upon early offer the best possibilities for complete dis- 
appearance of the bladder condition after the operation. Only 
too often the patient comes in very late in the course of the 
disease with the bladder in a bad state of contracture, so that 
the amount of relief obtained is small. Here, as in any other 424 
CLINICAL TUBERCULOSIS 
surgical condition, the key to the entire situation as regards 
ultimate cure is early diagnosis. 
Following operation, the amounts of urine voided rapidly 
diminish, so that the output returns to normal. Pyuria dis- 
appears in a large number of these cases, and the urine ultimately 
becomes free of pus. Tubercle bacilli may persist in the urine 
for a long time after operation, as was proved by Israel (117). 
After-Treatment. The after-treatment for bladder tuberculo- 
sis depends in a measure upon the amount of bladder involve- 
ment. In the largest number of instances, I have not resorted to 
the use of local treatment, which in so many instances is ex- 
tremely painful. The instillation of bichloride of mercury, in 
increasing amounts of from 5 to 20 cc and increasing in strength 
from 1:10,000 to 1:3000, has been used but it results in the pro- 
duction of very much pain. Other local applications that have 
been recommended are 5 per cent guaiacol or guaiamar injec- 
tions into the bladder; a warm solution of 6 per cent carbolic 
acid has also been advised, but has occasionally been followed 
by hematuria. In order to hasten the cure of tuberculous ulcer- 
ations, bladder fulguration and radium have been advised. A 
secondary operation on the bladder may be necessary in cases in 
which the symptoms persist in spite of the removal of the kid- 
ney. In women, a vesico-vaginal fistula can be carried out; in 
men suprapubic drainage may be indicated. 
(B) Genital Tuberculosis 
Tuberculosis of the genital tract is very often confused with 
tuberculosis of the urinary tract. Many times both occur in the 
same patient. In cases of tuberculosis of the genital tract there 
is present, in a large number of cases, definite evidence of tuber- 
culosis in other parts of the body. Thus Barney (169), who has 
made a careful study of this question, found tuberculosis of other 
organs in 55.8 per cent of his cases of tuberculosis of the epi- 
didymis. The lung was most frequently diseased, with a total of 
35 cases or 22.7 per cent. Keyes found a previous extensive 
tuberculous process in 36 out of his 100 cases. This evidence was 
most frequent in the lungs, bones, joints, tendons and glands. 
Pathogenesis. There is still some discussion regarding the 
beginning of genital tuberculosis in the male. The largest num- 
ber of contributors doubtless believe that tuberculosis of the 
genital tract is primary in the epididymis and that the process 
spreads from the epididymis to the prostate and seminal vesicles, TUBERCULOSIS OF GENITO—URINARY ORGANS 
425 
and in a definite number of instances, involves the testicle and 
bladder. The theory that tubercle bacilli are carried to the 
epididymis by the blood stream seems to be the view accepted 
by most authors. The fact that other blood-borne infections of 
the epididymis are seen, such as colon bacillus infections, would 
seem to lend support to the theory that it is a blood-borne dis- 
ease. Very often accessory factors have aided in the localization 
of the process to the epididymis, such as trauma or recent 
gonorrheal infection of the epididymis. 
Whether or not tuberculosis of the prostate is primary, hema- 
togenous, lymphogenous or perhaps deferential, in origin is not 
a definitely settled question. That tuberculosis in the genital 
tract begins primarily in the epididymis is not accepted by all, 
as there are adherents of the theory that tuberculosis begins pri- 
marily in the prostate and that it spreads from the prostate to 
the other parts of the genital tract. Equally unsettled is the 
question of how the tuberculous process spreads after it has 
reached the epididymis. Many believe that it spreads by way 
of the vas deferens. The opponents of this theory point to the 
fact that the vas deferens may be normal in instances in which 
tuberculosis is found in the epididymis, prostate gland, and 
seminal vesicles. Barney (169) believes that the spread is lym- 
phogenous. 
Pathology. The tuberculous process begins in the tail of the 
epididymis. From there it spreads and involves the body and 
later the head of the epididymis. The process may remain more 
or less localized for some time, and, indeed, the patient may state 
that a nodule has been present for many years. Not infrequently 
the nodule seems to be in a state of apparent healing. Later in 
the course of the disease, the process spreads to and involves the 
body of the testicle, the small tubercles increase in size and un- 
dergo caseation, and the disease extends beyond the confines of 
the epididymis and involves the vesicles, which become adherent 
to the epididymis. An abscess is produced which sooner or later 
opens externally through the skin and results in sinus formation. 
The sinus may heal, break open several times or several 
sinuses may be present. The tunica vaginalis usually presents a 
tuberculous hydrocele, the vas deferens becomes enlarged and 
hard, and in the late stages, irregular and beaded; the entire cord 
may be thickened, and the prostate becomes involved sooner or 
later. The surface of the prostate is irregular and its consistency 426 
CLINICAL TUBERCULOSIS 
is much increased. The seminal vesicles, in advanced cases, 
show thickening of the walls, are hard and nodular, and often 
there may be more or less evidence of a periseminal vesiculitis. 
Caseous nodules are formed; the wall may undergo fibrous in- 
duration so that the vesicle shrinks and produces a hard rigid 
mass. It is stated that calcification in tuberculous vesicles 
occurs; this, however, is rare. 
Tuberculosis lesions occur with about equal frequency on 
either the right or left side, and it is believed that they begin on 
the side corresponding to the involved epididymis. When the 
case is seen clinically, as a rule both sides are involved. 
Tuberculosis of the urethra is rare and occurs late in the course 
of the disease. Stricture formation occurs rarely, and results in 
symptoms of urinary difficulty, frequency, and obstruction. In 
late cases, the bladder is involved. The changes are in no wise 
different from those described in urinary tuberculosis. 
Symptoms. The onset is generally insidious so that the patient 
cannot state definitely when the disease began, except in the 
rare instances in which there is a definite and clear cut history 
of traumatism. An acute tuberculous epididymitis with sudden 
onset is rare. Although the disease generally begins as a unilat- 
eral one, the opposite side tends to become involved sooner or 
later, and a large number of patients return with involvement of 
the opposite side after the epididymis first involved has been 
removed by operation. The fact that the opposite side tends to 
become involved so frequently is one of the strong arguments in 
favor of the operation of epididymectomy in which attempt 
should be made to conserve the testicle. 
(1) Swelling. Often the first sign that attracts the patient’s 
attention is a slow, gradual, painless enlargement of one-half of 
the scrotum which is often associated with increased hardness. 
The increase in size is occasionally first noticed after traumatism 
and likewise after an attack of gonorrheal epididymitis. The 
patient may state that the testicle has never returned to its 
normal size. 
(2) Pain. Pain in the affected side may be absent and is more 
apt to be present during acute exacerbations. When the testicle 
becomes very large, there is apt to be not only pain in the tes- 
ticle but a dragging along the cord and a feeling of weight. 
(3) Suppuration. The tuberculous process tends to break 
down with resulting suppuration and the formation of one or TUBERCULOSIS OF GENITO—URINARY ORGANS 
427 
more fistulae. These may or may not persist, and often the 
fistulae heal up only to break down, or new fistulae may form in 
the vicinity. Keyes has stated that suppuration occurs early and 
rarely appears late. 
(4) Urinary Symptoms. Urinary symptoms may be absent 
for many years. Often it is the symptom that first attracts the 
patient’s attention to his illness. In the early cases, it is doubt- 
less due to the involvement of the prostate and vesicles which 
accounts for the dysuria and tenesmus. 
(5) Sexual Symptoms. Early there may be no disturbance in 
sexual function, and, even late, the sexual act can be performed 
and there is no marked diminution in sexual desire. On the 
other hand, azoospermia was found by Barney in 85 per cent of 
the cases. These were cases in which only one epididymis was 
involved clinically. This doubtless accounts for the high rate of 
sterility in this group of cases. 
(6) Involvement of the Vas Deferens. The vas deferens is 
involved in the late cases. It is very much enlarged, thickened, 
hard, beaded or nodular, and the entire cord may show 
thickening-. 
Other evidences of tuberculosis are often present, such as scars 
in the neck the result of an old gland tuberculosis, the presence 
of active or healed tuberculosis in lung, bone, joints, tendons, etc. 
Diagnosis. The history of a painless enlargement of the scro- 
tum and an enlarged nodular epididymis with a beaded condition 
of the vas deferens, the history of repeated attacks of suppura- 
tion, the presence of scars in the scrotum or the presence of a 
fistula make the diagnosis simple. 
Differential Diagnosis. The differential diagnosis calls for 
differentiation between syphilis and tumors, both of which begin 
in the body of the testicle. The Wassermann test is of value, 
in determining the presence or absence of syphilis, although it 
must not be forgotten that a patient may have both syphilis and 
tuberculosis of the testicle. Other pus infections of the epididy- 
mis should be ruled out, such as gonococcus infections and in- 
fections by the colon bacillus, staphylococcus, etc. 
Prognosis. The prognosis should be guarded in this as in 
urinary tuberculosis. According to statistics, 41 per cent of 58 
patients died of tuberculosis within six years. The more fre- 
quent causes of death are miliary and acute pulmonary tuber- 
culosis. 428 
CLINICAL TUBERCULOSIS 
Treatment. Dietetic-hygienic treatment, including rest, ease 
of mind, wholesome fresh air, etc., as is so successfully prescribed 
in other forms of tuberculosis, should be carried out. 
Tuberculin Treatment. Much discussion prevails regarding 
the value of tuberculin in the treatment of tuberculosis of the 
epididymis. There are many strong advocates for tuberculin 
treatment who report a large series of apparently cured cases, 
and there is an equally large group of adherents to the surgical 
form of treatment, however, tuberculin must be considered a 
most valuable therapeutic remedy in all post-operative cases. 
Surgical Treatment. Three types of surgical treatment may 
be considered: First: Incision and Drainage. In cases in which 
abscess formation has occurred, simple incision, curetting the 
cavity and packing it with iodoform gauze is the simplest form 
of treatment that has been recommended. It is opposed chiefly 
by the adherents of the tuberculin treatment who advise this 
form of treatment only when pus is present. 
Second: Conservative Operations. Epididymectomy is the 
choice of the operation in that it removes the tuberculous focus 
and allows the testicle to remain. It is the choice for several 
reasons, first, because the internal secretion of the testicle is 
conserved; second, because a large number of patients show 
involvement of the opposite side. If there is gross evidence of 
tuberculosis of the testicle, the testicle should also be removed. 
It has been stated that the testicle can overcome a tuberculous 
invasion if small in amount. 
The operation can usually be performed under local anesthesia, 
and the epididymis and vas deferens removed in toto. Following 
epididymectomy and vasectomy, it is supposed that the tuber- 
culous process of the prostate and vesicle becomes quiescent and 
rapidly shows marked improvement. It is, ordinarily, a simple 
operation, and when carefully performed under local anesthesia, 
it does not mitigate very much against the patient. 
Third: Radical Operation. The operation of epididymectomy 
and vasectomy is opposed on the grounds that it does not remove 
all the tuberculous infection in the genital tract. Opponents of 
this operation have suggested a radical procedure, which consists 
not only in the removal of the epididymis and vasa deferentiae, 
but, at the same time, removes both seminal vesicles and pros- 
tate through the perineum. This rather radical procedure has 
not met with general favor in this country.—H. L. K. CHAPTER 32 
TUBERCULOSIS OF THE SKIN 
General Consideration (24) (25) (26). The subject of tuber- 
culosis of the skin is one of comparatively recent date. Look- 
ing back a little over thirty years we find that only one form 
of tuberculosis of the skin was recognized, but since that time 
the subject has assumed enormous proportions and from year 
to year has increased in importance. This undoubtedly is 
due to the fact that finer methods of diagnosis have been in- 
troduced. By the injection of tuberculin intradermally the in- 
jection of tuberculous tissue into guinea pigs, the v. Pirquet, 
the Moro and particularly the Mantoux tests, it has been found 
that many diseases of the skin are most intimately related to 
tuberculosis in which this previously had not been suspected. 
The manisfestations of this disease are as protean as is Syphilis. 
There are now four recognized types or varieties of cutaneous 
tuberculosis in which the tubercle bacillus is usually present in 
the individual lesion: namely Lupus Vulgaris, Tuberculosis Ver- 
rucosa Cutis, Scrofuloderma and Tuberculosis Cutis Orificialis; 
in addition there are a number of different cutaneous lesions 
known as Tuberculides, which are ascribed to the toxins pro- 
duced by the tubercle bacillus generally at some distant focus 
in the body or as a result of embolisms of dead or attenuated 
bacilli. 
Etiology. The active cause of cutaneous tuberculosis is as 
elsewhere the Koch’s bacillus. Among the predisposing and con- 
tributing causes are dust, filth, dampness, overcrowding, poor 
housing conditions, and unhygienic surroundings, etc. The ca- 
chectic, run down and undernourished fall prey to the disease 
more readily than do the vigorous, healthy, and well nourished. 
Types and Varieties. The most important of the tuberculous 
disorders of the skin is Lupus Vulgaris, the result usually of 
direct inoculation, although the infection may also be carried to 
the skin by the lymph currents. The disease most commonly 
begins in childhood and usually attacks the face, especially the 
nose and area about the mouth. Children crawling about the 
429 430 
CLINICAL TUBERCULOSIS 
floors of the homes of diseased tuberculous individuals may- 
scratch their faces or pick their noses and inoculate themselves 
in this way. It has been known to follow vaccination, circum- 
cision, tattooing, piercing the ears for the wearing of ear 
rings, etc. 
A second variety occurring as warty lesions is classified as 
Tuberculosis Verrucosa Cutis and practically always follows 
Fig. 55. Lupus Vulgaris 
(Courtesy of Dr. J. F. Waugh) 
inoculation. Two forms of this are recognized, one known as 
the anatomical tubercle or postmortem wart, (Tuberculosis 
Cutis Necrogenica). This is occasionally observed on the hands 
of physicians and anatomists. It is intimately associated with 
the handling of dead human bodies and diseased cattle. It occurs 
usually on the fingers, especially on the dorsum of the thumb 
and index finger, as an indurated, horny, pigmented lesion the 
size of a split pea or a small bean. As a rule it persists as such 
a lesion for months or years. TUBERCULOSIS OF THE SKIN 
431 
The other type is more extensive, more papillomatous, and 
occurs not only on the hands but also on other parts of the 
body. These forms of cutaneous tuberculosis are found fre- 
quently in certain mining districts where miners, the victims of 
pulmonary tuberculosis, wipe their mouths with the back of 
their hands. 
Another, the third variety of cutaneous lesion is known as 
Scrofuloderma. This lesion is an involvement of the skin by 
direct contiguity from an underlying tuberculous structure such 
as tuberculous glands of the neck, joints and bones. 
A fourth recognized variety is Tuberculosis Cutis Orificialis 
or Tuberculous Ulcers. These ulcers occur in patients suffering 
from tuberculosis of the throat and lungs and are generally seen 
in the mouth, throat, nose and about the anus in patients with 
gastro-intestinal tuberculosis. 
Pathology. Lupus Vulgaris (29) and the other manifestations 
of cutaneous tuberculosis differ but little in their pathological 
structure. Their histological appearance is practically identical 
with tuberculous lesions in other parts of the body. In Lupus 
the tubercle is found in the deepest part of the corium. In the 
meshes of a reticulum are seen giant cells, which may or may not 
contain tubercle bacilli. Surrounding this is a zone of small 
round cells, with vesicular nuclei, and surrounding these in turn 
a zone of plasma and young connective tissue cells. The tubercle 
is surrounded by a capsule of collagenous tissue. The cells lying 
nearest the center degenerate, their protoplasm becomes homog- 
eneous and their nuclei lose their ability to take a stain satisfac- 
torily. Necrosis and caseation occur as a result of this. The 
cells at the periphery, however, have a marked power of regener- 
ation and finallv become converted into connective tissue. This 
appears clinically as scar tissue. This explains the occurrence 
of patches of tuberculous tissue where we see at the same time 
areas undergoing necrosis and at the same time at their borders 
areas of scar tissue. In Scrofuloderma the lesion differs in no 
essential way from tuberculosis of the internal organs. There 
are present round cells, epitheloid cells and giant cells deep 
down in the subcutaneous tissue. The nodule degenerates and 
breaks down and may break through the thin overlying epider- 
mis, giving rise to characteristic ulcers. The degeneration is 
more marked than in lupus and the bacilli while not numerous 
are more easily found than in Lupus. 432 
CLINICAL TUBERCULOSIS 
Bowen (165) states that in Tuberculosis Verrucosa Cutis the 
nodule is situated in the upper part of the papillary layer, often 
in the papillae themselves. 
The epidermis is always secondarily involved. Acanthosis or 
proliferation of the stratum mucosum is always marked and there 
is generally an edema of this layer also present. Oftentimes as a 
Fig. 56. Lupus Vulgaris 
result of the ulceration beneath, as in Scrofuloderma the epi- 
dermis is ulcerated and destroyed. 
1 he glands of the skin all suffer in the destructive processes 
going on in the corium and all may be destroyed. 
Diagnosis and Description of the Lesions (122) 
(1) Lupus Vulgaris is the most frequent as well as the most 
important of the tuberculous lesions. In about 80 per cent of 
cases it occurs on the face: in some cases on the upper extremity 
and in a lesser number on the lower. In 80 per cent of cases it 
occurs before the twentieth year, and in over 50 per cent in the TUBERCULOSIS OF THE SKIN 
433 
first decade of life. Girls are more susceptible than boys, prob- 
ably because they are more closely confined and frequent the 
house more. 
In the United States or perhaps better in America, Lupus is 
not at all a common disease: (it is becoming more so particularly 
in the seaboard cities) practically all of our cases come from 
abroad. It is common on the continent, especially in Southern 
Europe and is in a much more virulent condition there. It is also 
Fig. 57. Tuberculosis Verrucosa Cutis (Duration 2 Years). This Patient Has Also 
Laryngeal and Pulmonary Tuberculosis. The Cutaneous Disease began 
at the Ali of the Nose (Left Side). Author’s Patient 
common in India and the Scandinavian countries. The parts 
commonly attacked, in the order of their frequency, are the face, 
the nose, the cheeks, auricles of the ears, and lips. The disease as 
it occurs on the face may originate in the mucous membranes and 
thence extend to the skin, or originate in the skin and later affect 
the mucous surfaces. 
It generally begins as a small nodule, deep down in the corium, 
only slightly elevated above the level of the skin. In color it 434 
CLINICAL TUBERCULOSIS 
varies from a dark yellow to a yellowish red; it feels soft, is 
smooth or covered with a fine scale, and occasions no subjective 
sensations. When pressed with a diascope or glass slide a 
typical apple jelly brown color is seen. New nodules gradually 
form and by coalescence of these a plaque results. The nodules 
spread by peripheral extension. Their growth is very slow. 
In the ulcerative type which fortunately is rarely seen in this 
country, there is rapid extension with the formation of oval or 
circular ulcers, having irregular margins and dirty red granulat- 
ing floors. One type is known where fibrous tissue formation is 
Fig. 58. Tuberculosis Verrucosa Cutis 
the predominating feature. Often beyond the scars in many 
cases fresh nodules of the disease are seen. 
The scars of Lupus are irregular, indurated, deforming, yel- 
lowish white or reddish yellow in color. Many hypertrophic 
varieties are known. The disease lasts usually for years and 
relapses are common after what appears to be a cure. The 
general health may or may not be affected. Sometimes there is 
a coexistent bronchitis, or laryngeal or pulmonary tuberculosis. 
Differentiation. Lupus Vulgaris must be differentiated from 
the nodular syphilide of tertiary Syphilis, from Blastomycosis. 
Lupus Erythematosus, and Sarcoid of Boeck. TUBERCULOSIS OF THE SKIN 
435 
(a) The Nodular Syphilide occur as multiple, flat, round, cir- 
cumscribed, firm, dark red nodules, varying in size from a coffee 
bean to a large nut. Their surface is smooth or desquamating, 
they are asymmetrically placed, assuming semicircular, reniform 
or circular configurations and are commonly seen on the fore- 
head, the neck and the buttocks. They begin late in life and the 
Wassermann reaction is invariably positive. 
(b) Blastomycosis also occurs later in life. It begins as a 
verrucous papule or papulo-pustule that spreads more rapidly 
than Lupus. It forms distinctly elevated verrucous plaques, 
dark red in color, with sloping borders which are beset with 
many small abscesses. In these abscesses the causative organ- 
ism is found. The lesion is often covered with a heavy crust. 
Removal of this crust shows a moist verrucous surface covered 
with papilliform elevations. The lesions of Blastomycosis are 
commonly seen on the forehead and face, the region about the 
eyes being often affected. 
(c) Lupus Erythematosus, a tuberculide, may at times be con- 
fused with Lupus Vulgaris, but its more superficial character, its 
typical butterfly appearance, affecting the bridge of the nose, and 
spreading over the cheeks in the form of two wings, affecting the 
lobes of the ears and the scalp, its greater degree of color, its 
greasy adherent scales and the dilated follicles with comedone 
like plugs in them, makes its differentiation easy. 
(d) Sarcoid of Boeck also affects the face. It is classed as a 
tuberculide because of its appearance and histological structure. 
The lesions may be small or large nodules or plaques. They 
start as red, edematous or infiltrated spots, which are distinctly 
elevated, as much as a quarter of an inch, and which burn or 
itch. They grow purple and telangiectatic centrally, the margin 
turns brown or yellow, and scales and, as involution sets in they 
fade, leaving a brownish discoloration and a slight atrophy. They 
never break down. 
(2) Tuberculosis Verrucosa Cutis is a warty condition of the 
skin, the result of direct inoculation with the tubercle bacillus, 
and may affect any age. Infection may originate in several dif- 
ferent ways. It has followed tattooing, the wound of a sabre in 
duelling, the handling at autopsy of tuberculous cadavers, and 
the wiping of the mouth with the back of the hands. The hands, 
especially the fingers and dorsal surfaces are the commonest 
sites of infection. The disease begins upon a previous abrasion 436 
CLINICAL TUBERCULOSIS 
as a papule, pustule or vesicle with an infiltrated reddish areola. 
Plaques, oval or round in shape are formed. These vary in size 
from that of a small coin to an area several inches in breadth. 
The patches are verrucous, dry and covered with minute vegeta- 
tions and crusts. In color they are usually brown, dark brown 
or purple red and are devoid of sensation. The disease may last 
for months or years. Complications are rare. Healing is fol- 
lowed by a smooth scar. 
This condition resembles in some ways a patch of Blastomy- 
cosis. Blastomycosis, however, is generally more moist, the edge 
is more definitely defined and in the minute abscesses of its bor- 
der the fungus can be isolated. 
(3) Scrofuloderma is that type of tuberculosis which affects 
the corium in the shape of tuberculous abscesses, usually located 
over a broken down tuberculous gland, bone or joint. It is the 
result of extension of an underlying tuberculous focus to the 
skin. 
This type is seen most commonly in those who are in poor 
general health and are the subjects of tuberculosis of glands, 
bones and joints. It is most common in children and young 
adults. The lesions are single or multiple; the neck, groins and 
limbs are the parts commonly affected. The primary lesion is a 
swelling deep in the corium. As this increases in size the over- 
lying skin becomes reddened, thinned, and eventually breaks 
down, forming an ulcer. This ulcer has an irregular, oval or 
linear outline, with a thin, undermined edge. The floor is covered 
with pale, flabby granulations. The discharge from the ulcer is 
bloody, purulent or serous and often contains tubercle bacilli. 
The scars when the lesion heals, are irregular and fibrous. 
Scrofuloderma is a chronic process and may last for months or 
years. 
(4) Tuberculosis Cutis Orificialis, or tuberculous ulcers, are 
oval or circular indolent ulcers which occur in patients who are 
the victims of internal tuberculosis. These ulcers occur in the 
mouth, on the lips, about the anus, and occasionally in the ears. 
The ulcers are shallow, irregular in shape and size, of a reddish 
yellow color, and are at times exceedingly painful. 
Acute tuberculosis of the skin has been seen in children as 
nodules, vesicles, bullae, papules and pustules, which form 
crusted, deep circinate lesions, in practically all of which the 
tubercle bacillus has been found. TUBERCULOSIS OF THE SKIN 
437 
The Tuberculides. Under this title has been grouped those 
cutaneous eruptions which may occur in individuals believed to 
be infected with the tubercle bacillus. However, in only a few 
cases has the bacillus been demonstrated. They react to the 
various tuberculin tests when applied, and it is believed that the 
reactions are due to toxins which are derived from some distant 
tuberculous focus and which are circulating in the blood stream. 
Another theory recently advanced is that they are the result of 
embolisms of dead or weakened bacilli, weakened if alive in the 
struggle they had undergone against the defensive forces of the 
body in a glandular or joint focus. In many of these tubercu- 
lides the histological picture is that of tuberculosis. In this group 
are included Lichen Scrofulosorum, Folliclis, Acnitis, Acne 
Scrofulosorum, Acne Cachecticorum,1 Lupus Erythematosus, 
Erythema Induratum2 of Bazin and Sarcoid of Boeck. To this 
list Highman (14) in his recent work on Dermatology has added 
another class, tuberculides of presumptive tuberculous nature. In 
this class he includes Pernios, Pityriasis Rubra of Hebra, Angio- 
keratoma of Mibelli and a vague group resembling Malcolm 
Morris’ follicular eczema. 
(1) Lichen Scrofulosorum occurs in children or young adults. 
The eruption is a small, round, papular one. The papules are 
yellowish or brown red in color; in size from a pin head to that 
of a millet seed. Their summit is often covered with a tiny ad- 
herent scale, pustule or horny plug, which conceals a minute 
depression. The lesions are generally aggregated in oval groups, 
often have a crescentic form, occur on the trunk and abdomen, 
and cause no subjective sensations. Their course is chronic; 
•A tuberculid occasionally observed in patients suffering from active pulmonary tuber- 
culosis is Acne Variolaformis (89), so called, because these lesions resemble those of vari- 
ola or small pox. They occur usually in the form of postules tending to necrosis and are 
upon the forehead, scalp, face, etc. These lesions are seen on young patients suffering 
from chronic, protracted, but active pulmonary disorder, most particularly in the last 
months of life.—J. R. 
2 Erythema Nodosum and Tuberculosis. Etiology and Semeiology. This form of skin 
(89) lesion usually accompanies clinically a pulmonary, gland or joint disturbance, a typical 
exanthematous disease related to joint rheumatism, is supposed to be of toxic origin but is 
not a so called localized skin symptom of a constitutional or bacterial disorder partic- 
ularly tuberculosis. It has not been definitely established if there is an etiological con- 
nection between erythema nodosum and tuberculosis nor has it been proven that erythema 
nodosum is the direct result of either the tubercle bacillus or its toxins. It must however 
be admitted that the lesion is frequently found in children suffering from tuberculosis in 
one form or another. It is particularly a frequent accompaniment of tuberculous menin- 
gitis. It cannot be considered an early symptom nor a grave sign if found in active tuber- 
culous disease. Erythema Nodosum if present may produce a favorable soil which may 
then activate a latent tuberculous focus, as is observed in measles and other infectious 
diseases. True Erythema nodosum is found in children exclusively of tuberculous indi- 
viduals, but the proof that these lesions are themselves of a tuberculous nature is want- 
ing. Erytheme Polymorphe of French writers and other obscure skin lesions usually 
belong to this same category.—J. R. 438 
CLINICAL TUBERCULOSIS 
they often persist for months or years, and when they clear up 
they often leave scars. 
(2) Folliclis, a papulo-necrotic lesion, occurs especially on 
the hands, feet, elbows, and knees, sometimes on the palms and 
soles. The primary lesion is a papule or nodule, round in contour, 
varying in size from a pinhead to a small pea, red or purplish 
red in color, firm and painless. It is generally surmounted by 
a small vesicle or vesico-pustule, which crusts over, and when 
the crust is removed leaves a small ulcer. The ulcer when healed 
is replaced by a scar. Individual lesions may last only a short 
time, but crops continue to come and go, and in that way the 
lesions may last for years. 
(3) Acnitis differs from Folliclis in that the lesions affect the 
face, occurring in groups upon the cheeks, upper lip, chin, and 
forehead. They are red or brown red in color, in size from a 
pinhead to a pea, firm to the touch, and often capped as are the 
lesions of Folliclis with a small vesicle or pustule, which upon 
its disappearance leaves a depressed scar. They also occur in 
crops. 
(4) Acne Scrofulosorum consists of an eruption of small red 
papules, millet seed in size. The eruption occurs principally on 
the extensor surfaces of the limbs, and the papules as in the other 
tuberculides, are surmounted by a small pustule which becomes 
crusted over, forms an ulcer and leaves a scar. 
(5) Acne Cachecticorum occurs on the face, back, chest, and 
lower limbs. The lesions are small, pinhead sized papules and 
papulo-pustules, of a red color. They closely resemble a syph- 
ilide. They often persist for years and disappear leaving small, 
depressed scars. 
(6) Erythema Induration first described by Bazin as “Eryth- 
eme des Scrophuleux” most commonly affects young girls. This 
eruption occurs on the calves of the legs as deep seated nodules, 
which gradually break down, forming indolent, irregular shaped 
ulcers. These ulcers are deep and of variable size, with irregular 
edges, and a greyish red base. They run a chronic course, re- 
solve spontaneously, and tend to recur. 
(7) Sarcoid of Boeck occurs as small nodules or as large 
nodules or plaques. The eruption occurs primarily on the face, 
shoulders, and upper extremities. The lesions start as red, 
edematous or infiltrated spots which turn purplish or brownish. 
They are distinctly elevated, and are the seat of marked itching TUBERCULOSIS OF THE SKIN 
439 
and burning sensations. They fade very gradually leaving a 
brownish discoloration and a slight amount of atrophy. The 
course of the disease is a slow one and the eruption lasts for 
months and years. Arsenic has been of a great deal of value in 
the treatment. 
(8) Lupus Erythematosus is of two types, the discoid or 
localized and the disseminate or generalized. The latter is not a 
common form, (a) The discoid type begins as several pinhead 
to bean sized maculo-papules. They are pinkish to red in color 
and as they grow older become a deeper red, sometimes bluish 
red. They are covered with a dry, very adherent scale, greyish 
in color. They grow slowly and extend peripherally until they 
form definitely elevated plaques, of a bluish red color, covered 
with these dry, very adherent scales. There is considerable 
infiltration present and the patches, especially at the borders 
show a definite elevation. On removing the scales comedone 
like plugs are seen filling the gaping mouths of the sebaceous 
follicles. The disease attacks by preference the nose, cheeks, 
lobes of the ears and scalp, (b) The common form occurs as a 
plaque extending over the bridge of the nose onto the cheeks 
in the shape of a butterfly. There are few if any subjective sen- 
sations. The disease is chronic; the lesions may remain a long 
time without change or under treatment undergo rapid involu- 
tion. 
The Treatment of Cutaneous Tuberculosis 
General. In Scrofuloderma in which the skin is usually second- 
arily involved as a result of an underlying tuberculous gland, 
bone or joint, the treatment is always a surgical one. In all the 
other forms of cutaneous tuberculosis the treatment becomes a 
medical problem. Both general and local therapy are indicated. 
The general treatment must be the same as is now in common 
use in treating the differnt forms of chronic tuberculosis. Fresh 
air, thorough ventilation of the home and sleeping quarters, 
bodily hygiene, sufficient rest, sunshine, much time spent in the 
open, and good, wholesome food are all urgently indicated. 
The administration of efficient tonics is also a valuable ad- 
juvant. They stimulate gastric secretion and aid digestion. The 
two best probably are the Elixir of Iron, Quinine and Strych- 
nine in teaspoonful doses three times a day before meals and the 
Elixir Gentian Glycerinatum N.F. in like doses. The arsenical 
preparations are of decided value in the treatment of cutaneous 440 
CLINICAL TUBERCULOSIS 
tuberculosis, Fowler’s solution, or Liquor Arsenici Chloridi in 
5 minim doses, arsenious acid in 1/20 grain doses may be given 
three times daily. Cacodylate of soda has been used by some 
physicians with success. Of the various medicinal remedies 
used, none has given more satisfactory results than the use of 
tuberculin in proper dosage. The tuberculin therapy which is 
fully described in the chapter on tuberculin should be followed, 
giving old tuberculin in minute doses at first, gradually increas- 
ing. It will not be necessary to give very large doses. The tuber- 
culous individual’s tonic dose, evidenced by a feeling of well 
being, when reached, may be maintained for months. 
Local Treatment. The Finsen Lamp discovered by Prof, bin- 
sen of Copenhagen, is the best means at our disposal for treating 
lupus. (128) The use of phototherapy in the treatment of tuber- 
culosis of the skin marks an epoch in the treatment of this dis- 
ease. The procedure is based upon the destructive effects ultra- 
violet light has upon the diseased cells of lupus tissue. In the 
use of the ultra-violet rays the lamp must be brought into close 
contact with the skin under pressure in order to remove from 
the diseased area the blood, for this interferes with the passage 
of the rays. The various lamps are supplied with a window of 
quartz which does not, as does glass, interfere with the passage 
of the ultra-violet rays. 
The objections to this method of treatment are that in treating 
large areas the method is tedious, and that in treating lupus of 
the mucous membranes or ulcerative patches the method cannot 
be used because sufficient pressure cannot be exerted on these 
areas. 
X-Rays in experienced hands have been very successful in 
the treatment of the disease. The Kromayer quartz lamp has 
also been of value. In small patches Carbon Dioxide snow can 
be used with benefit. Adamson (172) has recently reported very 
good results in the treatment of some forms of lupus with the 
Liquid Acid Nitrate of Mercury. The actual cautery is at times 
of benefit but the method of choice when it can be used is the 
Finsen Light.—E. A. O. CHAPTER 33 
TUBERCULOSIS OF THE EYE AND THE MUCOUS 
SURFACES 
(A) Tuberculosis of the Eye 
General Consideration. Tuberculosis of the eye is not an un- 
common affection. While this organ is not particularly suscep- 
tible to the disease, any part of the eyeball or its appendages may 
become involved. Here, as elsewhere in the body, the disease 
may, especially in its incipiency, be difficult to diagnose. With 
the introduction of tuberculin as a diagnostic agent, inflamma- 
tory lesions of the eye of obscure origin are frequently proven to 
be tuberculous. (198-207) 
It is a striking fact that the eye is rarely involved in a case of 
open tuberculosis. It is equally striking that when the tubercu- 
lous process becomes generalized, the eye, as a rule, falls prey to 
the disease. The eye may become the seat of a tuberculous 
process in an otherwise apparently healthy individual. Tuber- 
culosis may cause inflammation of the eye by an active lesion 
in situ or by the action of the toxins of the disease liberated at 
remote foci. Possibly phlyctenular kerato-conjunctivitis may be 
an example of the latter type of disease. The microorganisms 
may enter the eye endogenously by way of the blood stream, or 
ectogenously by direct inoculation, as through an abrasion. 
Predisposing Factors. The predisposing factors entering into 
the contraction of the disease are: (a) Age—the disease being 
more frequent in children; (b) Trauma—in the presence of 
which the tubercle bacillus finds suitable soil for its propagation; 
(c) Familial tuberculosis—which subjects the individual to mas- 
sive doses of tubercle bacilli; (d) City-dwelling—for like rea- 
sons; (e) Tuberculosis of the other eye predisposes its fellow to 
a like infection. 
The tunica vasculosa which consists of the choroid, the ciliary 
body, and the iris is the tissue most frequently invaded. The 
hematogenously conveyed microorganism is arrested in the deli- 
cate capillary plexuses of the chorio-capillaris layer of the 
441 442 
CLINICAL TUBERCULOSIS 
choroid, in the ciliary processes, or in the region of the major or 
minor circle of the iris, in which location the tuberculous nodules 
first appear. From these points the disease characteristically 
invades adjacent and foreign tissue. 
Fig. 59. Section of the Eye (Schematic) (After Leber) Showing the Usual Seat of 
Beginning Tuberculous Disease of the Inner Eye and in the Order of Frequency at the 
Points of fc=Chorio-Capillaries, g= Ciliary Processes, h=Maior Circle of Iris, k=Minor 
Circle of Iris. 
Explanatory Notes 
A=Chorioid, B=Conjunctiva, H=Cornea, L—Lens, N=Retina, 0=Optic Nerve, 
Ora Serata, R=Internal Rectus, S—Optic Nerve Sheath, SO=Sclera. 
a=central artery, ai=central vein, b=retinal arteries, bi=retinal veins, cc=ciliary 
arteries, d=long posterior ciliary artery, di=anterior ciliary arteries, ei=anterior ciliary 
veins, f=chorioidal capillaries, g=ciliary bodies, h~circulus arteriosus iridis major, 
i=arteries of the iris, ii=veins of the iris, k=circulus arteriosus iridis minor, 
vorticosa, m=veins from the ciliary muscles, n=Schlemm’s canal, o and O]—posterior 
conjunctival vessels, p=anterior conjunctival vessels, q=marginal loops of the cornea. 
Symptoms: There are certain general clinical characteristics 
which usually attend the disease. They are: 
V 
1. Chronicity. 
2. Relative freedom from pain. 
3. The tendency to invade adjacent and foreign tissue. 
4. Little response to local treatment. 
5. Atypical lesions. TUBERCULOSIS OF THE EYE 
443 
Since the disease may involve any part of the organ or its 
appendages, it may be well to briefly point out some of the more 
common symptoms in the several locations. 
Tuberculosis of the Eyelids: Rarely seen in this country; 
when present, it usually is an extension of lupus of the skin. The 
lesions ulcerate, and the scar tissue formation following results 
in lid deformity. Swelling of the pre-auricular glands accompany 
the active lesion. 
The Conjunctiva: Tuberculosis of the conjunctiva may appear 
as a follicular conjunctivitis, as a subepithelial nodule, or as ex- 
cresences in the fornices. Either type usually ulcerates. His- 
tologically, giant-cell systems are found. The lesions are chronic 
and respond but little to local treatment. The cornea may become 
involved and the eye-ball lost by perforating lesions. 
Phlyctenular Keratitis. It has long been noted that a peculiar 
type of lesion of the bulbar conjunctiva occurs in children (oc- 
casionally in adults) who show evidences of tuberculous infec- 
tion. The disease is called phlyctenular kerato-conjunctivitis1 
by some writers; by others, conjunctivitis eczematosa or con- 
junctivitis scrofulosa. These terms are suggestive of the sup- 
posed etiology. In rural districts, a history may almost invar- 
iably be obtained of an intimate association of the child with an 
adult suffering from pulmonary tuberculosis, whereas in cities, 
where such a history is usually unobtainable, the child will give 
a positive reaction to tuberculin. The disease very rarely occurs 
in nursing babies and rarely persists after puberty; adults who 
have not had the disease in childhood do not exhibit the affection 
in typical form. 
These lesions are multiple, occur most frequently at the lim- 
bus of the cornea and appear as small red, superficial swellings 
covered by the epithelium of the conjunctiva; the vessels of the 
surrounding conjunctiva are engorged while the remainder of the 
conjunctiva may appear quite normal. The tiny tumor breaks 
primary lesion, the cause of phlyctenular disease, may be a tuberculous focus 
somewhere in the body. This may be an enlarged gland and the advisability of its 
removal, if practical, should be considered or, perhaps, a roentgen ray treatment be 
advised. According to some authors,89 secondary organisms are considered as playing a 
definite role, but how much, if any, has not been definitely established. A specific therapy 
has. been. found, most suitable in connection with a general treatment as stated above. 
It is advisable in the beginning to give tuberculin in very small doses and in gradually 
increasing amounts, so as to reach a cutaneous ananaphylaxis or anergy without reaction 
During the treatment the skin anergy may be only transitory for with a returning of 
allergy or skin sensitiveness there may also be return of the phlyctenular-eczematous con- 
dition .with greater virulence; hence the specific therapy demands the greatest exactitude 
in dealing with these lesions. The patient, during the treatment, must be under the con- 
stant care of the physician, and if any untoward symptoms appear the dosage must at 
once be lowered or, perhaps better, be entirely inhibited for a while.—J. R. 444 
CLINICAL TUBERCULOSIS 
down at the center, producing an ulcer, which usually heals 
promptly. When the lesion is located on the cornea great pain, 
photophobia, and lacrimation accompany its cycle. The result- 
ing desquamation may lead to a true ulcer of the cornea. These 
lesions are apt to appear in successive crops, continuing for 
months or even years. Resulting scars may disturb vision 
markedly, but very rarely cause blindness. 
The tumors are accumulations of round cells and are in no 
sense true tubercles, nor have tubercle bacilli ever been demon- 
strated in them. It is quite probable that they are the result of 
protein sensitization or anaphylaxis. Possibly they may be 
grouped with the dermatoses known as tuberculids. The disease 
usually responds promptly to strict and careful regulation of the 
diet, general hygience, and habits of the child, cleanliness, fresh 
air, sunlight, and good food, with perhaps a mild specific anti- 
tuberculosis impression, etc., without which local treatment is 
but of temporary value. 
The Cornea: The cornea is frequently the seat of primary 
tuberculosis, this from direct infection of the eye from without. 
Both suppurative and non-suppurative forms are seen. The sup- 
purative forms are characterized by superficial ulcers with pannus 
formation. Deep infiltration or ulceration may take place lead- 
ing to perforation of the cornea and loss of the eye-ball. A small 
percentage of the interstitial forms of keratitis may be tubercu- 
lous. The lesions are subepithelial at the beginning, frequently 
invading the substantia propria and leaving- behind dense opa- 
cities. All atypical forms of keratitis with low grade inflamma- 
ory reaction should suggest the possibility of tuberculosis. The 
cornea may, of course ,become involved secondarily. 
The Sclera: Tuberculous involvement of the sclera is prob- 
ably always a secondary process, the uveal tract being the seat 
of the primary lesion. A localized, congested, tender, nodular 
prominence appears on the sclera which may completely disap- 
pear or which may extend and involve the cornea. 
The Tunica Vasculosa: (a) The Ciliary Body and the Iris: 
Mayon, the English pathologist, removed the aqueous humor in 
thirty cases of irido-cyclitis and was able to isolate the tubercle 
bacillus in thirteen of them. The iris lesions may appear as dis- 
tinct nodules, small, greyish or yellowish, most frequently situ- 
ated at the root of the iris. They may be few or many. Again, 
there may be no visible changes in the iris, but posterior syne- TUBERCULOSIS OF THE EYE 
445 
chiae form, and deposits on the posterior surface of the cornea 
are conspicuous. Tuberculous granuloma may form and fill the 
anterior chamber leading to destruction of the eye. 
Tuberculous iritis may be not unlike other forms of iritis. The 
disease is usually characterized by little pain or inflammatory 
reaction and the tendency to be slowly progressive. With in- 
volvement of the ciliary body, the circumlental space may be- 
come occluded and the area bounded by the posterior surface of 
the iris, the lens, and the hyaloid membrane becomes filled with 
tuberculous tissue, while the vitreous may remain uninvaded. 
(b) Choroiditis. The best known form of tuberculous choroi- 
ditis is the type occurring in acute miliary tuberculosis. These 
lesions occurring shortly before death are probably always pres- 
ent as a part of the disseminated process. They are grouped 
usually at the posterior pole of the eye, but may be peripheric. 
In size they may vary from one-third to disc size. In color, they 
are greyish or greyish-yellow, and have soft, lightly defined mar- 
gins shading off into the normal retina. They are not pigmented. 
The retinal vessels arch but slightly over these areas. The 
lesions develop rapidly, new ones appearing from hour to hour; 
they are located in the coriocapillaris layer of the choroid and 
extend inwards to the lamina vitrea and outwards to the sclera. 
The media remain clear and the vision good when obtainable; 
the field is undisturbed and the retina uninvaded. Histologically, 
the lesions show typical giant-cell formation. 
Single conglomerate tuberculous masses may develop in the 
choroid, pushing the retina before it with increase of tension and 
resulting in destruction of the eye-ball. These are late manifes- 
tations of tuberculosis and are of grave significance. Exudative 
choroiditis may be tuberculous and cannot be differentiated from 
the non-tuberculous forms. 
(c) The Retina. Primary tubercle of the retina is rare, but tu- 
berculosis may be the cause of vascular changes resulting in re- 
curring hemorrhages into the retina or vitreous. The disease 
usually affects young adults, but may persist throughout life, 
giving rise to recurring extravasations of blood. The walls of 
the veins are usually involved, as is evidenced by a perivasculitis. 
The disease usually affects both eyes, and the prognosis is bad. 
The diagnosis is made by the use of tuberculin which must be 
most cautiously used lest the local reaction result in new 
hemorrhages. 446 
CLINICAL TUBERCULOSIS 
(d) The Optic Nerve. In association with tuberculous menin- 
gitis and general tuberculosis, miliary lesions may effect the pial 
sheath, the chiasm, or optic tract. The optic nerve head may 
become invaded secondarily to tuberculosis of the choroid. 
(e) The Orbit. The lower margin of the orbit is most fre- 
quently involved. A thickened area may be detected, the lids be- 
come edematous, the lesion finally shows fluctuation and breaks 
down. Denuded bone may be detected upon probing the wound. 
Diagnosis. In the diagnosis of tuberculosis of the eye, tuber- 
culin is of great value. The test is positive only in the event of a 
local reaction at the site of test, a focal reaction about the ocular 
lesion, and as systemic reaction. The ocular reaction manifests 
itself by a transient increase in the existing symptoms, i. e., in- 
creased photophobia and lacrimation, increased or new areas of 
infiltration of the cornea, increased ciliary injection, increased 
ciliary tenderness, increased cloudiness of the vitreous, increase 
in the size of the fundus lesions, or the appearance of new 
lesions. This so-called positive reaction may be followed by a 
negative one in which all these symptoms become ameliorated. 
All obscure eye lesions should suggest the possibility of tuber- 
culosis and the case should be tuberculin tested. 
Treatment. The treatment of tuberculosis of the eye presents 
difficulties which attend this disease in other organs. The gen- 
eral measures found to be useful in checking the disease else- 
where in the body should be adopted here. Locally, rest, the use 
of atropin when the uvea is involved and local stimulation by 
means of hot applications, etc., are indicated. When judiciously 
used, tuberculin often gives marvelous results. If the disease is 
detected in its incipiency, tuberculin often effects a prompt and 
complete cure.—G. W. R. 
(B) Tuberculosis of the Mucous Surfaces. Under this caption 
is usually considered tuberculous disease of those mucous sur- 
faces which can readily be inspected. This includes the tissues 
of the upper air passages, the ear, and the eye. The latter, how- 
ever, has been already considered fully in detail; hence we shall 
include here only a consideration of the mucous surfaces of the 
mouth and nose and, perhaps, of the ear. 
In tuberculous disease of such organs and tissues of the body 
as the intestinal canal, the lungs, the genito-urinary tract, etc., 
the mucous surfaces are always more or less involved in the 
tuberculous process; hence they are not considered here. TUBERCULOSIS OF THE EYE 
447 
Tuberculosis of the mucous membranes includes tuberculous 
disorders found in the mouth, the nose, and occasionally in the 
ear. In the mouth, the disease manifests itself as affecting the 
lips, the cheeks, the tongue, the gums and alveolar processes, 
the hard and soft palate, the uvula, the faucial tonsils, the pillars, 
the lymphoid tissue and posterior wall of the oropharynx; in the 
nose, usually the septum, the turbinated bodies, and the pharyn- 
geal tonsil of the naso-pharynx, and in the ear, the external 
meatus and the canal. 
The mucous surfaces of all these various structures are very 
similar to the mucous membranes of the other parts of the body. 
All the surfaces offer great resistance to invading bacteria; it is 
only when these membranes are not intact or when the bacteria 
appear in too great a number, are massive, that infection can 
take place. Usually for infection to take place here, a slight 
trauma is always necessary. The secretions of the mouth and the 
vibrissae of the nose also offer, in a measure, protection against 
bacillary invasion; the mouth secretions particularly contain 
bactericidal substances which inhibit, destroy, or weaken bac- 
terial implantation and growth. 
Tuberculosis of the various mucous membranes may be either 
primary or secondary. Primary tuberculosis of the mouth is 
extremely rare; it is only through injuries to these surfaces that 
it is possible of conceiving a bacillary implantation. The pri- 
mary form is occasionally observed, but even this is very in- 
frequent considering the great prevalence of pulmonary disease. 
Primary tuberculosis of the tonsils is occasionally observed. It 
occurs as a result of mouth inhalation of bacilli contaminating 
the air currents or in the taking of food containing the bacteria; 
but here, also, the inhibiting action of the crypts, follicles and 
their secretion is distinctly noticeable.2 
In a similar manner we can conceive of primary tuberculosis 
of the pharyngeal tonsil by the inhalation of air through the 
nasal passages. Microscopical examinations of tonsils after ton- 
sillectomy has often revealed the presence of the tubercle bacil- 
lus as a latent process, but tuberculous disease of the tonsils, is 
not frequently found. It seems that the bacilli pass through the 
tonils as through a sieve, and we find them in the regional, the 
cervical glands, which then frequently become tuberculously dis- 
2Bacilli do not readily enter the faucial tonsil; the epithelial covering (even within the 
crypts) seems to form a safe barrier. It is only through a massive infection that this 
protective mechanism becomes weakened and its inhibitive functions lost. 448 
CLINICAL TUBERCULOSIS 
eased and undergo degenerative changes. The portals, (the 
tonsils) may remain enlarged, but as a rule no other noticeable 
changes are observed. We can also readily conceive primary 
or direct infection in the non-tuberculous by the use of an un- 
sterilized tooth forceps immediately after the removal of a tooth 
from an actively tuberculous individual, and that can also apply 
to nasal or aural operations through unclean instruments. 
The Secondary Form of Tuberculosis of the mucous mem- 
branes is occasionally observed in the actively tuberculous when 
the sputum is bacilli laden, where, for instance, the removal of 
an offending tooth may be followed by a tuberculous ulceration 
about the gums and the deeper structures in and about the alveo- 
lar process. Tuberculous ulcers about the tongue, cheeks, 
mouth, nose, or ear in tuberculous subjects are occasionally ob- 
served ; these usually are secondary to slight trauma or abra- 
sions of the mucosa. Such ulcers are usually superficial, flat, 
pale, of irregular outline, covered with dirty, grayish-white 
secretions, generally situated upon a nodular base without in- 
flammatory border, and covered with red granulations inter- 
spersed throughout by grayish-yellow spots. The whole process 
is a slow one, advancing slowly and healing slowly. That these 
ulcerative surfaces are of a tuberculous nature is evidenced from 
microscopic sections in which we find collections of round cells 
interspersed with giant cells and occasionally tubercle bacilli. 
These ulcerative processes are extremely chronic, accompanied 
by little or no pain, and may exist without subjective symptoms 
for some time before the patient becomes aware of their pres- 
ence. This is particularly observed if the lesions are situated 
about the lips, gums, or tongue; not so, however, if on the 
pharynx where during the act of swallowing they become ex- 
tremely painful. Tuberculous ulcers following the removal of a 
tooth3 in an advanced case of pulmonary tuberculosis is alwavs 
accompanied by most excruciating pain, and here the ulcerative 
process usually invades the whole alveolar process. Tubercu- 
losis of the mucous surfaces is more frequent in men than in 
women in proportion of two to one; this is because men are 
3A most distressing case of tuberculosis of the mucous membrane of the mouth, which 
typically reflects what has been stated above, came under my observation recently. A 
tuberculous individual, third stage, far advanced, but still ambulatory, his sputum laden 
with tubercle bacilli, had five teeth removed, three from the upper jaw and two from the 
lower. Almost immediately, this was followed by tuberculous ulcers which invaded the 
entire depth of the alveolar processes. Owing to his poor physical condition, these ulcers 
spread with great rapidity over much of the surface of the jaws anH rums. The time 
from the removal of the. teeth until exitus was only two months, but during all that time 
he suffered most excruciating pain and distress unless relieved by anodynes. TUBERCULOSIS OF THE EYE 
449 
more careless about the hygiene of their mouths, picking their 
noses, putting the fingers in the ears, etc. 
Many of these ulcerative tuberculous processes are lupoid 
growths, if not typical lupus, and most are akin to the tuber- 
culids found in cutaneous lesions. Owing to their very slow 
growth they may resemble at first only small nodules or tumors 
which gradually undergo degenerative changes with tissue de- 
struction, when their true nature becomes revealed. 
The tuberculous processes about the nose are usually ob- 
served in two forms; one an infiltrative, ulcerative form and 
one of tumor formation. The septum here is frequently pri- 
marily infected, but may be secondarily from the bacilli laden 
sputum of the tuberculous individual. 
The external ear and the auditory canal may also be the seat 
of tuberculous disease, this is usually a secondary form, a finger 
infection. 
Treatment. Contemplated operations about the mouth, nose, 
eyes, or ears of an actively tuberculous individual should re- 
ceive the closest consideration and if about the nose or mouth 
should be undertaken only when we are assured that the sputum 
is entirely free from the Koch’s bacillus. Even under the most 
painstaking cleanliness and a strictly aseptic technic it is al- 
most impossible to avoid wound infection and owing to the ex- 
tremely great tendency of the ulcerative process to spread fol- 
lowing operative interference, cauterization, or curettage, it is 
advisable to be most cautious in the use of these measures. A 
general treatment, if not already instituted, must be secured at 
once. This is just as important here as it is in treating tubercu- 
losis in other parts of the body, and should be done in connec- 
tion with topical applications of appropriate remedies which tend 
to relieve pain and suffering. The use of a 2 to 5% cocaine solu- 
tion applied directly to the ulcer after it has been freed from se- 
cretions often gives prompt relief. Morphine sulphate may be 
used similarly, but is better given by mouth. A saturated solu- 
tion of pyoktanin blue applied directly to the ulcer, the use of 
iodine in the form of the tincture, or anesthesin or orthoform in 
powder form applied directly is often followed by most gratify- 
ing results. Lactic acid, applied and repeated in about three 
hours, if carefully used, is often very serviceable.—J. R. CHAPTER 34 
TUBERCULOSIS AND THE CARDIO-VASCULAR 
SYSTEM. 
1. Tuberculosis and the Heart. It goes without saying that 
a cardiac lesion may influence mechanically a tendency to dis- 
order in the pulmonary circuit, or, if the lungs are already dis- 
eased, to favor still more the disturbance. In practice, we 
usually observe two conditions, namely, either a stenosis of the 
pulmonary artery or a valvular lesion of the left heart. Pulmo- 
nary stenosis as a factor in tuberculous disease is now generally 
recognized, and individuals with a stenosis of the pulmonary 
artery, which is usually congenital, generally perish when they 
reach the age of puberty or about that time. In valvular lesions 
of the left heart, however, accompanying a tuberculous process, 
the disturbance is generally of mechanical origin, a faulty lymph 
and blood circulation. In some individuals, there is always a 
strong tendency to a mechanical disposition to blood and lymph 
stasis which favors a lessened excursion and aeration of the 
apices of the lungs, a disposition to tuberculosis. (135) 
Rokitansky, in 1846, promulgated an antagonism between pul- 
monary tuberculosis and disease of the left heart, namely, that 
within certain limits, a primary cardiac disease would inhibit the 
co-existence of a secondary pulmonary tuberculous disorder. 
Since Rokitansky’s time, many observations have been made by 
competent observers, and they have shown that both aortic and 
mitral disease may accompany pulmonary tuberculosis. 
Fremmolt, in 1874, reported on 8,000 autopsies, and showed 
that not infrequently there was a simultaneous appearance of 
cardiac disease and pulmonary tuberculosis. He arrived at the 
following conclusions: (1) The simultaneous appearance of 
chronic, cardiac disease and pulmonary tuberculosis is not as 
infrequent as is usually assumed. (2) Disease of the aortic 
valve (the left ostium arteriosum) is found to complicate pul- 
monary tuberculosis somewhat less frequently than affections 
of the mitral valve, (the left ostium venosum). (3) The simul- 
taneous disorder of more than one valve is extremely seldom. 
450 THE CARDIO-VASCULAR SYSTEM 
451 
Kryger, in 1,100 autopsies, frequently found healed pulmonary 
lesions in cardiac disease, and he concluded that a tuberculous 
process is seldom an accompaniment of cardiac disorder. Traube 
maintained that tuberculosis may exist with aortic lesions, but 
not with mitral stenosis. Lyden joined Traube in the belief 
that mitral stenosis and pulmonary tuberculosis do not occur 
simultaneously, but he also emphasized the infrequency of both 
mitral and aortic insufficiency with tuberculosis. Squire and 
Frankie, on the other hand, observed that pulmonary tubercu- 
losis and cardiac disease are frequent, both with mitral stenosis 
and other cardiac lesions. Fossier states that both disorders in 
the same individual are not infrequent, particularly with mitral 
disease, and that tuberculosis may develop at any stage of the 
cardiac difficulty; further, that in ordinary pulmonary tubercu- 
losis, the heart may be smaller, but when complicated with car- 
diac lesions there is no atrophy; if tuberculosis is present it may 
progress, independently of the cardiac disorder, sometimes slow- 
ly, sometimes more rapid, when the prognosis becomes more 
grave, the dyspnea greater and although the tuberculous process 
is not influenced by the cardiac disorder still it exerts a most 
unfavorable influence on the heart. 
Meisenberg in Curschman’s clinic found, in 4649 tuberculous 
individuals, 53 cases of co-existing heart lesion (1.14%), and 
mitral insufficiency was the most frequent single lesion. He fur-* 
ther observed that the pulmonary tuberculous process influenced 
the cardiac disorder unfavorably, but was in turn little, if at 
all, influenced by the heart lesion. In 33% of his cases, the car- 
diac lesion was the older disorder; in 4 cases, the tuberculous 
process was undoubtedly the older, and in the remaining cases 
it was most difficult to determine which was the primary disease. 
In none of his cases, however, was mitral stenosis the older 
lesion. Sauer, Berlin Pathological Institute, in .304 carefully 
selected mitral disorders, found 85% entirely free from tubercu- 
lous disease, in 12% a healed lesion, and only in 3% an accom- 
panying active pulmonary affection, and all of his cases showed a 
clinical induration, which confirmed the belief that indurated 
tissue does not offer a very favorable nidus for either the deposi- 
tion or the growth of the tubercle bacillus. 
It is evident that it becomes necessary to know which was the 
primary difficulty, the cardiac or the pulmonary, and it also be- 
comes evident that to a primary, perhaps already somewhat ad- CLINICAL TUBERCULOSIS 
452 
vanced, pulmonary tuberculous process, a cardiac lesion may be 
added secondarily, or the conditions may be most favorable, 
(in mixed infection and in ulcerative processes in the lungs), to 
bring about a cardiac disturbance. Hence from all that has been 
stated we may conclude that (1) Rokitansky’s theory of an an- 
tagonism existing between tuberculosis and cardiac disease is 
not tenable; (2) mitral stenosis is less frequently observed in 
combination with pulmonary tuberculosis than are the other 
valve lesions; (3) mitral insufficiency may bring about a cer- 
tain degree of immunity in tuberculosis when it favors the de- 
velopment of the brown induration in consequence of pulmonary 
stasis; (4) the progress of an existing tuberculous process will 
be neither modified nor inhibited by a co-existing cardiac dis- 
ease, but (5) the tuberculous process reacts very unfavorably on 
the cardiac disorder the more rapidly the tuberculous process 
advances. 
The fact remains that there exists a lessened disposition to 
the deposition and growth of the tubercle bacilli in mitral sten- 
osis. This is supposed to be the result of blood stasis in the 
lesser circulation, but there exists no stasis in well compensated 
mitral stenosis. Only with the appearance of decompensation 
does slowing of the blood current and stasis supervene; hence, 
the lessened disposition to the deposit of the tubercle bacilli can, 
according to v. Romberg only be explained on a mechanical 
basis, namely, that in mitral stenosis the smaller blood vessels 
in the pulmonary circuit are much distorted this lessens the 
mechanical opportunity of the tubercle bacilli, which are usually 
in clumps, forming small emboli ready to be deposited. In mitral 
stenosis, stasis is greater than in insufficiency. It may be noted 
here that hypertrophy of the left ventricle and pulmonary tuber- 
culosis are also antagonistic, that in aortic valve lesion and in 
arterio-sclerosis there is usually pronounced hypertrophy of the 
left ventricle. These conditions are generally found in ad- 
vanced age when clinical tuberculosis becomes more infrequent. 
2. Tuberculosis and the Pulmonary Circulation. The anatom- 
ical condition of the heart of the tuberculous individual has early 
been recognized. It has generally been described as small1, both 
!The small heart in the tuberculous. Heart proportional to body weight. Animals 
like cattle, antelope, etc., in which the heart is in proportion to the body weight as 1 is 
to 250 are very prone to tuberculous disease, whereas the sheep, whose proportion is as 
1 to 100, the deer, 1 to 90, are comparatively immune. In the human, an enlarged heart 
is extremely seldom found in the tuberculous subject, and in the gouty or podagric 
patient, who usually has an enlarged heart, tuberculosis is unknown as a concomitant 
disorder. THE CARDIO-VASCULAR SYSTEM 
453 
in size and in the thickness of its walls as well as the capacity of 
its ventricles. Peacock found the heart in the tuberculous 
smaller than that found in other chronic diseases, and Louis, 
Lannec, Stokes, and Rokitansky all speak of the small heart in 
the tuberculous which they attribute mainly to nutritional dis- 
turbances, to a lowering of the general muscle tone, the cachexia 
and the lessening of the quantity and quality of the blood. Engel 
demonstrated that the left heart becomes proportionately less 
in weight as compared with the right. Normally the right heart 
is to left as 1:2.82; in the phthisical, however, the right is to 
the left as 1:2.14. 
Of much importance to the theory of the small heart of the 
consumptive is the teaching of Benecke, namely, that with the 
small heart, the lumen of the arteries becomes smaller, causing 
a lessening of the blood supply through the pulmonary circuit 
and a weakening of the lung structure, either an inherited or 
acquired disposition. A primary constitutional anomaly favor- 
ing the tuberculous disease must be presupposed, the analogue 
of which is found in Virchow’s teaching of the inherited hypo- 
plasia in the arteries of the body as found in the thinness of the 
walls and in the lessening of their lumen as the pathogenesis 
in many cases of severe chlorosis. Brehmer pointed out that 
with a small heart, if the lung is too large, a relative anemia of 
the latter results, and, with a lessening of the propelling force, 
a mechanical predisposition to tuberculous disease is established. 
Decroix and Potain consider the small heart in the tubercu- 
lous a secondary process due to the cachexia induced by the 
malady. According to Muller, the small heart in the phthisical 
is not a congenital hypoplasia, but a progressive decrease in 
weight which runs parallel with the general emaciation of the 
whole body, particularly that of the muscular structure. The 
roentgen ray was called into use by Moritz and by exact ortho- 
diagraphic methods, he found, in a most remarkable degree, that 
the size of the heart is a very changeable factor, dependent upon 
the size of the body of the individual, on the sex, the age, the 
conformation of the chest, and, above all, upon the muscular 
development and the weight of the body. Sciallero, from an 
analysis of thousands of radiological plates, found the heart in 
the young suffering from malignant disease always small; in 
people somewhat advanced in years, however, or in those suffer- 454 
CLINICAL TUBERCULOSIS 
ing from inactive or arrested tuberculous disease, it was almost 
always normal and small only in few exceptions. 
Beck studied the relation of the body weight to tuberculosis 
and concluded that the volume of the heart as compared to the 
body weight becomes lessened. Kraus pointed out that the 
small heart, situated centrally, with large vessels is the typical 
heart of the contracted chest or the phthisical habitus. This all 
goes to prove that the heart of the tuberculous shows at autopsy 
a lessening in cardiac volume due to a cachexia. Landouzy de- 
scribes a “paratuberculous” condition, said to be noticeable in 
the heart and blood vessels of the descendants of the tuberculous, 
which may be due to a congenital smallness of the thoracic 
cavity. It has not, however, been definitely proven that a small 
heart is really a predisposing factor to tuberculous disease. If 
we assume a relative pulmonary anemia necessary to a tuber- 
culous disorder, we must first prove that a small heart is really 
incapable of supplying the needed blood to the lungs. 
Much interest has always been exhibited in the relationship 
of tuberculosis to the right heart, and Buhl definitely proved the 
appearance of an eccentric hypertrophy with dilatation of the 
heart in tuberculosis. In rapidly progressive cases, frequently, 
dilatation of the right heart is observed, particularly in chronic 
phthisis and in the fibroid variety. It has long been known that 
certain complications lead to enlargement of the right heart, and 
pleural adhesions, bronchial catarrh, and emphysema may be 
mentioned; complications in pulmonary tuberculosis, however, 
like chronic bronchitis, pleural adhesions, and fibrous induration 
of the pulmonary tissue, and, especially, emphysema all play a 
characteristic role in the dilatation of the right heart. Hirsch, 
following the views upheld by Muller, demonstrated that hyper- 
trophy of the right heart in tuberculosis is based mainly on 
mechanical changes in the pulmonary circuit, that is, from 
pleural adhesions, from emphysema, and, in a number of cases, 
from the contractions of the arterial lumen due to indurative 
or ulcerative, tuberculous processes. 
Dilatation of the right ventricle and accompanying enlarge- 
ment of the liver have only recently been advocated as early 
symptoms of pulmonary tuberculosis. It should here be men- 
tioned, as was first related by Turban, that an absolute cardiac 
dulness toward the right of the sternum is a very common and 
an early symptom of a right-sided apex tuberculosis with con- THE CARDIO-VASCULAR SYSTEM 
455 
traction, and this retraction of the lung border towards the right 
may leave the right heart exposed and thus may lead to error 
in the diagnosis of a cardiac hypertrophy or an enlargement to- 
wards the right. That we may assume a frequent hypertrophy 
of the right ventricle in tuberculosis is evidenced by accentua- 
tion of the second pulmonic tone. 
The heart may further be influenced by the tuberculous proc- 
esses in various ways, namely, by dislocation and distortion, an 
interference with the functions of the heart, causing both sub- 
jective and objective symptoms to be present. Cardiac palpita- 
tion, abnormally loud heart sounds, pain, pulse rapidity, etc., are 
frequently observed as a sequence of cardiac dislocation, result- 
ing from a tuberculous process as in apical fibrosis, an exudative 
pleurisy or a pneumothorax, and these symptoms are clearly the 
result of mechanical and not of toxic disturbances. 
Chronic changes in the heart structure, the endocardium, the 
myocardium, and the pericardium as well, have frequently been 
observed as complications in tuberculosis. Neuman, in 1,489 
autopsies on phthisical subjects, found five cases of chronic, 
interstitial, fibroid myocarditis, and Norris, in 41 carefully se- 
lected cases of phthisis, found in 14 the heart muscle histologi- 
cally normal, in 10 chronic, interstitial myocarditis, in 5 fatty 
degenerations, and in 3 brown induration and atrophy. Fatty or 
muscle degeneration have very frequently been described by 
pathologists as an accompanying disorder in chronic phthisis. 
Teissier emphasizes the frequency of the tuberculous etiology 
in many of the disorders of the valves of the heart. This is analo- 
gous to the teaching of Poncet that a tuberculous joint rheuma- 
tism, an arthritis, or an arthralgia is the result of the toxin action 
and not of bacillary origin. It is the bacillary toxins (the tuber- 
culin) circulating in the blood of the tuberculous which cause 
the change in the heart structure, both endocardial and myo- 
cardial. 
The heart alone is not influenced by the tuberculous process, 
the blood vessels also show the effect of the disturbance. 
We frequently observe in the tuberculous, thrombosis of veins, 
the direct effect of a bacillemia, the arteries are also frequently 
affected by the tuberculous process, and even arterio-sclerosis 
is very often found as a concomitant symptom in young phthisi- 
cal subjects. 456 
CLINICAL TUBERCULOSIS 
From clinical observation and study of pulmonary tuberculosis 
in its relation to the heart since Rokitansky’s time, the following 
deductions may be made. The heart in the phthisical may be 
normal and be displaced, more often to the right, either from 
pleural adhesions or exudates, or from chronic, fibroid, tuber- 
culous changes in the lungs. The displacement may be either 
sudden, as in natural pneumothorax or serous pleurisy, or it may 
be pushed to one side by a distended lung and drawn toward the 
contracted lung where often it may simulate a dextrocardia. In 
the beginning of the tuberculous process, the heart is usually 
normal in size, but with the progress of the disorder some 
changes are more or less noticeable, and the heart becomes atro- 
phied or, occasionally, hypertrophied. This hypertrophy is espe- 
cially observed in cases of old and chronic, fibroid phthisis in 
which a cardiac insufficiency accompanied by alarming symptoms 
is noticeable. 
In about 60% of the cases of pulmonary tuberculosis, auscul- 
tatory heart changes are demonstrable. In advanced pulmonary 
tuberculosis, accentuation of the pulmonic second sound has 
been long observed and functional murmurs are heard in about 
6% of all cases. The pulse is usually of low tension and rapid. 
Of all organic heart lesions, a pericarditis is the most frequent 
complication. This, however, may be tuberculous or non- 
tuberculous, more often of the dry than of the exudative form. 
Myocarditis is infrequent and usually non-tuberculous. A tuber- 
culous endocarditis is very infrequent; in fact, endocardial dis- 
ease in the course of tuberculosis is very seldom, although an 
individual suffering from endocarditis may be stricken with pul- 
monary tuberculosis. Pulmonary stenosis is always primary, 
mitral and aortic insufficiency generally primary, but mitral 
stenosis may be secondary. Mitral insufficiency is the most fre- 
quent cardiac disturbance encountered as a complication in pul- 
monary tuberculosis, and mitral stenosis is the least. Aortic 
insufficiency is also frequent, whilst aortic stenosis is very sel- 
dom. With the exception of pulmonary stenosis, a cardiac lesion 
appears to inhibit or lessen the tendency to tuberculous disease. 
3. Tuberculosis and Tachycardia. An organ in which the 
anatomical structure is subject to many changes must suffer in 
its proper functioning, and one of the first and most important 
observations made is that of the disturbance of the heart in 
tuberculosis. The rapid action of the heart, the accompanying THE CARDIO-VASCULAR SYSTEM 
457 
tachycardia, is a phenomenon resulting from the mechanical 
changes in the lesser circulation, and the more pulmonary tissue 
that is involved, the more rapid will be the heart’s action. Often 
in chronic cases where the process is arrested, even after many 
years, or in cases of extensive fibrosis or pleural thickening, 
slight exertion will bring about a rapid heart action. It is very 
evident that even in recent cases of pulmonary tuberculosis with 
extensive involvement a frequency of the pulse can be explained 
on mechanical grounds. A tachycardia which may appear inde- 
pendent of fever usually runs parallel with the severity of the 
disorder. Sterling mentions that a rapid pulse in the first stage 
of the pulmonary disorder proves the absence of a connective 
tissue wall about the tuberculous process. 
The clinical symptom of tachycardia in tuberculosis is the 
extremely abnormal lability of the pulse, and this lability re- 
mains for many years after all the symptoms of the pulmonary 
disorder have disappeared. This rapid heart action, even after 
complete inactivity, points to a remaining slight injury to the 
heart muscle or to the nervous apparatus of the heart. A con- 
stant, rapid pulse is one of the earliest symptoms of the tuber- 
culous disorder, and its constancy is of the greatest prognostic 
importance. 
Tachycardia in the tuberculous may be due to pressure upon 
the nerves of the heart such as accompanies enlargement of the 
tracheo-bronchial glands or to mediastinitis, pleuritis, pericar- 
ditis, etc., in all of which the heart’s rapidity is more or less due 
to mechanical causes. It is possible, although improbable, that, in 
the tuberculous, compression of the vagi is followed by tachy- 
cardiac; theoretically, compression is usually followed by lessen- 
ing of the pulse rate. Animal experimentation has shown the 
effect of severing the vagi, namely, that the severing of one has 
no effect on the heart’s action, but if both are severed the fre- 
quency of the pulse rate increases. It may be assumed that in 
tachycardia the fibres of the sympatheticus are compressed with 
the fibres of the vagi. In most instances the pulse remains always 
fast. 
Lawrason Brown called attention to the frequency of an aus- 
cultatory phenomenon observed in the heart of the tuberculous, 
notably, an impurity of the first mitral tone and a systolic mur- 
mur at the apex. The possibility of a slight dilatation of the 
heart as the cause of this systolic murmur has first been men- 458 
CLINICAL TUBERCULOSIS 
tioned by Fiirbringer. The accentuation of the second pulmonic 
in tuberculosis as a sign of pressure in the lesser circulation and 
of hypertrophy of the right heart has already been mentioned. 
4. Tuberculosis and Hypotension. A low tensioned pulse in 
persons of middle life is not a constant phenomenon in the tuber- 
culous individual, although hypotension is the general rule, a 
normal or high pressure is a favorable sign, as is a rise in pres- 
sure during the course of the disease. In rapidly progressive 
cases, the blood pressure is low and remains low. Blood pres- 
sure observation is one of the surest and safest signs to guide us 
and to point out the cases which can be healed or be arrested. 
These observations apply not only to pulmonary tuberculosis 
but to tuberculous pleuritis and peritonitis as well. 
In beginning tuberculosis, the blood pressure may be within 
normal limits, but in the third stage cases it is usually low; this 
applies most particularly to those rapidly progressing cases with 
cavity formation. Observation has proven that in progressive 
tuberculosis there is a proportional lowering of the pressure— 
this lowering of the pressure depends upon the activity or non- 
activity of the tuberculous process at the time. The explanation 
of this lowering of the blood pressure in tuberculosis is chiefly 
the result of changes in the muscular structure of the heart 
brought about by the elaborated toxins of bacillary origin and 
vaso-dilator action by the same bacillary products. 
With the lowering of the pressure, the rise in the frequency 
of the heart action goes hand in hand. This is due to a paralysis 
of the vaso-constrictors in consequence of which the frequency 
of the heart’s action is quickened in order to equalize the paretic 
condition in the circulation. In some supposedly normal sub- 
jects, the use of tuberculin has been followed by a lowering of 
the blood pressure, which generally reaches its minimum point 
in about eight hours, and returns to normal again in about three 
days. A logical deduction of the low tension in the phthisical is 
supposed to be based upon the hypofunctioning of the adrenals. 
Observations along this line have been made by Bignold, Lucien, 
Bernard, Loschke, and others, all of whom have observed an in- 
hibition of the Drooer functioning of these glands in tuberculous 
subjects. Tuberculous individuals with a favorable2 prognosis 
2Tt is a more favorable prognosis when the arterial tension in the tuberculous individual 
is found normal or above. A sudden rise in the pressure may be a forerunner of an 
impending hemorrhage and a sudden drop a sign of an acute or recurring exacerbation or 
perhaps the beginning of a generalized disease; The low blood pressure in the tuberculous 
may be explained by the presence of tuberculo-toxins in the circulation. THE CARDIO-VASCULAR SYSTEM 
459 
generally show a normal or high blood pressure, and if, in pa- 
tients suffering from arterio-sclerosis or nephritis, tuberculosis 
becomes a concomitant disorder the blood pressure will always 
remain high. It is a notable fact that in the tuberculous threat- 
ened with hemorrhage, or perhaps some days or weeks before 
the onset of the hemorrhage, the blood pressure usually becomes 
high. Neuman observed this in more than 86% of his cases. 
5. Blood Pressure Observations. (74) It is now generally 
conceded that pulmonary tuberculosis as clinically observed is 
usually accompanied by a marked diminution in the blood pres- 
sure, and that this lowering of the tension is ascribed to a toxe- 
mia, to the circulating in the blood-stream of various toxins of 
bacillary origin, and that the development and elaboration of the 
toxins during the progress of the disease and subsequent en- 
trance into the circulation in progressively increasing amounts 
will induce irritation and dilatation of the arteries, a vasomotor 
irritability, and subsequent paresis, and attendant diminution in 
the blood pressure. 
That tuberculin, the toxin elaborated during bacillary growth, 
has a definite influence on the circulation and on the arterial ten- 
sion and blood pressure has been amply demonstrated by F. 
Bauer, of Vienna, who, after repeated injections of tuberculin, 
and which reacted negatively, observed no variation in the blood 
pressure; if, however, the injection was followed by a positive 
reaction, at least a slight, sensible lowering of the pressure was 
always observable. The direct effect of the toxemia is to cause a 
rapidity of the heart’s action, accompanied by a weak pulse, a 
want of arterial tone, resulting in diminution of the internal pres- 
sure; hence, there is a corresponding lowering of the blood- 
pressure with the progress of the pulmonary lesion and attendant 
toxin absorption, and, inversely, with a lessening of the active 
tuberculous process, lessening of toxin elaboration and absorp- 
tion, a corresponding rise in the blood-pressure may be demon- 
strable. 
In most tuberculous patients, a distinct variation in pulse and 
tension is always clearly observable, whereas in a healthy in- 
dividual a very slight variation in pulse-rate and blood-pressure 
may be noticeable. The pulse-rate is, in health, somewhat lower 
while in the recumbent position, higher in the upright, and at a 
point midway between the two in the sitting, with a correspond- 
ing rise of the blood-pressure in the horizontal, a lowering of 460 
CLINICAL TUBERCULOSIS 
pressure in the vertical position registering a pressure between 
the two, in the sitting posture. In the tuberculous, there is al- 
ways noticeable the great extremes both in the pulse-rate and 
the blood-pressure observations. In taking the blood-pressure 
and pulse-rate of tuberculous patients in the three stages of the 
disease, nothing more striking can be demonstrated than that 
usually the arterial tension is lower and the pulse-rate higher 
in the actively progressive cases than in the chronic or arrested. 
From blood pressure observations Pottenger has formulated 
the following: 
1. In advanced pulmonary tuberculosis, the blood-pressure is 
low. 
2. Causes which favor this low blood-pressure are: (a) Tox- 
emia—the action of the toxins on the vasomotor dilators; (b) 
weakness of heart muscle, and (c) general emaciation. 
3. Causes which maintain a proper amount of tension are car- 
diac hypertrophy and thickening of the arterial walls. 
Nardi, of Padua, who thoroughly studied but a limited number 
of cases, 30 in all, arrived at like results. Of the 30 cases, 9 
showed a lowering of the tension; 12 were within normal limits, 
and 9 showed a hypertension. He divides all tuberculous cases 
into two groups: The first group, the energetic tuberculous with 
normal or overnormal pressure, a relatively large heart, a better 
development of the left ventricle, a good body development, a 
good resisting power, and a better prognosis. The second group 
is designated as the torpid tuberculous, with a pressure below 
normal, a relatively small heart, positive clinical picture, poor re- 
sisting power, and an unfavorable prognosis. He maintains that 
the prognostically unfavorable blood-pressure lowering in a cer- 
tain class of the tuberculous is the direct result of the faulty de- 
velopment of the heart, reviving Rokitansky’s theory of the small 
heart in the phthisical. 
In many of the suspected tuberculous in which the clinical pic- 
ture points strongly to a pulmonary tuberculous involvement, 
even before a physical examination is made, a fair diagnosis can 
often be made by blood-pressure and pulse-rate alone. With a 
fairly rapid but weak pulse in the lying, faster in the sitting, and 
still faster in the standing posture, a pronounced tachycardia, and 
an arterial tension which is best with the patient in the recum- 
bent, not so good in the sitting, and much poorer in the upright 
position, a fairly positive diagnosis of pulmonary tuberculosis THE CARDIO-VASCULAR SYSTEM 
461 
may be supposed. If to this be added a rise in temperature, loss 
of weight, of appetite, cough, and like symptoms, a positive diag- 
nosis from such blood-pressure findings and pulse-rate records 
can often be made tentatively without physical examination of 
the chest. 
In taking the pulse-rate and blood-pressure of 74 ambulatory cases at 
the tuberculosis clinic at Rush Medical College, representing the incipient 
tuberculous, the moderately advanced, and far advanced, as well as tenta- 
tive and non-tuberculous, quite a difference in results was tabulated. In 
the records of the 32 first-stage cases, representing the ages from 
sixteen in the youngest to thirty-six in the oldest, all taken in the three 
varying positions, one is impressed by the frequency with which the 
pulse-rate stands in inverse proportion to the blood-pressure. This varia- 
tion cannot be referred to as a mere coincidence. With a gradual rise of 
the pulse first from the lying to the sitting, then to the standing position, 
there is a proportional fall in the blood-pressure which is not in corre- 
lation with healthy records. If there be a rise of 10 beats from the 
lying to the sitting, and probably 10 more from the sitting to the stand- 
ing position, there will be in many cases a corresponding drop of about 
6 points in the blood-pressure from the lying to the sitting, and 6 
more points from the sitting to the standing position. In the 14 moder- 
ately advanced cases the inverse difference between the pulse-rate and the 
radial tension was still more noticeable in many of the cases. In the ad- 
vanced, old, chronic cases with much fibroid tissue changes and good re- 
sisting power, the variation in the pulse-rate in the three positions—lying, 
sitting, and standing—may be as great as in the early infected, active cases, 
but a decided difference in the blood-pressure was observable. Here a 
variation in pulse-rate in lying, sitting, and standing of 90, 102, and 110, 
respectively gave a uniform blood-pressure of 120 in assuming either 
lying, sitting, or standing position. 
Summarizing: 
1. Blood-pressure and pulse-rate in the tuberculous is only a 
symptom, and not a part, of the disease. 
2. Lowering of the blood-pressure may be interpreted as an 
early symptom of the tuberculous infection, even before the 
physical signs or even before elevation of temperature may be 
definitely demonstrable. 
3. The toxemia in the tuberculous, with its accompanying 
cardiac atrophy and degeneration, seems to favor hypotension 
and tachycardia, concomitant vasomotor dilatation, and a low 
blood-pressure, whereas even with a moderate toxemia in the 
tuberculous, with a relatively large heart, a better development 
of the left ventricle will favor normotension or hypertension, and 
consequently a high blood-pressure. 462 
CLINICAL TUBERCULOSIS 
4. Tuberculous patients with high blood-pressure, even though 
the cause of the increased pressure is an arteriosclerosis, primary 
or secondary to a chronic nephritis, do better than patients with 
subnormal or hypotension (Haven Emerson). 
5. In the tuberculous subject suffering from vasomotor dilata- 
tion induced by the circulating toxins in the blood, anything 
which will cause a contraction of the arterioles will increase vas- 
cular tension; hence, vasomotor pressor remedies may be given, 
the first and foremost of which is rest. 
6. Lowering of the blood-pressure in the active tuberculous 
may be a conservative act of nature—may be compensatory. Is 
it advisable to raise the pressure by the administering of blood- 
pressure-raising drugs? Would it be beneficial or harmful? 
7. A favorable prognosis may be expected if, during the treat- 
ment of the tuberculous, the blood-pressure obtains a steady and 
uniform rise, approaching nearer the normal as the disease is 
being arrested. 
8. The taking of the blood-pressure on the tuberculous patient 
in but one position is faulty, and will not lead to proper deduc- 
tions, consequently a change of position from the lying to the 
sitting and to the standing should be made while taking the 
pulse-rate and making proper blood-pressure observations. 
Early recognition of the flaring up of a latent or a quiescent focus is diagnosing early 
or beginning tuberculosis. In beginning tuberculosis the blood-pressure is lowered, the 
pulse-rate increased; in the second stage the pressure is lowered more and the pulse fre- 
quently increased. In the young and in the female the blood-pressure is higher propor- 
tionately than in men and in the aged. The pressure is increased by excitation and by 
cough and is lowered by exhausting labor or after a full meal. A rise in blood-pressure 
is prognostically a favorable sign in one in whom the pressure was previously low, and 
remaining low indicates a progression of the disorder. Low pressure is charcateristic of 
and constant in the active tuberculous, hypotonia is the rule. By means of blood- 
pressure notation the curable can be separated from the non-curable. Usually in cases 
with a tendency to cavity formation or the breaking down of tissue the pressure is low, is 
labile, not stabile. More than one reading is necessary. CHAPTER 35 
TUBERCULOSIS FOLLOWING TRAUMA AND SHOCK 
The Relation of Trauma and Shock to Pulmonary Tuberculosis. 
The Municipal Tuberculosis Sanitarium (Sanatorium) of the 
City of Chicago was completed and opened for the reception of 
patients in April, 1915. From the date of opening of the Sana- 
torium until the end of the year, that is, until December 31, 1915, 
covering a period of about nine months, the Central Free Dis- 
pensary of Rush Medical College admitted to the Sanatorium 
through its channels 257 patients. In looking over the records 
and histories of these 257 tuberculous individuals it was found 
that about 77 (30%) gave a history of having had an operation 
performed within a year or so previous to the onset of active 
tuberculous disease. The question now arose: Was the fre- 
quency of active pulmonary tuberculous disease in these individ- 
uals who had submitted to operation a mere coincidence or was 
the giving of the anesthetic, the shock incident to the operation or 
the operation itself a contributing factor in the etiology of tuber- 
culosis? It is not difficult to conceive that an operation attended 
by loss of much blood, owing to lowering of vitality may activate 
a previously latent tuberculous process, or that the administering 
of an anesthetic is too concentrated a form, say, ether in more 
than 8%, tuberculosis may be brought about. However, consider- 
ing the question of shock as a cause of tuberculous disease the 
problem becomes much more complicated. Regarding the ques- 
tion of shock as a factor, we must consider: (1) the definition 
and what are the causes of shock; (2) what are its signs and 
symptoms and (3) what influence has shock, and trauma as well, 
upon the quiescent tuberculous process so as to reactivate it? 
(A) What is the definition of shock and what are its causes? 
Shock is prostration, is collapse, is a profound stupor and is 
described as a sudden physical or mental disturbance, a state of 
profound mental or physical depression consequent upon severe 
physical injury or emotional disturbance. It may be brought 
463 464 
CLINICAL TUBERCULOSIS 
about by any injury to either body1 or mind, such as fear, grief, 
anxiety, worry, homesickness, even great joy, toxic drugs, like 
mercury, arsenic and tobacco, extremes of heat and cold, de- 
spondency, mechanical injuries to vital organs, the brain, stom- 
ach, viscera, testicles, ovaries, skin, joints, extensive burns, 
etc., and all severe pain capable of exhausting the vital powers. 
Some individuals predispose to shock, the sanguine temperament 
more frequent than the lymphatic, the overworked, the underfed 
more than the idle, the anemic and cachetic more than others. 
There may be various degrees of shock and the injury to one 
organ followed by greater shock than to another. In intestinal 
trauma the nearer to the pylorus the injury the greater the effect 
of nervous shock. Iliac obstruction in the dog may be followed 
by death after weeks but if duodenal, death may follow in a few 
hours. Shock is frequently induced by surgical operations, in 
all of which we recognize a traumatism to either body or mind. 
Trauma and shock are not synonymous; they are interrelated, 
interdependent, no trauma, no shock; shock follows trauma, 
hence tuberculosis following shock presupposes a previous 
mental or physical injury. 
(B) What are the signs and symptoms of shock? Trauma is 
always presupposed to shock, the individual suffering from shock 
presenting a state of extreme torpidity. Apathetic, face and skin 
pale, lips and nails cyanotic, clammy perspiration, pupils dilated, 
eyes staring, with a fixed look into the distance, nausea, vomit- 
ing, hiccough, respiration accelerated, irregular, respiratory 
wave shortened, both inspiration and expiration are quickened 
and the pause lengthened. Blood pressure and pulse are most 
interesting and pathognomonic. Tn surgical shock, the abnor- 
mally low blood pressure is the most essential, single phenom- 
enon, the arterial pressure may be reduced to or even below 50 
mm of mercury. A noted lowering of the blood pressure is often 
observed immediately on incising the skin of the abdomen. 
There is usually a pronounced reduction in body temperature, 
may drop from 1 to 3 degrees and lowering of the temperature 
below 96.8 is a very grave indication; pulse weak, and not pal- 
pable. The fall in temperature in shock is the result and not the 
cause of the low blood pressure. In profound shock the bulk of 
lit has repeatedly been proven that many. persons harbor within their bodies virulent 
tubercle bacilli but are not made sick by their presence in the body. In such individuals 
it is only necessary that disturbances or lowering of vitality, much physical and mental 
efforts, trauma and shock, weakening of the body by intercurrent disease, etc., to lead 
from a tuberculosis infection to a tuberculous disease. TUBERCULOSIS FOLLOWING TRAUMA AND SHOCK 
465 
blood does not circulate freely in the arterial system but accumu- 
lates in the venous trunks resulting in intravenous hemorrhages 
or in symptoms which simulate hemorrhage. Shock causes a 
vasomotor dilatation, a lessening of vasomotor tone a result of 
reflex paralysis or exhaustion of the vasomotor centers, an in- 
hibitive action of the sympathetic fibres of the vasomotor nerves, 
causing lowering of the blood pressure, the blood escaping into 
the veins and capillaries. The more highly organized the more 
prone to shock and a high strung, nervous temperament consti- 
tutes a most important predisposing cause. Shock is light in 
children, pronounced in the adult and grave in the aged. In 
shock all depends upon the circulatory apparatus and not the 
age of the patient. In the aged the arteries are hard and fibrous 
and the blood pressure usually high; in the young the arteries 
are soft and pliable and the blood pressure low. The new born 
is free from shock that is before the physiologic connection be- 
tween the central nervous system becomes established. In the 
new born there is a short period of immunity which is followed 
by the greatest period of susceptibility which gradually lessens 
until in adult life the resistance is greatest and again diminishing 
in old age. There is little difference in the sexes before puberty; 
after puberty, the female becomes less stable, especially at the 
menstrual period, the male growing more hardy. From puberty 
to the child bearing period the female is slightly more susceptible 
to shock, the female is more hopeful, more tractable as a patient. 
(C) What influence has trauma and shock upon the tubercu- 
lously infected individual? It is now generally admitted that 
there exists a close relationship of tuberculosis to accidents j1 
to trauma, to shock, but to bring about tuberculous disease in 
shock both trauma and bacilli are necessary. The view is held 
by many that an organ or tissue in order to become tuberculous, 
it must contain tubercle bacilli previous to the injury or be al- 
ready tuberculously diseased. It has been repeatedly proven 
that tuberculosis may develop in an organ entirely free 
from bacilli previous to injury. Virchow and Rokitansky as- 
sumed that muscle fibre possessed a specific immunity against 
tuberculosis; however, animal experimentation has demon- 
strated that if in an animal the muscles of the extremities be 
bruised, this then followed by an intravenous injection of virulent 
bacilli that in addition to the pulmonary tuberculosis a notable 
tuberculosis of the irritated muscle fibre is present. 466 
CLINICAL TUBERCULOSIS 
With an injury tubercle bacilli may enter the body or wounds 
become directly infected, and direct infection from without, ex- 
ogenous infection has followed vaccination, circumcision and 
even trivial injuries to the cuticle, but the chief cause of 
tuberculosis following injury and shock must always be endog- 
enous, that is, from within, the disease extending to an injured 
or weakened part owing to a lowering of body resistance. It is 
well known, for instance, that a tuberculous gland may bring 
about a metastatic infection after an injury to the gland. It be- 
comes necessary to differentiate if trauma and shock have pro- 
duced tuberculosis in a perfectly healthy but infected individual, 
or in one who was previously tuberculously diseased, but the 
process at the time was not active. Trauma and shock may be 
the necessary factors which' aggravate a previously existing 
process or make an active one more active or one which has be- 
come inactive or quiescent again active, much depending if the 
organism or even individual organs have been weakened from 
intercurrent conditions previous to the injury, like overwork, 
grief, homesickness and other causes as have already been enu- 
merated, all of which are important elements in the lower- 
ing of body resistance. 
Into this category may also be placed all those vicious condi- 
tions which if indulged in over protracted periods are generally 
followed by a lowering of the body’s vitality, especially long 
periods of dissipation and carousing, leading a vicious life, sexual 
and other excesses, irregular mode of living, abuse of the body, 
insufficient or unwholesome food, etc. 
Tuberculous disease as it relates to trauma and shock may be 
divided into two classes, either into (a) the class in which trau- 
matism itself, attended with little or no noticeable element of 
shock, is the causative factor or into (b) that class in which 
shock appears to be the main cause. 
(A) In cases of tuberculosis in which trauma per se seems 
to be the exciting cause the process usually runs a rapidly fatal 
course. I wish to cite a few cases from the literature to which I 
wish to add one that only recently came under my observation. 
Ferdinand Weil M.M.W. 1910, No. 3, reports two cases, one of 
which during life was considered septic, the other typhoid. In 
both there was fever, rapid pulse and high temperature, with 
indefinite chest findings and in both an abortion was performed a 
week or so before the onset of the symptoms. Death about 5 TUBERCULOSIS FOLLOWING TRAUMA AND SHOCK 
467 
weeks from the beginning of the disorder, postmortem confirmed 
the suspicion of miliary tuberculosis and in addition, in both in- 
stances the uterus was found to be the seat of a primary (?) 
tuberculous disease. Here undoubtedly, trauma to the uterus 
incident to the abortion brought about the entrance of tubercle 
bacilli directly into the lymph or blood stream resulting in dis- 
seminated tuberculous disease. Rose M.M.W. 1909, No. 38, re- 
ports a similar case, running a very rapid course, which during 
life was considered one of puerperal sepsis until the postmortem 
revealed its true nature. Marcus Posen; Monathschrift fur un- 
fallheilkunde 1910 No. 10, reports a case of chronic encapsulated 
tuberculous gland in the axilla followed, after a severe contusion 
of the shoulder and injury to the gland in a man 43 years of age, 
by miliary tuberculosis and exitus in three weeks from date of 
injury, accompanied by meningitis tuberculosa. F. Parker Weber 
Brit. Med. Jour., 1910, reports a most interesting case. A young 
man in apparently perfect health, on shipboard, returning from 
Africa, received a severe blow on the testicle on April 1, 1897, 
and died 25 days after from miliary tuberculosis, and the post- 
mortem showed distinct evidence of earlier lesions in the apices 
of both lungs, enlarged mediastinal lymph glands, evidence of an 
old pleurisy and a caseating mass in the testicle. The following 
case came to my attention a few years ago: 
Dr. D., aged 54, died January 9th, 1918, of miliary tuberculosis. He was 
of healthy, sturdy Scotch stock with negative family history as to tuber- 
culosis, had a family consisting of a wife and two daughters. About 10 
years ago one of his children was taken ill with a most severe type of ma- 
lignant scarlet and succumbed within a week of its onset. The shock inci- 
dent to the death of the child brought on a severe nervous disturbance 
which was followed by universal Alopecia. In late years, and up to the 
fall of 1917 he was enjoying unusually good health having gained some in 
weight; however, during the summer he complained of an occasional at- 
tack of sore throat, a slight pharyngitis. On September 1, 1917, while 
removing his collar he noticed a slight swelling on the left side of the 
neck below the jaw near the posterior horn of the hyoid; this was diag- 
nosed as an acute inflammation of the thyroid, an acute thyroiditis, and 
the swelling becoming somewhat painful and fluctuating, an incision was 
made September 6th, discharging about 15 cc of fluid pus. The gland 
continued discharging pus for some time when under gas an attempt was 
made to reach the bottom of the abscess so as to favor more rapid drain- 
age and healing and after this procedure the pus soon ceased to flow and 
in its place a clear serum, simulating synovial fluid, kept flowing from the 
sinus and which greatly irritated the skin about the neck and shoulder. 
He now began showing symptoms of denutrition and this was attributed 468 
CLINICAL TUBERCULOSIS 
to the constant loss of thyroid secretion, a disturbance in metabolism. 
Up to this time the physical examination of the lungs always gave nega- 
tive findings but now the examination revealed a dull area, note high, 
bronchial breathing, whispering voice increased, posterior to the left 
of the spine from the first to the fifth dorsal vertebra and beyond the 
parasternal line, and suspecting the presence of enlarged bronchial lymph 
glands a stereo-roentgenographic picture was taken which showed a dis- 
tinctly dense hilus shadow; in fact, the shadow was so dense that two care- 
ful and well-informed roentgenologists gave their opinion that it is more 
likely malignant than tuberculous. He now began to show a slight 
hacky, non-productive cough and after many attempts at securing a "little 
sputum finally succeeded one morning in raising a little pelicle which on 
examination showed many tubercle bacilli and now an examination of the 
fluid secreting from the thyroid gland was made and it also showed the 
presence of the Koch’s bacillus in large number. On December 5th, 1917, 
a second stereoscopic set of plates were taken showing unmistakably the 
presence of a miliary tuberculosis, death following within a month. 
(B) Cases of pulmonary tuberculous disease in which shock 
alone seems to be the exciting- cause. Reference has been made 
above that in surgical shock an abnormally low blood pressure is 
the most essential, single, phenomenon. It is well known that in 
pulmonary tuberculosis in either the active, inactive or arrested 
stage, low blood pressure is also a constant phenomenon; in fact, 
low blood pressure in an apparently healthy individual, with 
negative physical findings, is a most positive single sign of a 
present or future tuberculosis. From what has been stated we 
must acknowledge that shock causes a vasomotor dilatation, ac- 
companied by damming back of the blood in the veins and 
capillaries, a slowing of the blood current, a venous stasis. We 
all are also familiar with the picture of the contracted chest in the 
young adult with its small upper aperture and its great tendency 
and frequency to tuberculous disease. We have here a similar 
phenomenon, insufficient aeration, lymph and blood stasis, with 
a strong tendency to metastatic disease. With a rapid or normal 
blood current, if bacilli should have found their way into the cir- 
culating fluid, they do not find easy lodgement, besides the fast 
flow destroys many, whereas a slow current presents all the ele- 
ments favorable to deposition and growth of the tubercle bacillus, 
hence in shock the one symptom of low blood pressure, with 
stasis and vasomotor paralysis are just the factors which we all 
recognize as favoring the development of tuberculous disease. 
If the blood pressure in the tuberculous adult, with either an 
active, inactive, quiescent or arrested process is usually low and TUBERCULOSIS FOLLOWING TRAUMA AND SHOCK 
469 
if low blood pressure is an important phenomenon accompanying 
shock, then individuals who are on the borderline, in whom the 
physical signs are perhaps negative, perhaps slight prodromal 
symptoms or slight toxidity from slight tuberculin elimination 
and absorption, showing that somewhere in the economy a slight 
activity is taking place, pulse slightly accelerated, a slight varia- 
tion in temperature, blood pressure a trifle low, if in such an in- 
dividual, the blood pressure is still lowered by trauma and deep 
shock, which lower vitality and resistance, than the organ which 
already shows a lowering is usually the one which shows the dis- 
turbance and as at puberty and for some years beyond the lungs 
are most vulnerable, the other organs at this time in life have 
acquired a certain degree of immunity, it is now the pulmonary 
circuit which shows the effect of this induced shock. 
How shock may bring about tuberculous disease may be well 
illustrated by the following case histories: 
Case 1 and 2. Family consisted of Mr. D., aged 73; Mrs. D., aged 65, 
and four children, two boys and two girls; negative family history for 
tuberculosis. Miss A. L. D., age 27; occupation: bookkeeper; usual 
weight, 146 pounds; always enjoyed fairly good health and, with the excep- 
tion of an attack of chicken pox at the age of 2, had no other children’s dis- 
ease. In July, 1911, while on a vacation, she met with a very serious acci- 
dent. While riding in a street car at Niagara Falls, the car coming to a sud- 
den stop she was thrown violently forward, her face and mouth coming 
forcibly in contact with the back of the seat in front. Since childhood, she 
had a faulty formation of the teeth which at the time were being corrected, 
the teeth being held in proper position by gold wire. In striking on her 
mouth all these teeth became dislodged, this was followed by some hem- 
orrhage. She showed much excitement and nervousness at the time, 
reached home about two weeks after the injury and at once began com- 
plaining of frequent headaches, and at times displayed a most violent and 
irritable temper. She returned to her work in the fall of 1911 and in 
January, 1912, began to complain of a constant tired feeling (Prodromal 
Symptom). A slight cough appeared in the spring and in August, 1912, 
she discontinued her work, her symptoms now becoming more pro- 
nounced, a diagnosis of pulmonary tuberculosis was made and gradually 
progressing to the terminal stage, died October 1, 1913. During all this 
time the expectorations were very scanty, little cough, and towards the 
close she developed a painful pleurisy. Close confinement to her home, 
with close application and long hours at office work, perhaps illy-venti- 
lated, and an attended injury and shock in a person of sanguine or nervous 
temperament brought about a reactivation of a probable quiescent or healed 
lesion, or by lowering of vitality and resistance activated a latent process. 
Early in November, 1913, I was consulted by the sister of the dead girl 
and there in taking the family history I first learned of the sad fate and 
early demise of this girl. The following is a short history of Miss A. D., 470 
CLINICAL TUBERCULOSIS 
age 21, sister of the dead girl; occupation, bookkeeper. Rheumatism at 
the age of 14; asthma in 1907, continuing for 4 years; previous to that an 
Eczema lasting for 5 years; pneumonia, 1905; pleurisy 3 years ago. Ex- 
amination, November 19, 1913; pulse 92, temperature 99.8, weight 133 
pounds. Physical examination: evidence of an old pleurisy left lung, 
drooping of the left shoulder, right upper lobe anteriorly note high, voice 
conduction increased, inspiratory musical rales, interrupted breathing. 
Posterior muscle spasm. Kronig right 5 cm, left 5.5 cm; re-examina- 
tion, March 18, 1914: pulse 74, temperature 98.8, weight 141 pounds. From 
these findings and the family history I advised her to be under constant 
observation and care. Now seven years after she is in most excellent health, 
living under strictly dietetic-hygienic rules since the death of her sister. 
The brothers though advised of the gravity, refused positively to be ex- 
amined until in the summer of 1917 I was called to the home of Mr. D. 
to examine one of the sons, who at the time was suffering from pulmon- 
ary tuberculosis, second stage. He was sent to the Municipal Tuberculosis 
Sanatorium, where he remained but a short time, returning home; died, 
November 22nd, 1917, aged 29. 
History: Whooping cough at the age of 7, no other children’s diseases; 
occupation, R. R. clerk; usual weight, 168 pounds. In October, 1911, and 
at the age of 23 he met with a most serious accident. The Steamer Pere 
Marquette was foundered in Lake Michigan in a storm and out of a crew 
of 38 men only 5 were rescued, he being one of the five. He was in the 
cold water for nearly one hour before help arrived. One of the four men 
who were rescued with him shortly after became violently insane and is 
now confined in an asylum; this seemed constantly to pray upon his mind. 
In January, 1914, he began complaining of being tired, languid, even lazy. 
He would accept a position, fill it but a short time, then quit, always 
complaining of that tired feeling (Prodromal symptom). His family 
would remonstrate, but he appeared indifferent, moping and sitting about 
the house. Habits, good. In January, 1917, he began to show definite 
symptoms of active tuberculous disease, took to bed in June, and exitus 
letalis in November, 1917. His mother has since informed me that al- 
though he was an active and ambitious boy before, that ever since the 
accident he was constantly complaining of a tired feeling and that he was 
much indulged, because of this condition. Since the death of this boy, 
the other lad, now aged 28, has also come under my observation, and 
though his findings are negative, owing to his family history, it is advis- 
able to keep him under observation. 
Case 3. Mr. H. J., age 22; born in Chicago; vocation, accountant; usual 
weight, 158 pounds; first came under my care December 3rd, 1917. Chest 
examination warranted a diagnosis of chronic pulmonary tuberculosis, 
second stage. Pulse 120, temperature 99, weight 136)4, slight clubbing of 
the fingers; sputum, 2 to 4 tubercle bacilli in each field. History: Scarlet 
fever at the age of three, followed by otitis media, this for more than 17 
years continued, off and on, to discharge pus. Soon after puberty he be- 
gan leading an irregular life and at the age of 17 was a confirmed cigar- 
ette smoker, consuming from 15 to 20 cigarettes daily, remaining often out 
of doors the greater part of the night, returning home early in the morning TUBERCULOSIS FOLLOWING TRAUMA AND SHOCK 
471 
and, without rest or breakfast, go to work, and during all this time the 
ear trouble gave him much concern. At the age of 19, in 1914, he con- 
sulted a physician who advised the removal of the tonsils as a possible 
means of curing the chronic ear difficulty. In May, 1915, under local 
anesthesia, in the doctor’s office he had his tonsils removed. This was 
followed by a most severe hemorrhage, lasting for hours. He complains 
of a tired feeling since that time, and since the operation, 5 years ago, he 
has worked in all but 9 months. The ear still discharged after the removal 
of the tonsils and the physician suggested an autogenous vaccine. This 
was prepared and for more than 3 months he received 2 to 3 intracutane- 
ous injections every week which so irritated him that he positively refused 
to continue with the treatment. Was the loss of blood following the re- 
moval of the tonsils a contributing factor to his tuberculous disease? It 
is well known that every severe injury to the body, particularly if accom- 
panied by loss of blood, will reduce body resistance and often from an in- 
active to an active or from a latent to a manifest disorder is early notice- 
able. This patient died December 4th, 1921. 
Let us revert for a few moments to the records of the 257 
tuberculous patients who were sent in 1915 from the Central 
Free Tuberculosis Dispensary to the Municipal Tuberculosis 
Sanitarium, 77 of which gave a history of having had an opera- 
tion performed within a year or so previous to the onset of the 
tuberculous disease. Have these operations, on the 77 patients, 
been performed at a time in life when the patients’ vitality was 
at a low ebb or possibly at its lowest point? The greater num- 
ber were in a decade, covering the time from the 14th to about 
the 24th year, the operations consisting mainly of appendec- 
tomies, tonsillectomies, laparotomies, turbinectomies, removal of 
enlarged glands, etc. 
Immediately before, at puberty and for some years beyond 
when the physiological balance in the young individual is greatly 
disturbed by new or dominating, emotional and sensual im- 
pulses, when there is greatest danger of lowering vitality, would 
it not be advisable to delay all operations that are not necessarily 
life saving until this equilibrium has again been fully restored, 
or if it is deemed necessary to operate to do it in the younger 
years before the disturbance of this balance? An individual who 
presents a picture of, or perhaps some of the physical signs point- 
ing slightly to a suspicious tuberculous disorder, even if appar- 
ently healthy, and if in such a person we find a blood pressure 
not proportional to his age, in whom it would be most advisable 
to minister to the upbuilding of his body energy and resistance, 
and with it increase his blood pressure, would it not become 472 
CLINICAL TUBERCULOSIS 
most important that we guard against all such agencies which 
have the slightest tendency to lower this pressure? 
In preparing an individual for operation, we find that generally 
a careful examination of the heart and its sounds is made, a thor- 
ough urinalysis and a blood examination, the lungs are usually 
very hastily examined, but we seldom see even a casual or hur- 
ried blood pressure observation made. With beginning of pub- 
erty the greatest pulmonary tuberculosis morbidity and mor- 
tality begins. This is usually in the middle of the second decade 
of life and in the middle of the third a perceptible decrease in 
the tuberculosis mortality is beginning to manifest itself and at 
this time in adult life the period of greatest resistance is in evi- 
dence, and operation better borne, eliminating in a measure, at 
least, the element of shock. As operations2 play but a part in 
the production of shock, it becomes most important, particularly 
at the tender years towards and after puberty, to guard against 
all such conditions which may lower vitality and in that manner 
bring about an active tuberculous process from a quiescent or 
latent one and fear and fright, automobile and railroad accidents, 
grief and homesickness play as important a role in producing 
shock as do operations. We have learned that all physical and 
mental disturbances are factors in producing shock, hence avoid, 
particularly in young adults all such influences which may in- 
duce shock, which lower blood pressure, temperature and pulse, 
which lower vitality, lessen resistance, especially at a period, at 
puberty, when the balance is such that a little more in one direc- 
tion or a little less in another, may lead either to a state of per- 
fect health in one way or to a steady progressive with ultimate 
death in another, from pulmonary tuberculosis, the white plague, 
the great disorder of the human race, the one in which we all are 
so vitally interested. 
2An acute or perhaps latent infection existing at the time of the operation is responsible 
in a number of operative cases for a subsequent pulmonary tuberculosis, hence only to 
operate 'vhen the surgeon has the full assurance that there is no latent or acute tuber- 
culous infection. PART THREE 
LABORATORY DIAGNOSIS 
Laboratory Diagnosis in Tuberculosis 
Microscopical. Chemical. Biological, Etc. 
This comprises three chapters. First: a general consideration 
of the sputum, both the normal and that from the tuberculous 
subject and how to collect, prepare and stain it for microscopic 
examination. Attention is also given to the lymphocytic picture, 
so noticeable in the sputum of the tuberculous, as well as to the 
albumin reaction. Second: the hematology, here the blood as 
seen in tuberculosis is considered. The hemoglobin, the leuco- 
cytes and the erythrocytes of the normal as compared with the 
blood of the tuberculous subject; Arneth’s blood picture and its 
significance; the various theories and the demonstration of tu- 
bercle bacilli circulating in the blood stream. Under serology 
the complement fixation test only is considered, this somewhat 
in detail. In the last chapter, the various methods for staining 
and detecting the tubercle bacillus in the different body fluids, in 
excretions, secretions and in the excrements are considered. 
This consists in a microscopic examination of the urine, milk, 
bile, feces, pleural exudates, spinal and peritoneal fluids, etc. (7) 
(8) (16) (37). CHAPTER 36 
THE SPUTUM IN TUBERCULOSIS 
General Consideration. Secretions which are expelled from 
the mouth during the act of coughing bear evidence of a catarrhal 
condition along the respiratory tract. These secretions may be 
more or less fluid, may be very abundant and, as in bronchiec- 
tasis, may be expelled at certain intervals accompanied by much 
or little odor. The sputum from tuberculous patients is gen- 
erally odorless or, at most, of a faint mouldy character, most 
frequently colorless, white or yellowish-white; it may at times 
be tinged with green, the evidence of the presence of large num- 
ber of pus cells, and may also be slightly blood tinged or streaked 
with blood, though usually it is not bloody. It is most freely 
expelled in the early morning hours or on arising and becomes 
less as the day wears on and then occasionally there is an entire 
absence of all secretions. This does not, however, exclude nor 
disprove the existence of respiratory disease. 
In ordinary as well as in tuberculous sputum various morpho- 
logical elements are always present, the most abundant of which 
are: (a) Epithelial cells, plain pavement epithelium, chiefly from 
the buccal cavity; these cells are readily recognized under the 
microscope as flat, polygonal bodies with irregular outlines, and 
by their size and the large nucleus, (b) Pus cells,—these are 
variable in number, usually in proportion to an inflammatory 
process; they may, however, be so abundant so as to form the 
chief element. Erythrocytes may also be present in greater or 
lesser number depending upon whether much or little blood is 
exhibited, (c) In the exudative form of pulmonary tuberculosis 
with much tissue destruction and cavity formation, elastic fibres 
are usually present. These fibres appear either as isolated, de- 
tached filaments or collected in bundles, straight, coiled, or 
twisted, (d) Besides these elements, mucous corpuscles, fatty 
cells and fatty crystals, cell nuclei, granular debris, etc., occa- 
sionally bronchial casts, lung stones and fungous growths are 
demonstrable, (e) When a specimen of sputum has been prop- 
erly prepared, stained and is examined microscopically, the 
475 476 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
tubercle bacillus, if present, can be readily recognized, (f) The 
expectorated sputum is often contaminated with coal dust, which 
gives it proportionately a distinct blackish appearance. This is 
also often observed in perfectly normal sputum, (g) Biliary pig- 
ment in the presence of icterus may frecjuently be found in the 
sputum, as well as varying amounts of coloring matter derived 
from blood, (h) Another amorphous element of sputum is 
mucus, a secretion from the bronchial mucosa which gives 
sputum its viscid character. Albumin is occasionally present and 
presages an inflammatory condition of the bronchioles, alveolar 
ducts, or the air cells. The fluid portion consists chiefly of water 
and the more abundant the expectoration the more fluid or 
watery it is. 
Sputum is generally classified as to color and appearance into 
(1) mucous. This signifies a watery substance expectorated by 
perfectly healthy people, or perhaps more so in those suffering 
from bronchial catarrh. (2) Muco-purulent. This consists of 
both mucus and pus cells, the latter separating freely from the 
mucoid or watery portion as a sediment when the sputum is 
placed into a bottle and set aside for a short time. This form of 
sputum is frequently found in simple bronchial catarrh but most 
pronounced in pulmonary tuberculosis. (3) Purulent sputum; 
pus sputum. This form of sputum, generally homogeneous in 
character, consists almost entirely of pus, is derived from pul- 
monary cavities due to the breaking down of tissue, usually a 
concomitant in the rapidly progressing exudative type of pul- 
monary tuberculous disease. This, at times, may consist of pure 
pus, if pus in the pleural cavity has perforated the pulmonary 
structure and is discharging through a bronchus (empyema). 
(4) Bloody or sanguinous sputum. Sputum tinged or streaked 
with blood is usually from the mouth, teeth, throat or naso- 
pharynx, etc., and may also be tinged after a gastric or oeso- 
phegeal hemorrhage. If the sputum is mixed with much blood 
and is coughed up, it generally comes from a ruptured vessel in 
the lung tissue and is then known as a pulmonary hemorrhage. 
The Sputum in Pulmonary Tuberculosis. In acute miliary 
tuberculosis the sputum does not differ either in appearance, 
color or viscosity from that expectorated in ordinary catarrh of 
the bronchial tubes. In the proliferative type of the disease with 
but little or no destruction of tissue the expectorated material 
generally consists of the secretions of the bronchial tubes; con- THE SPUTUM IN TUBERCULOSIS 
477 
sequently, in appearance at least, it is not distinguishable from 
that of catarrhal disease; by microscopic examination, however, 
the presence of the tubercle bacillus may be demonstrable and 
albumin by chemical test, proven. 
The bronchial secretions at the beginning of the disorder are 
usually very scanty, and, as time goes on, the intensity of the 
bronchial catarrh increase. Simultaneously, degenerative changes 
take place in the bronchioles and the air cells and the resultant 
material of these changes now become mixed with the bronchial 
secretions and form part of the expectorated sputum. In propor- 
tion as the products of these degenerative changes are much or 
little, the expectorated material, the sputum, assumes the appear- 
ance which to the eye is usually designated as “Tuberculous 
Sputum.” This becomes practically more and more noticeable 
in the exudative type of the disease or what is commonly known 
as the broncho-pneumonic form. Here generally cavity forma- 
tion is the clinical picture, more or less rapid breaking down of 
tissue, with high fever, rapid pulse, much cough, loss in weight 
and appetite. 
The sputum becomes muco-purulent in proportion to the 
severity of the tuberculous process. In the cirrhotic or fibroid 
type of the disease the sputum again changes, assuming again 
the appearance of that which we usually see in ordinary or 
bronchial catarrh. Here, at times, there may be an entire ab- 
sence of sputum or the sputum may accumulate during the 
night and be freely, perhaps copiously, expectorated in the morn- 
ing. With bronchiectatic changes the sputum may accumulate 
in the dilated bronchi and, then, usually with change of posi- 
tion, large quantities of sputum are coughed up; this may be 
accompanied by little or much odor. We see from all this that 
sputum in pulmonary tuberculosis is subject to great changes in 
fluidity, consistency, viscosity, and from absence of to more or 
less watery, to muco-purulent, even to purulent or bloody, and 
from odorless to more or less mouldy, even to fecal. With the 
formation of cavities the sputum often changes, assuming a 
slightly greenish tinge and becoming more ropy, tenacious, and 
mixed with air bubbles, and here the muco-purulent material 
from the vomicae does not sink to the bottom of the vessel into 
which it is expectorated but remains suspended by means of the 
incorporated air. This sputum, under the microscope, shows 
many pus cells, staphylococci, streptococci, some diplococci, epi- 478 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
thelial cells, elastic fibres, debris, coal dust, etc., interspersed 
throughout with few or many tubercle bacilli. In the sputum of 
the tuberculous, proteolytic, amylolytic and lipolytic ferments 
can be demonstrated. 
How and When to Collect the Sputum. It is evident that the 
sputum of the tuberculous individual is subject to great varia- 
tions, hence we must aim at securing it at a time when the 
anatomical elements promise to be most positively present. The 
tuberculous person or the suspected is asked to secure the 
sputum in the early morning. The patient should have a clean, 
perhaps sterile bottle, cup, or container within easy reach, and 
when he has a coughing spell should raise the material from deep 
down the bronchial tubes and spit it into the vessel at hand. If 
the sputum is to be examined for the tubercle bacillus, the early 
morning or first sputum is desired. In collecting sputum for 
examination, it often becomes necessary to teach the patient how 
to expectorate. Very frequently the sputum secured is that from 
the buccal cavity, or perhaps, from the naso-pharynx, as the 
patient simply spits or hawks and what he brings out is put into 
a suitable container and sent to the doctor’s office or to the 
laboratory. Here the patient must be told that the material 
which he coughs up, brings up from the bronchial tubes, and not 
that which he spits or hawks up, is wanted. He should be told 
not to suppress the cough, but to favor expectoration and that 
what is wanted is not saliva from the mouth, but secretion and 
mucus from the deeper portions of his lungs. It frequently hap- 
pens that the sputum expectorated during the day may be free 
from tubercle bacilli or they may be so few as to escape detection, 
and frequently in a beginning case, or one in whom we suspect 
tuberculous disease, the bronchial secretions are very scanty or 
perhaps none at all. A little maneuver must then be resorted to 
so as to aid us in securing an amount sufficient for examination. 
The giving of 10 to 20 grains of potassium iodide in a little 
water in the evening may often produce in the morning most 
satisfactory results. To tuberculous individuals who cough quite 
frequently but do not raise sputum, the so-called dry cough, 
grain of morphine should be given at bed time; this has a tend- 
ency to quiet the patient and his cough as well, and on awaking 
in the morning he usually expectorates quite freely with the first 
fit of coughing. 
The sputum when collected in a suitable container should at THE SPUTUM IN TUBERCULOSIS 
479 
once, or as soon as possible, be sent to the laboratory for exam- 
ination, particularly so during the warm or summer months; 
during the winter or in cold weather it is not necessary to submit 
the sputum for testing at once as an interval of a few days does 
not vitiate a microscopic examination. Should it be necessary to 
send the sputum to some distant laboratory, the adding of a few 
drops of carbolic acid or a little formaldehyde is desirable, just 
sufficient to inhibit putrefactive changes while in transit. To a 
small amount of sputum, about a teaspoonful, in a wide mouth 
bottle add 2 to 5 drops of carbolic acid, cork securely and label, 
giving the name of the patient, time of collection and date, wrap 
in suitable material or make a package which will allow safe 
transit. 
All sputum not wanted for laboratory examination should be 
received in paper napkins or clean clothes and these deposited in 
suitable paper bags and destroyed in a furnace—this should be 
a daily routine duty. Especially constructed sputum cups, made 
from various materials, chiefly heavy paper, are now much in 
use and are most appropriate for the collection of sputum. These 
cups are emptied every day or oftener and the contents consigned 
to direct fire or to specially prepared crematories. These sputum 
cups, or any sputum container, must always be closed after the 
sputum has been deposited so as not to spread the infection, as 
through flies. Cuspidors, so frequently seen at the bedside of 
home patients, should be strictly tabooed; if used at all, they 
should be one-half filled with water to which a teaspoonful of 
pure carbolic acid has been added. 
To collect the sputum from children suffering from pulmonary 
tuberculosis is often fraught with great difficulty. Many chil- 
dren, while they do cough, do not expectorate, but seem to swal- 
low the sputum. It is often very necessary to make a micro- 
scopic examination of the sputum but most difficult to secure a 
sample. Asking the child to cough and spit out is of no use, as 
it simply will not do so. Here, occasionally, more drastic mea- 
sures must be resorted to. Place the child on a high stool or 
chair or preferably in the mother’s lap, have an attendant hold 
the child’s hands and feet, then place the head against your left 
side and with the left hand hold the child’s head in a firm posi- 
tion ; now ask the child to open its mouth, then place the thumb 
of the hand, which is holding the child’s head, firmly against 
the cheek, and press the cheek well in between the upper and 480 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
lower jaw. With the index finger of the right hand covered with 
sterile or clean gauze, in the child’s throat, move it about as if 
exploring the larynx and during the gagging which usually fol- 
lows quite an amount of sputum can be collected for examina- 
tion. The technic is quite similar to that for palpating a child’s 
posterior nares for adenoids, differing only in that the method is 
here reversed, the index finger pointing downwards instead of 
upwards. 
Examination of the Sputum. Microscopical and Chemical. 
(1) Microscopical: (a) The tubercle bacillus in the sputum. 
Preparing the sputum for microscopic examination. If the 
sputum is fairly fluid, homogeneous, and easily miscible, then 
shaking well in a closed container may be sufficient. Should it, 
however, be thick or tenacious, then the adding of equal parts 
of distilled water and shaking may suffice. In most of the 
laboratories in the Boston hospitals, the sputum submitted for 
examination is immediately shaken with equal parts of a 2% 
carbolic acid solution till a homogeneous mixture is obtained. 
It is then ready for spreading on the glass slide. This is 
known as the Boston Method. Some laboratory technicians 
select with a platinum loop or sterile applicator a small nodule 
or cheesy mass, place it upon the slide, and, by moderate pres- 
sure, rub it into a uniform pulp and spread it evenly. Others add 
a small amount of formaldehyde and mix it intimately with the 
sputum. If equal parts of either distilled water or carbolic acid 
solution and sputum have been mixed, the number of bacilli ob- 
served in a stained field should be multiplied by two. 
When the sputum is properly prepared then a few loopfuls are 
transferred to a glass slide, evenly spread, allowed to dry without 
heat, and passed through a bunsen or alcohol flame three times, 
after which it is ready for staining. The staining material in gen- 
eral use is a carbol-fuchsin solution. This dye stains the organisms 
a deep red, the bacillus holding this color with great tenacity. 
A few drops or sufficient to cover the sputum are placed upon 
such a prepared slide and, with a pair of forceps, the slide is held 
over the flame till the stain steams slightly. This is repeated 
several times, adding a little more stain. It is then washed in 
tap water and destained or decolorized. Tubercle bacilli do not 
stain readily but if once stained they do not readily destain. For 
destaining, usually a 25% solution of either nitric or sulphuric THE SPUTUM IN TUBERCULOSIS 
481 
acid is used. I much prefer destaining with Ebner’s fluid, a solu- 
tion of hydrochloric acid and salt in water and alcohol. Pour the 
fluid, drop by drop, upon the stained slide, held slightly slanting, 
until it flows away colorless, wash again in tap water, counter 
stain with methylene blue, wash, dry, and examine with a 1/12 
oil immersion lens. Many other stains may be used. A Gram 
stain is also serviceable. A staining method reported to give a 
larger percentage of positive results, at least 25% more, affording 
a slide which is more pleasing and more restful to the eye is the 
following. 
An Improved Staining Technic. A small amount of muco- 
purulent sputum is transferred to a glass slide and a drop of 5% 
solution of caustic soda added, and thoroughly mixed, using heat 
till a gelatinous mass is secured. This is now evenly spread, then 
placed into a drying oven, and when thoroughly dried, it is im- 
mersed in carbol-fuchsin solution warmed at 98.6° F. for 15 min- 
utes, washed with equal parts of Esbach’s fluid and water, de- 
colorized with 25% nitric acid and, when faintly pink, washed in 
water, then in 60% alcohol, and again in water. Counterstain 
with malachite green, 1 to 20 (1 part saturated alcoholic solution 
and 19 parts distilled water), for 30 seconds, rinse, dry, and 
examine. 
If in given sputum samples collected at various intervals from 
a suspected person, the tubercle bacillus, even after frequent 
examination, cannot be demonstrated, recourse should be had to 
some of the newer methods, which aim at a concentration of the 
sputum, assuming that the bacilli are but few in number. The 
Uhlenhuth or Antiformin method, the Ligroin method, accord- 
ing to Lange and Nitsche, and the Ellermann and Erlanderson 
method will all be found most dependable. These methods for 
the preparing of sputum are also advisable in those so-called 
closed cases in which we cannot demonstrate the tubercle bacillus 
after oft repeated examinations. In these cases the concentration 
of the sputum collected during the entire 24 hours will show 
very frequently that, after all, they were not closed cases, but 
that the bacilli were so few that they entirely escaped detection. 
Much’s Granular Stain. The granules left after the tubercle 
bacillus has undergone retrogressive changes are not stainable 
with the ordinary carbol-fuchsin solution and to detect the pres- 482 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
ence of these granules (ami they are still virulent) in sputum or 
tuberculous material Much has devised a modified Gram stain, 
which is now known as the Much’s granular stain. A slide is 
prepared in the ordinary way, then covered with Lugol’s solu- 
tion, heated over a flame until it begins to steam, and allowed to 
cool; this is repeated two or three times. It is then washed in 
tap water and dried between filter paper. Next, the specimen is 
similarly treated with gentian-violet solution and, after washing, 
is decolorized with 25% sulphuric acid solution, then alcohol or, 
preferably, at once with Ebner’s fluid, it is then rinsed in dis- 
tilled water, again dried between filter paper, immersed for 
about ten minutes in equal parts of acetone and alcohol, counter 
stained with methylene blue (1% solution), washed, dried, and 
examined. 
There is neither a diagnostic nor a prognostic value in the 
number of bacilli demonstrable in a given sample of sputum. 
The number of bacilli found on a simple slide is wholly depend- 
ent upon chance. There may be very many bacilli in a given 
field and, then again, there may be very few in the next; hence, 
any quantitative scale devised or suggested is valueless as to the 
condition of the disorder or as to the prognosis. The scrutinizing 
of ten fields on a given slide, as first suggested by Ritter, count- 
ing the number in each, dividing by ten, and estimating the aver- 
age number of bacilli in a single field in that manner is as de- 
pendable as any. Many laboratory diagnosticians make use of 
the Gaffky Scale for indicating the number of bacilli present 
and, from these findings, estimate the relative gravity of the pul- 
monary disease. All such scales are only arbitrary, expressing 
no true or definite condition as to amount of lung involved. The 
Gaffky Scale is as follows: 
No. I—If, over a complete smear, only from 1 to 4 T. B. are found. 
No. II—If, after examining many fields, a single bacillus is found. 
No. Ill—One bacillus in every field (average). 
No. IV—Two or three bacilli in every field (average). 
No. V—Four to six bacilli in every field (average). 
No. VI—Seven to twelve bacilli in every field (average). 
No. VII—Many bacilli in every field. 
No. VIII—Numerous bacilli. 
No. IX—Very numerous. 
No. X—Enormous numbers in every field. THE SPUTUM IN TUBERCULOSIS 
483 
Solutions used for staining and destaining tubercle bacilli: 
Ebner’s Fluid: 
Acid Hydrochloric, C. P 
Sodium Chloride, C. P., each 2.5 
Distilled water 100 cc. 
Alcohol 500 cc. 
Gentian—Violet Stain: 
Gentian—Violet 1 gram. 
Phenol, pure 5 grams. 
Alcohol 10 cc. 
Water, sufficient to make 100 cc. 
Esbach’s Fluid: 
Picric Acid 1 gram. 
Citric Acid 2 grams. 
Distilled water, sufficient to make 100 cc. 
Ziehl-Neelsen—Carbol-Fuchsin Stain: 
Fuchsin 1 gram. 
Carbolic Acid, pure 5 grams. 
Alcohol 10 cc. 
Distilled water, sufficient to make 100 cc. 
Lugol’s Solution: 
Iodine, pure 5 grams. 
Iodide of Potassium 10 grams. 
Water sufficient to make 100 cc. 
Methylene Blue—A 1% Aqueous Solution. 
(b) The Small Lymphocytes in Tuberculous Sputum. (82) 
Since the discovery of the tubercle bacillus, the examination of 
the sputum of the suspected tuberculous individual has rested 
mainly in a demonstration of either the presence or absence of 
these micro-organisms, and often the diagnosis has been based 
entirely on these findings, particularly in cases of doubtful physi- 
cal signs. It is now well known that a sputum negative as to 
Koch’s bacilli does not exclude pulmonary tuberculosis, but with 
the presence of albumin by chemical test, even in the absence of 
the tubercle bacillus, we may arrive at fairly definite conclusions. 
An anatomical element (other than the tubercle bacillus) is al- 
ways present in samples of sputum obtained from tuberculous 
individuals; this is a preponderance of small lymphocytes. Such 
sputum is then always found to be albuminous. 
Sputum lymphocytosis is evidence of a chronic pulmonary dis- 
order for in the acute pulmonary disturbances, the polymorpho- 
nuclear type greatly predominates. As early as' 1907,' Wolff- 
Eisner directed our attention to an increase of these' cellular 
bodies in the sputum of pulmonary tuberculosis. He states that 484 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
this noticeable increase in the small lymphocytes can be ob- 
served in every early case of pulmonary tuberculosis and that 
this total increase may number anywhere from 30 to 90%; that 
these small lymphocytes are always present, often long before 
the tubercle bacillus can be demonstrated, and that a sputum 
lymphocytosis is generally a forerunner of a tuberculous process. 
(2) Chemical Examination of the Sputum. (78) The Albumin 
Test. The Albumin Content in the Sputum of the Tuberculous. 
This is equally as important as the microscopical. If a micro- 
scopical examination determines the presence of the tubercle 
bacillus in the sputum then, in all probability, it is no longer a 
beginning case, the stage of incipiency has long passed, and the 
diagnosis is positively made. If, however, the signs and the 
clinical picture point to a suspicious pulmonary tuberculous dis- 
ease and if microscopic examination does not prove the presence 
of the tubercle bacillus, then a chemical examination should be 
made to prove the presence or absence of albumin. A positive 
albumin content of the sputum, which is negative for bacilli, will 
usually give a positive intradermal tuberculin test. 
The presence of albumin in the tuberculous sputum was first 
demonstrated by Rogers and Levy-Valenci in 1910. They re- 
ported on the sputum examination of 1200 cases of pulmonary 
disease representing the three stages, and only 17 gave a nega- 
tive albumin reaction. They concluded from these observations 
that the sputum of the tuberculous generally is albuminous and 
that the absence of albumin always permits the elimination of 
tuberculous disease, but that the presence of albumin does not 
always allow a positive assumption that a suspected individual 
is actively tuberculous, because albumin is found in sputa of 
persons suffering from other lung affections. It is significant, 
however, that for a non-tuberculous person a negative albumin 
content is always a positive finding. 
About the same time, similar observations were made by 
Lessieur who reported on 190 cases of pulmonary tuberculosis, 
in all of which he found an albumin positive sputum. He states 
that sputa containing the bacillus of Koch by direct microscopic 
examination will invariably give a positive albumin reaction; 
if, however, the sputa give a negative albumin test that 
microscopically or by any other method the tubercle bacillus can 
not be demonstrated. He further states that the albumin test is 
usually negative in all those affections which do not invade the THE SPUTUM IN TUBERCULOSIS 
485 
pulmonary parenchyma, but is always constant in the pneu- 
monias, in pulmonary tuberculosis, and is often positive in cardio- 
renal disease. According' to the observations of Rodriguez Alves, 
a positive albumin reaction is demonstrable in every phase of 
pulmonary tuberculous disease from the very incipient to the far 
advanced. 
The sputa, collected from 108 clinical patients both suspected and 
ambulatory tuberculous, at the Rush Medical College Dispensary, were 
examined chemically for the presence or absence of albumin. The 
results confirmed the findings of the earlier investigators. A chemical 
examination of the sputum of both the tuberculous and the suspected 
deserves of wider application. It is undoubtedly of great value in those 
very early cases when the clinical picture is not positive, where a positive 
sputum test may point to a positive tuberculous involvement and where 
the absence of an albumin reaction means negative as to tuberculosis. 
The Great Importance of Properly Collecting the Sputum for 
Chemical Examination. The sputum should be collected, as 
stated above, early in the morning on arising. The patient should 
be asked to rinse the mouth with a few mouthfuls of warm water 
so as to free the mouth and throat from all adhering secretions. 
He should then cough up deep from the lungs and put the ex- 
pectorated material into a clean, sterile, wide-mouthed bottle and 
close it securely with a well fitting pork. He must be specifically 
instructed not to collect the secretions from the mouth or throat, 
not the ordinary saliva, but the material which he coughs up and 
which comes from the lungs and bronchial tubes. A sputum 
submitted for testing should be examined at once or, at least, 
within six or eight hours, that is, before fermentative changes 
have taken place. In cold weather, a sputum one day old may 
still be suitable. No chemical antiseptic or preservative should 
be added to the so collected sputum. 
Directions for Making the Albumin Test. As the technic is so 
simple, the results so satisfactory and the necessary apparatus so 
few, a chemical examination of the sputum should become the 
routine method in every case of either suspected or early pul- 
monary tuberculosis. 
Put 5 cc of sputum into a glass cylinder of about 25 cc capacity 
(glass cylinder must be supplied with a well fitting ground glass 
stopper), add 5 cc of distilled water and about 10 drops of glacial 
acetic acid, replace the stopper, shake well, and set aside. Shake 
occasionally during the next 20 to 30 minutes, then proceed to 
filter. If the sputum is suitable for filtration it will have sep- 486 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
arated into three distinct layers, reminding one very much of an 
expressed stomach content ready for testing. Should the middle 
or watery portion of the sputum solution still be a little opaque, 
showing the presence of some remaining unprecipitated mucin, 
add a few drops more of the glacial acetic acid, again shake well, 
and set aside as before. The fluid portion now appearing clear, 
proceed to filter it through a plain, wetted filter, and test the clear 
filtrate for albumin in the usual way by either Heller’s test or the 
heat test, either of which is very satisfactory; at my hands, 
however, the ferrocyanide test has proven most reliable and 
accurate. If, to an acidified albuminous solution of sputum in a 
test tube, a drop of 10 per cent ferrocyanide of potassium solution 
is added, an approximate idea of the amount of albumin can at 
once be gathered by observing the drop of ferrocyanide solution 
carrying down the precipitated albumin, and one can also notice 
the difference between a massive albumin content and one in 
which only a small amount of albumin is present by the manner 
in which the precipitated albumin falls to the bottom of the tube. 
From personal observations, I have arrived at the following 
conclusions: 
1. If the chemical examination of the sputum is albumin posi- 
tive but tubercle bacilli negative, with physical findings obscure 
and indistinct, the intradermal injection of tuberculin will often 
change both to positive. 
2. A positive albumin reaction and a positive tuberculin test 
are of far more importance diagnostically than the negative 
clinical examination; also, the negative value of the albumin and 
the tuberculin tests is of far greater, of more positive value than 
the negative clinical examination, because a negative clinical 
diagnosis may still be doubtful, may not be positively negative. 
3. A single positive sputum finding can not be considered 
positively and diagnostically tuberculous, but a single negative 
albumin reaction can assuredly be considered as non-tuberculous. 
4. A negative sputum for albumin is also generally micro- 
scopically negative for the tubercle bacilli; usually in the open 
or infectious cases both albumin and bacilli will be found in the 
sputum, while in the closed or non-infectious cases albumin 
minus the bacilli will be present. 
5. The positive albumin reaction is a sure indication of an 
inflammatory invasion of the pulmonary parenchyma which may 
be tuberculous, pneumonic, or congestive, and the reaction is THE SPUTUM IN TUBERCULOSIS 
487 
always negative when the inflammatory process has not affected 
the substance of the lung, as in acute and chronic bronchitis and 
asthma; hence, the reaction is of most importance in those cases 
in which the pulmonary infection is not yet manifest and the 
differential diagnosis lies between tuberculosis and simple bron- 
chial catarrh. 
6. Albumin in the sputum is often the forerunner of the 
tubercle bacillus, and albumin may be found in the sputum many 
months before the bacilli make their presence known; hence, a 
positive sputum content, though bacilli negative, with but 
meager or very slight physical findings, favors a possible in- 
cipient or preincipient tuberculous diagnosis. 
7. Like all clinical signs, it must be considered with all the 
other signs, both subjective and objective, to arrive at positive 
conclusions. 
(3) Combined Microscopical and Chemical Sputum Examina- 
tion. 
In suspected or beginning pulmonary tuberculosis, the pres- 
ence of a lymphocytic picture of the sputum under the micro- 
scope should stimulate a persistent search for the tubercle bacillus, 
and although they may be so few that they may escape detection 
entirely, even after oft repeated examinations, such lymphocytic 
sputum, if carefully observed at frequent intervals over long 
periods of time, will demonstrate sooner or later the presence of 
the tubercle bacillus. If we combine with these microscopic ex- 
aminations a frequent chemical sputum test, we may arrive at a 
positive conclusion and clinch our diagnosis far in advance of 
being able show the presence of the tubercle bacillus. 
“One hundred and ninety-nine samples of sputa collected at the Rush 
Medical College Dispensary were submitted to examination. First a 
careful microscopic search for the tubercle bacillus, then a study of the 
presenting microscopic sputum picture as to the preponderance of the 
small corpuscular element, and, lastly, a chemical examination for the 
presence or absence of albumin was made. The result of these observa- 
tions may be briefly tabulated as follows. In fifty-three specimens 
tubercle bacilli were present—these samples were undoubtedly from 
individuals suffering from pulmonary tuberculosis; forty gave a distinct 
lymphocytosis and positive albumin content in variable amounts. Thirty- 
four were albumin positive and negative for both tubercle bacilli and 
lymphocytes. Seventeen were bacilli negative but showed a positive 
lymphocytosis of more than 50%. Again, seventeen were free from 
bacilli, lymphocytes, or albumin—these were samples from positively 
non-tuberculous persons. From the remaining thirty-eight sputa samples, 488 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
we have the following reports. The sputum was either too bloody for a 
reliable albumin test or it was distinctly leucocytic, or the lymphocytic 
picture was not sufficiently clear to be classed as positive, etc.” 
The parallelism between the lymphocytic sputum pictures on 
the one hand, and the positive albumin content of the expectora- 
tions on the other, in the absence of tubercle bacilli, was evident 
in so many of the above conducted chemical and microscopical 
examinations that on these findings alone a fairly positive diag- 
nosis of pulmonary tuberculosis could be made, and, from the 
observation and study on these 199 samples of sputa secured 
from both tuberculous and non-tuberculous subjects, we are 
justified in permitting the following conclusions: 
(1) A sputum lymphocytosis showing under the microscope 
50% or more of small lymphocytes with a moderate amount 
of albumin by chemical test speaks very strongly for the presence 
of pulmonary tuberculosis. 
(2) In beginning cases of pulmonary tuberculosis, even before 
positive physical signs are present, a sputum lymphocytosis can 
be demonstrated and with this an albumin content in varying 
amounts. The tubercle bacilli may be entirely absent or only 
occasionally a single bacillus found. 
(3) The presence of lymphocytes in preponderant amount, with 
a positive albumin test, in a sputum sample is simply the fore- 
runner or near the beginning of positive findings, and tubercle 
bacilli, if not already present in the expectorations, will soon be 
found. 
(4) In sputum with a positive albumin reaction and giving a 
lymphocytic picture in the absence of the tubercle bacillus is con- 
firmatory evidence that the sputum is from a person suffering 
from pulmonary tuberculosis. 
A careful microscopic study of every sample of sputum under 
examination should first be made for either the presence or 
absence of the tubercle bacillus; if this should be negative, and 
a preponderance of the small lymphocytes and a positive albumin 
reaction be found, we are justified in assuming that the source of 
this expectoration is from a positively tuberculous individual. CHAPTER 37 
THE BLOOD IN TUBERCULOSIS 
Hematology 
General Consideration. Examination of the blood of a person 
with uncomplicated pulmonary tuberculosis reveals surprisingly 
little significant information. When secondary infection sets in 
a definite change becomes evident. (1) (45). 
The Hemoglobin. In pulmonary tuberculosis, as a rule, the 
hemoglobin is normal or slightly reduced, even in the presence of 
pallor or marked cachexia; there are, however, individuals who 
show a marked reduction in hemoglobin, but these are excep- 
tions. A hemoglobin below 75 is very uncommon, even during 
the active stage of the disease. We say that as a general rule 
the hemoglobin index in tuberculosis is good. This, however, 
does not always apply to the disease in children; where very 
frequently the hemoglobin is quite perceptibly reduced. In bone 
and joint tuberculosis in children, the hemoglobin is often con- 
siderably reduced, but usually not in children suffering from pul- 
monary disease. 
The Erythrocytes. It is a significant fact that even in case of 
active tuberculous disease the red corpuscles are practically nor- 
mal in number with a good color index. An initial rise in ery- 
throcytes is occasionally seen in tuberculous patients after the 
first few hours of residence in a high altitude. This increase, 
following a residence in such altitudes is only a natural com- 
pensatory phenomenon—it is part of the process of maintaining 
the normal oxidation at such heights. In cavity formation with 
an accompanying fever, the red blood corpuscles are reduced, but 
where there is no fever, they are usually normal or perhaps 
slightly increased. 
The Leucocytes. The white cell count varies but little from 
the normal, either in a count made at sea-level or at a high alti- 
tude. Usually the lymphocytes are somewhat increased, the 
count averaging, perhaps, somewhat higher at the high altitudes 
than at the lower levels; these appear to be increased in number 
489 490 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
in the very early and in the favorable cases. The leucocyte count 
at sea-level is given by some as 4,000 to 5,000. This is regarded 
by many very competent observers as being too low and that 
6,000 to 7,000 is nearer correct. The leucocytes usually remain 
normal in number and a leucocytosis is very exceptional. If, 
during a period of observation in a tuberculous individual in 
whom the leucocyte count has always been within normal limits, 
a sudden increase should be observed, it would suggest a be- 
ginning cavity formation. This results from the organisms of 
the secondary infection. So long as the leucocyte count is nor- 
mal, cavity formation can be excluded, hence, a distinct leu- 
cocytosis in the course of active pulmonary tuberculous disease 
indicates the probability of cavity formation. It follows from 
this that a high leucocyte count is generally found in those cases 
with a bad prognosis.1 
The Blood as a Whole in Pulmonary Tuberculosis. In com- 
paratively few individuals suffering from pulmonary tuberculosis 
do we find both the red corpuscles and the hemoglobin dimin- 
ished. The blood of the tuberculous person, however, as stated 
above, may show many changes if the products of mixed infec- 
tion or if complications occur with the disease. The presence of 
organisms of secondary infection, septic conditions, prolonged 
diarrhoea, etc., all may have a more or less pernicious influence 
on the circulating blood. So long as the pulmonary disease re- 
mains purely tuberculous, very little change in either the number 
or the quality of the erythrocytes or the leucocytes is observed; 
the change only becomes apparent when secondary infection or 
complications occur. 
According to Grawitz (89) the blood picture in the three stages 
of the disease,varies greatly; if the diseased process in the lungs 
progresses, if there is much or little fever, or if cavities are 
present or absent. He notes the following changes. In the first 
stage of the disease, with infiltration and no signs of cavities, the 
erythrocytes are slightly decreased, the hemoglobin, about nor- 
mal or perhaps slightly lessened, and the leucocytes are not 
changed. In the second stage, without fever, no complications 
and perhaps slight or beginning cavity formation, the erythro- 
cytes are not changed, there is no change in the hemoglobin, but 
1 (Tt should be noted in this connection that the injection of tuberculin is usually 
followed by a transitory increase of the leucocytes this again changes in a few days, 
when the mononuclears again begin to increase slowly.) THE BLOOD IN TUBERCULOSIS 
491 
the leucocytes are perceptibly increased. In the third stage, with 
hectic fever, the erythrocytes are greatly decreased, the hemo- 
globin, very much lessened or decreased, and the leucocytes, 
greatly increased. In female patients, in the first stage of the 
disease, there is frequently a decrease in the hemoglobin even in 
the presence of a normal leucocyte “count.” In children, the 
clinical picture frequently seen during the second stage of the 
disease is that of oligemia. Such children appear pale, the skin 
is dry, the parts are much retracted, there seems to be a lessening 
of the whole blood quantity. In the third or cachectic stage, there 
is an increase in the leucocytes during the whole period of fever, 
due to the presence of pyogenic organisms. Some observers note 
that an improvement in the tuberculous condition is generally 
associated with an increase of the lymphocytes at the expense 
of the polymorphonuclears. If the patient grows worse then the 
polynuclears increase and the lymphocytes decrease. 
In beginning tuberculous disease there is a gradual increase of 
the lymphocytes, and, as the disease progresses and assumes the 
form of mixed infection, the lymphocytes begin to decrease; with 
arrest of the disease there is again an increase of the lympho- 
cytes. The polymorphonuclear leucocytes increase as the disease 
progresses, especially if toxic symptoms of mixed infection are 
manifest. Eosinophiles are increased if the disorder shows a 
healing tendency, decreased if the disease progresses. This pic- 
ture keeps pace with the defensive powers of the organism. 
Arneth’s Blood Picture of the Polymorphonuclear Leucocytes 
in Tuberculosis. 
According to Arneth there is a characteristic change in the 
blood of the active tuberculous which consists in an increase 
of the polymorphonuclear neutrophiles. The percentage of 
mononuclears (5%) to polynuclears (95%) in normal blood is 
about as 1 is to 20. In the blood of the tuberculous there is 
usually an increase in the mononuclears with a corresponding 
decrease of the polynuclears. This is dependent upon the as- 
sumption that the polynuclears are the chief elements in the war- 
fare against the invaders and their toxins, that in this warfare 
many are destroyed; which liberate the contained antibodies, 
which now stimulate the production and formation of the mono- 
nuclears, the more youthful cells. (It should be mentioned that 
this theory is by no means generally accepted.) The neutro- 
philes, on account of their great preponderance, play a,n impor- 492 
CLINICAL TUBERCULOSIS 
tant role. Arneth’s theory is that the cells with the greater num, 
ber of nuclei or of nuclear divisions play the leading part in com- 
bating infection and disease, and that the cells with the fewest 
number of nuclei are the immature or not yet fully developed 
cells, and that they take only a proportional part in the combat. 
In health, there is a constant and definite proportion of the 
various cells to one another and in their number of nuclei; this, 
in disease, is greatly disturbed, the younger or more youthful 
cells predominating, and when such a change is observed in the 
blood picture, it indicates that the blood forming mechanism, 
the hematopoietic system, is greatly disturbed and can not meet 
the demands of the fight. It is thought from this that the poly- 
nuclears are the chief resisting cells of the body, being the first 
to show their activity in resisting the effect of infectious toxins, 
that the mononuclear are simply the reserve forces. 
If a large number of blood examinations are made, selecting 
the blood from healthy individuals, a picture distinct and definite 
will be produced which is quite characteristic. One will readily 
observe that the nuclei in the polynuclear cells vary greatly as to 
the number of nuclear divisions, that the leucocytes containing 
three nuclei are most numerous, those with two nuclei are also 
fairly numerous, but less so than those with three, those with 
four nuclei less than those with two, that a fair proportion have 
a single nucleus, and but few have five. The average number, 
from a great many series of examinations, is as follows, per 
hundred cells: 
Number of nuclei 1, 2, 3, 4, 5. 
Number of cells 5, 35, 41, 17, 2. 
In health 
From this count, Arneth suggested as an index the taking of 
the sum total of one and two dividing it by 3, 4 and 5, this gives 
40/60 or 2/z. In the blood from tuberculous individuals, a con- 
siderable change in the polymorphonuclears from that of the 
healthy can be observed; the number of cells with a single 
nucleus increase considerably, those with two nuclei also in- 
crease, whereas those with three, four, or five perceptibly de- 
crease, according to the following scheme: 
Number of nuclei 1, 2, 3, 4, 5. 
Number of cells 16, 57, 26, 1, 0, 
with an index of 73/27 or approximately 7/3 
In tuberculosis THE BLOOD IN TUBERCULOSIS 
493 
For these various indices, Arneth suggested the following 
arbitrary values: 
Normal blood cells with one and two nuclei = 40 to 55. 
Tending to bad “ “ “ “ “ “ =55 to 70. 
Bad " “ “ “ “ “ =70 to 85. 
Very bad “ “ “ “ “ “ =85 and over. 
We note here in the blood of the tuberculous a shifting of the 
nuclear cells from right to left,2 that is, an increase of the mono- 
nuclears as well as the binuclears at the expense of the other 
polynuclear cells. This neutrophilic blood picture becomes of 
great prognostic value. If in the course of frequent blood exam- 
inations, the picture should show a gradual reversion from left to 
right, back to the normal, to the original type, fewer mononu- 
clears and more polynuclears, then the prognosis would be much 
better, and inversely, with an increase of the mononuclears, the 
prognosis becomes proportionally grave, the fight against the 
disease being lost; hence, a rising Arneth index is regarded as 
indicative of a bad prognosis and a falling one as good and 
favorable. 
The Arneth scale is discussed here because of the massive 
literature that has been written on the subject. It should be 
borne in mind that a large number of misconceptions have arisen 
from it and numerous conclusions have been read into it, many 
of which are quite foreign to the original intention of Arneth. 
The Arneth scale is primarily a blood picture of the patho- 
genesis of general infection. He observes that when infection 
becomes ascendant there is an increase in the number of young 
forms of the neutrophiles containing but one granule, and a 
diminution of the older forms of the four and five lobed nuclear 
leucocytes. 
The Tubercle Bacillus in the Blood Stream. (186) 
There is no question in the study of the tubercle bacillus in 
which we find a greater difference of opinion than that concern- 
ing either the presence or absence of the bacillus in the blood 
stream. There is no doubt that in agonal or terminal cases the 
2Arneth calls this a shifting of the blood picture to the left. Today we correlate this 
observation with injury to the hematopoietic system. It is part of the pathological altera- 
tion caused by the infection. Experimentally a similar blood picture can be produced by 
the administration of radium, X-ray, benzene and mustard gas, all of which have been 
shown to be leucotoxic agents. Today the leucocytes and lymphocytes of the blood are 
not regarded as important factors in resistance to tuberculosis although they may present 
evidence of the disease. Mallory and his pupils, also Klotz and his pupils have advanced 
the conception that the wandering endothelial phagocyte, is the significant cellular element 
in resistance to tuberculosis and this view is rapidly gaining headway. 494 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
tubercle bacillus is frequently present in the blood current and 
can readily be demonstrated, but there exists much doubt if in 
beginning cases, or as some observers endeavor to show in the 
non-tuberculous, the bacillus is also present. 
The bacillus was first isolated from the blood stream by 
Weichselbaum from three cases of miliary tuberculosis at au- 
topsy, and by Meissel and others in acute miliary tuberculosis 
during life, but they were not able to demonstrate the bacillus in 
the blood from patients suffering from chronic tuberculosis. 
Later, other observers were able to show rod shaped organisms 
in the blood in the chronic form of the disease, Schnitter in 32%, 
Lippmann in 44%. In 1913, Brown offered a report at the meet- 
ing of the National Tuberculosis Association from observations 
made at the Trudeau Sanatorium. His observations were on 94 
cases; bacilli were found in the blood in 4% of the incipient 
cases, in 19% of the moderately advanced and in 64% of the far 
advanced. 
Kurashige of the Academy of Medicine, Osaka, Japan, exam- 
ined the blood of his associates at the clinic, all apparently in 
perfect health. In 20 out of a total of 34 (59%) he asserts that 
he was able to demonstrate a bacillus in the blood. More sur- 
prising to him was the fact that some time later, in about 8 
months, three developed a pleuritis, two had an initial hemor- 
rhage, and in four others, animal experimentations gave tuber- 
culous infection. From this, Kurashige concluded that very fre- 
quently in cases of pulmonary tuberculosis, the tubercle bacillus 
can be demonstrated in the blood stream, without resultant 
miliary disease. In a second report, he reaffirms his previous ob- 
servation, emphasizing that the tubercle bacillus in the blood of 
the tuberculous person may be a constant phenomenon, and in a 
third communication, he states that the great source of tubercle 
bacilli in mother’s milk is from the blood in which they always 
circulate. 
Sturm states that in 40 to 50% of all tuberculous persons even 
in the early stage, the tubercle bacillus can be demonstrated but 
that their presence bears no relation to the severity of the disease; 
that 50% more are stainable by the Much modified Gram stain 
than by the Ziehl-Neelsen. Rumph (186) of Ebersteinburg, 
Baden Sanatorium, found four positive cases out of 18 examined 
(22.2%) and raised the questions whether these rods, found in 
the blood are morphologically and tinctorially changed, whether THE BLOOD IN TUBERCULOSIS 
495 
the bacilli found in the blood are dead, weakened, dissociated, de- 
stroyed or devoid of a staining capsule, or whether the bacilli 
stain as bright and perfect when separated from the blood as they 
do in sputa. To answer these questions, his associate, Zeissler, 
examined the blood of 25 female patients who were in the in- 
cipient stage of the disease and found these so-called rods or 
tubercle bacilli in every instance namely, in 100%. He then 
examined the blood from‘seven supposedly healthy subjects and 
here also he found these same rods, again 100%. He next in- 
jected 35 animals with blood secured from a like number of 
tuberculous individuals in whose blood these same particular 
rods were found. Only three pigs became positively tuberculous, 
(8.5%), the others remained negative. The infection in one pig 
was from a case with a healed tuberculous lesion, the second pig, 
from a case of closed tuberculosis first stage, and the third, from 
a third stage case. All animals were killed thirty-one weeks after 
the injection. 
Krause, reporting his findings on 100 patients in the first, 
second and third stage of the disease, states: Out of 55 in the 
first stage of the disease, the sputum was positive in only 10, the 
blood, negative in all; in fifteen second stage cases, with thirteen 
sputum positive and two negatives, the bacillus could be shown 
in the blood of five, all others negative; in thirty patients, far 
advanced, the sputum was positive in all, and the bacillus was 
found in the blood in 18 cases. 
According to Liebermeister, the negative results obtained by 
animal experimentation for the purpose of detecting the presence 
of the tubercle bacillus in the blood depends upon various causes. 
The bacilli in the circulating fluid are comparatively few, and 
the greater part of the morphologically demonstrable bacilli are 
either weakened, damaged, or probably dead, besides the blood 
serum contains immunizing substances in relative stronger con- 
centrations, the less diseased the condition of the individual is. 
In this manner, the animal is injected with a fluid which contains 
comparatively little virulent material suspended in a medium of 
great immunizing power. When injecting three or more guinea 
pigs with blood obtained from one and the same patient, at the 
same time, in equal amounts, and under precisely similar condi- 
tions, he observed that occasionally only one or, at the most, two 
pigs became tuberculously infected. This goes to prove that 
positive results point undoubtedly to live and virulent tubercle 496 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
bacilli in the blood, but it does not show that a negative result 
proves the absence of bacilli. The rapidity of the blood current 
may inhibit the growth of or even kill the bacilli, or the injected 
bacilli may not be capable of propagation, or, may perhaps, be 
lifeless or dead, or the immunizing substances in the blood may 
have inhibited their growth. Liebermeister succeeded in 40% of 
his animal experiments, in producing inoculable tuberculosis 
from blood of active tuberculous persons. 
Technic for Preparing Blood for Microscopic Examination. 
(A) The apparatus. 
The necessary apparatus and solutions are the following: 
(1) Centrifuging tube of 25 cc. This is known as the Zeissler 
Fig. 60—Zeissler Tube. Used in demonstrating tubercle bacilli in the blood stream. 
tube. It is graduated and supplied with a well fitting glass 
stopper (see cut above). 
(2) A sterile needle or syringe for securing the blood. 
(3) A laking solution. This consists of a 0.2% of neutral 
potassium oxalate solution. Dissolve 2 grams of neutral potas- 
sium oxalate in 1,000 cc pure, double distilled water, set aside in 
a closed container for 24 hours, filter rapidly through a thin, 
white, pleated, filter, after which it is ready for use. 
(4) Pure concentrated antiformin. 
(5) A quantity of 60% alcohol. 
(6) Necessary pipettes, glass slides, flasks, etc., all scrupulously 
clean and free from dust. 
The greatest care, accuracy, precision and cleanliness is re- 
quired. All the necessary glassware should be washed in soda 
solution, then placed in sulphuric acid, rinsed in pure distilled 
water, then in absolute alcohol, and carefully put away in a dust 
proof compartment. The distilled water used for making the 
neutral potassium oxalate solution should be repeatedly distilled 
and of such purity as is now being used in lumbar puncture. 
(B) The technic. 
Having secured 5 cc of blood, put it at once into a Zeissler 
tube, add 25 cc of the potassium oxalate solution, shake re- 
peatedly for about 15 minutes, and centrifuge, using a high speed, THE BLOOD IN TUBERCULOSIS 
497 
electric machine. After centrifuging fully one-half hour, pour off 
the supernatant fluid, add 10 cc of pure distilled water to the 
sediment in the tube, and shake until a uniform emulsion is ob- 
tained; now add a drop of pure, concentrated antiformin, shake 
well, and set aside for a few minutes, after which add another 
drop and shake as before. This is to clarify the fluid; it usually 
requires but a few drops of the antiformin. After each drop 
added, shake, set aside and note if the solution is clear; this is 
generally found perfectly so in about one-half hour, after which 
the tube is filled with sufficient 60% alcohol and again centri- 
fuged. Now pour off or with a large pipette remove all of the 
fluid portion, and in the sediment at the point of the tube these 
rods will be found. Remove one-half of this sediment with a 
hypodermic syringe and inject it at once into an experimental 
animal. Of the remaining half place equal parts on two glass 
slides, dry, fix, and stain one with the Ziehl-Neelsen the other 
with the Much granular stain. It becomes necessary to add a 
little albumin to fix the material on the slide.—J. R. 
Serological and Immunological Considerations of the Blood. 
Let us compare tuberculosis to some other infectious fevers 
with reference to the presence of the so-called immune bodies. 
Tetanus produces a toxin of extreme potency and two forms have 
been identified. A neurotoxin or tetanospasmin and a tetanoly- 
sin; none such exist in tuberculosis. Diphtheria produces a very 
potent toxin, a very small amount of which is fatal to the guinea 
pig; tuberculosis produces no such toxin. Rabies produces a 
toxin whose potency can easily be increased or diminished by 
certain cultural procedures; tuberculosis produces no such toxin. 
Typhoid fever produces specific antibodies—agglutinins which 
are specific against the cultures of typhoid bacilli in a dilution of 
1 in 2,500; in tuberculosis the agglutinins occasionally reach a 
strength of 1 in 50, but these agglutinins are not always present 
in the blood of tuberculous individuals and frequently they occur 
in normal sera. There is not sufficient evidence on hand to re- 
gard them as being identified with immunity in tuberculosis if 
any immunity exists at all. In pneumonia and epidemic menin- 
gitis there are specific agglutinins against the various types of 
the respective organisms; in tuberculosis thus far no one has 
demonstrated a specific agglutinin against the human tubercle 
bacillus that will not in the same dilution agglutinate the bovine 498 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
bacillus. In certain infectious diseases one attack is generally- 
regarded as conferring a permanent active immunity; in this 
group are typhoid fever, scarlet fever, small pox, measles, syphilis 
and others; this is not so in tuberculosis; all forms of contact 
with the disease render the organism only more susceptible to it. 
In certain other infectious diseases, a passive immunity can be 
conferred by the injection into the host of a suitable vaccine or 
its derivative products; in this group are smallpox, rabies, 
typhoid fever and to a slight extent diphtheria; no such immunity 
can be conferred in tuberculosis. 
There yet remains to be demonstrated a single method of con- 
ferring passive immunity in tuberculosis in human beings, al- 
though every possible method has been tried. Dead cultures of 
all strains and all varieties have been tried as a basis of a pro- 
tractive vaccine; so have living bacilli of both virulent and atten- 
uated cultures, the bacilli and its products have been chemically 
split and divided in every conceivable way. There have been 
made water soluble extracts and alcohol soluble extracts, saline 
extracts and glycerine extracts, the bacilli have been used whole 
and macerated, triturated and inspissated and we are just as far 
today as our forefathers were in the days of Hippocrates so far 
as conferring passive immunity by any form of biological product 
which may be administrated to human beings. We are inclined 
to state quite definitely that there is no way of conferring passive 
immunity in tuberculosis; nor does one attack of the disease pro- 
tect the organism against subsequent attacks; in fact the reverse 
is more likely to hold true. Every form of contact with this dis- 
ease only renders the subject more susceptible to it. 
From an immunological point of view we are inclined to follow 
others who state that there are no demonstrable immune bodies 
in tuberculosis; yet from a general biological point of view we 
are forced to conclude that there must be some form of bio- 
chemical protective mechanism or else we should all be dead of 
the disease. Just what this biochemical protective mechanism is 
we don’t know but we feel that it is not antibody protection as 
we ordinarily understand immune phenomena. It is this bio- 
chemical protective mechanism or portions of it that we demon- 
strate by the indirect means of complement fixation. 
Complement Fixation in Tuberculosis. 
General Considerations. The discovery of the tubercle bacillus 
by Robert Koch in 1882 added a link to the scientific chain of THE BLOOD IN TUBERCULOSIS 
499 
evidence which placed the pathological diagnosis of tuberculosis 
upon a practically infallible foundation. If the tubercle bacillus 
was found in the diseased tissues it made the diagnosis of tuber- 
culosis certain. Unfortunately, in the majority of cases, tuber- 
culosis is an internal disease and only in the advanced or ulcera- 
tive stages does it yield products to the external world suitable 
for diagnosis. The almost general presence of the tubercle 
bacillus in man, as determined by postmortem examination, adds 
a complicating influence to a clear definition of the disease. 
The clinician is principally concerned in the separation of 
tuberculous infection from tuberculous disease. He wants to 
know definitely whether his patient has active or inactive tuber- 
culosis, whether the disease is progressing or not, if it has any 
influence on the individual’s physical ability, and what the prob- 
able outcome will be in the patient, under observation. In short, 
he would like a functional, diagnostic, and prognostic analysis 
of his patient. In view of the fact that the tubercle bacillus is so 
difficultly accessible in the human body, the search for the causa- 
tive organism has been augmented by innumerable attempts to 
ascertain its presence by other means, and to determine whether 
or not it is causing destruction of the body tissues. 
With the advent of serology, all of its methods were tried in 
an attempt to gain this information. The tuberculin test, al- 
though valuable in young children, was soon discarded as a diag- 
nostic or prognostic agent in adults. Likewise, the precipitin 
and agglutination tests in tuberculosis were short lived, while 
the opsonic index method never did gain favor on account of the 
difficulties in technic and interpretation. Of the immunological 
tests, the complement fixation test has been probably the most 
elaborately studied and has given the most encouraging results. 
In order to comprehend the technical details of this test a few 
words on the history of the discovery may be helpful. 
Historical Data in Complement Fixation. The complement fixa- 
tion test is a reaction belonging in the immunological class of 
antibody reactions. The earliest observations on antibodies 
might be stated to be those made by Sir John Hunter, the cele- 
brated English physician, who noted that unheated blood, on 
standing, did not putrefy as readily as heated blood. This ob- 
servation paved the way for numerous others which followed, 
subsequently but rather slowly, but which eventually led to the 500 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
discovery by Richard Pfeiffer in 1894 of the Pfeiffer phenomenon. 
He noted that in a guinea pig which had been injected subcu- 
taneously a number of times with cholera vibrio, and subse- 
quently was given an intraperitoneal injection of cholera vibrio, 
there resulted changes in the intraperitoneally injected organ- 
isms which did not occur in those organisms also injected intra- 
peritoneally in an animal which had had no previous inoculation. 
Those changes consisted in a peculiar granular appearance of the 
cholera vibrio and a final destruction by lysis of their bodies. 
Metschnikoff and Bordet in 1895 demonstrated that this lysis 
could occur in the test tube provided the organisms were mixed 
with the serum from an animal previously given several injec- 
tions of cholera vibrio. Bordet in 1898 elaborated on this work 
and demonstrated that red corpuscles would likewise undergo 
lysis both in animals previously injected with the foreign red 
corpuscles and in vrcro when the serum of these animals was 
mixed with the homologous erythrocytes. He also demonstrated 
that in the typical in vitro red corpuscle lysis or hemolysis three 
constituents were necessary: (1) the specific red blood corpuscles 
which had been injected into the animal for immunizing pur- 
poses; (2) the serum of an animal that had been injected with 
these red corpuscles and thus had become and (3) 
the constituent found in all normal serums previously discovered 
by Buchner and called the alexin of Buchner, or, in our present 
terminology, the complement. Here then, we have the produc- 
tion of a specific lytic substance to an antigen, the red corpuscles 
which can produce an easily visible reaction (hemolysis), and it 
is this reaction which really laid the foundation for the Bordet 
and Gengou phenomenon of complement fixation. 
Bordet and Gengou simultaneously noted in 1900 that red 
blood corpuscles, bacteria, or any antigenic substances could be 
sensitized by placing them in an immune serum (produced by 
injecting these same antigenic substances into animals) which 
had been heated for thirty minutes at 56° C, leaving the sub- 
stance—“sensibilitrice” as they called it—(or amboceptor) un- 
injured, as it is thermostabile, and adding fresh serum containing 
complement (the latter being thermolabile and easily destroyed 
by heating at 56° C. for thirty minutes). The reaction between 
these three substances was a definitely quantitative one and could 
therefore be used for determining the presence of any bacterial 
antibody or red cell antibody complex. THE BLOOD IN TUBERCULOSIS 
501 
Antigens. According to Hektoen an antigen is any substance 
which when injected into an animal body causes the formation 
of specific antibodies. As typical examples of antigens, we have 
most of the pathogenic bacteria, pathogenic protozoa, many al- 
buminous bodies (i. e., venoms, enzymes, etc.), and bland pro- 
teins, (i. e., egg white, edestin, etc.). The action of a specific 
antibody, while specific, is strictly quantitative, depending upon 
the amount of amboceptors. As proof of this there exists the 
typical Neisser-Wechsberg phenomenon of deviation of comple- 
ment which must not be confused with complement fixation. In 
the complement fixation, we have the union of complement with 
one lytic complex (antigen and amboceptor) to avoid its binding 
by another similar complex (antigen and amboceptor), but differ- 
ing in specificity only; while in complement deviation, an excess 
of amboceptors binds the complement and thus avoids the action 
of the complement upon the antigen. Neisser and Wechsberg in 
1901 found that a small amount of immune serum renders normal 
serum more bactericidal, but a greater addition of immune serum 
robs it of most and sometimes of all of its bactericidal power in 
vitro. 
Bearing in mind the elements necessary for the mechanism of 
the complement fixation test, and also the definitely quantitative 
relations essential between the antigen, the immune body or 
antibody (amboceptor) and complement, we can intelligibly dis- 
cuss complement fixation. 
The Wassermann Reaction. 
If, for instance, we wish to diagnose a certain disease by deter- 
mining the presence of its specific antibody as, for instance, that 
caused by the cholera vibrio, we can do this in an indirect man- 
ner by making use of the red blood corpuscle complex which is 
easily visible to the naked eye. Let us, for example, call the 
antigen for cholera vibrio C, the immune body produced in the 
animal which has been injected with this organism Cl and the 
complement CO. If we mix C, the known, Cl, the unknown, and 
CO in quantitative relation, incubating for a certain period of 
time to allow fixation or binding, we get a combination of C, Cl, 
and CO which completely fixes CO and removes from it the 
ability to react with any other lytic complex. If, then, we add to 
this red blood corpuscles, (e. g., human corpuscles) in a definite 
amount which we will call R, and an immune serum produced in 502 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
the rabbit by injecting with human red blood corpuscles, (this 
serum having been heated at 56° C. for thirty minutes to destroy 
the native complement) we have all the essentials for the pro- 
duction of hemolysis except complement. It is easy to see how 
the presence or absence of complement, dependent on its being 
bound in the cholera system that is complete, or not being bound 
in the cholera system which is incomplete, will give us a means 
of determining the presence of the unknown cholera immune 
bodies or antibodies used in diagnosis by complement fixation. 
Now we can substitute in this system any other complex as, for 
instance, syphilitic antigen and the serum from a suspected 
syphilitic patient and, by means of the red blood corpuscle sys- 
tem, always keeping in mind the quantitative relations in this 
system, can determine whether or not we have the serum of a 
syphilitic patient. 
The Wassermann reaction, as we know it today, is one of the 
most practical of all complement fixation tests, but it was not 
the earliest application of complement fixation. Wassermann 
and Briick first applied bacterial extracts as antigens to tubercu- 
losis, but found the test for tuberculosis impractical. These in- 
vestigations occurred at a period when active search was being 
made for the spirocheta pallida, which was discovered by 
Schaudinn and Hoffmann in 1905. It then occurred to Wasser- 
mann that the fixation of complement test could be applied to 
the diagnosis of syphilis. His first results were published in 1906 
together with those of Neisser and Briick. A report was also 
made at that time of experiments in monkeys in which salt solu- 
tion extracts of syphilitic tissues were used as antigens. 
The Complement Fixation Test in Tuberculosis. 
The first application of complement fixation in tuberculosis 
was made by Widal and LeSourd (107) in 1901. They obtained 
fixation of complement in certain cases of tuberculosis, using as 
antigens homogeneous suspensions of tubercle bacilli of the Ar- 
loing-Courmont strain. In 1903, Bordet and Gengou (126) 
demonstrated the presence of an antibody capable of uniting with 
tubercle bacilli and fixing complement in the sera of tuberculous 
animals. Wassermann and Briick, (118) in 1906, demonstrated 
the presence of an antibody to tuberculin as antigen in patients 
treated with tuberculin, and, as a result of this, developed the THE BLOOD IN TUBERCULOSIS 
503 
idea of antituberculin being formed as a result of tuberculin 
treatment. 
About the best study up to 1913 was that made by Elizabeth 
Fraser (156) who compared a large variety of antigens prepared 
from tubercle bacilli and concluded that those prepared from 
living human bacilli were most reliable for tests in human tuber- 
culosis. 
Dudgeon, Meek and Weir, (155) in 1914, also tested a large 
number of antigens and found the bacilli or their products the 
most suitable antigens. McIntosh, Fildes and Radcliffe,(159) 
after testing a large number of antigens, also concluded that the 
bacillary emulsion prepared from live bacilli was best. 
Craig (129) employed as antigen an alcoholic extract of several 
strains of human tubercle bacilli grown on a special egg medium, 
the antigen being an extract of bacilli and medium. Since then, 
alcoholic extracts have innumerable times been proved imprac- 
tical, and a recent paper by Lucke,(149) in 1916, corroborated 
these earlier findings.(108) 
In 1916, Corper (108) described an autolysate antigen which 
was prepared by autolyzing tubercle bacilli in physiologic saline 
for ten days at'incubator temperature. The supernatant, clear, 
yellow autolysate was found to contain antigenic properties equal 
to that of a bacillary emulsion prepared from the same cultures 
and to possess the advantage of having a wider range between its 
antigenic and anticomplementary unit, than the bacillary emul- 
sion. 
In 1917, Corper and Sweany (109) compared the findings with 
the autolysate and Miller’s (151) bacillary antigens, and found 
very little difference between the number of positive results ob- 
tained by means of these two antigens. They concluded that it 
is absolutely impossible to differentiate active from inactive 
tuberculosis by means of this test, and that the main value of the 
test was for differential diagnostic purposes in conjunction with 
the other findings in the case. 
While the foregoing studies were being carried on by other 
investigators, Petroff of Saranac Lake was busy devising new 
antigens in the hope of finding an ideal antigen which would 
prove reliable. Beginning with a culture of bacilli grown upon 
a potato medium which did not finally prove satisfactory, he pre- 
pared four new antigens (143) a potato filtrate prepared from 
the filtered extract of a potato broth culture medium upon which 504 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
tubercle bacilli had been grown, a sodium hydroxide extract of 
tubercle bacilli, a methyl alcohol extract of tubercle bacilli, and 
finally a hot, glycerol “extract.” (120) He maintained that in 
order to get good results a variety of antigens should be used. 
In 1918,(150) Brown and Petroff, using these antigens, found 
a positive complement fixation in 72 per cent of 478 patients on 
whom a diagnosis of tuberculosis was made; 51% of the in- 
cipient cases; 73% of the moderately advanced, and 81% of the 
far advanced. When activity was present, 81% gave positive 
reactions, and when absent, 61%, while 90%, in whom tubercle 
bacilli were found in the sputum, were positive. They concluded 
that patients with a negative reaction could be allowed to exer- 
cise more freely than those with a positive reaction. Besides 
the comparative studies carried out by Fraser, Corper and 
Sweany, Petroff, and others, the work of Miss Lange (158) at 
Johns Hopkins Hospital is worthy of mention. 
During 1918, there appeared a significant contribution by 
Heiman (157) as a result of a study of the complement fixation 
test for tuberculosis on children. He used Petroff’s and Miller’s 
antigens on the serums from 50 children ranging in age from 
six months to twelve years. Sixteen of these were tuberculous, 
six were suspects, and twenty-eight were non-tuberculous. Six 
cases of pulmonary tuberculosis (two with miliary) were nega- 
tive with both antigens; one case of tuberculous peritonitis was 
negative; in six cases of tuberculous meningitis, four were nega- 
tive and two, positive; seven cases of pleural effusion, of which 
one was definitely tuberculous, were all negative. Among the 
twenty-eight cases with no tuberculosis, three gave a strong 
positive reaction, one a slight reaction, and one a suspicious re- 
action. Heiman concludes that the test in children was of no 
value, but believes that a further improvement in technic may 
eventually make it of some value. 
In 1919, there appeared several significant articles on comple- 
ment fixation in tuberculosis. Young and Givler,(93) who used 
three antigens (Corper’s autolysate, Petroff’s methyl alcohol, 
and Wilson’s bacillary suspension (95)) comparatively in a study 
of tuberculous, normal, and syphilitic serums, concluded that the 
three antigens did not differ greatly in the percentage of positive 
findings in known cases of pulmonary tuberculosis, while clin- 
ically normal individuals reacted to the extent of 11% with all 
the antigens. A fairly high percentage of luetic serums also gave THE BLOOD IN TUBERCULOSIS 
505 
positive tuberculosis tests with all three antigens in the absence 
of demonstrable tuberculosis. Paul A. Lewis,(154) who made 
an effort to apply absolute quantitative methods to the study of 
this reaction, found that the serums of certain tuberculous in- 
dividuals gave strong positive reactions, while others entirely 
failed to give a reaction. The serums of certain persons to all 
intents and purposes normal gave strong reactions also. He 
concludes from his work that the numerical relations are such 
as to make it unsafe to apply the complement fixation reaction 
to the diagnosis of tuberculosis except as a matter of the most 
limited confirmatory interest. 
Having thus reviewed the views upon complement fixation in 
tuberculosis of some of the most reliable and most efficient in- 
vestigators in the tuberculosis field and, from their observations 
and conclusions, we can sift out the following important points 
regarding this test in tuberculosis. 
1. In spite of the fact that there is a large variety of tuber- 
culosis antigens, there is very little difference between them in 
so far as their reliability and efficiency is concerned, especially 
with regard to the positive results obtained by their use. The 
essential point of importance is that they must be prepared from 
tubercle bacilli (preferably polyvalent) or suitable products 
thereof. 
2. The percentage of positive tests obtained with the serums 
in cases of tuberculosis increases with the advancement of the 
disease, although very far advanced or moribund cases are likely 
to give a comparatively lower percentage of positives than might 
be expected from their stage of the disease. 
3. Active cases of tuberculosis give a higher percentage of 
positive reactions than inactive cases, but the difference is not 
sufficiently great to be of diagnostic value. 
4. Sputum positive cases of pulmonary tuberculosis give a 
higher percentage of positive reactions than sputum negative 
cases, but here also, there is not sufficient difference to be of 
diagnostic value. 
5. In the presence of syphilis, or in a case with a serum giving 
a positive Wassermann reaction, the tuberculosis complement 
fixation test, if positive, is of very dubious value because a high 
percentage of luetic serums give cross fixation with practically 
all the tuberculosis antigens. 506 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
6. It is advisable to use the complement fixation test for 
tuberculosis with reserve, and, in the terms of Lewis, to apply 
the test in diagnosis as a matter of the most limited confirmatory 
interest. 
7. It is possible, however, that from the standpoint of prog- 
nosis, according to Brown and Petroff, the test is valuable in 
that repeated tests at definitely spaced intervals may help to in- 
dicate the cases that may be allowed to exercise more freely. 
Technic of the Complement Fixation Test for Tuberculosis. 
The technic for performing the complement fixation test for 
tuberculosis consists essentially of the technic employed in per- 
forming the Wassermann test, with the exception that the luetic 
antigen is substituted by one of the common tuberculosis anti- 
gens. 
For the complete details of the preparation of the red corpuscle suspen- 
sions, immune serums, inactivations, etc., the student is referred to the 
texts written on the Wassermann reaction, or to good text books on clin- 
ical and laboratory diagnosis. H. J. C. CHAPTER 38 
THE URINE, MILK, FECES, BILE, PLEURAL EXUDATES, 
SPINAL AND PERITONEAL FLUIDS, ETC., 
IN TUBERCULOSIS. 
Bacilli. (A) In the Urine; (B) In Mother’s Milk; (C) In the 
Feces; (D) In the Bile; (E) In Exudates and Fluids, etc. 
The Urochromogen Test; Lime Salts Elimination; 
Cytodiagnosis; Inoscopy, Etc. 
Examination of the Urine in Tuberculosis. 
(A) Characteristics of Normal or Healthy Urine. (39) 
Urine, the fluid eliminated by the kidneys, received tempo- 
rarily in the bladder reservoir, in health, is voided at practically 
regular intervals. This fluid, consisting chiefly of water, is 
separated by the kidney filters, the glomeruli and the solids and 
coloring matters, consisting of various mineral compounds and 
retrogressive protein bases, are secreted by the epithelium of the 
renal tubules. The latter, the proteins of the urine, represent 
the continuous waste taking place in the economy, a physio- 
logical process; consequently by means of urinary exam- 
inations, we are in a position to estimate the daily output as com- 
pared with the intake, all within normal physiological limits. In 
disease all this undergoes very noticeable changes, serious dis- 
turbances in metabolism effecting the urinary secretions, hence 
a study of the urine in the diseased individual often gives us more 
accurate information than may be obtained by either the ther- 
mometer or the pulse. In health, the daily excretion of urine 
averages 1500 cc, or about 50 ounces, the solid constituents, in- 
organic matter and mineral salts contained, about 70 gramms or 
2Yz ounces. In 1000 parts of urine there are approximately 35 
parts of solid to 965 of water. A 24 hour specimen of urine is 
usually of a straw or light wine color, specific gravity of about 
1.020, usually acid in reaction, and when freshly voided has a 
peculiar, slightly aromatic odor, and is always microscopically 
clear.1 
iTo readily determine the total solids in the urine, multiply the last two figures of the 
specific gravity by 2.33. For instance, the specific gravity of the urine is 1.020, then 
multiply 2.33 x 20 = 46.50. This gives the total solids in 1000 cc, equal to 46.60 grams 
to the litre. 
507 508 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
(B) Characteristics of the Urine in Pulmonary Tuberculosis. 
Here the urinary output is greatly influenced by such condi- 
tions as pyrexia, diarrhoeal disturbances, night sweats, copious 
expectorations, vomiting, hemorrhage, etc., in all of which the 
volume of urine may be greatly decreased; it may, however, even 
be augmented if during such disturbances the intake of fluid is 
greatly increased. In the diarrhoeas, often accompanying active 
pulmonary tuberculous disease, the kidney elimination may be 
lessened by one-half of the usual daily quantity; this is also 
seen if so-called hectic fever is present; again, in those instances 
of active disease when the ingestion of food is almost imme- 
diately followed by vomiting, the urinary flow also becomes 
greatly reduced. This is again observed in the rapidly pro- 
gressing, in terminal cases, and in the miliary form of the disease. 
So long as the appetite is good and the ingestion of food or- 
dinary in amount, requiring the usual intake of water then there 
is no perceptible lessening of the urinary elimination. The de- 
crease only becomes apparent when the disease is running a 
rapid course, when exacerbations and remissions follow in rapid 
succession. It is then1 that we observe a variation in the 
amount, color, and the general appearance as well. Then again, 
as in the normal, a large intake of fluid, as in the exclusive 
milk diet, the volume of urine is greatly increased, the urine ap- 
pearing almost water white. 
In pulmonary tuberculous disease whether accompanied by 
renal disorder or not, the urine often cannot be differentiated in 
amount, color, reaction, specific gravity, etc., from that passed by 
a healthy person, but by both chemical and microscopic tests 
the difference becomes quite evident, and the presence of the 
tubercle bacillus, the albumin, the abnormal lime salts, the 
nature of the coloring matter all become interesting factors in 
the examination of the urine in tuberculosis. 
Tubercle Bacilli in the Various Fluids and Solids of the Body. 
(A) Methods for Demonstrating Tubercle Bacilli in the 
Urine. (94) As early as 1882, Damsch inoculated guinea pigs 
with the urine of suspected tuberculous individuals to establish 
a diagnosis of renal tuberculosis, and in 1883, Babes demon- 
strated tubercle bacilli in the urine of patients suffering from 
genito-urinary tuberculosis. The method then in use was the 
sedimentation, or as it was called, gravitation method and later, 
centrifugalization (187) was the method of selection. From the URINE IN TUBERCULOSIS 
509 
sediment in the urine glass or in the centrifuging tube, smears 
were made, dried, fixed, and stained in the usual way. The 
gravity method is still the one most in general use, and the 
technic as outlined by Walker in 1904 is the one chiefly used. 
From an exhaustive study of renal tuberculosis, he was able to 
demonstrate the bacilli in every one of the 50 cases studied. 
Walker’s (141) Method is as follows: 
(1) The specimen is allowed to settle in a conical urine glass 
for twelve hours. 
(2) The sediment from the conical glass is taken up by means 
of a pipette and two drops placed on clean, sterile glass slides. 
(3) The slides are put on a frame above a Bunsen flame and 
slowly allowed to dry—avoid rapid heating. 
(4) The slides are passed through the flame in the ordinary 
manner so as to fix the specimen. 
(5) They are then placed in a 5% acid (HC1) alcohol solution 
and allowed to remain for five minutes. This dissolves the urin- 
ary salts. 
(6) The slides are then washed in running tap water to re- 
move all traces of acid and alcohol. 
(7) The smears are now stained in the ordinary way" with 
carbol-fuchsin and decolorized with Gabbett’s Methylene blue. 
(8) Wash in tap water, dry, and examine. 
Other methods in use are, the Uhlenhuth, Antiformin, the 
Ellerman and Erlandsen, Pancreatin and Sodium Carbonate di- 
gestion, the Lange and Nitsche, Ligroin, the Kozlow, ether and 
acetone, the Petroff, Acetic and Tannic Acid methods, etc. 
A modified method similar to Walker’s which perhaps may 
promise more definite results is one in general use at The Rocky 
Glen Sanatorium.(191) The following instructions are given: 
Acid Fast Bacilli in the Urine. Urine was collected from 
female patients only. The patients were instructed to urinate into 
three vessels, the first two were discarded as they were intended 
to act as a wash for the meatus and vulva. The third specimen 
was used for the test. The tests were made upon women only as 
there is less apt to be smegma bacilli about the meatus in women 
who are in an institution, than in men. 
(1) The urine is centrifuged for one hour at a rapid speed. 
(2) A small amount of the sediment is placed upon a clean 
glass slide. The slide is permitted to dry slowly over a bunsen 
flame. 510 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
(3) As the sediment dries, a very small amount of egg al- 
bumin is stirred into it. If the specimen contains albumin it will 
not be necessary to add egg albumin. 
(4) When the specimen is perfectly dry, pass through the 
flame ten or twelve times. 
(5) Dip the slide in a 5% acid alcohol (HC1) solution. This 
will dissolve some of the uric acid salts. Wash in tap water. 
(6) Dry slide, and again pass through flame. 
(7) Steam 10 minutes with a carbol-fuchsin solution. 
(8) Wash slide thoroughly with distilled water. 
(9) Decolorize slide for 1 minute in a 1% acid (HC1) alcohol 
solution. 
(10) Wash off thoroughly with water. 
(11) Counter stain with a methylene blue solution containing 
25% sulphuric acid (Gabbet’s stain). (This acts as a counter 
stain and also as a second decolorization to make sure that none 
but true acid fast bacilli hold the carbol-fuchsin stain. Gives 
more decolorization than used for sputum analysis). 
(12) Wash, dry, and examine slide. 
To secure urine from male tuberculous patients and to avoid 
contamination with the smegma bacillus, it is advisable to secure 
the urine by catheterization. 
The acid fast bacilli when present in abundance will almost 
always occur in large groups surrounded by a peculiar capsule 
or halo. Only one or two such large groups may be found on an 
entire slide. If not present in abundance, they may be grouped 
together, and in most cases they are typical, absolutely, of the 
tubercle bacillus. In patients with negative sputum, mostly first 
stage cases with very little active chest findings, the organisms 
may appear somewhat shorter than the bacillus usually found in 
sputum, but when the urinary sediment is injected into guinea 
pigs, pure cultures of typical tubercle bacilli are reproduced. 
Mark’s observations cover 150 cases with 600 urinary examina- 
tions, 45% first stage, 20% second stage and 35% third stage 
cases. 40% of the cases showed acid fast bacilli in the urine at 
some time only, and in 60%, the bacilli were found in every test. 
These laboratory observations are of special interest. He found 
that incipient cases with negative sputum, ones that had few ac- 
tive findings, the most constant common symptom being “tired 
feeling,” showed a larger percentage of acid fast bacilli in the 
urine than any other. Cases with positive sputum in the in- THE URINE, MILK, ETC., IN TUBERCULOSIS 
511 
cipient and moderately advanced classes seldom showed acid fast 
bacilli. His interpretation is that when bacilli are expectorated 
there is less tendency of their getting into the blood current, and 
that in cases in which the condition is active but no connection 
with a bronchus the organisms may gain entrance to the blood, 
being filtered out by the kidneys without any apparent kidney 
disturbance. Other observers have also described the tubercle 
bacillus present in the urine in the absence of positive renal 
disease.(115) 
May not the kidney permeability, which we occasionally observe in 
children and young adults (which in the literature is described as ortho- 
static albuminuria) and which I have considered as a prodromal (78) 
symptom (see Chapter XI, “Symptomatology”), give after all a bacilli 
positive urine in which the bacteria may be demonstrated if we only 
search diligently and persistently? The urine test for albumin can be 
made by any of the well known methods—the Heller test, the Acetic Acid 
and the Ferrocyanide test, etc. This is fully given in the chapter on the 
Sputum in Tuberculosis, and as the tests there given are all applicable 
to urinary examinations, the reader is referred to its pages. 
(B) The Demonstration of Tubercle Bacilli in Mother’s Milk. 
Judging from the nature of pulmonary tuberculous disease it is 
presupposed that tubercle bacilli may be present in the milk of 
the pregnant tuberculous woman. Available and reliable statis- 
tics from the literature regarding the bacteriology of human 
milk, however, are very meagre and even what has been done by 
different observers reveals a lack of concerted conclusions. Ac- 
cording to Holt, tubercle bacilli have been demonstrated by 
Rogers and Gamier in the milk of a woman with advanced pul- 
monary tuberculosis, but that ordinarily they are not present un- 
less the mammary glands are tuberculously diseased, and Marfan, 
referring to this case and a case reported by Demme, states that 
these are the only two authentic cases of children being infected 
from the mother’s milk, but he contends that nevertheless the 
tuberculous mother in the interest of both herself and offspring 
should not nurse her child. Bandelier and Roepke state, “The 
danger of infection from mother’s milk is very small when com- 
pared with the much greater one, the natural, the most intimate 
relationship existing between the mother and child.” 
Wang and Coonley, (131) reported their observations on 28 
tuberculous women after childbirth. These examinations were 
made twice each week securing from each patient from 3 to 5 
cc of milk, testing the same not later than two hours after it 512 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
was withdrawn. From each specimen secured, separate smears 
were at once made, and the balance reduced with a weak antifor- 
min solution. The milk was mixed with equal parts of a 5 to 10% 
antiformin solution, immediately placed into an incubator for one 
hour, then centrifuged at high speed for 10 minutes, the super- 
natant portion removed, the sediment in the tube thoroughly 
mixed with distilled water, and recentrifuged for 10 minutes. 
From this second sediment a few drops were placed on a glass 
slide, egg albumin added, dried, fixed, and stained in the usual 
way. The sediments secured from fifteen patients in this manner, 
after the smear preparations were injected into guinea pigs intra- 
peritoneally; these were all negative. The milk secured in this 
series was from patients in the moderately or far advanced stage 
of the disease, ranging in age from 19 to 40. The total number 
of microscopic milk examinations made was 450, taken bi- 
weekly; all were negative but one, this from a pulmonary- 
orthopedic patient. The woman insisted upon nursing her child 
and now, \y2 years after, this child appears perfectly healthy 
and is well developed. From these observations they concluded 
that tubercle bacilli (living?) are infrequently found in breast 
milk of the tuberculous woman who has no mammary disease; 
that though the possibility of infection from this source is slight, 
it is best to interdict nursing, for both mother and child, as per- 
haps toxic substances, other than bacillary, in the milk, may have 
a most deleterious effect on the young organism. 
In all probability, if the tuberculous process is not very extensive, per- 
haps only few tubercle bacilli are circulating in the blood current, then 
few or none will enter the milk from this source; perhaps those that may 
enter are dead, destroyed, weakened, or non-virulent, and the milk will 
not infect the nursing child. In advanced tuberculosis, when the milk 
glands themselves have become tuberculous, and there is a great possibil- 
ity of their contents contaminating the milk, the danger to the child 
becomes enormous, hence to guard the child and in the interest of the 
it becomes imperative that the mother must not, if tubercu- 
1c i s’v diseased, nurse her child. 
In this connection the following observations made on animals 
may be apropos. The Royal English Commission on Human 
and Bovine Tuberculosis in its third report in 1909 makes this 
statement: “If milk from clinically tuberculous animals is in- 
jected into the experimental animal, the result will always give a 
positive reaction even if on postmortem the udder is found free 
from tuberculous disease; if, however, the milk from a cow in THE URINE, MILK, ETC., IN TUBERCULOSIS 
513 
which the only sign is the positive tuberculin test is injected into 
such a test animal, the result will always be negative; hence 
clinically tuberculous cows without disease of the udder may 
contaminate the milk with tubercle bacilli, but more often the 
milk is entirely free.” 
It should be mentioned here, that the examination of milk for tubercle 
bacilli, secured from milk producing animals, cows, goats, sheep, etc., does 
not differ from the method given by Wang and Coonley for testing the milk 
of the tuberculous mother. 
(C) Tubercle Bacilli in. the Feces.2 Tubercle bacilli if 
found in the feces are generally of pulmonary origin. In active 
pulmonary tuberculous disease when the sputum is bacilli laden, 
many will find their way into the oesophagus, thence into the 
stomach, from there into the intestinal tract, and be passed out 
with the stool. As a rule the bacilli in this passage are not de- 
stroyed nor dissolved; they are found to be very resistant 
against the digestive ferments and are not influenced by decom- 
position processes. In primary intestinal tuberculosis, bacilli 
may frequently be passed with the stools. However, if the retro- 
peritoneal or the mesenteric glands are tuberculously diseased and 
are subject to degenerative changes still the bacilli infrequently 
find their way from this source into the intestinal tract. 
The character of the stool usually speaks for or against enteric 
disease. A stool containing much mucus, blood, and some pus, 
a thin discharge or diarrhoeal stool, is in all probability from a 
patient suffering from intestinal tuberculosis, v. Jaksch is of 
the opinion that a positive diagnosis of ulcerative, intestinal 
tuberculosis can only be made if the bacilli are constantly present 
in the stool, particularly if they are present in pure culture if in 
large groups and always if pus is present. If in the surface 
washings of a fully formed stool the tubercle bacillus can be 
demonstrated, it in all probability is from the intestinal walls, 
from the intestinal mucosa, and points strongly to intestinal 
tuberculosis. If, however, in a fully formed stool the bacilli are 
found in portions from the interior, these in all probability are 
from the ingested sputum and are of pulmonary origin. The 
giving of an opiate, therefore, to lessen peristalsis so as to tem- 
porarily check the bowels may insure a well-formed, solid stool, 
sThe smegma bacillus is said to be frequently found in the anal orifice and may become 
mixed with the stools; this should be borne in mind when making fecal examinations. 514 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
and here the examination of either surface or interior may point 
to the source of the bacilli. 
A very practical method for examining feces for the presence 
of the tubercle bacillus, based upon the suggestion of Hamburger, 
is given by3 Strassburger.(192) This method is based upon the 
fact that in order to remove bacteria from a fluid it is advisable 
to lower its specific gravity, particularly so if only few organisms 
are present and this lowering of the specific gravity is readily 
accomplished by the addition of alcohol. Equal parts of water 
and absolute alcohol lower the specific gravity to 0.8975 at 15° C. 
Accordingly, a small particle of fecal matter about the size of a 
pea is rubbed up well in a mortar with a small quantity of dis- 
tilled water, centrifuged for a very short time to eliminate prac- 
tically most of the coarser particles, the bacilli remaining in the 
supernatant fluid; this cloudy fluid is now poured off, mixed with 
an equal volume of 95% alcohol, and then well centrifuged, the 
fluid portion decanted or removed, and the sediment in the tube 
fixed and stained in the usual way. To lower the specific gravity 
of a fluid, equal parts of alcohol, ether, and fluid may be em- 
ployed ; this favors the separation of the bacteria still more. 
Animal Experimentations. The tubercle bacillus can usually be demon- 
strated in the feces in about 46% of clinically tuberculous cows. In exam- 
ining the feces of cattle microscopically for tubercle bacilli, however, it 
should be remembered that there may always be an element of doubt, 
because saprophytic, acid fast bacilli are always present. 
(D) Tubercle Bacilli in the Bile and Gall Bladder. In the liver 
the anatomical picture of tuberculosis is usually that of the 
miliary form, a tuberculous hepatitis. In the gall bladder tuber- 
culosis is usually a chronic, ulcerative, tuberculous cholecystitis, 
the result of irritation by stone. The lodgment of the tubercle 
bacillus in the mucosa of the gall bladder is a secondary affair 
from tuberculous foci in other organs. If tubercle bacilli do not 
circulate through the blood stream then they can not be excreted 
through the bile and gall bladder, tuberculosis is then an impos- 
3The above method, given by Strassburger for removing tubercle bacilli from feces by 
the use of alcohol, can be applied to other fluids with equal satisfaction. In urine, both 
albuminous and albumin free, the use of alcohol is indicated. In urine containing ’much 
epithelial cells and pus germs, which may be considered heavy bodies, if centrifuged, the 
bacilli will, during sedimentation, be carried down into the tube. If to such urine 
before centrifuging a double volume of alcohol is added, all cellular elements and bac- 
teria as will be more rapidly deposited. To spinal fluid (Liquor Cerebrospinalis) the 
addition of alcohol precipitates the albumin content in a fine flocculent form. This 
undoubtedly favors the removal of all cellular bodies, or rapid sedimentation. In pleural 
exudates the albumin content is usually so great, the albumin sedimentation so enormous 
that the bacteria for future demonstration would become lost; here the dilution of the’ 
exudate with equal parts of distilled water is advisable before adding alcohol. When 
desirous of testing any other fluid, even sputum, for tubercle bacilli, it may be treated 
similarly, using absolute alcohol as a diluent to lower the specific gravity. URINE IN TUBERCULOSIS 
515 
sibility—Joest’s views are somewhat different. From extensive 
animal experimentation and study he concludes that tubercle 
bacilli enter the gall bladder from primary foci in the liver 
through the bile ducts. . The tuberculous processes are not in the 
tubules but near them and so they become enlarged, break 
through, their contents becoming mixed with the bile. He main- 
tains that this is similar to tuberculous disease of the female 
breast where the tuberculously diseased milk glands pour their 
contents into the ducts and contaminate the milk. 
Maxson (1910) questions if tubercle bacilli are ever excreted 
through the bile and concludes, from personal observation in 12 
cases supplemented by 20 cases by Rosenberger, as follows. (97) 
That while the circulation of tubercle bacilli in the blood and 
their excretion in the bile is not proved, the evidence is suffi- 
ciently strong to make it very probable. (Since then it has been 
proven that tubercle bacilli very often circulate in the blood.) 
These 32 observations proved that no matter what the clinical 
diagnosis in the case was, if autopsy revealed the presence of a 
tuberculous lesion in either lung, pleura, or peritoneum, the acid 
fast bacilli could be demonstrated in the bile. 
Maxson’s technic is as follows: 
(1) Add four parts of 15% antiformin solution to one part of 
bile. Allowed to stand about fifteen minutes in incubator is pre- 
ferred. 
(2) Add equal parts of distilled water. Shake well. 
(3) Add ligroin to a depth of about 10 mm. 
(4) Allow to stand until sharp separation occurs. 
(5) From the turbid zone which appears just below the ligroin 
transfer ten loopfuls to a clean warm glass slide, allowing the 
ligroin to evaporate between each loopful. Put the loopfuls on 
the same spot on the slide. 
(6) Fix by heating slide, wash well, stain with carbol-fuchsin, 
decolorize with acid alcohol, counterstain with methylene blue, 
wash, dry, and examine. 
(E) Tubercle Bacilli in Exudates and Other Body Fluids. 
The demonstration of the tubercle bacillus in exudates, transu- 
dates, spinal, meningeal, peritoneal, etc., fluids, does not differ 
very materially from the procedures employed for the identifica- 
tion of bacilli in milk, urine, etc. The usual methods in all are 
by sedimentation, concentration, centrifugalization all of which 
have been given somewhat in detail in this chapter under special 516 
CLINICAL TUBERCULOSIS 
headings to which the student is referred. In the part on 
Inoscopy (also this chapter) the method of sedimentation is 
fully described; this may also be successfully employed in search- 
ing for bacilli in any of the various body fluids. 
The Urochrome or Coloring Matter of the Urine in Tubercu- 
losis. (68) The normal yellow coloring matter of the urine is 
known as urochrome, the derivative of which appear as two 
separate substances, one of which can be separated from the 
urine by lead acetate; the other is not so separated, therefore, 
they are not identical. These substances are designated uro- 
chromogen (A) and urochromogen (B) and by oxidation are 
changed to urochrome. Both urochromogen A and urochromo- 
gen B are proteinoid substances or protein derivatives, oxidation 
products from the destruction of protoplasmic albumin. Of these 
two precursors of urochrome, urochromogen A can, by means 
of potassium salts be oxidized into urochrome; the other, 
or urochromogen B, if present, gives the Ehrlich or diazo re- 
action which is dependent upon the presence and amount of 
urochromogen in the urine; one is identified in the freshly voided 
urine, the other develops after the urine is kept for 24 hours in 
the incubator. 
Urochrome results from albumin changes, but the presence of 
its precursors in greater amounts is evidence of toxic destruction 
going on in the organism. In the tuberculous individual, in the 
urine of which urochromogen can be demonstrated, it shows that 
the reduction of organic albumin is not only quantitatively in- 
creased, but that it deviates qualitatively from the normal, hence 
an increased urochromogen in the urine is, in every sense, of 
toxic origin, and here the toxins of bacterial origin play the 
leading role. The influence of these toxins is manifested by a 
destructive condition of the normal oxidative processes going 
on in the urine, leading not to urochrome, as in the normal 
process, but to the production of the lower oxides of urochrome. 
In 1910 Moriz-Weisz called attention to a new reaction in the 
urine in connection with the well-known diazo or Ehrlich’s. It 
is designated as the urochromogen, or better as the perman- 
ganate test, and is based upon the original Ehrlich’s, upon the 
presence of urochromogen B but acts more promptly than the 
diazo, reacting with urochromogen A, with which Ehrlich’s re- 
acts only after the urine is kept in a moderately warm place for 
24 hours. Urochromogen A is only a lower oxide leading up to THE URINE, MILK, ETC., IN TUBERCULOSIS 
517 
the formation of urochromogen B. As the diazo only gives the 
reaction with the latter, and not with the former, the perman- 
ganate test is quicker and more readily positive as it gives the 
reaction with both chromogens. The technic for demonstrating 
the permanganate reaction is very simple and more sensitive 
than the diazo reaction. How this reaction is really brought 
about is still in dispute. To fresh urine in a urine glass add 
twice its volume of distilled water, fill two equally sized test 
tubes about £4 full, to one add three drops of 1:1000 perman- 
ganate of potassium solution; the other is kept as control. By 
comparing the two test tubes on holding them up to the light, 
the difference in the color reaction becomes readily apparent. If 
now a few more drops are added the color may be greatly in- 
tensified. Should the urine contain much bile pigment, bilirubin, 
etc., it is advisable to add a quantity of ammonium sulphate be- 
fore applying the permanganate test. In the examination of a 
great number of specimens of urine, both normal and patho- 
logical, the permanganate test has been considered a specific in 
proving the presence of the lower oxides of urochrome. 
From numerous observations made by clinicians it is now the 
consensus of opinion that, especially in pulmonary tuberculosis, 
a positive urochromogen reaction shows an acutely destructive 
lesion or process going on in the organism and that a negative 
reaction in positively pulmonary cases appears to indicate at 
least, a temporary cessation of all activity. In ordinary chronic, 
non-active, fibroid cases the reaction is negative and becomes 
again positive upon a re-exacerbation of the tuberculous process 
or upon the entering of a new acute intercurrent disturbance. 
The freshly voided urine from an active tuberculous individual 
will give a negative diazo; if, however, the urine is placed in an 
incubator for 24 hours it often becomes strongly positive. The 
tuberculous organism is incapable of producing the urochrome 
which the healthy body produces, but in its place it produces a 
lower oxide, an incompletely oxidized substance, which in all 
probability is a form of peptonoid or a polypeptonized body un- 
changed and which in a warm place in 24 hours is oxidized to the 
higher urochromogen B form. 
Roy C. Heflebower,(166) the first in this country to test the 
value of the permanganate of potassium reaction on the urine, 
observed the test on 39 tuberculous individuals in tuberculosis 
sanatoria and arrived at the following conclusions: (1) The fre- 518 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
quency and constancy of the diazo and urochromogen reaction 
in the urine are proportional to the severity of the disease; a 
constant negative reaction indicates a mild case, whereas a con- 
stant positive reaction is evidence of a severe and serious dis- 
order. (2) The urochromogen reaction is more frequent, more 
constant, than the diazo, therefore, a better index. (3) The in- 
tensity of both reactions proves, when constant, a severe tuber- 
culosis. 
Corper, Callahan, and Marshak (160) reported their observa- 
tions before the National Tuberculosis Association in 1916 on 
350 patients at the Municipal Tuberculosis Sanatorium of Chi- 
cago representing the three stages of the disease, and they con- 
cluded as follows: 
(1) Cases dying from pulmonary tuberculosis give a positive 
diazo and urochromogen test at some time during the last six 
months of their illness. Whenever both tests are negative during 
this period, death is found to be due to some intervening condi- 
tion, such as pulmonary hemorrhage, tuberculous meningitis, 
etc. 
(2) Cases of chronic, fibroid tuberculosis generally give both 
reactions negative, except when same is explicable by some acute 
exacerbation, acute intercurrent infection, or acute pleural effu- 
sion. 
(3) In active cases of pulmonary tuberculosis when both re- 
actions are positive and remain so for most of the succeeding 
examinations, it is of grave prognostic import. When both re- 
actions are negative in active cases no stress can be laid upon the 
findings. 
(4) There seems to be no regularity between the presence of 
either reaction, its disappearance to be displaced by the appear- 
ance of the other or by both. 
(5) The presence of a urochromogen reaction in cases showing 
no clinical symptoms is of no prognostic value. No diazo re- 
actions were obtained in clinically inactive cases, whereas a num- 
ber of urochromogen reactions were obtained in such cases. 
Lime Elimination in Tuberculosis. The increased lime con- 
tent in the urine of the tuberculous. Demineralization. Decal- 
cification. According to the elaborate studies of Senator, as 
early as 1877, the urine of the tuberculous contains relatively 
more lime salts than that of healthy individuals. He states it to 
be a positive fact that in pulmonary phthisis an abnormal quan- THE URINE, MILK, ETC., IN TUBERCULOSIS 
519 
tity of calcium is excreted in the urine. Robin contends that 
with the very beginning of tuberculous disease the affected in- 
dividual shows an increased demineralization, that the increase 
of lime salt elimination can be of great diagnostic value in the 
pretuberculous stages of the disease, that is while prodromal 
symptoms only are present. Sobatta, 1911, states that de- 
mineralization may be considered an acquired disposition in the 
pregnant and the diabetic, hence there is a heightened tendency 
to tuberculous disease; and that a lime salt reduction in the or- 
ganism exists more or less in all cases of pulmonary tuberculosis. 
This creates the tuberculous disposition, hence, therapeutically., 
lime salts are indicated. It is believed by most physiolo- 
gists (101) that the lime content of blood serum of healthy in- 
dividuals is always maintained at a constant level, that in the 
human blood the variation is from 9 to 10 mg per 100 cubic 
centimeters.4 
A. C. Crofton contributed a very interesting paper on the 
“Increased Urinary Calcium Excretion in Tuberculosis,” before 
the Sixth International Congress on Tuberculosis. He contends 
that in considering the calcium elimination we must distinguish 
between that which is eliminated by body changes, the endog- 
enous calcium, and the lime which is brought to the body by 
way of foodstuffs, the exogenous, both of which are eliminated 
through the blood and kidneys. The calcium elimination from 
the body changes is usually constant, does not fluctuate very 
much from day to day, while the exogenous calcium excretion is 
inconstant, fluctuates much from day to day, is dependent upon 
the amount of lime taken in with the food and that but little of 
this lime is eliminated in the urine, the greater bulk passing out 
with the feces. To check up the excreted lime from body changes 
and that from the ingested foods, his examinations were con- 
ducted on dogs that were injected with live tubercle bacilli, then 
fed on food,'the accurate calcium content of which was known. 
Comparing the increased calcium content in the urine after de- 
ducting the quantity of lime passed with the stools, he was able 
to observe a steady lime starvation. From the time of inocula- 
tion to the death of the animal, a progressive increase in calcium 
output was shown. He then made similar observations on the 
human. In advanced cases of tuberculosis with destruction of 
4I am not aware that similar observations have been made on the tuberculous to see if 
this equilibrium is here also maintained; if not, it may in part account for the lime salt 
starvation in these patients. 520 
LABORATORY DIAGNOSIS IN TUBERCULOSIS 
lung tissue the urinary excretion of calcium is markedly in- 
creased, the figures are always higher than in the normal. 
The quantitative determination of calcium in the urine accord- 
ing to McCruddin (16) is as follows. The urine if alkaline must 
be made neutral or slightly acid with hydrochloric acid and fil- 
tered or if turbid or faintly acid add 10 drops of pure HC1. Two 
hundred cc of the clear acid urine are treated with 10 cc of a 
2.5% oxalic acid and 8 cc of a 20% sodium acetate solution. Al- 
low the mixture to stand over night at room temperature or 
shake vigorously for 10 minutes. Filter off the precipitated cal- 
cium oxalate and wash it cl-free with 0.5% ammonium oxalate 
solution. Save the filtrate if desired for the determintion o£ 
magnesium. The precipitated calcium oxalate is then dried on 
filter paper at 100° C, is placed into a weighed platinum crucible, 
burned over a bunsen flame until the filter paper is completely 
ashed. The blast-lamp is then applied and the crucible is then 
dried in a desiccator and weighed. The increase in weight rep- 
resents the calcium oxide (CaO) in 200 cc of urine. A simple 
calculation will yield the amount of CaO in the 24 hours speci- 
men. 
Cytodiagnosis in Tuberculosis. (89) A study of the character, 
number, and kind of cellular elements found in pleural effusions, 
in spinal, peritoneal, endocardial fluids, or in various other serous 
effusions is known as cytodiagnosis. It, like all other methods 
of diagnosis, can not be taken singly. It is only in connection 
with the clinical history and physical findings that it becomes 
a valuable aid in the study of tuberculosis. An enormous 
amount of good work along these lines has been done, especially 
by French clinicians. Widal and Ravaut of Paris offer the fol- 
lowing. The examination of a pleural exudate in which certain 
cellular bodies are present in varying amounts may offer impor- 
tant points in etiology, diagnosis, and pathogenesis. A few 
cubic centimeters of pleural fluid are withdrawn by aspiration, 
defibrinated, and centrifuged, (a) In idiopathic pleurisy the ex- 
clusive picture is a preponderance of the small lymphocytes with 
perhaps a few red corpuscles: (b) in tuberculous pleurisy we 
may find a few deformed polynuclears, but principally lympho- 
cytes; (c) in streptococcus, sero-fibrinous pleurisy the polynu- 
clear-neutrophiles are much in evidence; (d) in pneumococcus 
pleurisy red blood corpuscles and a few lymphocytes are seen, 
but the polymorphonuclears are most abundant and a few mono- THE URINE, MILK, ETC., IN TUBERCULOSIS 
521 
nuclear cells of endothelial origin are also present; (e) in trau- 
matic pleurisy and the aseptic pleurisies complicating heart and 
kidney disease large endothelial cells single and in groups are 
present. 
In tuberculous meningitis there is a constant and perceptible 
lymphocytosis in the spinal fluid which is pathognomonic of 
tuberculous disease. Kretschmer (111) reports the case of a 
soldier who died of tuberculous meningitis in which the tubercle 
bacilli were demonstrable in the spinal cord, but failed to be 
shown in the examination of the withdrawn spinal fluid. Here 
the centrifuged fluid gave a differential count of 75% of small 
lymphocytes and 25% neutrophiles. 
The cellular elements or constituents in the different fluids 
vary as to the nature of the disease, i. e., acute or chronic. In 
acute diseases the polynuclears generally predominate, whilst 
in chronic disorders like tuberculosis the lymphocytes are usu- 
ally in preponderant numbers, hence a large number of poly- 
morphonuclear cells is indicative of a marked or recent inflam- 
mation (acute infection), and a considerable quantity of the 
mononuclear element, the small lymphocytes, signify either a 
mild degree and a late stage of inflammation or the presence of 
a chronic non-inflammatory process (tuberculous). The diag- 
nostic value of cytology may be summed up by the cytologic 
formula formulated by Widal and Ravaut. 
(a) A preponderance of the small lymphocytes in a fluid 
(exudate) either pleural, spinal, peritoneal, endocardial, etc., 
means a tuberculous effusion (chronic). 
(b) A preponderance of the polymorphoneutrophiles in a fluid 
means (exudate), that it is of acute and infectious origin (acute). 
(c) A predominence of endothelial cells in a fluid occurring 
especially in sheets or plaques means that the effusion is of 
mechanical origin (transudate). 
Inoscopy. (89) Inoscopy is a method, the object of which is 
to demonstrate in an exudate or transudate the presence of bac- 
teria, chiefly tubercle bacilli, and here advantage is taken of 
spontaneous clotting. This method as first suggested by Jousset 
is most dependable and offers good results if the technic is ac- 
curately followed. Spontaneous coagulation or clotting of an 
exudate takes place usually in a very short time and, at the same 
time separates from the fluid portion all the morphological ele- 
ments present. If now this coagulum is redissolved by means of 522 
TUBERCULOSIS 
an alkali or much better, as is now done (artificially digested) 
by means of a pepsin solution, the tubercle bacilli may be readily 
separated by centrifugalization. 
The coagulated mass from 100 cc of exudate requires about 
100 cc of the following pepsin solution for digestion: 
Pepsin 8.5 grams 
Hydrochloric Acid U.S.P 1.0 cc 
Glycerine 10.00 cc 
Water a. s. ad 100 cc 
The coagulum is put into a beaker or flask, and the pepsin 
solution added. It is then placed into a warm room or a 
thermostat, shaking the mixture occasionally. In 2 or 3 hours 
complete digestion has taken place. Only digestion of the albu- 
minous matter is accomplished, the tubercle bacilli and the 
nuclei of the leucocytes remaining intact and the virulence 
of the bacteria but little affected. From the sediment in the 
centrifuge tubes, smears are prepared and stained in the usual 
way. Inoscopy is equally applicable in the examination of 
the blood; even the sputum from the suspicious tuberculous may 
be so examined. To fluids which may be suspected of containing 
tubercle bacilli but which do not coagulate spontaneously, a 
coagulable substance such as horse serum may be added to re- 
move the bacteria, and sputum, urine, bile, etc., may all be most 
satisfactorily examined by this method. 
MISCELLANEOUS 
We shall here first consider a few such topics that in some ivay are 
related to the various questions of Tuberculosis. Chapter XXXIX 
gives the calory values of the different foods, the carbohydrates, fats 
and proteins and includes a dietary table; Chapter XXXX, the defi- 
nitions of such words, terms and phrases as are now in general use in 
the conversation and in the literature of Tuberculosis. Next, a table 
showing the normal standard weights at the different ages from 18 
to 55 inclusive as compared with the height, and a table for making 
the Standard Tuberculin Dilution is appended. This is followed 
by an index giving the names of authors with page index, by a 
bibliographic index and closing with a general index or index of 
subjects. CHAPTER 39 
CALORIES 
Calories, the Food Values of Proteids, Fats, and Carbohydrates 
as Expressed in Heat Units. 
All humans in health and in disease, must be supplied with cer- 
tain quantities of food to keep up the body’s existence. Food is 
the fuel which the body requires to maintain its weight and its 
energy. Food is to the body what fuel is to the boiler, and like 
it, is consumed in producing heat and force. (31) (32) 
Generally speaking, in the human, the fuel, necessary to pro- 
duce force and energy, to sustain life, is measured in units of 
heat—this is spoken of and known as calories. These heat units 
or calories may vary in quantity or amounts according to the 
size, age, activity, work, etc., of the individual. One group or 
class of foods may be much more in demand by the organism at 
a given time in life than another; for instance, carbohydrates 
are much more essential in child life, whilst during the energetic 
and active period of adult life, proteids as a rule are the more 
necessary elements of food. The active and the ambitious re- 
quire more calories per day than the indolent and the lazy; more 
calories are consumed during the cold than during the warm 
days. Age and sex also play most important roles. In early 
infant life the number of calories required by the male and in the 
adolescent, when the male usually becomes more active than 
the female, there may be a difference of more than a thousand 
calories per day. The average daily requirement in men being 
about 3500 calories as against 2500 in women. 
By calorie1 is understood the amount of heat which is required 
Un estimating the number of calories necessary for the body’s upkeep we must also 
consider certain undetermined chemical substances, in all probability labile albuminous, 
known as vitamines. The presence of these bodies is most essential, their absence from 
food products is prone to lead to various disorders and diseases like Rickets, Beri-Beri, 
Xerophthalmic, etc. What effect the presence or absence of vitamines may have on the 
tuberculous organisms is still somewhat speculative.- We must, nevertheless, concede 
their great importance in the treatment of disease when we consider their significance to 
the normal and vital functions of the body. Up to the present nothing definite is known 
concerning these bodies. However, we know that their presence is necessary to the growth 
and development on the one hand and to the keeping of the body in a healthy condition 
on the other. Vitamines are of two kinds (or perhaps three), a fat soluble which is neces- 
sary to body growth and a water soluble, which possesses antagonistic properties like 
antineurotic or antiscorbutic, etc. In foodstuffs these bodies are readily destroyed by long 
cooking, in pickling, in frozen meat, in shredded grains, like in rice, keeping food in salt 
brine, etc. _ ... 
In estimating a dietary for the tuberculous these bodies should receive consideration 
and foods which require long cooking, or pickling, should be excluded and the use of 
raw fruit and vegetables and milk, nuts, eggs, etc., be encouraged. 
523 524 
MISCELLANEOUS 
to raise the temperature of one gram (15 minims) of distilled 
water one degree, and by means of this standard all food stuffs 
are estimated in heat units, or better, calories. The oxidization 
or consumption of one gram each of proteids, fats and carbo- 
hydrates has yielded respectively 4.1, 9.3 and 4.1 calories. Ac- 
cording to the pioneer research work as first elaborated by Carl 
Voit of Munich and which is still accepted as most competent, 
a healthy individual of average weight, 70 to 75 kilos (150 to 165 
pounds), performing moderate muscular labor, requires about 
118 grams of proteids (483.8 calories), 56 grams of fats (520.8 
calories) and 500 grams of carbohydrates (2050.0 calories) or a 
total of 3054.6 calories, or heat units. 
Life cannot be indefinitely sustained by one single kind of 
food. It requires, to maintain body energy and life, that the 
various food materials, (proteids, fats and carbohydrates) be 
taken as the body needs them during the various periods of exer- 
cise or rest. A proportional daily intake of food in calories to 
meet these requirements, to sustain the body’s vital processes 
without hindrance, is given in the following table. In addition 
to proteids, fats, and carbohydrates, many mineral salts, water, 
vegetable and fruit acids, etc., are required to maintain com- 
fortably a proper functioning of the various organs and tissues 
of the body; coarse food or roughage in the form of green vege- 
tables is necessary to aid in the proper movements of the bowels, 
lime salts for the upbuilding of the bony structure, water for the 
blood plasma and tissues of the body, etc. 
The table given here shows some of the various food materials 
consisting of proteids, fats and carbohydrates expressed in calorie 
values or units of heat per pound, as yielded to the body. 
One pound of olive oil yields approximately 4464 calories 
One pound of butter yields approximately 3605-3816 calories 
One pound of bacon yields approximately 3101 calories 
One pound of ham (smoked) yields approximately 1920-2485 calories 
One pound of beef (roast) yields approximately 1620-1714 calories 
One pound of lamb (chops) yields approximately 1665-1771 calories 
One pound of lamb (roast) yields approximately 900-960 calories 
One pound of steak (tenderloin) yields approximately 1300-1344 calories 
One pound of pork (chops) yields approximately 1752 calories 
One pound of mutton (leg roast) yields approximately 1420 calories 
One pound of turkey (roast) yields approximately 1295 calories 
One pound of chicken (roast) yields approximately 869 calories 
One pound of chicken (fricassee) yields approximately 855- 907 calories 
One pound of fish (bluefish cooked) yields approximately 670 calories 
One pound of fish (Spanish mackerel) yields approximately 715 calories 
One pound of fish (salmon) yields approximately 915- 950 calories 
One pound of oysters yields approximately 230- 250 calories 
One pound of eggs (boiled) yelds approximately 765- 811 calories 
One pound of mushrooms (boiled) yields approximately 1262 calories 
One pound of cheese (American) yields approximately 2173 calories 
One pound of cheese (full cream) yields approximately 1950-2064 calories 
One pound of marcaroni with cheese yields approximately 1531 calories 
One pound of cream yields approximately 1282 calories THE CALORIES IN TUBERCULOSIS 
525 
One pound of milk yields approximately '. 32S- 346 calories 
One pound of milk (malted, prepared) yields approximately 300 calories 
One pound of milk (skimmed) yields approximately 178 calories 
One pound of milk (butter) yields approximately 173 calories 
One pound of sugar yields approximately.... 1968 calories 
One pound of potatoes (boiled) yields approximately 440- 466 calories 
One pound of potatoes (chips) yields approximately 2827 calories 
One pound of potatoes (sweet, boiled) yields approximately 979 calories 
One pound of bread (white) yields approximately 1296 calorjes 
One pound of bread (graham) yields approximately 1282 calories 
One pound of bread (brown) yields approximately 1050-1109 calories 
One pound of bread (ginger) yields approximately 1670 calories 
One pound of bread (whole wheat) yields approximately 1140 calories 
One pound of bread (rolls) yields approximately 1395 calories 
One pound of cake yields approximately 1776 calories 
One pound of pie (apple) yields approximately 1270-1392 calories 
One pound of pudding (rice) yields approximately 720 calories 
One pound of rice (boiled) yields approximately 525- 538 calories 
One pound of oatmeal yields approximately. 302 calories 
One pound of crackers (soda) yields approximately 1925-2035 calories 
One pound of crackers (graham) yields approximately 2095 calories 
One pound of beans (baked) yields approximately 600- 955 calories 
One pound of beans (lima) yields approximately 768 calories 
One pound of beans (canned) yields approximately. 634 calories 
One pound of corn (stewed or green) yields approximately 480 calories 
One pound of peas (dried) yields approximately 1644 calories 
One pound of honey yields approximately.... 1608 calories 
One pound of prunes (stewed) yields approximately 1675 calories 
One pound of raisins yields approximately 1699 calories 
One pound of dates yields approximately 1709 calories 
One pound of apricots yields approximately 1056 calories 
One pound of rhubarb yields approximately 739 calories 
One pound of grapes yields approximately 355 calories 
One pound of bananas yields approximately 317 calories 
One pound of apples yields approximately 307 calories 
One pound of figs yields approximately 1560 calories 
One pound of current jelly yields approximately 3550 ca ones 
One pound of oranges yields approximately 254 calories 
One pound of squash yields approximately.._ 331 calories 
One pound of beets (cooked) yields approximately 1°5- 197 calories 
One pound of tomatoes yields approximately 105- 110 calories 
One pound of celery yields approximately 91 calories 
One pound of lettuce yields approximately 96 calories 
One pound of cabbage yields approximately 24 calories 
One pound of turnips yields approximately 19 calories 
The following list from the Modern Health Crusade appeared 
in the April, 1920, number of the Bulletin of the National Tuber- 
culosis Association. The calorie values of the various articles 
of diet as here given are expressed in teaspoonful, tablespoonful, 
piece, slice, cup, etc., and are especially recommended in the 
treatment and care of the puny, the sickly, the underfed, the 
undernourished, and the suspected tuberculous child. 
Cereals 
Calories 
Rolled oats 1 cup 147 
Bread 1 slice 202 
Bread with butter 1 slice 230 
Bread with peanut butter 1 slice 221 
Ginger bread 1 slice 281 
Corn bread 1 slice 194 
Shredded wheat 1 HO 
Farina 1 CUP 
Rice 1 CUP 180 
Cream of wheat 1 CUP 16!) 526 
MISCELLANEOUS 
Cornmeal mush 1 cup 169 
Cracked wheat 1 cup 198 
Hominy 1 cup 143 
Macaroni and cheese 1 cup 302 
Barley soup 1 cup 131 
Hot biscuit 1 104 
Griddle cakes 1 101 
Meats 
Meat loaf 1 slice 209 
Roast lamb 1 slice 333 
Hamburger steak 1 slice 138 
Beef stew 1 cup 691 
Sardine 1 65 
Frankfurter 1 180 
Fish chowder 1 cup 372 
Brown gravy cup 36 
Roast beef 1 slice 333 
Cheese fondue 1 cup 529 
Meat balls and rice 1 cup 169 
Baked fish 1 slice 201 
Pot roast 1 slice 240 
Codfish balls 1 88 
Corned beef 1 slice 608 
Smoked pork 1 slice 827 
Vegetables 
Boiled onions 1 49 
Pea soup 1 cup 279 
Escalloped potatoes 2 heap’g tbs. 242 
Escalloped tomatoes 1 cup 198 
Baked beans 1 cup 385 
Beets 1 83 
Cabbage salad 1 cup 32 
Lettuce 4 leaves 8 
Peas and carrots 1 cup 69 
Bean loaf 1 cup 547 
Tomatoes 2 (raw) 41 
Greens 1 tfe, 28 
Lima beans 1 cup 326 
Potato salad ) cup 143 
Lentils 1 cup 269 
Baked potato 1 147 
Boiled cabbage 3 tbs. 100 
Spinach 2 tbs. 57 
Boiled potato 1 143 
Bean soup 1 cup 505 THE CALORIES IN TUBERCULOSIS 
527 
Desserts 
Syrup 1 tsp. 117 
Rhubarb sauce 1 tb. 78 
Cream toast 1 slice 348 
Ginger cookie 1 41 
Apple tapioca 1 cup 235 
Custard 1 Cup 362 
Junket 1 cup 208 
Cake 1 piece 164 
Jelly 1 htsp. 113 
Oatmeal cookie 1 115 
Fruit cookie 1 110 
Fruit cake 1 slice 192 
Fruit shortcake 1 slice 350 
Cheese 1 cu. inch 90 
Fudge 2 pieces 221 
Cornstarch pudding 2 htsp. 166 
Indian pudding 2 htsp. 225 
Steamed fruit pudding 2 slices 569 
Bread pudding 1 cup 380 
Fruit 
Prunes 5 143 
Apple sauce 3 tbs. 136 
Baked apple 1 120 
Baked banana 1 144 
Apricot or peach sauce 3 tbs. 218 
Dates 10 269 
Berries (with 1 tsp. sugar) 3 htbs. 120 
Orange 1 75 
Banana 1 90 
Drinks 
Milk 1 quart 695 
Milk 1 glass 220 
Cocoa 1 cup 126 
Coffee 1 cup 00 
Tea 1 cup 00 
For convenience this supplemental list is added here, giving 
the food values or calories in ounces instead of in pounds. 
CALORIES PER OUNCE 
Apricots 13 
Parsnips 15 
Carrots 13 
Celery 5 
Onions 16 
Turnips 8 
Farina 105 
String Beans 9 
Lima Beans 90 
Corn Flakes 103 
Spaghetti 103 
Cheese 106 
Olive Oil 200 
Oleomargarine 204 
Sugar 106 
Molasses 79 
Potatoes 18 
Eggs 45 528 
MISCELLANEOUS 
Butter Beans 22 
Kidney Beans 92 
Navy Beans 96 
Tomatoes (Cans) 5 
Beets 22 
Corn 27 
Cornmeal 100 
Corn Syrup 80 
Barley ,....•. 103 
Radishes 5 
Peas (Canned) 14 
Peas (Split or dried).......... 93 
Lettuce 5 
Cauliflower . 8 
Cabbage 9 
Sauer Kraut 9 
Parsley .... 4 
Grapes . 20 
Jelly 50 
Peaches 14 
Rice 102 
Tapioca 99 
Raisins -• • • • 95 
Dates 80 
Milk 20 
Butter 214 
Flour 98 
Corn Starch 103 
Chocolate 130 
Bread (Fruit) 75 
Bread (Bran) 65 
Bread (W. Wheat) 70 
Bread (Rye) 62 
Crackers (Graham) 103 
Crackers (Soda)... 118 
Oats, Rolled 112 
Wheat, Puffed 103 
Wheat, Cracked 105 
Ginger Snaps 100 
Peanut Butter 175 
Lard 204 
Lamb 54 
Beef and Soup Bone 59 
Pork fresh (lean) 41 
Pork fresh (fat) 78 
Salt Pork .... 222 
Bacon • 169 
Apples > • 15 CHAPTER 40 
DEFINITION OF WORDS, TERMS, AND PHRASES USED 
IN CONVERSATION AND IN THE LITERATURE 
ON TUBERCULOSIS 
These words and phrases are usually found in the writings on 
topics on tuberculosis and are used by physicians doing special 
tuberculosis work; in general medicine they are but little used. 
The medical student interested in this problem should familiarize 
himself with these terms so as to be able to use them properly. 
It is most painful to the ear when a speaker (or perhaps a writer) 
refers'to a tubercular disorder when he really means a tuber- 
culous condition. The following words, terms, and phrases are 
now in general use. (9) (10) (11) (12) (54) (55) (56) 
Tuberculosis, Tuberculous and Tubercular. These three words 
have their origin in common and are derived from the same root; 
namely, from tuber or tubercle, a small swelling or nodule. 
The word tuberculosis (from tubercle, a small nodule and osis, 
a morbid condition) is now generally recognized as referring to a 
pathologic process or a disease somewThere in the human body 
which is produced by the tubercle bacillus. We are all agreed 
as to when to use the word tuberculosis; that is, when we refer 
to the disease entity.produced by the Koch bacillus; but we are 
not all in harmony as to when we should say tubercular or when 
tuberculous. A lesion found anywhere in or about the body and 
which if represented by small nodules, is said to be tubercular. 
Cruveilhier, as early as 1862, produced small nodules in the 
lungs, liver, etc., (see Chapter 1) by means of minute droplets of 
mercury; and particles of dirt, fabric, silica, etc., often produce 
in the human body, especially in the pulmonary tissue, similar 
minute bodies. Even the ova of the tape worm are frequently 
found imbedded in the abdominal viscera producing similar small 
nodules. These are all correctly described as tubercular nodules 
or as tubercular tissue. Leprosy is a tubercular disease; small 
nodular masses are found in and about the cuticle brought about 
by the leprosy bacillus. Even nodular masses produced in the 
lungs by the presence of the tubercle bacillus may rightly be 
529 530 
MISCELLANEOUS 
called a tubercular affair if we do not know their source. Hence 
anything on or within the body in the form of small nodules may 
with propriety be referred to as a tubercular condition. If, how- 
ever, tubercles or small nodules are brought about by the pres- 
ence of the Koch bacillus, then by common usage, we make a 
distinction; that is, if we know that the pathological process any- 
where in or on the body is brought about by the tubercle bacillus, 
then it is correct to refer to it as a tuberculous affair. 
Briefly, then, when we speak in a general sense of nodular 
masses in or about a tissue or organ, we should say tubercular; 
but when we allude to or speak about the disease entity brought 
about by the tubercle bacillus, that is, when we speak in a spe- 
cific sense, then only is it correct to say tuberculous, and wrong 
to speak of it as tubercular. Tuberculous is the adjective ap- 
plied to lesions regardless of their form, caused by the tubercle 
bacillus; tubercular, the adjective which is applied broadly, in- 
cludes every condition and describes the appearance of the lesion 
regardless of its etiology. 
Tuberculously infected and tuberculously diseased. These ex- 
pressions are very frequently used synonymously. They are, 
however, distinct, have separate and very different meanings. 
Generally speaking, we say that we are all infected, but few are 
tuberculously diseased. The tuberculously infected individual 
gives evidence that at some time in life he came in contact with 
the virus, that is, with the tubercle bacillus; that the bacillus has 
found a resting place or nidus somewhere in his body, become 
perfectly contented, made its presence known in the lymph 
tissue, after which it assumed a more or less passive existence. 
The great majority of us go about our affairs in our daily life 
wholly unconscious that somewhere in our interior, we have a 
colony or group of these invaders. We recognize today that 
nearly all are tuberculously infected and that people living in 
large congested districts in cities are all infected. By means of 
the diagnostic tuberculin test we can prove the existence of these 
micro-organisms and their toxins in our bodies. If we go about 
our affairs in a hygienic, careful and healthy way, as is the rule 
in the majority of individuals, we never become cognizant of this 
infection. Should we, however, become careless about ourselves, 
as so frequently happens in early adolescence, with late hours, 
indulgence in drink, excesses of all kinds with fatigue or ex- 
haustion (even too much football, baseball, golf, dancing, swim- PHRASES, ETC., USED IN TUBERCULOSIS 
531 
ming, etc.) with insufficient rest for recuperation, then the body 
lowers the barriers which for years perhaps have kept the in- 
vaders within their confines, and we find that the individual in 
addition to being tuberculously infected is now also tubercu- 
lously diseased. 
In the tuberculously infected, as a rule, there are no symptoms 
except perhaps now and then a few enlarged glands; in the 
tuberculously diseased, symptoms usually play a leading role. 
Briefly, then, we may state that every body is tuberculously in- 
fected, approximately 100%. Of this number about 60% go 
through life unaware of the infection and about 30% at some 
time during their existence become also tuberculously diseased. 
In these, with care, treatment, and obedience to the principles of 
hygiene, the disease becomes again arrested and they then again 
remain only tuberculously infected; in the remaining 10% the 
infection is followed by active tuberculous disease and this class 
remains throughout life not only tuberculously infected, but 
chiefly tuberculously diseased. 
The open and the closed cases of pulmonary tuberculosis. An 
individual who presents himself for examination and who gives 
a history of some previous pulmonary disorder, pneumonia, 
pleurisy, etc., perhaps months or even years ago, of having lost 
weight, with poor appetite, with cough at times, slight tempera- 
ture, clinical findings positive, and with tubercle bacilli in the 
sputum would be designated an open case of pulmonary tuber- 
culosis. Should, however, all the above mentioned signs and 
symptoms, with positive clinical findings be present, but with 
repeated negative sputum findings, then the case in all proba- 
bility would be called a closed case of pulmonary tuberculosis. 
In the so-called open cases, identical with the infectious, there 
is a free communication from the diseased area in the lungs to 
the outer atmosphere; the necrotic tissue and bacilli have an out- 
let into the bronchial tubes and are expectorated with the 
sputum. These, known as the open or sputum positive cases, 
become the chief source of spreading infection and disease, and 
are the highly dangerous ones. In the closed or sputum negative 
cases, although the physical findings are positive or perhaps only 
slightly positive and which are usually the more or less slow 
cases, there exists no communication between the tuberculous 
area and the outer world, the tuberculous tissue is still walled 
off, and although there may be cough and expectoration, tubercle 532 
MISCELLANEOUS 
bacilli are not present in the sputum. Such individuals are not 
dangerous to any community so long as they remain closed or 
sputum negative, but the examining physician must always bear 
in mind that closed cases may at any time become open; hence 
in all such cases it becomes the imperative duty of the examining 
physician to make at least one sputum test every thirty days. 
In short, then, the open cases of pulmonary tuberculosis are 
those in which the sputum is tubercle bacilli positive; in these 
there is a direct communication between the tuberculous area in 
the lung tissue and the outer atmosphere. The closed or sputum 
negative cases are those in which the physical findings may or 
may not be positive; here the pathologic area in the lung ap- 
pears to be walled off and as yet there is no free communication 
with the bronchial system. 
Phthisis and Tuberculosis. A very fine distinction in the use 
of these two words is often made. Some maintain that phthisis 
refers to the chronic form of the disease and tuberculosis to a 
more acute, a more recent affair. The word “consumption,” so 
much in use by the laity, is undoubtedly derived from the pic- 
ture seen of the phthisical, and not of the tuberculous individual. 
The patient with marked cachexia, pronounced emaciation, fixed 
and immovable chest, prominent ribs, much loss in weight, skin 
pale and dry, with a facial expression which denotes difficult or 
labored breathing, is said to be a phthisical subject, but a patient, 
regardless of how long the disease has existed, who is suffering 
from chronic pulmonary disorder and does not show much dis- 
turbance, has a fairly good appetite, no less in weight or perhaps 
very little, and is able to be about, perhaps following his avoca- 
tion, is said to be tuberculous. If a patient is running a tempera- 
ture, pulse rapid, cough pronounced, expectorations free, many 
bacilli in the sputum, with ulceration and destructive processes 
going on in the lungs, with definite cavities, then we should say 
that such a patient is phthisical. On the other hand, if we should 
find one or both apices involved, localized rales, temperature not 
very high, pulse about 100, with little or no evidence of lung 
destruction, we say that such a person has tuberculosis. 
Note the distinct difference in the use of these words in path- 
ology. If in cutting through a lung or kidney we find many 
cavities, much tissue destruction with pus and caseous material, 
we refer to it as a phthisical lung or kidney. If, however, at 
autopsy we find the organs diseased, evidence of a tuberculous PHRASES, ETC., USED IN TUBERCULOSIS 
533 
process going on, but with very little or no tissue destruction, 
and no cavities, we speak of it as tuberculosis of the lung or kid- 
ney. Hence, the severity of the disease, regardless of duration 
or chronicity, tells us when to say phthisis and when tubercu- 
losis.1 
Sanitarium and Sanatorium. Sanitarium (from sanitas, health). 
A health station; a place or institution where the conditions are 
such as especially to promote health and vigor. The word is 
often incorrectly employed for sanatorium (from sanare, to heal), 
which is a hospital or place for curing those who are sick, espe- 
cially a private hospital. Gould’s Dictionary.) 
Sanitarium, an establishment for the treatment of diseased 
persons, especially a private hospital for convalescents or those 
who are not extremely ill. 
Sanatorium, from sanatorius, conferring health. 
(Dorland’s Medical Dictionary.) 
Sanitarium, (sanitary; L. sanitas, health). A health station 
or retreat. Sanatorium, from sanatary. (sanatorium, L. Sanare, 
to heal) : an establishment for the treatment of the sick, a rest 
for invalids. Sanitary and sanatary should not be confused. 
Sanitary has the more general meaning of pertaining to health, 
while sanatary signifies conducive to health. (Webster.un- 
abridged.) 
These are the definitions of the words “Sanitarium” and “Sana- 
torium” as found in our standard dictionaries. There exists still 
a great deal of uncertainty as to when to use the one and when, 
the other. It is becoming more and more accepted that when we 
refer to an institution for convalescent patients, a rest cure, a 
retreat, or a place where those are treated who are suffering from 
a nervous breakdown or from mental disorders, etc., we speak of 
a sanitarium, whilst those who are suffering from pulmonary 
tuberculosis, in the beginning or in the moderately advanced 
stage, and who desire to be hospitalized, are said to be assigned 
to a sanatorium. There are, however, exceptions to this rule 
which cannot always be altered. For instance, the large institu- 
tion in the City of Chicago for the care of the tuberculous is 
known as the Municipal Tuberculosis Sanitarium. The word 
lln this connection, it may be worthy of note to state that many well-known lung 
specialists make very little, if any, distinction in the use of these terms, using the word 
“phthisis” in a broad and general sense. They assert that any lesion in the lungs, 
regardless of size, or amount of involvement, if brought about by the Koch’s bacillus 
should be spoken of as a phthisical process and that the words “consumption,” “tuber- 
culosis,” “scrofula,” etc., have no special meaning, that they all refer to one and the 
same condition in the lungs, and that is “phthisis.” 534 
MISCELLANEOUS 
“sanitarium” was written into the bill, permitting the community 
to erect such an institution, at the time it was presented before 
the legislature in Springfield for passage. After its passage, it 
was not deemed advisable to make the change from “sanitarium” 
to "sanatorium,” owing to the fact that the change might affect 
the bill as it stood, so its promoters allowed it to stand. It 
should, however, read "Sanatorium” and not "Sanitarium,” to be 
in accordance with common usage. 
The use of the word tubercular in connection with a sana- 
torium, or a hospital, is not good language, and should not be 
used; there exists no such thing. To say "tubercular sana- 
torium,” "tubercular hospital,” does not mean an institution 
where patients suffering from pulmonary tuberculosis are being 
taken care of, but it signifies a building or structure on or in 
which nodular masses are being developed or growing. 
Ambulant, Ambulatory. From ambulant, to walk; conveying; 
pertaining to walking. 
These words are very frequently used when referring to tuber- 
culous patients who are not suffering from far advanced disease. 
A patient who is suffering from pulmonary tuberculosis and is 
being treated at the physician’s office, at a tuberculosis clinic, or 
dispensary, i. e., who is in a condition to come for treatment, is 
said to be an ambulatory tuberculous individual, whilst a patient 
whose condition does not permit him to come for assistance, but 
who must be taken care of at the sanatorium or his home is 
spoken of as a stationary, home, or bedfast patient. So long as 
the patient’s pulmonary condition remains quiescent and he is 
able to walk about, he is ambulatory, but in those cases in which 
the disorder progresses, the patient passes automatically into the 
bedfast or non-ambulatory class. 
Hilum pi. Hila and Hilus, Hilar, Etc. A difference of opin- 
ion exists amongst clinicians and teachers concerning the cor- 
rect use of these words. By the term Hilum we designate 
the depression, pit or recess observed in some organs, that is 
where blood vessels, etc., enter and leave the organ, as for 
instance, the hilum of the lung, kidney, liver, spleen, etc. 
Many writers and teachers maintain that the word Hilus has 
no place in literature in referring to these depressions and 
that the word hilum only should be used. Some dictionaries, for 
example, Gould’s, describes the word Hilum but does not men- 
tion the term Hilus. Both words are now so freely used in the PHRASES, ETC., USED IN TUBERCULOSIS 
535 
literature on tuberculosis that to both a distinct and definite 
place must be assigned. When referring to the depression or 
when used in the sense of a noun, say Hilum, like “the hilum of 
the lung,” “the liver,” etc., but when used in a generic term or 
as an adjective, say Hilus, like hilus tuberculosis, hilus disease, 
the hilus glands are enlarged, etc., plural the hilar shadows, etc. 
Allergy and Anergy. Allergy (opposite Anergy) or Allergie 
(opposite Anergie), Anaphylaxis (opposite Ananaphylaxis), Hy- 
persusceptibility, Sensibilitrice, Protein Sensitization, The Theo- 
bald Smith phenomenon, etc., are all more or less similar terms, 
expressing a similar phenomenon. 
In the chapter on Tuberculin (see Chapter XXIV), reference 
was made to the experimental work done by Koch. We may 
briefly refer here to these observations. When an animal (or a 
human) is injected with a body foreign albumin, in not too great 
an amount, no obvious effect is observed. If, however, after a 
given interval a second injection of the same albumin, even in a 
less quantity is administered, a severe reaction is noticeable, 
which may be so severe as to cause death in a comparatively 
short time. This reaction is referred to as shock, as anaphylactic 
shock, or simply as anaphylaxis. The first injection sensitized 
the animal to that particular albumin and the reaction is specific 
for that and no other. To this reaction, Richet (1903) applied 
the name “anaphylaxis” (from ana-phylaxis—against—protec- 
tion). This term is not well chosen as it does not express the 
phenomenon of sensitization or hypersensitiveness. 
Later when v. Behring discovered the hypersensitiveness to 
toxins and accurately described the phenomenon, he suggested 
the name allergy. The word “allergy” signifies that the body, 
after coming in contact with a foreign albumin undergoes a 
change, and becomes sensitized to a subsequent contact with 
that same albumin. This phenomenon is observed in the tuber- 
culously infected individual who, harboring in his organism a 
foreign albumin or protein (tuberculin), reacts when he comes 
in contact with a similar protein through either the skin or 
mucous surfaces. This is a specific reaction. 
Tuberculin. (A) The positive and negative reaction. When 
tuberculin is applied, diagnostically, to an individual who previ- 
ously has come in contact with the tuberculosis virus or perhaps 
is already slightly tuberculously diseased, a reaction is mani- 
fested at the point of application by the appearance of an area 536 
MISCELLANEOUS 
of hyperemia. The results are identical if the medicament is 
applied either to the mucous membrane or to a cutaneous surface, 
and the conjunctival or Calmette, the percutaneous or Moro, the 
cutaneous or v. Pirquet, and the intracutaneous or Mantoux are 
all, if the application proves positive, followed by a more or less 
reddened zone, indicating that the reacting individual some time 
in life came in contact with the tubercle bacillus. We designate 
this as a positive reaction. If, however, in a suspected individual 
the repeated application of tuberculin is not followed by a re- 
action, no reddened area, no systemic disturbance, then we say 
that the tuberculin test is negative. This, however, should not 
always be construed as signifying that the tested individual has 
never come in contact with the disease producing germs, because 
in advanced cases of pulmonary tuberculosis, and in recent infec- 
tions in which the newly infected organism has not been called 
upon to develop defense agencies, the tuberculin application is 
generally always negative. 
Briefly, then, when tuberculin is used for diagnostic purposes, 
and its application is followed by an area of redness, it is said to 
be positive; if not, negative. Hence, we speak of a positive or a 
negative tuberculin reaction or test. 
(B) The positive and negative phase. On the other hand, if 
tuberculin is given for curative purposes, therapeutically and not 
diagnostically, and if during the course of treatment, the patient 
evinces a feeling of well being, becomes much improved, his 
tuberculous process seems to be arrested, the activity becomes 
less (evidence of an immunizing response) we designate such 
findings as the positive tuberculin phase. If, however, during 
such a course of treatment, or perhaps if the therapeutic dose 
given produces untoward results such as a slight increase in 
fever, some malaise, nausea, or aggravated clinical symptoms, 
or after long use of tuberculin, no improvement in the clinical 
picture is noticeable, does not seem to influence the disorder in 
any way, then we allude to this as the negative tuberculin phase. 
In short, when tuberculin is used for diagnostic purposes we 
speak of either a positive or a negative reaction; if, however, 
given therapeutically, we observe its effect on the tuberculously 
diseased individual and speak then of a positive or a negative 
phase. 
Manifest Tuberculosis. (Evident tuberculosis.) This expres- 
sion is very much in use in foreign literature and is now used by PHRASES, ETC., USED IN TUBERCULOSIS 
537 
many phthisio-therapeutists. This term is usually applied when, 
in a given case of pulmonary tuberculosis, the conditions are 
such that by means of a chest examination the physical signs 
can be demonstrated to be positive. It indicates that the tuber- 
culosis is active. 
Latent Tuberculosis. This is the direct opposite of manifest 
tuberculosis. In writings on tuberculosis, it is also often re- 
ferred to as hidden, obscure, occult, pretuberculous, etc. It ex- 
presses an inactivity of the disease, and is said to follow after 
infection, the infection remaining quiet or latent, not active, until 
some body disturbance takes place when the infection is followed 
by manifest disease. So long as the infection remains as it is, 
presenting no symptoms or signs of activity, it is called latent. 
Clinical Tuberculosis. When both subjective and objective 
symptoms are present, and when by physical examination the 
disease is demonstrated, it is referred to as clinical tuberculosis. 
If, in the examination of the chest, the physical signs are ob- 
scure, not definite, the diagnosis doubtful, then it is not spoken 
of as clinical tuberculosis. Clinical tuberculosis may or may not 
be active, but the physical signs are positive. Hence, we may 
say that clinical tuberculosis is tuberculosis with or without ac- 
tivity ; manifest tuberculosis, tuberculosis with activity; and 
latent tuberculosis is suspected pulmonary tuberculosis in which 
the lesion is not clearly demonstrable by physical examination. 
Tuberculous Lesions. This denotes the physical changes 
which have taken place in the lungs after infection. It usually 
refers to the spots or areas in the lung which are now tuber- 
culous, are now abnormal or infiltrated. 
Immunity and Virulence—see Chapter 9—Immunity. 
Infection—see Chapter 5—Infection and Contagion. 
Subjective and Objective Symptoms—see Chapter 11—Symp- 
tomatology. 
The definitions of the words “quiescent,” “arrested,” “cured,” 
etc., are here fully given in the definition of the terms, “in- 
cipient,” “moderately advanced,” and “far advanced,” as sug- 
gested by the National Tuberculosis Association. 
Terms Used in Definition of Incipient Tuberculosis. 
1. Slight Constitutional Disturbance. Slight loss of appetite, 
of strength, of weight, lassitude; possibly slight acceleration of 
pulse or possibly slight elevation of temperature. The impair- 538 
MISCELLANEOUS 
ment of health may be so slight that the patient does not look or 
feel sick in the ordinary sense of the word. 
2. Slight Elevation of Temperature. Maximum temperature 
after rest for one hour, never over 99.5 to 100° F. by mouth, (or 
100.5° per rectum). 
3. Slight Acceleration of Pulse. Maximum pulse rate not over 
90 after rest for one hour, sitting or lying, except when due to 
causes other than tuberculosis. 
4. Absence of Tubercule Bacilli or “closed case.” Each 
monthly examination (if the sputum be negative) should consist 
of a careful microscopic examination, with a mechanical stage, 
of two smears, devoting at least three minutes to each smear, 
made from selected particles (from at least different parts) of the 
sputum on each of three successive days. The morning sputum 
should always be obtained, or, better, the minute bits that some 
arrested patients raise at very infrequent intervals. It is not yet 
deemed wise to insist on digestion and centrifugalization, or on 
inoculation of guinea pigs. If bacilli are present, the case is 
called “open” for the following 30 days. 
5. Infiltration. Physical signs of slight prominence of the 
clavicle, lessened movement of chest, narrowing of apical reson- 
ance with lessened movement of base of lung, slight or no change 
in resonance, distant or loud and harsh breathing with or without 
some change in the rhythm, (i. e., prolonged expiration), vocal 
resonance possibly slightly increased, or fine or moderately 
coarse rales present or absent. 
6. Apex. That portion of the lung situated above the clavicle 
anteriorly and the third dorsal spine, posteriorly. 
7. A Small Part of One Lobe. An area of one or two inter- 
costal spaces, or an area not exceeding 6 to 8 cm. (2 or 3 
inches) in extent, according to the size of the patient. 
Terms used in Definition of Moderately Advanced Tubercu- 
losis. 
1. Marked Impairment of Function, Either Local or Consti- 
tutional. Local: Marked dyspnea on exertion limiting seriously 
the patient s activity. Constitutional: Marked weakness, anemia, 
tachycardia. 
2. Moderate Extent of Localized Consolidation. An area of 
one-half lobe or less, which may involve both apices; marked 
dulness, bronchial or decidedly broncho-vesicular breathing; 
markedly increased vocal resonance; rales usually present. These PHRASES, ETC., USED IN TUBERCULOSIS 
539 
signs are apt to be sharply limited as to area instead of gradually 
shading into normal physical signs. 
3. Evidence of Destruction of Tissue. Presence of tubercle 
bacilli or elastic fibers in the sputum, or the presence of the 
physical signs of a cavity. There are no absolutely certain phy- 
sical signs of a cavity but a combination of any four of the 
following signs is to be taken as indicative of a cavity: (1) 
cracked pot note; (2) amphoric breathing; (3) intense whisper- 
ing pectoriloquy; (4) a veiled puff or post tussive suction; (5) 
bubbling or resonant rales. “Physical signs of softening” do not 
admit of any definition apart from that of cavity formation, and 
the term should not be used. 
4. Disseminated Fibroid Deposits. More or less localized 
areas of fibrous tissue, producing on physical examination some 
change or dulness in the percussion note, more or less increase 
of vocal resonance, harsh, suppressed, or broncho-vesicular 
breathing, rales usually sibilant or sonorous, but at times fine or 
moderately coarse. 
5. Serious Complications. These should be limited to tuber- 
culous complications, such as meningitis, pharyngitis, laryngitis, 
(except slight thickening of the posterior interarytenoid space, 
and superficial ulceration of a vocal cord), enteritis, peritonitis, 
nephritis, cystitis, orchitis, adenitis, (unless very slight), etc. 
Terms Used in Definition of Far Advanced Tuberculosis. 
1. Marked consolidation indicates dulness merging into flat- 
ness, bronchial or tubular breathing, and other signs of consoli- 
dation as defined above. 
Classification of Terms Used Upon the Discharge of Patient. 
(a) Apparently Cured (formerly “cured”). All constitutional 
symptoms and expectoration with bacilli absent for a period of 
two years under ordinary conditions of life. 
(b) Arrested. All constitutional symptoms and expectoration 
with bacilli absent for a period of six months; the physical signs, 
those of a healed lesion. 
(c) Apparently Arrested (formerly “apparently cured”) All 
constitutional symptoms and expectoration with bacilli absent 
ior a period of three months; the physical signs, those of a healed 
lesion. 
(d) Quiescent (formerly “arrested”). Absence of all constitu- 
tional symptoms; expectoration with bacilli may or may not be 540 
MISCELLANEOUS 
present; physical signs stationary or retrogressive; the foregoing 
condition to have existed for at least two months. 
(e) Improved. Constitutional symptoms lessened or entirely 
absent; physical signs improved or unchanged; cough and ex- 
pectoration with bacilli usually present. 
(f) Unimproved. All essential symptoms and signs unabated 
or increased. 
(g) Died. 
Terms Used in Definition of “Apparently Cured.” 
1. Constitutional Symptoms (absent). These include eleva- 
tion of temperature, loss of weight, loss of strength, night sweats, 
chills, tachycardia, cyanosis, loss of appetite, amenorrhea, etc. 
2. Physical Signs of Healed Lesion. These may embrace 
every physical sign of infiltration or consolidation (see above) 
with the exception of rales, which must be permanently absent, 
except possibly a few fine rales at the base, probably atelectatic 
or marginal in origin, at one apex, or over a small part of one 
lobe. Rales in the latter two places are to be heard only during 
the cough, at the end of a prolonged expiration, or late in inspira- 
tion which follows the cough. 
Terms Used in Definition of “Improved.” 
Constitutional Symptoms Lessened or Entirely Absent. By 
this is meant an improvement in the general condition as shown 
either by a gain in both weight and strength or by reduction of 
previous febrile temperature at normal without loss of strength. 
Terms Used in Definition of “Unimproved or Progressive.” 
Essential Symptoms and Signs. These include, among others, 
weight, strength, appetite, night sweats, hemoptysis, pleurisy, 
dyspnea, temperature, pulse rate, dulness, changes in vocal 
resonance and respiratory movement, rales. 
Terms Used in Definition of “Cured.” 
Ordinary Condition of Life. This term as used implies that 
the patient is able to live in an environment where he is able to 
support himself without the assistance of others, or to live in his 
former surroundings and pursue his former occupation. 
Terms in Definition of “Onset.” 
Catarrhal, Pleuritic, Insidious, Hemorrhagic, Febrile, etc. 
Definition of Term “Temperature on Admission.” 
Average maximum temperature for the first seven days. 
Definition of “General Condition on Admission and on Dis- 
charge.” PHRASES, ETC., USED IN TUBERCULOSIS 
541 
Favorable, Unfavorable. 
Definition of Term, “Temperature on Discharge/’ 
Average maximum temperature for the last two days. 
Definition of Term “Digestion on Admission and on Dis- 
charge.” 
Impaired or unimpaired. 
TABLE OF NORMAL STANDARD WEIGHTS—MALES 
Inches 
Stripped and Without Shoes 
Normal Weight of an Individual According to Height and Age 
60 
61 
62 
63 
64 
65 
66 
67 
68 
69 
70 
71 
72 
73 
74 
75 
76 
5 ft. 
5 1 
ft. 6 in. 
6 ft. 
Age 
Aee 
18 
108 
111 
115 
118 
122 
126 
130 
134 
139 
143 
148 
153 
157 
156 
167 
172 
177 
18 
19 
108 
112 
116 
119 
123 
127 
131 
135 
140 
144 
149 
154 
158 
163 
168 
173 
178 
19 
20 
109 
113 
117 
120 
124 
128 
132 
136 
141 
145 
150 
155 
159 
164 
169 
174 
179 
20 
21 
110 
114 
116 
121 
125 
129 
133 
137 
142 
146 
151 
156 
160 
165 
170 
175 
180 
21 
22 
111 
115 
117 
122 
126 
130 
134 
138 
143 
147 
152 
157 
161 
166 
171 
176 
181 
22 
23 
111 
115 
119 
123 
127 
130 
135 
139 
144 
148 
153 
158 
162 
167 
172 
177 
182 
23 
24 
112 
116 
120 
123 
128 
131 
136 
140 
145 
149 
154 
159 
163 
168 
173 
178 
183 
24 
25 
113 
117 
120 
124 
128 
132 
136 
141 
146 
150 
155 
160 
164 
169 
174 
179 
184 
25 
26 
114 
118 
121 
125 
129 
133 
137 
142 
146 
151 
156 
161 
165 
170 
175 
180 
185 
26 
27 
114 
119 
120 
126 
130 
134 
138 
142 
147 
152 
157 
162 
166 
171 
176 
181 
186 
27 
28 
115 
119 
122 
126 
130 
134 
139 
143 
148 
153 
158 
162 
167 
172 
177 
182 
187 
28 
29 
116 
119 
123 
127 
131 
135 
140 
144 
149 
154 
159 
163 
168 
173 
178 
183 
188 
29 
30 
116 
120 
124 
128 
132 
136 
140 
144 
149 
154 
159 
164 
169 
174 
179 
184 
189 
30 
31 
117 
121 
124 
128 
132 
137 
141 
145 
150 
155 
160 
165 
170 
175 
180 
185 
190 
31 
32 
117 
121 
125 
129 
133 
137 
142 
146 
151 
156 
161 
165 
171 
176 
181 
186 
191 
32 
33 
118 
122 
125 
130 
134 
138 
142 
147 
151 
156 
162 
166 
171 
176 
182 
186 
191 
33 
34 
118 
122 
126 
130 
134 
139 
143 
147 
152 
157 
162 
167 
172 
177 
182 
187 
192 
34 
35 
119 
123 
126 
131 
135 
139 
144 
148 
153 
158 
163 
167 
173 
178 
183 
188 
193 
35 
36 
119 
123 
127 
131 
135 
140 
144 
149 
153 
158 
164 
167 
173 
178 
183 
188 
193 
36 
37 
120 
123 
127 
132 
136 
140 
145 
149 
154 
158 
164 
169 
174 
179 
184 
189 
194 
37 
38 
120 
124 
128 
132 
136 
141 
145 
150 
154 
159 
165 
169 
175 
180 
184 
189 
195 
38 
39 
121 
124 
128 
133 
137 
141 
146 
1 50 
155 
160 
165 
170 
175 
180 
185 
190 
195 
39 
40 
121 
125 
128 
133 
137 
141 
146 
150 
155 
160 
165 
170 
176 
180 
185 
190 
196 
40 
41 
121 
125 
129 
133 
138 
142 
146 
151 
156 
160 
165 
171 
176 
181 
186 
190 
196 
41 
42 
122 
125 
129 
134 
138 
142 
147 
151 
156 
161 
166 
171 
177 
181 
186 
191 
196 
42 
43 
122 
126 
130 
.134 
138 
143 
147 
1 52 
157 
162 
167 
172 
177 
182 
187 
192 
197 
43 
44 
122 
126 
130 
135 
139 
143 
147 
152 
157 
162 
167 
172 
178 
182 
187 
192 
197 
44 
45 
123 
126 
130 
135 
139 
143 
148 
153 
157 
162 
168 
173 
178 
183 
187 
192 
198 
45 
46 
123 
127 
131 
135 
139 
144 
148 
153 
158 
162 
168 
173 
178 
183 
188 
192 
198 
46 
47 
123 
127 
131 
135 
140 
144 
149 
153 
158 
163 
168 
173 
179 
183 
188 
193 
198 
47 
48 
123 
127 
131 
136 
140 
144 
149 
153 
158 
163 
169 
174 
179 
183 
189 
193 
199 
48 
49 
123 
127 
131 
136 
140 
145 
149 
154 
159 
163 
169 
174 
179 
184 
189 
193 
199 
49 
50 
124 
128 
132 
136 
140 
145 
149 
154 
159 
163 
169 
174 
180 
184 
189 
193 
199 
50 
51 
124 
128 
132 
137 
141 
145 
150 
154 
159 
164 
170 
174 
180 
184 
189 
194 
200 
51 
52 
124 
128 
132 
137 
141 
145 
150 
154 
159 
164 
170 
175 
180 
184 
189 
194 
200 
52 
53 
124 
128 
132 
137 
141 
145 
150 
155 
160 
164 
170 
175 
180 
185 
190 
195 
200 
53 
54 
124 
128 
132 
137 
141 
145 
150 
155 
160 
165 
170 
175 
180 
190 
190 
195 
200 
54 
55 
124 
128 
132 
141 
148 
150 
155 
160 
165 
170 
175 
180 
185 
190 
195 
196 
200 
55 
Deduct about 10% from above 
: weight in case of i 
female. 542 
CLINICAL TUBERCULOSIS 
No. 0 Take 1 cc O. T. and 9 cc Na Cl. Solution (phenolized) =No. 0 and 1 cc No. 0=1 in 10 (dg. 0.1 or 0.1)=1 in 10 or a 10% Solu- 
tion =1% grain per cc 
No. 1 Take 1 cc No. 0 and 9 cc Na Cl. Solution (phenolized) =No. 1 and 1 cc No. 1=1 in 100 (eg. 0.01 or 0.01)=1 in 100 or a 1% So- 
lution...: =1/6 grain per cc 
No. 2 Take 1 cc No. 1 and 9 cc Na Cl. Solution (phenolized) =No. 2 and 1 cc No. 2=1 in 1000 (mg. 0.001 or 0.001)=1 in 1000 or a 
1/10 of 1% Solution =1/60 grain per cc 
No. 3 Take 1 cc No. 2 and 9 cc Na Cl. Solution (phenolized) =No. 3 and 1 cc No. 3=1 in 10.000 (dmg. 0.0001 or 0.1 mg.)= 1 in 10.000 
or a 1/100 of l%Solution =1/600 grain per cc 
No. 4 Take 1 cc No. 3 and 9 cc Na Cl. Solution (phenolized)=No. 4 and 1 cc No. 4=1 in 100.000 (cmg. 0.00001 or 0.01 mg.)=l in 
100.000 or a 1/1000 of 1% Solution=l/6000 grain per cc 
No. 5 Take 1 cc No. 4 and 9 cc Na Cl. Solution (phenolized)=No. 5 and 1 cc No. 5=1 in 1.000.000 (mmg. 0.000001 or 0.001 mg.)=l in 
1.000000 or a 1/10.000 of 1% Solution=l/60.000 grain per cc 
The diagnostic or probationary dose of Tuberculin equals 1/10 cc of No. 1 (0.001) this is approximately 1/60 grain. Giving a less amount 
than the diagnostic or probationary dose of Tuberculin equals 1/20 cc of No. 1 (0.0005) this is approximately 1/120 grain, etc. 
The Therapeutic Dose of Tuberculin 
The initial therapeutic dose of Tuberculin usually equals 1/10 cc of No. 5 (0.001 mg'.) this is approximately 1/600.000 of a grain. If a 
smaller dose is desired, then the initial therapeutic dose of Tuberculin usually equals 1/20 cc of No. 5 (0.0005 mg.) this is approximately 
1/1.200.000 of a grain, etc. 
We see that the diagnostic dose of Tuberculin is really 10.000 times that of the initial therapeutic dose. 
TABLE OF STANDARD TUBERCULIN DILUTIONS AND THEIR EQUIVALENTS 
The Diagnostic Dose of Tuberculin MISCELLANEOUS 
543 
Fig. 61. The Road to Health for the Tuberculous, illustrating the six indispensable and 
necessary factors for the bringing about of an arrest of the Pulmonary Tuberculous 
disease. 
Designed by a patient now suffering from Pulmonary Tuberculosis and who is religiously 
observing these six rules and that to the letter, confident that by so doing her tuberculous 
process will become promptly arrested. 
For description of these six most important and necessary rules see page 207, Chapter 
19, “The Cure of the Tuberculous.” INDEX OF NAMES OF AUTHORS AND CON- 
TRIBUTORS WITH PAGE INDEX 
Adamson, 440 
Albee, F. H., 406 
Albrecht, E., 36 
Albrecht, H., 36 
Areteus, 3 
Aristotle, 3 
Arloing, F., 257, 502 
Arndt, C., 262 
Arneth, 473, 491 
Auengrubber, Leopold, 125 
Avicenna, 3 
Babes, 508 
Baccelli, 341 
Bacon, C. S., 352, 359 
Baer, 247 * 
Baglivi, 229 
Baillie, Mathew, 5 
Baldwin, E. R., 276 
Balfour, A., 22 
Bandelier, B., 511 
Bang, 23 
Bardeleben, v. H., 350, 359 
Barney, 424, 425, 427 
Barry, 230 
Bauer, F., 459 
Baumgarten, v., 21, 56 
Bayle, 5 
Bazin, 438 
Behring, v. E., 8, 296, 535 
Benecke, 453 
Beraneck, E., 314 
Bernard, 458 
Bertrand, 256 
Bickersteth, 230 
Bignold, 458 
Bonnett, 256 
Bordet, 500 
Bowditch, Vincent, 276, 353 
Bowen, 432 
Brauer, Ludolph, 231 
Brehmer, Herman, 212, 274, 453 
Bridge, Norman, 269 
Broussais, 5 
Brown, Lawrason, 33, 457, 494 
Briick, 502 
Buchner, 500 
Buhl, 6, 454 
Callahan, 518 
Calmette, A, 8, 22, 325 
Carnot, 365 
Carson, James, 229 
Carstens, J. H., 348 
Casselberry, Wm. E., 373 
Celsus, 3,255 
Chaveaux, 7 
Cheyne, 403 
Constatt, 230 
Coonley, 511 
Cornet, 8, 17,196, 270, 276, 305 
Corper, H. J., 506, (HJC) 503, 518 
Courmont, 502 
Craig, C. F., 503 
Crofton, A. C., 519 
Cruveilhier, 6, 529 
Damoiseau, 338 
Damsch, 508 
Daus, S., 234 
Davis, 273 
Davis, C. Henry, 361 (CHD) 
DeCroix, 453 
D’Espine, 289 
De la Camp O., 298 
Demme, 511 
Deny, 313 
Dettweiler, 212, 270, 275 
DeWitt, Lydia M., 251 
Deyche, 253, 314 
Diebel, 350 
Douglas, S. A., 348 
Dudgeon, 503 
Dunham, K., 172 
Dunton, 273 
Ebright, 419 
Ehler, 230 
Ehrlich, 250,251,316 
Ellermann, V., 481, 509 
Ellis, 338 
Emerson, Haven, 462 
Engel, 453 
Enos, 385 
Erlandson, A., 481, 509 
Esbach, 481 
Esherich, 327 
Fabricius, 4 
Faure, 256 
Felker, 420 
Ferran, Jaime, 15 
Fildes, 503 
Finkler, 250 
Finson, Niels R., 257, 440 
Floyd, C. F., 232, 353 
Fluegge, 17 
545 546 
AUTHORS’ AND CONTRIBUTORS’ INDEX 
Forester, 4 
Forlanini, Carlo, 230, 233, 244 
Fossier, 451 
Fracastori, 4 
Fraenkel, A., 270, 276 
Frankie, 451 
Frankenthal, 360 
Fraser, Elizabeth, 503 
Fremolt, 450 
Freudenthal, Wolff, 386 
Freund, 111, 249 
Friedench, 248 
Friedlander, 7 
Friedmann, F. F., 315 
Furbringer, 458 
Funk, 349 
Gabrilowitch, 314 
Gaffky, 482 
Galenus or Galen, 3 
Garland, 338 
Gamier, 511 
Gengou, 500 
Ghon, A., 36, 291 
Giepel, 353 
Gilbert, 365 
Gilver, 504 
Goldscheider, 141 
Graetz, 262 
Grawitz, 490 
Grocco,339 
Gwerder, 247 
Hamburger, Franz, 305 
Hamman, Louis, 232 
Harras, 249 
Harris, J. E. J., 348 
Hart, 249 
Hauser, 352 
Heflebower, Roy C., 517 
Heiman, H., 504 
Heise, 189 
Hektoen, 501 
Herodotus, 255 
Herriott, 277 
Hervouet, 35 
Hewson, William, 229 
Hibbs, R. A., 406 
Highman, 437 
Hippocrates, 3, 195, 229, 255, 273 
Hirsch, 454 
Hoffmann, 386, 502 
Holt, 511 
Houghton, 230 
Hunter, John Sir, 499 
Hyman, 23 
Israel, 424 
Itard, Jean Marie Gaspard, 229 
Jacob, P., 249 
Jacobi, A., 353 
Jaksch, v., 513 
Joest, Ev 515 
Joseph, 420 
Jousset, 521 
Kapsammer, 410 
Kenyon, E. L., 387 (ELK) 
Keyes, 424, 427 
Kirkbride, 273 
Kisch, 262 
Klebs, Edwin, 7 
Klencke, 6 
Klotz, 493 
Koch, Robert, 7, 250, 308, 310, 311 
Kocher, A., 257 
Koranyi, F. v., 289 
Kornfeld, 422 
Kortum, 6 
Koster, 7 
Kozlow, 509 
Kraus, 454 
Krause, 495 
Krause, Allen K., 329 
Krause, Robert B., 251 
Kretschmer, Herman L., 428 (HLK) 
521 
Kroenig, 140, 141, 143 
Kryger, v., 451 
Kupferle, 353 
Kurashige, 494 
Kiister, 411 
Kiiss, 35 
Kutschera, v. 
Laennec, Rene, Theophile Hya- 
cinthe, 5, 149, 195, 229, 454 
Landis, 351 
Landouzy, L., 336, 454 
Lange, 481, 509 
Lange, Miss Linda, 504 
Lannelongue, 7 
Lapham, Mary E., 232 
Lebert, 6, 256, 276, 350 
LeCounte, 256 
Lemke, A. F., 230 
LePeyre, 256 
Leschke, E., 253, 314 
LeSourd, 502 
Lessieur, 484 
Lewis, Paul A., 251, 505 
Levy-Valenci, 484 
Liebermeister, 270, 495 
Liehe, 276 
Linden v. Countess, 251 
Lippmann, 494 
Lobal, 256 
Lobenstine, R. W., 350 
Lockard, L. B., 385 
Loeb, Jacque, 254 
Loschke, 458 
Louis, 453 
Lowenstein, 318 AUTHORS’ AND CONTRIBUTORS’ INDEX 
547 
Lucien, 458 
Lucke, 503 
Lukens, Robert McD., 386 
Lunton, 273 
Luton, 250 
Lyden, v., 451 
Malgal, 259 
Mallory, 493 
Mangetus, 5 
Mantoux Ch., 8, 324, 326 
Maraeliano, 316 
Marfan, A. B., 511 
Mark, Louis, 510 
Marmoreck, 316 
Marshak, 518 
Mathews, 350, 352 
Matthews, H. B., 43 
Maxson, Louis H., 515 
May on, 444 
McCruddin, 520 
McIntosh, 503 
McSweeny, 351 
McVicker, 23 
Meek, 503 
Meissel, 494 
Meissen, 251,276 
Meisenburg, 451 
Metschnikoff, 500 
Metz, A. R., 305 (ARM) 
Miller, H. R., 353 
Miller, J. A., 503 
Miller, W. S., 40 
Morgagni, 4 
Moritz, 453 
Moriz-Weisz, 516 
Moro, Ernest, 326 
Morris, Everett, 243 (EM) 
Morton, 6 
Morton, Richard, 4 
Much, Hans, 151,253,314, 481 
Muller, C., 453, 454 
Murphy, J.B., 230, 234, 246 
Nardi, 460 
Naumann, 459 
Neisser, 290, 501, 502 
Neumann, 455 
Nitsche, 481, 509 
Norris, Charles, 347, 352, 353 
Norris, G. W., 455 
Novak, 353 
Oliver, Edward A., 440 (EAO) 
Ollier, 257 
Osier, 336 
Otis, E. O., 272 
Page, Charles, 276 
Pankow, 353 
Pannwitz, 349 
Panwitz, 257 
Paracelsus, 4 
Parola, Luigi, 230 
Parrot, 35 
Paterson, Marcus, 8, 280 
Peacock,453 
Penzoldt, F., 276 
Petroff, S. A., 503, 509 
Petruschky, 289, 317, 324 
Pfeiffer, Richard, 500 
Pinel, 273 
Piorry, 232 
Pirquet, v. C., 8, 291, 296, 326 
Pliny, 3 
Polak, J. O., 350, 352 
Poncet, 257, 455 
Ponndorf, 311 
Posen, Marcus, 467 
Potain, 453 
Pottenger, F. M., 76, 460 
Pratt, Joseph H., 276 
Proyer, John A., 264 
Radcliffe, 503 
Ramadge, 230 
Ranzal, 353 
Rauchfuss, 339 
Ravaut, 520, 521 
Raw, Nathan, 8, 313 
Reed, Eva Charlotte, 273 
Reeder, William G., 446 (WGR) 
Rest, 365 
Rhoden, 276 
Richet, 535 
Ridard, R., 263 
Rieder, 164 
Ritter, 482 
Robin. A., 519 
Robinson, 232 
Rodriguez, Alves, 485 
Roentgen, Wm. K., 164 
Roepke, O., 511 
Rogers, 484, 511 
Rokitansky, 7, 450, 452, 453, 460 
Rollier, 257, 263. 
Romberg, v., 452 
Romer, P., 327 
Rose, 467 
Rose Cassie Bell, 293, 193 (CBR) 
Rosenberger, Rundle C., 515 
Rosenthal, 164 
Rosthorn, v., 350 
Rothschild, 232 
Roux, 257 
Rumph E., 494 
Rush, Benjamin, 5, 273 
Ryerson, Edwin W., 409 (EWR) 
Sahli, 317 
Sansum, 358 
Sauer, K., 451 
Sauerbruch, v. F., 231, 247 
Saugmann, Prof. Chr., 240,244 548 
AUTHORS’ AND CONTRIBUTORS’ INDEX 
Scarborough, 349 
Schaudinn, 502 
Schlimpert, 351 
Schmorl, 353 
Schnitter, 494 
Schroetter, v. Herman, 231, 257, 262 
Schueppel, 7 
Schultzen, 269, 270, 271 
Sciallero, 453 
Senator, 518 
Sergent, Emil, 350 
Sissons, 35, 47 
Sloan, Martin T., 232 
Smith, 290 
Smith, E., 22 
Smith, Theobold, 8 
Sobatta, 519 
Spaeth, 230 
Spengler, Carl, 253, 313, 314, 328 
Spengler, Lucius, 231 
Spitzer, 43 
Squire, 451 
Steger, 116 
Sterling, 457 
Sternberg, 346 
Stiller, 115 
Stokes, 453 
Strauss, 251 
Stroutz, 247 
Sturm, 494 
Sweaney, 503 
Sylvius, 4 
Teissier, G., 455 
Thompson, St. Clair, Sir, 374, 381 
Tracy, Susen E., 274 
Traube, 451 
Trembley, Charles C., 349, 359 
Trousseau, 365 
Trudeau, Edward L., 8, 275 
Tuffier, 247 
Turban, 349 
Turban, K., 270, 276, 454 
Turek, 256 
Tussenbrock, Catherine van, 358 
Uhlenhuth, 481 
Ullmann, 397 
Veit, 359 
Velden, R., van den, 364 
Villemin, 6 
Virchow, 6, 453, 465 
Voit, Carl, 524 
Walker, 509 
Walther, 276 
Wang, 511 
Wang, S. L., 351 
Wassermann, 501, 502 
Webb, Gerald, 232 
Weber, H., 276 
Weber, Parker F., 467 
Wechsberg, 501 
Weichselbaum, 494 
Weigert, 7 
Weil, Ferdinand, 466 
Weinberg, 353 
Weir, 503 
Wells, H. Gideon, 251 
Weiss-Moriz, 516 
Wheaton, C. L.. 118, 278, 283 (C. 
L. W.) 
Widal, 502, 520, 521 
Wildbolz, H., 410 
Wilder, 358 
Williams, Mary Hamilton, 306 
Wilms, 247 
Wilson, M. A., 504 
Winternitz, 257, 286 
Wolff-Eisner, 311, 326, 483 
Wollenstein, Martha, 353 
Woodruff, I. O., 353 
Woodyatt, 358 
Wright, 281, 318 
Wunderlich, 230 
Wyman, 273 
Young, 504 
Zeissler, 495 
Ziemann, H., 22 
Zirkel, 353 BIBLIOGRAPHIC INDEX 
The literature consulted: (a) Books, Monographs, etc.; (b) Annals, 
Transactions from Medical Assemblies, Reprints, etc.; (c) Medical Jour- 
nals, Pamphlets, Reports, Essays, etc.; (d) addendum. 
The figures in parenthesis ( ) given throughout the text refer to the respec- 
tive number appearing before the quoted book, pamphlet, etc., in this index. 
(a) Books, Monographs, etc. 
1. A Guide to the Clinical Examination of the Blood. Richard C. Cabot, 
M. D., Boston. 
2. Anatomy, Descriptive and Surgical. Henry Gray, F. R. S. 
3. Anatomy, Hand Atlas of Human Anatomy. Werner v. Spalteholz, 
1903. 
4. Anatomy, Surgical. Manual of Surgical Anatomy. Medical Depart- 
ment, U. S. Army and Navy. 
5. Anatomy. Text-Book of Anatomy. D. J. Cunningham, F. R. S. 
6. A Text-Book of Diseases of the Nose and Throat. D. Braden Kyle, 
M. D., Philadelphia, 1909. 
7. A Text-Book upon the Pathogenic Bacteria. Joseph McFarland, 
M. D. 
8. A Treatise on Diagnostic Methods of Examination. Professor Her- 
mann Sahli (American Edition). 
9. Dictionary; The American Pocket Medical. W. A. Newman Dorland, 
M. D. 
10. Dictionary; An illustrated, of Medicine, Biology and Allied Sciences. 
George M. Gould, M. D. 
11. Dictionary; International, of the English Language. Webster’s Un- 
abridged. Noah Porter, D. D. 
12. Dictionary; The American Illustrated Medical. W. A. Newman Dor- 
land, M. D., 1917. 
13. Dictionnaire Encyclopedique des Sciences Medicales. Paris, 1876. 
14. Dermatology. Highman, M. D., McMillan, 1921. 
15. Der primaere Lungenherd bei der tuberkulose der Kinder. Anton 
Ghon, 1912. 
16. Diagnostic Methods. Dr. Ralph W. Webster, Sixth Edition, 1920. 
17. Diagnostisch—therapeutisches Taschenbuch der tuberkulose. Dr. D. 
Epstein, 1910. 
18. Die Heliotherapie der Tuberkulose. A. Rollier, Leysin, 1913. 
19. Die Immunitatswissenschaft. Dr. Hans Much, 1911. 
20. Die Klinik der Tuberkulose. Drs. B. Bandelier and O. Roepke, 1912. 
21. Die Prognossenstellung bei der Lungentuberkulose. Drs. Kuthy and 
Wolff-Eisner, 1914. 
22. Die Tuberkulose. Dr. G. Cornet, 1907. 
23. Diseases of the Bronchi, Pleura and Lungs. Nothnagel’s Encyclo- 
pedia. 
24. Diseases of the Skin. Oliver S. Ormsby—Lea & Febiger. 
25. Diseases of the Skin. William Allen Pusey. 
26. Diseases of the Skin. Stelwagon—W. B. Saunders. 
549 550 
BIBLIOGRAPHIC INDEX 
27. Diseases of the Upper Respiratory Tract. P. Watson Williams, M. D., 
London, 1907. 
28. Friihdiagnose und tuberkulose—Immunitat. Dr. A. Wolff-Eisner, 
1909. 
29. Histopathology of Diseases of the Skin. Unna. 
30. History of Medicine. Fielding H. Garrison, M. D., 1913. 
31. Lectures on the Diagnosis and Treatment of Diseases of the Chest. 
E. Fletcher Ingals, A. M., M. D. 
32. Lehrbuch der Lungentuberkulose. Dr. Alfred Moeller, 1910. 
33. Lungenchirurgie. Drs. C. Garre and H. Quincke, 1912. 
34. Manual of Physical Diagnosis. James Tyson, M. D. 
35. Muscle Spasm and Degeneration. Dr. F. M. Pottenger, 1912. 
36. Orthopedic and Reconstructive Surgery. F. H. Albee—W. B. Saun- 
ders, 1919. 
37. Pathological Technique. Mallory & Wright, 1908. 
38. Pathology of the Skin. Macleod. 
39. Practical Urinalysis and Urinary Diagnosis. Charles H. Purdy. 
40. Principles and Practice of Physical Diagnosis. John C. DaCosta, Jr., 
1908. 
41. Pulmonary Tuberculosis. Maurice Fishberg, M. D., N. Y., 1919. 
42. Pulmonary Tuberculosis. Edward O. Otis, M. D., Boston, 1917. 
43. Physical Diagnosis. Richard C. Cabot, M. D., 1909. 
44. Taschenbuch der Diagnostik and Therapie der Lungen-tuberkulose. 
Dr. Heinrich Gerhartz, 1913. 
45. Taschenbuch der Klinischen Haematologie. Dr. v. Domarus, 1912. 
46. The Diagnosis and Treatment of Pulmonary Tuberculosis. Dr. Fran- 
cis M. Pottenger, 1908. 
47. The Principles and Practice of Medicine. William Osier, M. D. 
48. The Suppression of Tuberculosis. Prof. E. v. Behring. Translation 
by Charles Bolduan, 1904. 
49. Treatise on Orthopedic Surgery. Royal Whitman. Lea & Febiger, 
1919. 
50. Tuberculosis, a Treatise by American Authors. Arnold C. Klebs, 
1909. 
51. Tuberculin Treatment. Drs. Clive Riviere & Egbert Morland, 1912. 
52. Uber Tuberkulinbehandlung. Prof. Dr. Hermann Sahli, 1913. 
(b) Annals, Transactions from Medical Assemblies, 
Reprints, etc. 
53. Annals of Otology, Rhinology and Laryngology. Wolff Freudenthal. 
The Possibilities of Curing Advanced Laryngeal Tuberculosis. Vol. 
29, p. 545. Sept., 1920. 
54. Transactions of the Sixth International Congress on Tuberculosis. 
Washington, D. C., 1908. 
55. Transactions of the National Association for the Study and Preven- 
tion of Tuberculosis. 1905 to 1917 inclusive. 
56. Transactions of the National Tuberculosis Association. 1918 to 1922 
inclusive. 
57. Transactions of the American Laryngological Association. Present 
day Aspects of Laryngeal Tuberculosis. H. Arrowsmith, 1917, BIBLIOGRAPHIC INDEX 
551 
58. Transactions of the American Laryngological Association. The Prog- 
nostic Importance of Tuberculosis of the Larynx by Sir St. Clair 
Thompson, M. D., p. 12. 1919. 
59. Transactions of the Robert Koch Society for the Study of Tubercu- 
losis. From February 11, 1913, to April 20, 1916. 
60. Transactions, Lectures on Tuberculosis. Delivered before the “Theo- 
dore B. Sachs’ Tuberculosis Study Class,” 1916. 
61. Reprints. Artificial Pneumothorax in Pulmonary Tuberculosis. Le- 
Roy S. Peters. 111. Medical Journal, Oct., 1916, and N. Y. Medical 
Journal, 1919. 
62. Reprint. An Intensive Method of Treating Tuberculosis. The Milk 
Treatment. J. H. Crewe, Mayo Clinic, Nov. 14, 1917. 
63. Reprint. Induced Pneumothorax. Its use in the treatment of Pul- 
monary Tuberculosis with a report of 202 cases. Everett Morris. 
The Review of Tuberculosis—Vol. 2, Oct., 1918. 
64. Reprint. Integument Atrophy. A sign of Diagnostic Importance in 
early Pulmonary Tuberculosis. Clarence L. Wheaton, Journal A. M. 
A., Vol. 54, p. 2133, 1910. 
65. Reprint. Pregnancy in Tuberculosis. Edward M. Heacock, 111. Med. 
Journal, February, 1917. 
66. Reprint. Pulmonary Tuberculosis. A. F. Lemke. Journal A. M. A., 
1899. 
67. Reprint. Surgery of the Lung. J. B. Murphy. Journal A. M. A., 
vol. 31, p. 151. 341 July, 1898. 
68. Reprint. The Significance of the Diazo and the Urochromogen Re- 
action in Pulmonary Tuberculosis. Stephen A. Douglass. Ohio State 
Med. Journal, 1917. 
69. Reprint. Tuberculosis and Pregnancy. S. A. Douglass and J. E. J. 
Flarris. The American Review of Tuberculosis, 1917. 
70. Reprint. Work for the Tuberculous. David A. Stewart. Manitoba 
Sanatorium. The American Review of Tuberculosis, 1920. 
The Author's Reprints 
71. Reprint No. 3. Corn Oil in the Treatment of Pulmonary Tubercu- 
losis. Journal A. M. A., Vol. 51, p. 39, July 4, 1908. 
72. Reprint No. 4. The Care of the Tuberculous at The Central Free 
Dispensary of the Chicago Tuberculosis Institute. Journal A. M. A., 
Vol. 53, p. 1390, Oct. 23, 1909. 
73. Reprint No. 5. A Contribution to the Study of Pulmonary Tuber- 
culosis in its Relation to Albuminuria. Transactions of the Sixth 
Annual Meeting of the National Association for the Study and Pre- 
vention of Tuberculosis, 1910. 
74. Reprint No. 6. Hypotention and Tachycardia in the Tuberculous. 
Transactions of the Seventh Annual Meeting of the National Asso- 
ciation for the Study and Prevention of Tuberculosis, 1911. 
75. Reprint No. 7. The Therapeutic Application of Tuberculin in the 
Treatment of Ambulatory Pulmonary Tuberculosis. Journal A. M. 
A., Vol. 57, p. 93, July 8, 1911. 552 
BIBLIOGRAPHIC INDEX 
76. Reprint No. 8. The Value of Tuberculin in the Diagnosis and Treat- 
ment of Pulmonary Tuberculosis. Illinois Medical Journal, Dec., 
1911. 
77. Reprint No. 9. The Pathogenesis of the Glandular or Primary 
form of Infantile Tuberculosis. Illinois Medical Journal, Jan., 1913. 
78. Reprint No. 10. The Albumin Analysis of the Sputum. Its great 
value as a reliable and positive diagnostic laboratory method for 
differentiating Pulmonary Tuberculosis from other Pulmonary Dis- 
eases. Medical Record (N. Y.), April 26, 1913. 
79. Reprint No. 11. The present Status of Tuberculin and its Therapeutic 
Limitations. Illinois Medical Journal, June, 1913. 
80. Reprint No. 12. Pulmonary Hemorrhages. Various methods for 
Treating and Controlling. Mechanical, Medical, and Opotherapeu- 
tical. Prophylaxis. Chicago Medical Recorder, May, 1916. 
81. Reprint No. 13. An Anomalous Temperature Curve in the Moder- 
ately Advanced Tuberculous. Journal A. M. A., Vol. 62, pp. 915, 
March 21, 1914. 
82. Reprint No. 14. Early Recognition of Pulmonary Tuberculosis by a 
study of the Lymphocytic Picture and Albumin Content of Sputum. 
Journal A. M. A., Vol. 63, p. 2283, Dec. 26, 1914. 
83. Reprint No. 15. The Cutaneous Tuberculin Vaccination Method. 
Transaction of the eleventh annual Meeting of the National Associa- 
tion for the Study and Prevention of Tuberculosis, 1915. 
84. Reprint No. 16. What Constitutes a Proper Carbo-Hydrate and Pro- 
tein Diet in the Treatment of the Tuberculous. Illinois Medical Jour- 
nal, June, 1915. 
85. Reprint No. 17. The Therapeutic Value of the U. S. P. Tincture of 
Iodine in the Treatment of Tuberculosis and other Infectious Dis- 
eases. Transaction of the Twelfth Annual Meeting of the National 
Association for the Study and Prevention of Tuberculosis, 1916. 
86. Reprint No. 18. The Course of the Tuberculous Disease at Different 
Ages. Illinois Medical Journal, Dec., 1917. 
87. Reprint No. 19. The Use of the Tincture of Iodine in Intensive Dos- 
age in the Treatment of Tuberculosis and other Infectious Diseases. 
Illinois Medical Journal, June, 1919. 
88. Reprint No. 20. Why have both the Primary Focal Infection and 
the subsequent Pulmonary Tuberculous Disease their origin nearly al- 
ways in the air vesicles and not in the Bronchial Tubes? Illinois 
Medical Journal, April, 1920. 
89. Zentralblat, Internationales, fiir die gesamtte. 
(a) Tuberculose Forschung, Vol. 3, 1909. 
(b) Tuberculose Forschung, Vol. 4, 1910. 
(c) Tuberculose Forschung, Vol. 5, 1911. 
(d) Tuberculose Forschung, Vol. 6, 1912. 
(e) Tuberculose Forschung, Vol. 8, 1914. 
(c) Medical Journals, Pamphlets, Reports, Essays, etc. 
90. A Classification to Facilitate the Selection of Patients for work in a 
Tuberculosis Sanatorium. Wm. T. Cannon. BIBLIOGRAPHIC INDEX 
553 
91. A Clinical Study of the Children of Tuberculous Parents. J. A. 
Miller and I. O. Woodruff, Journal A. M. A., Vol. 52, pp. 1016, 1909. 
92. A Clinical Study of the Transmission and Progress of Tuberculosis 
in Children through Family Association. C. F. Floyd and H. I. 
Bowditch. Arch, of Pediatrics. Vol. 26, p. 177, 1909. 
93. A Comparison of Certain Antigens and the Complement-fixation 
Tests in Pulmonary Tuberculosis. H. C. Young and J. P. Givler. 
The American Review of Tuberculosis, p. 476, 1919. 
94. A Consideration of the Methods for Demonstrating Tubercle Bacilli 
in the Urine. Ernest M. Watson. American Journal of Med. 
Sciences, p. 636, 1918. 
95. A Contribution to the Study of the Complement-fixation Reaction 
in Tuberculosis. M. A. Wilson, J. Immunology, Vol. 3, p. 345, 1918. 
96. Anatomische Unersuchungen von Friihstadien der chronischen 
Nierentuberkulose. Wildbolz H. & Wegelin. Zeitschrift fur Uro- 
logische Chirurgie, Vol. 11, p. 201, 1914. 
97. Are Tubercle Bacilli excreted through the Bile? Louis H. Maxson, 
University of Penn. Med. Bulletin 23, p. 225, 1910. 
98. Artificial Pneumothorax as a treatment of Pulmonary Tuberculosis. 
Samuel Robinson & Cleaveland Floyd. Arch. Int. Med., Vol. 9, p. 
452, 1912. 
99 Artificial Pneumothorax in Pulmonary Tuberculosis. N. Y. Medical 
Journal, March, 1919. 
100. Beitrage Zur Heilung der Tuberkulose. Dr. Ponndorf, Miinchen. 
Med. Wchnschr., Vol. 61, pp. 750, 826, 1914. 
101. Calcium Content of the Blood, Editorial, J. A. M., Vol. 75, p. 941, 
1920. 
102. Childbirth and Tuberculosis. E. S. McSweeney and S. L. Wang. 
Journal A. M. A., Vol. 70, p. 368, 1918. 
103. Clinical Observations derived from the examination of over three 
thousand chests, checked by stereorentgenograms. K. Dunham. The 
American Review of Tuberculosis, Vol. 8, p. 489, Oct., 1917. 
104. Comparative Results obtained in the Treatment of Pulmonary Tuber- 
culosis. Hugh M. Kinghorn. Journal A. M. A., Vol. 72, p. 13, Jan., 
1919. 
105. Die Diagnose der Form der Lungentuberkulose. Ernest Romberg. 
Munich. Med. Wochenschr., Vol. 61, pp. 1833 to 1835, 1914. 
106. Complement Fixation in Tuberculosis. A. M. Stinson Bull, of Hy- 
gienic Laboratory, U. S. Public Health Service. No. 101, pp. 7-28, 
Aug., 1915. 
107. Complement Fixation in Tuberculosis. Sherman & Miller. Edin- 
burgh Med. Journal, Vol. 10, p. 81, 1913. 
108. Complement Fixation in Tuberculosis. H. J. Corper. J. Infec. Dis., 
Vol. 19, p. 315, 1916. 
109. Complement Fixation Tests in Tuberculosis. H. J. Corper & H. C. 
Sweany. J. A. M. A., Vol. 68, p. 1598, 1917. 
110. Concerning Apparent Cures of Renal Tuberculosis. E. L. Keyes. 
J. Surg. Gynec. & Obst., Vol. 18, p. 214, 1914. 
Trans. Am. Urolog. Asso., Vol. 7, p. 17, 1913. 554 
BIBLIOGRAPHIC INDEX 
111. Demonstration of Tubercle Bacilli in Spinal Cord of Patient suffer- 
ing from Tuberculous Meningitis. H. L. Kretschmer, J. A. M. A., 
Vol. 74, p. 247, 1920. 
112. Desirability of Preventing Sterility in Young Women when operated 
for Tuberculous Peritonitis. J. H. Carstens, J. A. M. A., Vol. 73, 
p. 23, 1919. 
113. Diagnostic Value of the X-ray in advanced Pulmonary Tuberculosis. 
Max Biesenthal and Emmett P. Carroll. Illinois Med. Journal, Vol. 
33, p. 101, 1918. 
114. Die Tuberculose der Verschiedenen Lebensalter. Dr. Karl E. Ranke, 
Munich. Med. Wochenschrift, 215, 1913. 
115. Ein neues Verfahren zum microscopischen Nachweis von Tuberkel 
bacillen in Harn, E. de Vos. Inaug. Disert. Rostock, 1891. 
116. Epiglottidectomy: The Rational Treatment of Epiglottidean Tuber- 
culosis. Lorenzo B. Lockard. The Laryngoscope, p. 113, 1912. 
117. Erfahrungen iiber primare Nierentuberkulose. Israel J. Deutsche 
Med. Wochenschrift, Vol. 16, pp. 684-687, 1890. 
Vol. 24, pp. 443-445, 1898. 
118. Experimentelle Studien iiber die Wirkung von Tuberkelbacillen- 
Preparaten auf den tuberkulos erkrankten organismus. A. v. Wasser- 
mann & C. Briick. Deutsche Medicinische Wochenschrift, Vol. 32, 
p. 449, 1906. 
119. Glucose Tolerance in Health and Disease. Woodyatt, Wilder and 
Sansum. Arch. Internal Medicine, Vol. 19, p. 311, 1917. 
120. Glycerin Extract of Tubercle Bacilli as Antigen in Complement 
Fixation. S. A. Petroff, Am. Rev. Tuberc., Vol. 2, p. 523, 1918. 
121. Heliotherapy in Laryngeal Tuberculosis. C. W. Mills and A. M. 
Forrester. The American Review of Tuberculosis, Jan., 1919. 
122. Histological Studies in some types of Skin Tuberculosis. Fordyce, 
Journal Cutaneous Disease, 1914. 
123. Immunity and Immune Therapy. Dr. Erich Leschke Internationales 
Zentralblat. Vol. 6, p. 499, 1912. 
124. Intervenous Injection of Hypertonic Glucose Solution in Influenzal 
Pneumonia. Wills & Blankinship. Journal A. M. A., Vol. 74, p. 75, 
1920. 
125. La Zomotherapie dens le traitement de la Tuberculose. P. Barbier, 
Zentralblat fur Tuberkulose, Vol. 4, p. 433, 1910. 
126. Les Sensibilisatrices du bacille tuberculeux. J. Bordet and O. Gengon 
Comptes Rendus de L’Academie Des Sciences, Vol. 137, p. 351, 1903. 
127. Localization of Pulmonary Lobes by the X-ray. Kennon Dunham. 
Med. Record 97, p. 1077, 1920. 
128. New Method of Treatment of Lupus Vulgaris. Heidingsfeld. Jour- 
nal A. M. A., Oct. 17, 1914. 
129. Observations upon Complement-Fixation in the Diagnosis of Pul- 
monary Tuberculosis. Charles F. Craig, Am. J. Med. Sc., Vol. 150, 
p. 781, 1915. 
130. Occupation for Chronic Patients. Wm. Rush Dunton. Public 
Health Nurse Quarterly, Vol. 9, p. 385, Oct., 1917. BIBLIOGRAPHIC INDEX 
555 
131. Occurrence of Tubercle Bacilli in Breast Milk of Tuberculous 
Women. Stanley L. Wang and Frederick Coonley, Sea View Hos- 
pital, Staten Island, N. Y., Journal A. M. A., Vol. 69, p. 531, Aug. 
18, 1917. 
132. Operative Treatment of Tuberculosis of the Larynx. T. Ruedi, 
British Med. Journal, June 21, 1919. 
133. Pulmonary Tuberculosis and the Pregnant Woman. A. Jacobi, N. 
Y. State Med. J., Vol. 13, p. 192, 1913. 
134. Pulmonary Tuberculosis as an Obstetrical Complication. C. S. 
Bacon, Journal A. M. A., 1905, 1912 and 1913. 
135. Pulmonary Tuberculosis in its Relation to Diseases of the Heart and 
Blood Vessels. A Review of the Literature. Dr. H. Grau-Ronsdorf. 
Internationales Zentralblat. Vol. 5, pp. 227-276-387, 1911. 
136. Pulmonary Tuberculosis treated with Ultra-violet Light. E. Zueblin. 
Am. M., Vol. 14, pp. 210-216, 1919. 
137. Pregnancy in the Tuberculous. C. C. Norris. Proc. Am. Gynec. 
Society, 1914; Am. Journal Obst. N. Y., Vol. 73, p. 997, 1916. 
138. Physical Reconstruction Applied to the Treatment of Pulmonary 
Tuberculosis. Frank Billings. Transaction, National Tuberculosis 
Association, 1919. 
139. Raw Meat and Raw Meat Juice in the Treatment of Consumptive 
Disease. J. Hericourt. Lancet, January 7th, 1911. 
140. Recognition of pure Pneumothorax without exudate in Pulmonary 
Tuberculosis. Hermann v. Schroetter, Vienna, 6th International 
Tuberculosis Congress, Washington, D. C., Vol. 1, p. 1165, Sec. 11, 
1908. 
141. Renal Tuberculosis. George Walker, Johns Hopkins Hospital Re- 
port, Vol. 12, p. 455, 1904. 
142. Some Essential Points in the Anatomy of the Lung. W. Snow 
Miller. Am. Journal Roentgenology, June 17th, p. 269. 
143. Serological Studies in Tuberculosis. S. A. Petroff, Am. Rev. Tuberc., 
Vol. 1, pp. 33-50, 1917-18. 
144. So-Called Incipient Tuberculosis. The Author, Journal A. M. A., 
Vol. 66, p. 592, 1916. 
145. Social Aspects of Reconstruction for the Tuberculous. Estes Nichols. 
Transaction, National Tuberculosis Association, 1919. 
146. Stereo-roentgenography—Pulmonary Tuberculosis. Kennon Dun- 
ham, Am. Journal Roentgenology, June 17, p. 280. 
147. Surgical Treatment of Pulmonary Tuberculosis. Fr. v. Sauerbruch, 
Marburg, 6th International Tuberculosis Congress, Washington, D. 
C., Vol. 2, p. 82, Sec. Ill, 1908. 
148. Surgical Treatment of Tuberculous Nephritis. E. Kiister. Internat. 
Clin., Vol. 3, pp. 33-42, 1899. 
149. The Antigenic Properties of Tubercle Wax. Balduin Lucke, J. Im- 
munology, Vol. 1, p. 457, 1916. 
150. The Clinical Value of Complement-fixation in Pulmonary Tubercu- 
losis based on a study of 540 cases. S. A. Petroff and Lawrason 
Brown. The American Review of Tuberculosis, p. 525, 1918. 556 
BIBLIOGRAPHIC INDEX 
151. The Clinical Value of Complement-fixation in Tuberculosis. H. R. 
Miller, J. A. M. A., Vol. 67, p. 1519, 1916. 
152. The Course of the Tuberculous Disease under the influence of Ar- 
tificial Pneumothorax. Lucius Spengler, Davos., 6th International 
Tuberculosis Congress, Washington, D. C. Vol. 1, p. 1169, Sec. 
11, 1908. 
153. The Diagnosis of Tuberculous Laryngitis. Julius Dworetzky, A. 
M. A., Section on Laryngology, Rhinology and Otology, 1917. 
154. The Complement-fixation Reaction as applied to Tuberculosis. Paul 
A. Lewis. The American Review of Tuberculosis, p. 129, 1919. 
155. The Complement-fixation Reaction in Tuberculosis. L. S. Dudgeon, 
W. Meek, H. B. Weir, Journal of Hygiene, Vol. 14, pp. 72-75, 1914. 
156. The Complement-fixation test in Tuberculosis. Elizabeth Fraser, 
Ztschr. F. Immunitatsforsch. u. Exper. Therap., Jena., Orig., Vol. 
20, p. 291, 1913. 
157. The Complement-fixation test for Tuberculosis in Infancy and 
Childhood. Heiman H. Arch. Pediat., Vol. 35, p. 342, 1918. 
158. The Complement-fixation test for Tuberculosis. Linda B. Lange. 
The American Review of Tuberculosis, p. 541, 1918. 
159. The Diagnostic Value of the Complement-fixation Reaction in 
Tuberculosis. J. McIntosh, P. Filds & J. A. D. Radcliffe. Lancet, 
Vol. 2, pp. 484-490, 1914. 
160. The Diazo and Urochromogen Reactions in Pulmonary Tubercu- 
losis. H. J. Corper, F. F. Callahan and M. I. Marshak. Tr. Nat. 
Ass. Study and Prev. Tuberc. N. Y., Vol. 12, pp. 295-301, 1916. 
161. The Friedmann Treatment for Tuberculosis. John F. Anderson 
and A. M. Stimson. Bull, of the Hygienic Laboratory U. S. Public 
Health Service, No. 99, Oct., 1914. 
162. The Hot Morning Bath for the Tuberculous. Norman Bridge. 
Transaction. National Association for the Study and Prevention of 
Tuberculosis, p. 516, 1906. 
163. The Larynx in One Hundred Cases Dying of Pulmonary Tubercu- 
losis. A clinical post-mortem study. George Fetterolf. The Laryn- 
goscope, Vol. 26, p. 37, Jan., 1916. 
164. The Nature of Resistance to Tuberculosis. Allen K. Krause. The 
American Review of Tuberculosis. Vol. 1, p. 65, April, 1917. 
165. The Pathology of Cutaneous Tuberculosis. Bowen, Boston Med. 
and Surg. Journal, Nov. 12, 1891. 
166. The Prognostic Value of the Urochromogen and Diazo Reactions 
in Pulmonary Tuberculosis. Roy C. Heflebower. Am. J. Med. 
Sec. 143, p. 221, 1912. 
167. The Relation of the Pathology of Pulmonary Tuberculosis to the 
Roentgen Findings. Kennon Dunham, Am. Journal Roentgenology, 
June 17, p. 280. 
168. The Rollier Treatment of Tuberculosis. Clarence L. Hyde and 
Horace LaGrasso, N. Y. Medical Journal, Vol. 105, p. 11, 1917. 
169. The Symptomatology of Renal Tumors. A study of seventy-four 
cases. J. Dellinger Barney, Massachusetts General Hospital, Boston 
Med. and Surg. Journal, Vol. 188, p. 300, 1913. BIBLIOGRAPHIC INDEX 
557 
170. Treatment of Hemoptysis in Tuberculosis. M. Rothschild. Calif. 
State J. M., Vol. 9, pp. 288-291, 1911. 
171. The Treatment of Pulmonary Tuberculosis by Graduated Rest and 
Exercise. Marcus Paterson, London Practitioner, Jan., 1913. 
172. The Treatment of Lupus Vulgaris with Acid Nitrate of Mercury. 
Adamson, British Medical Journal, Nov., 1920. 
173. The Use and Abuse of Pulmonary Gymnastics. Edward O. Otis. 
Transaction. National Association for the Study and Prevention of 
Tuberculosis, p. 387, 1906. 
174. The Value of Tuberculosis Complement Fixation in Clinical Tuber- 
culosis. B. Stivelman. The American Review of Tuberculosis, p. 
546, 1918. 
175. Traite de la Phthisie Pulmonaire. Gaspard Laurent Bayle, Paris, 
1812. 
176. Treatment of Laryngeal Tuberculosis. Julius Dworetzky, Long 
Island Med. J., May, 1918. 
177. Treatment of Painful Dysphagia in Tuberculous Laryngitis. Robert 
McD. Lukens, N. Y. Medical Journal, Feb. 23, 1918. 
178. Treatment of Vertebral Tuberculosis by Fusion Operation. Russell 
A. Hibbs, Journal A. M. A., Vol. 71, p. 1372, Oct. 26, 1918. 
179. Tuberculosis and Pregnancy. Charles C. Trembley, 1912. 
180. Tuberculosis and Pregnancy. H. v. Bardeleben, Med. Klin. u. 
Therap., Vol. 12, p. 440, 1913. 
181. Tuberculosis and Pregnancy. J. O. Polak and H. B. Matthews. In- 
ternational (S. G. and O.) Abstract of Surgery, Vol. 21, p. 233, 1915. 
182. Tuberculosis and Pregnancy. Veit. Zentralblat f. Gynaekologie, Vol. 
30, p. 1217, 1906. 
183. Tuberculosis in Child Life. A Review of the Literature from 1907 
to 1909. Dr. Bauer, Internat. Zentralblat, Vol. 4, p. 227, 1910. 
184. Tuberculosis in its Relation to Pregnancy, Labor and the Puer- 
perium. B. W. Lobenstine. Am. Journal Obst. N. Y., Vol. 67, p. 
363, 1913. 
185. Tuberculosis of the Kidney. G. Kapsammer, Am. Journal Obstetrics, 
Vol. 68, pp. 499-529, 1913. 
186. Uber des Vorkommen von Tuberkelbazillen im Blutstrom. Dr. E. 
Rumpf in Ebersteinburg. Munich. Med. Wochenschrift, 1912. 
187. Uber den wrerth der Centrifuge bei Harnuntersuchung Albert Albee. 
Berlin Klin. Wochenschrift, p. 531, Mai, 30, 1892. 
188. Uber Nierentuberkulose. F. Kornfeld. Verhandlungen des Kong- 
resses fur innere Medizin, Vol. 25, pp. 580-599, 1908. 
189. Uber w'eitere Fortschrite in der momentanen Roentgenphotographie, 
Rieder H. and Rosenthal J. Mtinchen Med. Wochenschrift, Vol. 52, 
p. 806, 1905. 
190. Zur Behandlung der Tuberkulose (aus dem Waldsanatorium Davos), 
F. Jessen, Zetschr. F. Tuberk., Vol. 24, p. 197, 1915. 558 
BIBLIOGRAPHIC INDEX 
(d) Addendum 
191. The Rocky Glen Tuberculosis Sanatorium, McConnelsville, Ohio, 
Correspondence. Louis Mark, Medical Director. 
192. Uber den Nachweis von Tuberkelbacillen in den Faeces. J. Strass- 
burger, Munich. Medicinische Wocheschr., Vol. 47, p. 533, 1900. 
193. Roentgenotherapy of Peripheral Tuberculous Adenopathy. Albert 
E. Weil, Paris. American Journal of Roentgenology, Sept., 1917. 
194. Tuberculous Adenitis and Its Treatment by Roentgenotherapy. Rus- 
sell H. Boggs. American Journal of Roentgenology, Sept., 1918. 
195. Principles Involved in the X-ray Treatment of Tonsils. W. D. 
Witherbee, New York Medical Journal, March 16, 1921. 
196. Roentgen-Ray Treatment of Surgical Tuberculosis. A. van Ree. 
Nederlandsch Tijdschrift v. Sencesekinde Amsterdam, p. 1983, Nov. 
13, 1920. Reprint in Journal of the A. M. A., February 5, 1921. 
197. Teaching of Physical Diagnosis. Author, Journal A. M. A., Vol. 50, 
p. 767, 1908. 
198. Text-Book of Ophthalmology. Fuchs. 
199. Pathology of the Eye. Parsons. 
200. Pathology of the Eye. Collins and Mayou. 
201. Bacteriology of the Eye. Axenfeld. 
202. Erfahrungen und Gendenken uber Tuberkulose und Tuberkulin. 
Heine, Medizinische Klinik, 1912. 
203. Klinische Monatsblatter fur Augenheilkunde, Vol. 37, 1900. Birch- 
Hirschfeld. 
204. Arch. d’Opht., 1885, p. 193. Pands and Vassaux. 
205. The American Encyclopedia of Ophthalmology. 
206. Medical Ophthalmology. Knapp. 
207. Disease of the Eye. Morris and Oliver. 
208. Hull Physiological Laboratory. Loeb, Jacques, March 30, 1898. 
209. Encymes in the Nucleus. Albert P. Matthews, Physiological Chem- 
istry, Chicago, p. 180, 1915. 
210. Pfleuger’s Archives. W. Spitzer, Bonn, Breslau, Vol. 67, p. 615, 
1897. 
211. Annals de Medecine et Chirurgie Infantalis, Mai, 1914, No. 9. R. 
Ridard, Paris. 
212. Arch. f. Klin. Chirurgie, 1914. Vol. 104, p. 2. Kisch u. Graetz. 
213. Corr. Bd. f. Schweitz, 1914, No. 25 and 36. C. Arndt, Bern. GENERAL INDEX 
Abdominal pain, 227 
Aberrant types, 95 
Aberrations, 142 
Abnormal auscultatory murmurs, 
152 
Abnormal chest on inspection, the 
109 
chest, palpation of the, 121 
chest, percussion of the, 136 
chest, sounds, 153 
vocal sounds, 157 
voice sounds, 157 
Academic questions in tuberculosis, 
the, 1 
Acid fast bacilli in the urine, 509 
Acne cachecticorum, 438 
scrofulosorum, 438 
variolaformis, 438 
Acnitis, 438 
Acquired tuberculous immunity, 
the, 62 
Active tuberculosis, X-ray plate, 
the, 177 
Acute broncho-pneumonia, differ- 
entiation, 90 
miliary tuberculosis, 73, 75 
miliary tuberculosis in children, 
294 
Adaptation characteristics, 14 
Administration of tuberculin, when, 
how, 317 
of tuberculin, methods, 319 
Advanced far, tuberculosis—third 
. stage, 73 
moderately, tuberculosis—sec- 
ond stage, 73 
Advancing tuberculosis, X-ray 
plate, the, 176 
Adventitious sounds, 153 
Aerogenous route, the, 17 
Air, wholesome, fresh, 209 
Albumin test, the, 485 
Albumose-free tuberculin, 314 
Allergy, 534 
Ambulant, ambulatory, 534 
Ambulatory cases, the, 202 
treatment, 199 
Amenorrhoea, in tuberculous 
women, 347 
Animal experimentation, 23, 514 
inoculation in urinary tubercu- 
losis, 419 
Anaphylaxis and ananaphylaxis, 535 
Anergy, 534 
Angulus Ludovici, 106 
Ludovici promiens, 114 
Antigens, 501 
Apparatus for the inducation of 
lung compression, 239 
Appendicitis, differentiations from 
renal tuberculosis, 421 
Appropriate exercise, 210 
Arc light, 255 
Arneth’s blood picture, 491 
Artificial pneumothorax, 228 
pneumothorax, complications in, 
243 
Associated therapeutic measures, 
250 
Atria of infection, 16 
Atrophy, integument, 117 
Atypical forms of pulmonary tuber- 
culosis, other, 99 
types, 95 
Auscultate, how and when to, 158 
Auscultation, 145, 148, 289. 338 
of the normal thoracic sounds, 
149 
methods of, 148 
Auscultatory catarrhal signs, 153 
murmurs, abnormal, 152 
sounds, errors in, 159 
sounds, the normal, 149 
Autoserotherapy, 344 * 
Baccelli’s sign, 341 
Bacillen emulsion, B. E.:, 313 
Bacilli acid fast in urine, 509 
in the bile and gall bladder, 514 
in the body fluids, 507 
in the exudates and other body 
fluids, 515 
in the feces, 513 
in the mothers’ milk, 511 
Bacillus tuberculosis avium, 10 
tuberculosis bovinus, 10 
tuberculosis humanus. 9 
tuberculosis piscium, 10 
leprae, 10 
pseudotuberculosis, 11 
smegmatis, 10 
tuberculoides, 11 
Bad housing conditions, 26 
559 560 
INDEX 
Basal meningeal tuberculosis in 
children, 295 
Bedfast cases, the, 203 
Begin tuberculin treatment with 
very small doses, 331 
Beraneck’s tuberculin, T.B.K., 314 
Bile in tuberculosis, the, 507 
Birth control among the tubercu- 
lous, 354 
Blastomycosis, differentiation, 435 
Bleeding from the lungs, 362 
Blood as a whole in the tubercu- 
lous, the, 490 
immunological and serological 
considerations of the, 497 
in pulmonary tuberculosis, the, 
489 
picture, Arneth’s, 491 
pressure, 86 
pressure observations, 450 
stream, tubercle bacilli in the, 
493 
Bone and joint tuberculosis, 395 
and joint tuberculosis, compli- 
cations, 402 
and joint tuberculosis, diag- 
nosis, 397 
and joint tuberculosis, symp- 
tomatology, 397 
and joint tuberculosis, treat- 
ment, 403 
Bony structure, X-ray plate, the, 
167 
Borders of the lungs, the, 131 
Boston staining method, the, 480 
Boullion filtrate, Deny’s B. F., 313 
Breath sounds, the normal, 149 
Breathing, the cycle of, 163 
the mechanism of, 161 
the rhythm, normal, 163 
spino-tracheal, 290 
Broncheal gland tuberculosis, 286 
Bronchophony, whispering, 146, 157 
Bronchus apicalis posterioris, 60 
Calories, 523 
Capacity, the vital, 194 
Carcinoma, metastatic, the X-ray 
plate, 181, 189 
of the larynx, 380 
Care of the tuberculous, the, 199 
of the tuberculous, general, 202 
of the tuberculous, surgical, 228 
Caseation, 58 
Caseous foci of tuberculosis, the, 
89 
Cases, the ambulatory, 202 
the bedfast, home or house, 203 
the sanatorium, 204 
suitable for lung compression, 
Catarrhal auscultatory signs, 153 
Causes, mechanical, 26 
of death in renal tuberculosis, 
422 
Cavernous, cheesy type of tuber- 
culous kidney, the, 414 
Characteristic signs and symptoms, 
90, 91, 93 
Characteristics, cultural, 12 
infecting, 13 
of normal urine, 507 
of the tubercle bacillus, 11 
of the urine in pulmonary 
tuberculosis, 508 
pathogenic, 13 
special adaptation, 14 
tinctorial, 12 
Chemical examination of the spu- 
tum, 484 
Chemotherapy, 250 
iodine in, 253 
organic acids in, 253 
Chest, abnormal, palpation of the, 
121 
abnormal, percussion of the, 
136 
contracted, the, 111 
deformities, 110 
infantile type, the, 111 
normal, palpation of the, 120 
normal, percussion of the, 133 
phthisical, the, 112 
plate, X-ray, the normal, 165 
stenotic, the, 111 
the, how to examine, 105 
Children, the palpable glands in, 
302 
tuberculosis in, 284 
Chondrotomy, 249 
Choroiditis, tuberculous, 445 
Chromoscopy in renal tuberculosis, 
420 
Chronic nodular type, tuberculous 
kidney, 414 
simple laryngitis, 380 
Ciliary body, tuberculosis of the, 
444 
Cirrhotic form, the, 92 
Classification of patients on exami- 
nation, schema, 72, 73 
of terms used upon the dis- 
charge of a patient, 539 
of the various forms, 88 
schematic, 72 
Clinical forms of tuberculosis, 88 
forms of tuberculous enteritis, 
389 
manifestations, 285 
nomenclature, 89 
results in heliotherapy, 261 
tuberculosis, 69, 537 
varieties, 88 INDEX 
561 
Colic in renal tuberculosis, 412 
Collecting sputum for chemical 
examination, 485 
Combined sputum examination, 487 
Communicable diseases, 29 
Complaint present, 104 
Complement fixation in tubercu- 
losis, 498 
fixation technic in tuberculosis, 
506 
fixation test in tuberculosis, 502 
Complications in artificial pneumo- 
thorax, 243 
in bone and joint tuberculosis, 
402 
Composition of the bacillus, 14 
Compression of the lungs, 228 
of the lungs, cases suitable for, 
236 
Congenital immunity, 62 
Conjugal tuberculosis, 27 
Conjunctival tuberculin test, the, 325 
Conjunctiva, tuberculosis of the, 443 
Consumption, 71 
Contact cases, 27 
Contagion and infection, 29 
Contentment, 208 
Contour of the thorax, the X-ray 
plate, 167 
Contracted chest, the, 111 
Contraindications in the use of tu- 
berculin, 324 
Controlling pulmonary hemorrhage, 
practical rules for, 367 
Cornea, tuberculosis of the, 444 
Costa fluctuans decima, 115 
Cough, 82, 221 
Course of laryngeal tuberculosis, 
the, 374 
of renal tuberculosis, the, 442 
of tuberculous disease, the, 50 
Cracked pot sounds, 142 
Croupous pneumonia, differentia- 
tion, 91 
Cryptogenetic route, the, 22 
Cultural characteristics, 12 
Cutaneous route, the, 20 
tuberculin test, the, 326 
tuberculosis, treatment of, 439 
vaccination method, the, 323 
Cycle of breathing, a, 163 
Cystoscopy in renal tuberculosis, 419 
Cytodiagnosis, 507 
in tuberculosis, 520 
Decalcification, 518 
Definition of “general condition on 
admission and on discharge,” 
540 
of term “digestion on admis- 
sion and on discharge,” 541 
of term “temperature on dis- 
charge,” 541 
of words and phrases used in 
conversation, etc., 529 
Deformities, chest, ,110 
Demineralization, 518 
Densities, generalized, the X-ray- 
plate, 190 
localized, the X-ray plate, 188 
Deny’s boullion filtrate, B.F., 313 
Dermal route, the, 20 
Description of the tubercle bacillus, 
11 
of tuberculous skin lesions, 432 
D’Espine’s sign, 290 
Diagnosis differential of bone and 
joint tuberculosis, 397, 401 
of genito-urinary tuberculosis, 
the, 427 
of gland tuberculosis, the, 288 
of miliary tuberculosis, 97 
of pulmonary tuberculosis, the, 
100 
of renal tuberculosis, 417 
of tuberculosis of the eye, 446 
of tuberculosis of the skin, 432 
of tuberculous laryngitis, 379 
of tuberculous peritonitis, 391 
of tuberculous pleurisy, 338 
prima vista, 109 
Diagnostic dose of tuberculin, the, 
542 
injection of tuberculin in renal 
tuberculosis, 419 
methods (special) in renal 
tuberculosis, 419 
purposes, tuberculin for, 325 
quality of the X-ray plate or 
screen, the, 165 
Diaphragmatic pleurisy, 345 
Diaphragm, the, on the X-ray 
plate, 168 
Diarrhoea, 227 
Diathesis, 24 
Dietetic-hygienic treatment, the, 
199,212 
Different ages, the disease in the, 
50 
Differential diagnosis,genito-urinary 
tuberculosis, 427 
diagnosis, renal tuberculosis, 
421 
diagnosis, tuberculous laryngitis, 
379 
diagnosis, tuberculous peritonitis, 
391 
diagnosis, tuberculous pleuritis, 
339 
diagnosis, X-ray plate, the. 117 562 
INDEX 
Differentiation of pleurisy from 
lobar pneumonia, 340 
of skin lesions, 434 
tuberculosis from acute 
broncho-pneumonia, 90 
tuberculosis from lobar pneu- 
monia, 91 
Dilutions, tuberculin, the, 330 
Directions for the albumin test, 485 
Discovery of tuberculin, the, 308 
Disease tuberculous in children, 
primary, 285 
tuberculous in children, second- 
ary, 293 
tuberculous in children, tertiary, 
296 
Disposition, 24 
idiopathic, 24 
non-specific, 25 
other noticeable, 27 
specific, 24 
toxipathic, 25 
Disturbances, gastro-intestinal, 226 
mental, 26 
Dosage, standard tuberculin, the, 
333 
Dropheart, 169 
Dyspnoea, 83, 224 
Early tuberculosis, the X-ray plate 
in, 173 
Ease of mind, 208 
Ebner’s fluid, 483 
Effect of heliotherapy on the human 
body, the, 258 
of insolation on individual or- 
gans, the, 259 
of maternal tuberculosis on the 
fetus, 352 
of pregnancy on tuberculosis, 
350 
of tuberculosis on pregnancy, 
349 
Elimination of lime salt in tuber- 
culosis, 507 
Empyema, 344 
Encapsulation, 58 
Endotoxin, 314 
Enterogenous route, 18 
Errors in auscultatory sounds, 159 
sources of, 142 
Erythema induratum, 438 
nodosum, 437 
Erytheme des scrophuleux, 438 
polymorphe, 437 
Erythrocytes in tuberculosis, the, 
489 
Esbach’s fluid, 483 
Estimation of the vital capacity, 196 
Etiology of tuberculosis, the, 9 
of tuberculosis of the skin, 429 
of tuberculous laryngitis, 369 
Exercise and rest, 280 
appropriate, 210 
Examination of the sputum, chem- 
ical, 484 
physical, in gland tuberculosis, 
288 
physical, in tuberculous pleur- 
isy, 337 
Expectoration, 82 
Experimentation, animal, 23 
Explanation, Koch’s of the tuber- 
culin reaction, 310 
of the tuberculin reaction, 310 
Exploratory puncture in pleurisy, 
341 
Extra-uterine infection, 50 
Exudative form of tuberculosis, the, 
89 
Eye, tuberculosis of the, 441 
Eyelid, tuberculosis of the, 443 
Facies, phthisical, the, 118 
Factors, hereditary, 21 
predisposing in eye tubercu- 
losis, 441 
predisposing in genito-urinary 
tuberculosis, 411 
the psychic, 208 
Family history, 103 
Far advanced tuberculosis — third 
stage, 73, 75 
Fate, ultimate of tubercle, 60 
Feces, in tuberculosis, the, 507 
tubercule bacilli, in the, 513 
Fever, 219 
Fibro-caseous forms of tuberculosis, 
the, 91 
Fibroid form of tuberculosis, the, 92 
phthisis, the X-ray plate in, 184 
type, renal tuberculosis, 414 
Findings in the normal chest (X- 
ray plate), 165 
Fistulae-in-ano, 87 
Foci of infection, primary, 35 
Food values or calories, 523 
Formation of the tubercle, 56 
Fowl tuberculosis, 10 
Frequency of tuberculosis in chil- 
dren, the, 305 
of tuberculous pleurisy, the, 336 
of urination in renal tubercu- 
losis, 412 
Friction rubs, 154 
Friedmann’s prophylactic and cura- 
tive vaccine, 315 
Functional kidney test, the, 420 
Gabbett’s stain, 509 
Gaffky’s scale, 482 INDEX 
563 
Gall stones, differentiation from 
renal tuberculosis, 421 
Gastric distress, 83 
Gastro-intestinal disturbances, 226 
General care of the tuberculous, the, 
202 
Genesis of the tubercle, 56 
Genital tuberculosis, 424 
tuberculosis, symptoms of, 426 
Genitogenetic route, the, 20 
Genito-urinary organs, tuberculosis 
of the, 410 
tuberculosis, predisposing fac- 
tors, 411 
Gentian-violet stain, 483 
Gibbus, 108 
Glands, the groups of, 301 
palpable in children, the, 302 
Gland tuberculosis, 286 
tuberculosis, diagnosis of, 288 
tuberculosis, physical examina- 
tion, 288 
tuberculosis, signs and symp- 
toms of, 287 
tuberculosis, the tuberculin ther- 
apy in, 299 
Glandulae tracheo-bronchialis, 286 
Graduated labor, 28 
Graves’ disease, 81 
Grocco’s sign, 339 
Groove, Harrison’s, 106 
Sibson’s, 106 
Grouping of the various forms, 88 
Groups of glands, the, 301 
Gymnastics pulmonary, 269 
pulmonary, how to practice, 271 
Habitus asthenicus, 115 
paralyticus, 112 
phthisicus, 112 
Harrison’s groove, 106 
Health and disease, 199 
Heart and tuberculosis, the, 450 
drop, 169 
Heliotherapy, 255 
effect on the human body, 258 
in tuberculosis, 257 
posological considerations, 259 
technic, the, 261 
Heller’s test for albumin, 486 
Hematogenous infection, 17 
in renal tuberculosis, 411 
Hematology, 489 
Hematuria in renal tuberculosis, 413 
Hemoglobin in tuberculosis, the, 48 
Hemorrhage, 83, 227 
in tuberculosis, 362 
pulmonary, the X-ray plate in, 
183 
Hereditary factors, 27 
Heredity, 24 
Hila, hilum, hilus, hilar, 534 
Hilus shadows, on the X-ray plate, 
the, 170 
Hip and knee joint tuberculosis, 
treatment, 405 
Histology and pathology, 56 
Historical data, concerning the pri- 
mary foci in the lungs, 35 
data in artificial pneumothorax, 
228 
data in complement fixation, 
499 
data in physiotherapy, 273 
data in roentgenology, 164 
History family, 103 
of tuberculosis, the, 3 
personal, 103 
present, 103 
taking in tuberculosis, 102 
Hoarseness, 86 
Home or house cases, the, 203 
treatment, the, 199 
Housing conditions, bad, 26 
How and when to auscultate, 158 
and when to collect the spu- 
tum, 478 
to examine the chest, 105 
to practice pulmonary gymnas- 
tics, 271 
Hydropneumothorax, x-ray plate 
int 192 
Hydrothorax, x-ray plate, in, 186 
Hypersensitiveness, 67 
susceptibility, 535 
Hypotension and tuberculosis, 458 
Idiopathic disposition, 24 
pleurisy, 335 
Immediate results of lung compres- 
sion, 244 
Immune Koerper, 68 
Immunity, 61 
acquired tuberculous, the, 62 
congenital, 62 
Immunization, the various methods 
of, 65 
Immunological consideration of the 
blood, the, 497 
Incidence of tuberculosis among 
the tuberculous women, the, 
348 
Incipient tuberculosis — the first 
stage, 72, 75 
Indications, tuberculin in general- 
ized tuberculosis, 317 
tuberculin in localized colonies, 
316 
tuberculin, the diagnostic, 316 
tuberculin, the therapeutic, 316 564 
INDEX 
Infantile type of chest, the, 111 
Infecting characteristics, 13 
Infection and contagion, 29 
extra-uterjne, 50 
hematogenous, 17 
lymphogenous, 17 
sources of, 201 
urogenous, 412 
Infectious diseases, 26 
Infiltration in tuberculous laryngi- 
tis, 376 
Influence, toxic, 26 
Inoculation, animal in renal tuber- 
culosis, 419 
Inoscopy, 507, 521 
Insolation, diagram for, 264 
Inspection, 105, 106, 109, 288, 337 
abnormal chest, the, 109 
normal chest, the, 106 
Integument atrophy, 117 
Intracutaneous tuberculin test, the, 
327 
Intra-uterine infec.tion, 50 
Iodine in chemotherapy, 253 
Iris, tuberculosis of the, 444 
Keratitis phlyctenular, 443 
Kidney tests, functional, 420 
tuberculosis of the, 410 
tuberculosis, the age in, 410 
tuberculosis, the frequency of, 
410 
tuberculosis, the sex in, 410 
Koch’s bacillus, 9 
views or explanation of the tu- 
berculin reaction, 310 
Koerper immune, 68 
Kypho-scoleosis, 113 
Kyphosis, 108, 113 
Laboratory diagnosis in tubercu- 
losis, 473 
Labor graduated, 280 
Lactotherapy, 216 
LaLois des adinopathie similaires, 
35 
Lamp, quarts, 255 
Laryngeal phthisis, 369 
tuberculosis, 369 
tuberculosis, physical manifes- 
tations of, 374 
Laryngitis, chronic simple, 380 
syphilitic, 380 
tuberculosa, 369 
tuberculous, 380 
Larynx, carcimona of the, 380 
lupus of the, 381 
Latent tuberculosis, 537 
Law, Parrot’s, 35 
Ponndorf’s, 311 
Le foyer pulmonaire primitif, 35 
Lesions of the kidney other than 
tuberculosis, 421 
of other abdominal viscera, 421 
tuberculous, 537 
Leucocytes in tuberculosis, the, 489 
Lichen scrofulosorum, 437 
Light arc, 255 
of the sun, 259 
sun, 255 
sun treatment, 255 
Lime salt elimination in pulmonary 
tuberculosis, 507, 518 
Litten’s phenomenon, 117 
Lobar pneumonia, differentiation, 91 
Location (the usual) of the tu- 
bercle, 60 
Lordosis, 108 
Loss in weight, 85 
Ludwig’s angle, 106, 114 
Lugol’s solution, 483 
Lung compression, 228 
compression, immediate results, 
244 
compression, ultimate results. 
244 
markings, the x-ray plate, 171 
stones, 60 
the borders of the, 131 
Lupus erythematosus, 439 
erythematosus, differentiation, 
435 
of the larynx, 381 
vulgaris, 432 
Lymph-nodes, tuberculosis of the, 
284 
Lymphocytes (small) in tubercu- 
lous sputum, the, 483 
Lymphogenous infection, 17 
Manifestations, clinical in tubercu- 
losis, 285 
Manifest tuberculosis, 536 
Mantoux, tuberculin test, the, 327 
Maragliano’s serum, 316 
Markings lung, the x-ray plate, 171 
Marmoreck’s serum, 316 
Massage pulmonary, 269 
Maternal tuberculosis, the effect on 
the fetus, 352 
Measurements of the chest, 194 
Mechanical causes, 26 
treatment of pulmonary hem- 
orrhage, 363 
Mechanism of breathing, the, 161 
Mediastinum, the x-ray plate of the, 
169 
Medical treatment of pleurisy, 342 
treatment of pulmonary tuber- 
culosis, 199 INDEX 
565 
treatment of pulmonary hem- 
orrhage, 363 
treatment of tuberculous peri- 
tonitis, 393 
Meningitis, tuberculous, 295 
Menstruation, 85 
Mensuration, 194 
Mental disturbances, 26 
symptoms, 85 
Metastatic carcinoma, the x-ray 
plate, 181, 189 
sarcoma, the x-ray plate, 182 
Methods of auscultation, the, 148 
of palpation, the, 119 
of percussion, .the, 132 
Microscopical examination of the 
blood, the, 496 
examination of the sputum (tec- 
nic for), 480, 487 
Miliaris disseminata, 96 
Miliary tuberculosis, 90 
tuberculosis, acute, 73, 75 
tuberculosis in children, 294 
tuberculosis, the x-ray plate in, 
180 
tuberculous enteritis, 388 
Milk cure., the, 216 
in the tuberculous, the, 507 
mother’s, demonstration of the 
tubercle bacillus in, 511 
Mind, ease of, 208 
Miscellaneous, 522 
Moderately advanced tuberculosis, 
second stage, 73, 75 
Mohrenheim’s fossa, 106, 114 
Moro tuberculin test, the, 326 
Morphology, 11 
Much’s granules, 15 
granular stain, 481 
Mucous surfaces, tuberculosis of 
the, 446 
surfaces, tuberculosis treatment 
of the, 449 
Murmurs, succussion, 195 
National Tuberculosis Association, 
schema, etc., 72 
Negative tuberculin reaction, the, 
328 
New tuberculin, T. R., 373 
Night sweats, 84, 223 
Nodular form of tuberculosis, the, 
91 
syphilide, the differentation, 435 
Nomenclature, clinical, 89 
Nonspecific disposition, 25 
Normal auscultatory sounds, the, 
149 
breath sounds, the, 149 
chest findings, the x-ray plate, 
165 
chest on inspection, the, 106 
chest on palpation, the, 120 
chest on percussion, the, 133 
chest plate, the x-ray, 165 
chest variation from the x-ray. 
172 
vocal resonance, 156 
vocal sounds, 156 
voice sounds, 156 
Nursing and tuberculosis, 354 
Obedience, 218 
Objective symptoms, 82 
Observations on blood pressure, 
459 
on compression of the lungs, 
234 
Occupational therapy, 273 
Old tuberculin O. T., 312 
Operations, genito-urinary tubercu- 
losis, results of, 423 
Operative treatment of bone and 
joint tuberculosis, 405 
Ophthalmic tuberculin test, the, 325 
Opotherapy, 365 
Optic nerve in tuberculosis, 446 
Orbit, in tuberculosis the, 446 
Organic acids in chemotherapy, 253 
Organotherapy in pulmonary hem- 
orrhage, 365 
Other atypical forms of pulmonary 
tuberculosis, 99 
noticeable dispositions, 27 
noticeable tendencies, 27 
therapeutic methods for ad- 
ministering tuberculin, 323 
Otitis media. 87 
Pain, 83, 412, 426 
reflex, 400 
Painful and tender points, 123 
Palpation, 119, 289, 337 
methods of, 119 
of the abnormal chest, 121 
of the normal chest, 120 
Palpatory percussion, 144 
Paracentesis, 341 
Paratuberculous, 454 
Parrot’s law, 35 
Partial antigens or partigens, 314 
Pathogenic characteristics, 13 
Pathogenisis of gential tuberculo- 
sis, 424 
of urinary tuberculosis, 411 
Pathology and histology, 56 
Pectus carinatum, 106 
excavatum, 106 
Pelvic disease in women, differenti- 
ation from renal tuberculosis,422 
Percussion, 125, 144, 289, 337 
methods of, 132 566 
INDEX 
of the abnormal chest, 136 
of the normal chest, 133 
palpatory, 144 
Percutaneous tuberculin test, the, 326 
Peritoneal fluids in tuberculosis, 
the, 507 
Peritonitis tuberculosa, 388 
Personal history, 103 
Phenomenon, Litten’s, 117 
Theobald Smith, the, 535 
Phlyctenular Keratitis, 443 
Phototherapy, 255 
Phrenicotomy, 247 
Phthisis, 71 
and tuberculosis, 532 
bacillus, the, 9 
confirmata, 72 
desperata, 72 
incipiens, 72 
fibroid, x-ray plate in, 184 
pulmonalis, 71 
pulmonum, 71 
Phthisical chest, the, 112 
facies, the, 118 
Physical examination of gland tu- 
berculosis, 288 
manifestations of laryngeal tu- 
berculosis, 374 
Physiotherapy, 273 
rational, 276 
Pirquet v. tuberculin test, the, 326 
Placental transmission, 21 
Plate, the diagnostic quality, x-ray, 
165 
normal chest, x-ray, 165 
Pleomorphism, 11 
Pleural exudate in tuberculosis, the, 
507 
Pleurisy, diaphragmatic, 345 
pain, 227 
sacculated, 345 
surgical treatment of, 344 
Pleuritis idiopathica, 335 
tuberculosa, 335 
Pneumohydro thorax, x-ray plate, 192 
Pneumoliths, 60 
Pneumolysis, 247 
Pneumonectomy, 246 
Pneumonia, x-ray plate, the, 178 
Pneumonotomy, 246 
Pneumothorax, artificial, 228 
the x-ray plate in, 191 
Points, painful and tender, 123 
Polyvalent tuberculin, 313 
Ponndorf’s law, 311 
Porta infectionis, 16 
Portals of infection, 16 
Position of patient, 105 
Posological consideration in helio- 
therapy, the, 259 
Post-influenzal changes, x-ray plate, 
179 
Pottenger’s sign, 116 
Pott’s disease, 399, 402 
Prediposition, 24 
Pregnancy, effect of tuberculosis 
on, the, 350 
with tuberculosis, treatment of, 
358 
Present complaint, 104 
history, 104 
Pressure, blood, 86 
Prima vista diagnosis, 109, 113 
Primary foci of infection, the, 35 
stage of tuberculous disease in 
children, the, 285 
tuberculosis, 285 
tuberculosis of the larynx, 374 
tuberculosis, treatment of, 296 
tuberculous disease, 52 
Problem, tuberculosis a threefold, 
206 
Prodromal symptoms, 80 
Prognosis in genital tuberculosis, 427 
in renal tuberculosis, 422 
in tuberculous peritonitis, 392 
in tuberculous pleurisy, 341 
Proliferative form, the, 91 
Prophylactic treatment of tubercu- 
lous laryngitis, the, 381 
vaccine, Friedmann’s, 315 
Prophylaxis in pulmonary hemor- 
rhage, 366 
lymph nodes, in tuberculosis of 
the tracheo-bronchial, 296 
of tuberculosis in pregnancy, 355 
Protein sensitization, 535 
Pseudobacillus, the, 11 
Psychic factors, the, 208 
Pulmonary circulation and the heart, 
the, 452 
gymnastics, 269 
gymnastics, how to practice, 271 
hemorrhage, 183, 362 
massage, 269 
tuberculosis, 71 
tuberculosis, clinical forms, 88 
tuberculosis, hydrotherapy, 266 
tuberculosis, relation to trauma 
and shock, 463 
tuberculosis, the blood as a 
whole in, 490 
tuberculosis, the closed cases, 
531 
tuberculosis, the open cases, 
531 
tuberculosis, treatment of, 199 
Pulse, 85, 221 
Puncture, where to, 341 
Pyelitis in renal tuberculosis, 411 
Pyuria in genital tuberculosis, 412 INDEX 
567 
Quartz Lamp, 255 
Radiotherapy, 255 
Rales, dry and moist, 153 
Rational physiotherapy, 276 
Rauchfuss’ sign, 340 
Ray, X-, 255 
Reaction of the sun’s rays, the, 260 
the tuberculin, 309 t 
the tuberculin explanation of, 
310 
Wassermann, the, 501 
Reconstruction, 273 
of the tuberculous in civil life, 
278 
therapy, 280 
Reflex pain in bone and joint tuber- 
culosis, 400 
Rehabilitation, 273 
of the handicapped, 277 
Relation of trauma and shock to 
pulmonary tuberculosis, the 
463 
of x-ray to the diagnosis of pul- 
monary tuberculosis, the, 164 
Renal tuberculosis hematogenous, 
411 
tuberculosis lymphogenous, 412 
tuberculosis urogenous, 412 
Resonance normal voice, 156 
normal, vocal, 156 
Rest, 210 
and exercise, 280 
Results of operation, genito-urinary 
tuberculosis, 423 
Retina, tuberculosis of the, 445 
Rhonchi, 154 
Rhythm, normal breathing, 163 
Rib resection, 344 
Road to health for the tuberculous, 
the, 543 
Roentgenology, 164, 290 
Roentgenotherapy, 255 
Route, aerogenous, 17 
cutaneous, 20 
cryptogentic, 22 
enterogenous, 18 
genitogenetic, 20 
Sacculated pleurisy, 345 
Sanatorium cases, the, 204 
cases, treatment of, the, 199 
Sanitarium and Sanatorium, 533 
Sarcoid of Boeck, 438 
of Boeck, differentiation, 435 
Sarcoma metastatic x-ray plate, 182 
Saugmann’s critical study, 31 
Schema for classification of patients 
on examination, 72 
Schematic classification, 71 
Sclera, tuberculosis of the, 444 
Scoliosis, 108 
Scrobiculus cordis, 106 
Scrofuloderma, 436 
Secondary form of the disease, the, 
293 
stage of tuberculous disease in 
children, the, 293 
tuberculosis, 293 
tuberculous disease, 52 
Sensibilitrice, 535 
Sensitization, 67 
Serological consideration of the 
blood, 497 
Serum Maragliano’s, 316 
Marmoreck’s, 316 
therapy, the, 316 
Shadows, hilus the x-ray plate, 170 
Shock and trauma, 27 
definition and cause, 463 
influence on the infected, 465 
signs and symptoms of, 464 
the main factor, 466 
Shortness of breath, 224 
Sibson’s groove, 106 
Sign, Baccelli’s, 341 
D’Espine’s, 290 
Grocco’s, 339 
Litten’s, 117 
Pottenger’s, 116 
Rauchfuss’, 340 
Smith’s, 290 
Wheaton’s, 118 
Signs and symptoms, characteristic, 
90, 92, 93 
and symptoms of gland tuber- 
culosis, 287 
auscultatory catarrhal, 153 
Sleeplessness, 225 
Smith, Theobald, phenomenon, the, 
535 
Softening of the Tubercle, 58 
Sore throat, 227 
Sounds, abnormal chest, 153 
abnormal, vocal or voice, 157 
adventitious, 153 
auscultatory, errors in, 159 
normal, vocal or voice, 156 
splashing, 195 
Sources of error, 142 
of infection, 201 
Specific disposition, 24 
therapy, the, 299 
Spengler’s tuberculin I. K., 314 
Spinal fluids in tuberculosis, the, 507 
Spinalgia, 289 
Spinal tuberculosis, treatment of, 403 
Soino-trachael breathing, 290 
Spirometry, 196 
Splashing sounds, 195 568 
INDEX 
Sputum, collection for chemical ex- 
amination, 485 
examination, chemical, 484 
examination, combined, 487 
examination, microscopical, 487 
how and when to collect, 478 
in tuberculosis, the, 475 
lymphocytosis, in tuberculosis, 
483 
preparing for microscopical ex- 
amination, 480 
tubercle bacilli in the, 480 
tuberculous, 477 
Stage, first, 72 
primary tuberculous disease in 
children, 285 
second, 72 
secondary tuberculous disease 
in children, 293 
tertiary tuberculous disease in 
children, 296 
third, 72 
Stain, carbol-fuchsin, 483 
gentian-violet, 483 
Much’s granular, 481 
Ziehl-Neelson, 483 
Staining technic, improved, 841 
Standard tuberculin dilutions, 542 
tuberculin dosage, 333 
Stenotic chest, the, 111 
Sterility in tuberculous women, 347 
Sternberg’s Symptom, 346 
Stigmata of tuberculosis, the, 110 
Stone in renal tuberculosis, 411 
Structure of the tubercle, 56 
Structures, bony, the x-ray plate, 
167 
Subcutaneous structure, the x-ray 
plate, 167 
Succussion, 194 
sounds or murmurs, 194 
Sulcus, Harrison’s, 106 
Sunbaths, 255 
Sunlight, 255 
Sun’s rays, reaction of the, 260 
Surgical treatment of pleurisy, the, 
344 
treatment of pulmonary tuber- 
culosis, the, 228 
treatment of tuberculous peri- 
tonitis, the, 393 
Symptom, Sternberg’s, 346 
Williams’, 93 
Symptomatic treatment of peribron- 
chial gland tuberculosis, 298 
treatment of pulmonary tuber- 
culosis, 219 
Symptomatology of bone and joint 
tuberculosis, the, 397 
of tuberculous disease, the, 79 
Symptoms, mental, 85 
of activity, 80, 82 
of genital tuberculosis, 426 
of latency, 80 
of miliary tuberculosis, 98 
of pulmonary hemorrhage, 362 
of reflex pain in bone and joint 
tuberculosis, 400 
of reflex siens, group 2, 77 
of renal tuberculosis, 412, 414 
of tuberculosis of the eye, 442 
of tuberculous laryngitis, 378 
of tuberculous peritonitis, 389 
of tuberculous pleurisy, 336 
objective, 82 
prodromal, 82 
subjective, 82 
Syphilitic laryngitis, 380 
Tabes mesenterica, 388 
Table of normal standard weight, 
541 
of standard tuberculin dilutions. 
542 
Tachycardia, 227, 456 
Technic for heliotherapy, 261 
for preparing blood for micro- 
scopic examination, 469 
for the induction of lung com- 
pression, 239 
Maxson’s, 515 
Temperature, 84 
tendencies, other noticeable, 27 
Terms used in classification upon 
the discharge of a patient, 539 
used in definition of apparently 
cured, 540 
used in definition of cured, 540 
used in definition of far ad- 
vanced tuberculosis, 539 
used in definition of improved, 
540 
used in definition of incipient 
tuberculosis, 537 
used in definition of moderately 
advanced tuberculosis, 538 
used in definition of onset, 540 
used in definition of unimproved 
or progressive, 540 
Tertiary tuberculosis, 296 
tuberculosis, treatment of, 300 
tuberculous disease, 53 
Theory, the Wolff-Eisner, 311 
Therapeutic dose of tuberculin, the, 
542 
measures, associated, 250 
Therapy, general, the 199, 207 
occupational, 273 
specific, the, 299 INDEX 
569 
vocational, 273 
The tubercle bacillus, 9 
Thoracic organs, topography, of 
the, 125 
Thoracometry, 174 
Thoracoplasty, 235, 248 
Thoracotomy, 246 
Thorax infantilis, 11 
paralyticus, 112 
phthisicus, 112 
Three fold problem, tuberculosis, a, 
206 
Throat consumption, 369 
Time, a factor, 217 
Tinctorial characteristics, 12 
Topography of the thoracic organs, 
125 
Toxaemia, group 1, 77 
Toxic influence, 26 
Toxipathic disposition, the, 25 
Tracheo-bronchial lymph node tu- 
berculosis, 284, 286 
lymph node tuberculosis, treat- 
ment of, 296 
Transmission, placental, 21 
Trauma, 463 
and shock, 27 
and shock, tuberculosis follow- 
ing, 463 
influence on the infected, 465 
Traumatism, a causative factor in 
tuberculosis, 466 
to the genito-urinary organs, 411 
Treatment light, the, 255 
of ambulatory cases, 199 
of bone and joint tuberculosis, 
403 
of constitutional conditions in 
tuberculous adenitis, the, 303 
of cutaneous tuberculosis, the, 
439 
of genital tuberculosis, general 
and surgical, 428 
of genito-urinary tuberculosis, 
the general, 423 
of genito-urinary tuberculosis, 
the surgical, 423 
of hip and knee joint tubercu- 
losis, 405 
of local conditions in tubercu- 
lous adenitis, the, 304 
of pleurisy, medical, 342 
of pleurisy, surgical, 344 
of pregnancy with tuberculosis, 
358 
of pulmonary hemorrhage, 363 
of pulmonary hemorrhage, me- 
chanical, 363 
of pulmonary hemorrhage, med- 
ical, 363 
of pulmonary tuberculosis, the, 
199 
of pulmonary tuberculosis, the, 
surgical, 228 
of pulmonary tuberculosis-, the, 
symptomatic, 219 
of spinal tuberculosis, the, 403 
of the primary point of inva- 
sion in tuberculous adenitis, 
the, 304 
of the secondary form of tuber- 
culosis in children, 300 
of the tertiary form of tuber- 
culosis in children, 300 
of tuberculosis, 199 
of tuberculosis, medical, 199 
of tuberculosis, symptomatic, 219 
of tuberculosis of the eye, 446 
of tuberculosis of the mucous 
surfaces, 449 
of tuberculosis of the tracheo- 
bronchial lymph nodes, the, 
296 
of tuberculosis of the tracheo- 
bronchial lymph nodes, symp- 
tomatic, 296 
of tuberculosis with pregnancy, 
355 
of tuberculous adenitis, the, 303 
of tuberculous peritonitis, the 
medical, 393 
of tuberculous peritonitis, the 
surgical, 393 
operative, of bone and joint tu- 
berculosis, 406 
rest and exercise, 280 
the dietetic-hygienic, 212 
the home cases, 191 
the sanatorium cases. 199 
Tubercle bacilli in the bile and gall 
bladder, 507 
bacilli in the bile and gall blad- 
der, methods for demonstrat- 
ing, 514 
bacilli in the blood stream, 493 
bacilli in the exudate and other 
body fluids, 507 
bacilli in the exudate and other 
body fluids, methods for dem- 
onstrating, 515 
bacilli in the feces, 507 
bacilli in the feces, method for 
demonstrating, 513 
bacilli in the mother’s milk, 507 
bacilli in the mother’s milk, 
methods for demonstrating, 
511 
bacilli in the urine, 418, 508 
bacilli in the urine, methods for 
demonstrating, 508 INDEX 
570 
bacilli in the various body fluids, 
508 
genesis of the, 56 
location of the, 60 
structure and formation of the, 56 
Tubercular, 529 
Tuberculids, 437 
Tuberculin, 293, 307, 404, 423 
administration, 317 
albumose-free, 314 
bacillen emulsion B. E., 313 
Beraneck T. B. K., 314 
B. O. T., 313 
dilutions, 330 
dilutions, standard table of, 542 
for diagnostic purposes, 325 
injection, diagnosic in renal tu- 
berculosis, 419 
methods for administering, 319 
new T. R., 312 
old, 312 
polyvalent, 313 
positive and negative reaction, 
the, 535 
positive and negative phase, the, 
536 
reaction, the negative, 328 
reaction, the positive, 309 
reaction, the positive, explana- 
tion of the, 310 
Spengler’s I. K., 314 
standard dosage, the, 333 
test, the Mantoux or intracuta- 
neous, 327 
test, the Moro or percutaneous, 
326 
test, the ophthalmic or conjunc- 
tival, 325 
test, the v. Pirquet or cutane- 
ous, 326 
tests, the various, 325 
the therapeutic dose, 542 
the diagnostic dose, 542 
the discovery of, 308 
therapeutic contraindication, 324 
therapeutic indications, 316 
therapy in gland tuberculosis, 
the, 299 
Tuberculins, various kinds of, 312 
Tuberculinum purum, 314 
Tuberculosis, 529 
active, the x-ray plate, 177 
acute miliary, 73, 75 
acute miliary, in children, 294 
advancing, the x-ray plate, 176 
among pregnant women, the 
incidence of, 348 
and hypotension, 458 
and nursing, 354 
and pleurisy, 335 
and pregnancy, 347 
and pulmonary hemorrhage, 362 
and tachycardia, 456 
and the cardiovascular system, 
450 
and the heart, 450 
and the pulmonary circulation, 
452 
Association National, schema, 
etc., 72 
a threefold problem, 206 
atypical types, 95 
basal meningeal in children, 295 
bronchial gland, 286 
clinical, 69, 536 
clinical forms, 88 
complement fixation in, 498 
conjugal, 27 
cutis necrogenica, 430 
cutis orificialis, 436 
early x-ray plate, 173 
far advanced, third stage, 73 
following trauma and shock, 463 
pallinarum, 10 
genital, 424 
genital pathogenesis, 424 
genital symptoms of, 426 
heliotherapy in, 257 
in children, 284 
in children, the frequency of, 
305 
incipient—first stage, 72 
in pregnancy prophylaxis of, 355 
latent, 536 
manifest, 536 
maternal on the fetus, the effect 
of, 352 
miliary form, the, 96 
miliary x-ray plate, 180 
moderately advance, third stage, 
73 
of bones and joints, 396 
of the abdomen, 388 
of the conjunctiva, 443 
of the cornea, 444 
of the eve. 441 
of the eye and mucous surfaces, 
441 
of the eye, symptoms of, 442 
of the eyelids, 443 
of the genito-urinary organs, 
410 
of the kidneys, 410 
of the larynx, 369 
of the larynx, primary, 374 
of the mucous surfaces. 441, 446 
of the peritoneum, 388 
of the sclera, 444 
of the skin, 429 INDEX 
571 
of the skin, diagnosis of, 432 
of the spine in adults, 406 
of the tracheo-bronchial lymph 
nodes, 284, 286 
of the tunica vasculosa, 444 
of the urinary tract, 410 
on pregnancy, the effect of, 349 
primary form, the, 285 
pulmonary, 71 
secondary form, the, 293 
stigmata of, 110 
tertiary form, the, 296 
the bile in, 507 
the blood in, 489 
the feces in, 507 
the milk in, 507 
the peritoneal fluid in, 507 
the pleural exudate in, 507 
the spinal fluid in, 507 
the urine in, 507 
treatment of, 199, 207 
typical types, 89 
verrucosa cutis, 430, 435 
with pregnancy, the treatment 
of, 355 
Tuberculous, 529 
birth control among the, 354 
disease, primary, 52 
disease, secondary, 52 
disease, symptomatology, 79 
disease, tertiary, 53 
disease, the course of, 50 
enteritis, 389 
enteritis, prognosis of, 392 
enteritis, symptoms of, 389 
immunity, the acquired, 62 
immunization, the various meth- 
ods of, 65 
in civil life, reconstruction of 
the, 278 
kidney, the cheesy, cavernous 
type, 414 
kidney, the fibroid type, 414 
kidney, the nodular type, 414 
kidney, the ulcerative type, 414 
laryngitis, 369, 380 
laryngitis, infiltrative type, 377 
laryngitis, miliary form, 378 
laryngitis, prognosis in, 381 
laryngitis, symptoms of, 378 
laryngitis, treatment of, 381 
laryngitis, treatment (a) pro- 
phylactic, 381 
largyngitis, treatment (b) gen- 
eral and local, 382 
laryngitis, tumor formation, 376 
lesions, 537 
meningitis in children, 295 
peritonitis, 388 
pleurisy, 325 
pleurisy, course of the disease, 
337 
pleurisy, diagnosis, 338 
pleurisy, diagnosis, differential, 
339 
pleurisy, frequency of, 336 
pleurisy, physical examination, 
337 
pleurisy, symptoms of, 336 
soldier, the, rehabilitation of, 277 
sputum, 477 
the care of the, 199, 202 
Tuberculously diseased, 530 
infected, 530 
Types of bacilli, 9 
of tuberculosis, atypical or aber- 
rant, 95 
of tuberculosis, typical 89 
Ulcertive type, tuberculous kidney, 
the, 414 
Ultimate fate of the tubercle, the, 60 
result of lung compression, 
244 
Ureteral catheterization in renal tu- 
berculosis, 419 
Urinalysis, 418 
Urinary distress, 227 
tract, tuberculosis of the, 410 
tuberculosis, pathogenesis of, 
411 
tuberculosis, pyelitis in, 411 
tuberculosis, stone in, 411 
Urine, characteristics of healthy, 507 
characteristics in pulmonary 
tuberculosis, 508 
in tuberculosis, 507 
tubercle bacilli in, 418 
tubercle bacilli, methods for 
demonstrating, 508 
Urochrome of the urine in tubercu- 
losis, the, 516 
Urochromogen test, the, 507 
Urogenous, renal tuberculosis, in- 
fection in, 412 
Vaccination method, cutaneous, 323 
Vaccine, Friedmann’s, 315 
Variations from the normal x-ray 
plate, 172 
Varieties of tubercle bacilli, 9 
of tuberculosis of the skin, 429 
Various kinds of tuberculins, 312 
methods of tuberculosis immu- 
nization, the, 65 
other therapeutic methods for 
administering tuberculin, 323 
tuberculin tests, the, 325 
Vital capacity, 194, 196 
capacity, estimation of the, 196 572 
INDEX 
Vocal resonance, normal, 156 
sounds, normal, 156 
Vocational therapy, 273 
Voice sounds, normal, 156 
Wassermann reaction, the, 501 
What led to the discovery of tuber- 
culin? 308 
Wheatons’s sign, 118 
When to ausculate, 158 
Whispering bronchophony, 144, 146, 
157 
Wholesome fresh air, 209 
Williams’s symptom, 93, 142 
Wintrich’s note, 142 
Wolf?-Eisner theory, the, 311 
X-ray, 255, 420 
relation to d:agnosis, etc., 164 
Ziehl-Neelsen stain, 483 
Zomos, 215 
Zomotherapy, 215