IHE  PRESENT  STATUS
OF THE
PATHOLOGY
CONSUMPTION  AND TUBERCULOSIS.
BY
J. IIILGAKD TYNDALE, M.I).
OF NEW YORK CITY.
GEORGETOWN flfep&ITY.  > ?nc
          NEW
TROWS PRINTING AND BOOKBINDING GO.
        205—213 Bast 12th Street.
             1878. 
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ARMY MEDICAL LIBRARY
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THE PRESENT STATUS

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OF THE
PATHOLOGY
CONSUMPTION AND TUBERCULOSIS.
J. HILGAED TYNDALE, M.D.,
OF NEW YORK CITY.
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         NEW YORK:
TROW'S PRINTING AND BOOKBINDING CO.,
        205—213 East 12th Street.
             1878. 
     The following is a series of papers, written  at  short intervals
to a fellow-practitioner in a small town.  At his suggestion they are
now submitted to the profession at large, with  such slight alterations
as the circumstances of the case seemed to  call for.
                                                        J. H.  T.


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CONTENTS.
                                                    PAGE
Introductory..........,.............................   3
Catarrhal Pneumonia.................................  11
Croupous  Pneumonia..................................  18
Desquamative  Pneumonia..............................  26
Interstitial Pneumonia................................  31
Caseous Pneumonia....................................  38
Peribronchitis........................................  45
Tuberculosis.........................................  51
Relation of Tuberculosis to Scrofulosis................  67
Phthisis Pulmonalis...................................  73
Therapeutics..........................................  90
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GEORGETOWN. UNIVERSITY.
               THE PRESENT STATUS
                           OF THE

Pathology  of  Consumption  and  Tuberculosis.
                     INTRODUCTORY.

    In the present series of papers I propose giving a condensed
 outline of the present accepted theories in regard to the pathol-
 ogy of pulmonary phthisis.
    Consumption  has existed since time immemorial, or, at least,
 as far back as medical history reaches.  Whether it has decreased
 or increased cannot be accurately determined.
    Theories have been  built up,  only to  be replaced by others;
 many a talent has gone  to its grave, and yet it would  seem as if
 we were still far, very far removed from the truth—at least  so
 far as practical therapeutical results are concerned.
    Lately, however, considerable  light has  been shed upon the
 subjects of phthisis  and  tuberculosis by a number of authors, and
 it is from this accumulated material that it will be my endeavor
 to present a correct and distinct outline of the present status  of
 the pathology of pulmonary phthisis, or consumption, according
 to the latest accepted  theories, confining my own observations  to
 a few points, which will be duly chronicled in their proper place.
    We should dismiss from our mind the idea that the  pathology
 of phthisis will ever be brought down to represent one single con-
 dition and its consequences.
    In order to properly  comprehend upon  what ground our
present theories rest, it may be well to give a rapid sketch of the
past history of consumption.
   Consumption—decline—must needs exist where there is either 
4
consumption and tuberculosis.
 too great a waste  or a lack of supply.  Where too  much is  ex-
 pended, where the body is  reduced by discharges or  secretions of
 any kind, we  have decline, even though the supply may still  be
 normal.   The oldest pathologists have always held that consump-
 tion takes its origin from  various forms of disease and various
 organs, and this general idea is correct to-day.
    It was when autopsies became more frequent and small gray
 nodules were found in the lungs and digestive tract, that the
 theory gained ground that  all  consumptive  processes owed  their
 origin to the formation of  nodules of tubercular substance.  All
 consumptions were tuberculous.   This was the opinion of  Laen-
 nec, who, besides the small gray  nodules, described certain other
 larger  knots, together with solid infiltrations of considerable ex-
 tent, which were in nowise connected with tubercle.   The first
 were denominated yellow tubercle, and considered quite distinct
 from the gray (true tubercle).  Infiltrations and indurations were
 pronounced to be concomitants of both yellow and gray tubercle,
 and both were said to undergo the same processes of degeneration,
 by formation of caverns  and leading rapidly to destruction.  In
other words, the division was  into  tubercle proper (miliary tuber-
cle of present date) and infiltrated tuhercle (infiltration generally),
both subject to caseous degeneration, which process  was denomi-
nated " tuberculization."
    Laennec's  theory is the basis from which all else has  since
taken shape,  and the microscope has partly laid bare the  more
minute structure of his two tuberculizations.
    The establishing of pathological anatomy as a special branch
of our science made us acquainted  with  the  various forms of
degenerations—fatty, amyloid,  the  proliferation  of connective
tissue with subsequent contraction, cirrhotic conditions.   Based
chiefly on the latter form,  it was held that this was a  decided
step towards  the ultimate  cure  of phthisis, to  wit:  by cicatriza-
tion of cavities.  But we are forced to agree with Prof. Ruehle,
of Bonn, when he says: " The fact of a phthisical patient dying
of dropsy instead  of consumption can never satisfy the sincere
therapeutist."
    Next in order of theories we have the resemblance of con-
sumption to inflammatory  processes, based upon the illustrations
of Carwell (1838).   It was demonstrated to how great an  extent
the  smallest bronchi and the alveoli of the lungs were affected in 
INTRODUCTORY.
5
tuberculosis; how the changes pass into the neighboring paren-
chyma, the bronchi become dilated, and by dilatation finally form
cavities.   Again, much stress was laid upon the proliferation of
connective tissue and its consequent  cicatrization by induration.
The fact, however, remained, that breaking down of the products
of  chronic  inflammation  was by far  the  most frequent result,
both in the greater  number of  cases as well as in the  extent of
tissue  involved; in  short, that  cheesy metamorphosis was the
prominent characteristic.   Thus originated chronic  pneumonia
with cheesy degeneration  (caseous pneumonia).   The conclusion
derived from this was the  recognition of tubercle in two distinct
forms  once  more, namely:  miliary tubercle  (the tuberculum
nodule),  and the infiltrated  tubercle, recognized  as the result of
the cheesy degeneration of inflammatory products.
    It was not  long thereafter that miliary  tubercle was found to
be a new formation (neoplasm), and since the products of inflam-
matory processes could not be placed with neoplasmata, it became
plain that the  term " tubercle "  would not  answer for  both con-
ditions.
    In order, therefore, to  determine whether tubercle and cheesy
products were identical, inoculation upon  animals was resorted
to,  and with the following  result:  inoculation of the products
of  cheesy  degeneration  produced  both  miliary  tubercle  and
cheesy products in the inoculated animal.   Right here it is well
to bear in mind the possibility (and, according to late researches,
the probability) of  having  genuine tubercle  intermingled with
cheesy products in the mass to  be inoculated.  The inoculation
of  miliary  tubercle,  however, produced miliary tubercle alone,
so that, as to whether cheesy products can   be brought about by
tubercle  direct, or as a subsequent result, has as yet not  been defi-
nitely settled.*
    So it  would seem that thus far, at least, the identity of the
two remains undisturbed, that  in a general sense tubercle and
caseous degeneration are convertible.
    It has been demonstrated that in animals a cheesy infiltration
may call  forth tubercle-efflorescence, the same as in  the human

  * The latest investigations in regard to inoculation will be spoken of in  a
chapter on tuberculosis, where prominent authors will be cited to show a histo-
logical difference  between miliary tubercle from a  previously existing cheesy
centre, and the tubercle of inoculation with an indifferent substance. 
6
CONSUMPTION AND TUBERCULOSIS.
being, where general or local miliary tubercle (e. g., of the me-
ninges, meningitis basilaris) can be produced by the presence of
cheesy  aggregations, usually having their  seat in  lymphatic
glands.
   What has been said will suffice to make it clear to your mind
that a thorough  knowledge of the acute  inflammatory conditions
of the lung must of necessity precede an investigation  into  the
pathology  of  consumption and  tuberculosis.   In  subsequent
papers, therefore, it will be my endeavor to sketch the acute lung
affections (catarrhal, croupous, etc.), following them to their pos-
sible terminations, and add to these the primarily chronic inflam-
mation of the lung (interstitial pneumonia);  next treat  of that
chronic condition which may result from either of the foregoing,
namely: Caseous pneumonia; and lastly, of tuberculosis proper,
both as an acute infectious disease, as well as in its relation  to
caseous degeneration and to scrofulosis.
   Before closing this first paper, I feel it incumbent upon me to
draw attention to a few of the more salient points in the anatom-
ical  and physiological relations of the lung, so necessary to a
thorough understanding of  the pathology of  phthisis, the  more
as a few points  I will mention  are of recent origin,  and dwelt
upon in the work of Buhl, of Munich, from whom I quote :
   " In sifting  the  inflammatory conditions  of the respiratory
organs, you will rind  some of them taking place and  running
their characteristic course in the epithelial surface of bronchi and
lung alveoli.   These processes may thence be termed superficial.
Other conditions manifest themselves in the walls proper of  the
bronchi and the adjacent actual parenchyma of the lungs them-
selves.  Not  that  there is  a strict division into superficial and
parenchymatous inflammations, since  in many processes  both  are
more or less affected, but one of these processes is always second-
ary to the other."
   A very important point, and one to which I desire to draw
attention particularly, is the epithelial layer of the alveoli and its
physiological character.  Buhl,  in  his excellent  work, while  ac-
knowledging the existence of epithelium, both in foetal and adult
age, ascribes  to  it the characteristics of  lymphatic endothelium,
spread over the inner surface of  the alveoli,  and not those of a
continued  bronchial epithelium.   He proves this  by  drawing
attention  to the form  and size, and  the  oft-asserted fact of  its 
INTRODUCTORY.
7
being " interrupted," which  is likewise, and  only found, in the
endothelium of serous membranes.  Accordingly, bronchial epi-
thelium passes into alveolar endothelium, as tubular epithelium is
followed by endothelium in the peritoneum.
    Another  striking  proof  is  found  in  the experiments  of
Sigorsky (Centralblatt, 1870, No. 52), showing the existence of  a
network of lymphatic vessels, consisting of  canaliculi and stel
late knots uniting them in the alveolar walls, which knots com-
municate with the volume  of the  alveoli  by means of minute
openings.  It would appear proper, therefore, to look upon the
alveolar pouches as wide lymph-spaces, filled with air and lined
by endothelium, which endothelium is wanting in the lymphatic
network of the  alveolar walls.   These relations are of impor-
tance for the exchange of gases in respiration, since the inspired
air meets with no absolute resistance within the walls of  the air-
cells, which would not merely permit of diffusion of gases through
the capillary walls, but of a direct  entrance  into the open lym-
phatic network of the  alveoli.
    Lastly, attention has been  called by several  authors to the
analogy between the alveolar epithelium and the  endothelium of
the lymphatics, more especially as regards their products  in path-
ological processes.  It is well to remember that  authors, speak-
ing of  superficial  inflammations, thereby designate such forms,
the products of which are chiefly generated in the epithelium or
pass over its surface ;  while  the products of  parenchymatous in-
flammations are interstitial and peribronchial.
    The vascular system  of  the respiratory organs, likewise, calls
for a moment's attention.   It  is well  never to lose sight of the
fact, that the arteries proper of the  lungs are  not the only ones,
but that the  bronchial arteries likewise may play an important
part.  The bronchial arteries have a share  in the capillaries of
the pulmonary organs, and therefore  take  a part in the  disturb-
ances of nutrition of lung tissue.  The  bronchial arteries run an
interstitial,  interlobular course, finally branching  out  on  the
pleurae, while the arteries of the lung proper form the great bulk
of capillaries in the alveoli.
    It follows, therefore, as a general rule, that peribronchial in-
flammations and  parenchymatous infiltrations of the lungs are
within the territory of the bronchial arteries, whereas the super-
ficial inflammatory conditions (exclusive of the bronchi) are wTith- 
8
CONSUMPTION  AND TUBERCULOSIS.
in the territory of the pulmonary arteries.  It further explains
the involving of  the pleura and bronchi in original maladies of
luno-  parenchyma, as well  as  the possibility of an  extension of
bronchial or pleuritic disease upon lung parenchyma, and on the
other hand  the well established regularity in the appearance and
character of one or the other  of  the  diseases named, to wit:
Primary disease of lung parenchyma is more diffused, more con-
tinuous in accordance with the  capillary distribution ;  in  other
words, it is lobar; whereas, primary disease of the bronchi always
leaves certain  branches  free, and  even when spreading to the
lung parenchyma will, at first, be lobular, or even remain so.  In
other words, diseased lobules  are contiguous to, and surrounded
by, relatively healthy ones.
    The same thing may be said of thromboses and emboli.   Or-
dinary thromboses occur in the usually dilated capillaries, which
are fed by the arteries of the lungs,  and create lobar trouble, the
so-called pyaemic plugs (emboli) in the finer arteries of the lungs
are, though small, distinctly lobar as  regards their seat and extent.
    Intermediate between the lobar and  lobular form, we  place
such  disorders which originate  in  the lymphatics.  Of  these,
Prof. Buhl says:  " As the finest ramifications  of the lymphatics
follow the course of the bronchial arteries in the alveolar walls,
running  their course interlobular, interstitial  and peribronchial,
congregating at length  partly in the subserous pleural tissue,
partly in the lobes of the  lung, so is their pathological  progress
either continuous and diffused, or  confined to lesser spaces, to
mere points; or thirdly, both conditions may exist  simultane-
ously and a doubt may arise as to whether they should be called
lobar or lobular."
    There remains still another point for examination.  It is that
an  acute pulmonary trouble will present itself quite different
from a chronic one.   Inflammations, either superficial or paren-
chymatous, whether lobar or lobular, will present quite different
features when of acute than when of chronic origin.   If acute,
of recent and  sudden origin when  examined, they differ widely
from chronic inflammations, whose  chief  characteristics are de-
generations of great  extent when  superficial.  On the other hand
they are characterized by proliferation of  connective tissue, cica-
trization, etc., when  such chronic inflammations are  parenchy-
matous, interstitial or peribronchial. 
INTRODUCTORY.
9
   In either case, it will be well to remember, that in an inflam-
matory process, whether acute or chronic, where secretions are
not expelled, but remain in the respiratory passages, as well  as
when tissue is being disintegrated or destroyed, the contact  of
atmospheric air  (peculiar to  the  respiratory organs) exercises a
disintegrating effect  upon  the  infiltrations, in which the whole
body participates.  This  is seen  in the  shape of fungi, which
enter the blood  and lymphatic vessels through the decomposing
tissue. 
 
CATARRHAL PNEUMONIA.
11
                CATARRHAL  PNEUMONIA.

    You will remember I stated in my first article, that a catar-
 rhal process of the lung  tissue proper (of  the  alveoli) was an
 impossibility, on account of certain anatomical conditions.   Still
 the term  catarrhal pneumonia has become so fixed in our nomen-
 clature, as to mislead many practitioners in regard to the patho-
 logical conditions  passing under that name.
    French  physicians first  drew  a line  of distinction between
 catarrhal pneumonia and croupous  pneumonia.  Among  Ger-
 mans,  Ziemssen has furnished the  best  and most comprehen-
 sive view of the  subject in  his  " Pleurisy and Pneumonia in
 Infancy."
    Niemeyer, in his chapter on  catarrhal  pneumonia, opens by
 saying that since no mucous membrane with mucous follicles ex-
 isted in the alveoli, it was in reality a catarrh of the finer ramifi-
 cations of the bronchi.   Notwithstanding the extensive researches
 of  Bartels, Rokitansky and others, the pathology of catarrhal
 pneumonia has been all but comprehended. According to  Roki-
 tansky the minute bronchi  and the final termini of the bronchi
 are the seat of  an  intense inflammatory process.  Adding to this
 dictum the result of the investigations of other authors, we may
 say : It is an acute disease, attacking the lower lobes, beginning
 at their borders and subsequently passing forward and upward.
    Juergensen, on the contrary (see Ziemssen's Cyclopoedia), in-
 sists that in order  to comprehend the etiology of  catarrhal  pneu-
 monia, it is necessary to limit the definition thus: " Catarrhal
 pneumonia is always a  secondary process and  never has its pri-
 mary origin in the alveoli.   As a rule, it is preceded by inflamma-
 tion of the bronchial raucous membrane.  The only exception to
 this rule is in the inhalation of  strong irritants, such as chlorine,
 where  the effect may be  simultaneously produced in  bronchial
 and alveolar mucous membrane."  It will occur at once, that a
 question  of etiology of such importance should not be left in
doubt,  if  possible, especially since it must needs have a direct
bearing upon  the  possibility of  its being a  basis for phthisis.
These points will be touched upon in their proper place. 
12
CONSUMPTION AND TUBERCULOSIS.
    All  observations tend to establish that catarrhal pneumonia is
most frequent in children under five years of age.
    I will here positively assert, that catarrhal pneumonia is the
only form of inflammation of the lungs ever occurring before the
age of puberty.   Croupous pneumonia never occurs  before this
age.  This may seem heresy.  Much as I regret it, the extent of
the subject will not allow me to enter upon this question.
  Acute catarrh of the lesser branches, as well as of the most
minute termini of the bronchi, is, like  all catarrhs, superficial,
accompanied by edematous  swelling and redness of the mucous
membrane.  The immediate result of the foregoing is excessive
secretion of  mucus,  largely  diluted with  serum, occasionally
mixed with blood corpuscles and liquor sanguinis.  In time, with
the diminution of serum, the secretion becomes muco-purulent
and purulent.
    This short outline of the pathology of catarrhal  pneumonia
will show the propriety of denominating this disease by the name
of broncho-pneumonia, according to Niemeyer and others.  There
is still another  term for this disorder—capillary bronchitis.   It
is the one mostly used in this country for defining the  progress of
bronchial catarrh in the bronchial ramifications or capillaries.
    Let  us  now pass to the  actual  pathological  processes  of
catarrhal pneumonia.  That the alveolar walls are a continuation
of the bronchial ramifications, has been dwelt upon by Oppolzer,
Niemeyer and others, both of whom, strengthened by Buhl, have
taken occasion to dwell upon the  fact, that this continuation,
however, involves  a complete  change  in the  character of  the
alveolar lining.   Bronchial mucous membrane  is composed  of
several  layers, has  alveolar membrane, which,  as has been pre-
viously  stated,  is very  much like  lymphatic endothelium,  has
pavement epithelium, and consists of a single layer.
    In  accordance with  this  anatomical arrangement will  be
found the pathological conditions.  It is easy of comprehension,
that an actual catarrh of the middle and finer  bronchi, and the
clogging up of these with mucus and pus, must needs  involve the
alveoli in a decidedly modified degree.   I will first give an exact
outline  of  the  accepted pathological conditions, and then pass
to the causes  and  their effects, such  as are  closely allied to
catarrhal pneumonia.
   In examining an acutely diseased lung, we find different parts 
CATARRHAL  PNEUMONIA.
13
of the lung in  different  conditions.   We find, 1st, lobules, which
upon section present  a smoothly cut surface, not  granular as in
croupous pneumonia.   Corresponding  to the lobule, this smooth
surface is found to be part of  a well solidified,  condensed de-
posit, for the most part situated in the periphery of the  lung.
On pressure, a fluid, at  first bloody, then of pale gray color, es-
capes, mixed with hyperplastic epithelial cells, part of which are
already  undergoing fatty  degeneration.   The  chief  component
part of the infiltration, the gray fluid (for epithelium^ secondary in
quantity) is a secretion of thick mucus, very rich in pus corpuscles.
    2d. Parts in which the quantity of blood is greater than in
the foregoing, the pleurae even  showing ecchymotic  spots.   On
section, serum  mixed  with blood and air bubbles  escapes freely.
This is acute oedema of the lung.
    3d. In other lobules the air-cells appear distended with air,
quite pale, and showing vascularity in  their periphery only, as if
enclosed by blood-vessels (local emphysema).
    4th.  On  the  borders of  the  lung  and toward the  root, the
alveoli are collapsed, retracted, entirely or nearly emptied of air,
and of bluish red color.  These are atelectatic parts.
    Of  the  above four conditions found in lobules, only the first
(filling up of the  lobules with mucus and pus) is the immediate
and actual result of  catarrhal pneumonia.  Acute oedema,  local
emphysema and atelectasis  are  merely concomitant  conditions,
the same as accompany other inflammations.  Again, all four con-
ditions may alternate  with perfectly healthy tissue, thus showing
the lobidar character of the existing inflammation.
    It will naturally be concluded from the above, that, since the
mucus  and  purulent products  are  found  in  the alveoli,  they
must be products of  their structures.  This  may  be  partly true
with  respect to the pus, since the alveolar  capillaries  may per-
mit of migration of white (pus) corpuscles, as  well as other cor-
puscles.  As it is pretty well established that alveolar epithelium
does not produce mucus,  the greater part, if not all of the se-
creted product must have originated in the smallest bronchi and
have  been transferred by  respiratory motion and  gravitation to
the alveoli.  That the alveoli are at the  same  time in a state of
inflammatory irritation, may be allowed.
   Catarrhal  pneumonia  should, therefore, be  defined as: A
CAPILLARY BRONCHITIS (SO-CALLED BRONCHIOLITIS),  IN  WHICH  THE 
14
CONSUMPTION AND TUBERCULOSIS.
MUCOUS AND PURULENT SECRETIONS OF THE BRONCHI ARE TRANSFERRED
BY  RESPIRATION  AND  GRAVITATION TO  A  NUMBER OF  ALVEOLAR
LOBULI, CAUSING THE LUNG TO PARTICIPATE  BY COLLATERAL 03DEMA,
LOCAL EMPHYSEMA, ATELECTASIS, AND HYPERJEMIA.
   It is not my purpose to dwell at large  upon prognosis, etc.
As  stated in the first article, I will chiefly  confine  myself to
pathological conditions.
   A favorable termination is due to the above-mentioned fact,
i. e., the non-participation (at least  in  a direct manner) of the
true parenchyma in the inflammatory process.  The normal con-
dition is regained by fatty degeneration of the  products of the in-
flammation, together with their expectoration through the bronchi,
accompanied by the absorption of the  pus-corpuscles (white blood-
corpuscles) still remaining.  Renewed active  circulation in the
capillaries, reabsorption of serous infiltration into the lung paren-
chyma and bronchial mucous  membrane, restitution of local em-
physema, expansion of collapsed  parts by the entrance of atmos-
pheric air and regeneration of the lost epithelial cells, take place.
   Thus I have merely  sketched the  favorable  termination of
this kind of  pneumonia, in order to transfer  your attention to the
changes which occur when absorption, etc., does not supervene*
and which changes pave the way to pulmonary consumption.
   The  factors which should govern  our prognosis have been
well condensed by Juergensen, as follows:
   1st.  The  more acutely a catarrhal pneumonia runs its course,
the less  the danger of an unfavorable termination.
   2d. The  younger the patient in  number of  years preceding
the age  of puberty, the greater the danger to life.
   3d. The  danger to life is in exact proportion  to the extent of
the pneumonic process.
   4th.  Any reduction in the general resisting power of the pa-
tient increases the danger to his life.
   It is not my province to dwell upon other possible  termina-
tions, for example gangrene, as that  would not be appropriate to
our subject, which  is to confine ourselves  to such conditions as
lead to pulmonary consumption  or phthisis.
   Where the inflammation passes into the chronic  condition, as
frequently happens to debilitated persons, quite small  sections of
the parts involved may linger  behind others entering upon reso-
lution, and thus pass into the chronic stage.    • 
CATARRHAL PNEUMONIA.
15
   In speaking of the restitution of local emphysema, as well as
of collapsed parts, it  must be borne in  mind  that, inasmuch as
elogged-up bronchi exist in such parts, residues may readily be
left behind.  This is true of incapsulated epithelium, as well as of
the mucous  and purulent  secretions, all of which then  tend to
caseous degeneration  and pigmentary degeneration.
   Authorities differ  in regard to the frequency of cheesy degen-
eration of  these products.  Niemeyer states that it  occurs very
frequently.  Bartels and Ziemssen  have  seen each two cases only
where non-restitution resulted  in cheesy products and the subse-
quent  development of tubercle  from that centre.  Buhl places
this  occurrence among  the rare events.   As a  substantiating
proof  he calls attention  to the fact that cheesy degeneration  is
chiefly found in the upper lobes and their apices, while, as above
related, the products of catarrhal  pneumonia are found  in the
lower lobes.   Then the catarrhal products only clog up the finer
bronchi, are not traversed by lung-tissue proper, nor is any of it
included in the cheesy degeneration, as  is nearly always the case
in true caseous degeneration.   Buhl goes on to say,  that " the
bronchiolus encasing  the  cheesy mass is dilated and  thickened,
forming, as it were, a fibrous capsule for the mass."
   Mark now that this  process of incapsulation  of the cheesy
mass is not one of the effects of catarrhal pneumonia (although
the products  of the  cheesy mass itself  is), but the result of the
activity displayed  by the surrounding parts  (connective-tissue
vessels), irritated  by the  existing inflammatory products.  This
irritation is not of a very acute character, and tends to the forma-
tion and subsequent contraction of connective tissue.  This is
true chronic peribronchitis, of which more will be said in a future
article.
   Next let  us dwell  a short  time upon a point in connection
with the origin of lobular cheesy masses, which  are produced by
the wandering of catarrhal secretions from the lesser bronchi into
the  alveoli.   The same process, as  asserted  by some  writers, is
brought about by the entrance of foreign bodies into the alveoli.
In the category of  foreign bodies,  they include extravasated
blood, croupous and  diphtheritic membranes.  It is claimed that
by inspiration they are driven into the smallest bronchi and lung
alveoli, and there, by continued irritation, give rise to superficial
epithelial disturbances. 
 16              CONSUMPTION AND TUBERCULOSIS.

    To  these  products may be added the pus of purulent bron-
 chitis and that from cancers, as well as all products of  ulceration
 (such as epithelium from cancer of  the lip), particles of cartilage
 from necrosis of the larynx, or particles, in fact, from  any destruc-
 tive process.
    Let us dispose of these pathological products  before consider-
 ing such as are introduced from without.  It is well, while allow-
 ing for their ability to cause superficial inflammation, to discrimi-
 nate between each one  of these products.   It should be borne
 in mind that extravasated blood is often coughed up within  the
 next few days succeeding a hemorrhage, while the blood that
 remains is apt to become  purulent  so rapidly as to suggest  the
 probability of its  expectoration before its  presence could have
 caused  any great damage.   Products of a chronic character (pus
 from cancers), continually supplied for a long time, are more apt
 to degenerate.
    With regard to croup and diphtheria,  which  affect  the laryn-
 geal and tracheal mucous membrane, opinions differ.*
    Foreign bodies introduced from without should be  briefly
 touched upon.  The inhalation of dust has of  late received con-
 siderable attention.  Ever since Prof. Tyndall's lecture on " Dust
 and Disease," and Zenker's essay on  " Pneumonokonioses,"  this
 subject has created lively interest.   The  presence, under certain
 conditions of the atmosphere, of atoms of lime,  silicates,  carbon,
 various metals, has caused Zenker to  base  thereupon  his theory
 of " foreign body pneumonia."   These atoms have been found to
 exist in the alveoli.   Of course, in the majority  of cases their
 presence is harmless,  but I can readily imagine that in a  broken-
 down  constitution, or in cases  in which  the innervation of the
 alveoli is disturbed, pathological processes may supervene.
    Mention is made  of still another  ending of  catarrhal pneu-
 monia, which is a rare one.  I refer to atrophy of the alveoli and
 to bronchial dilatation.   This condition supervenes mostly in the

   * Prof.  Jacobi; who is  the best authority on this  subject, tells  me that the
 decomposed material is carried downward by the force of inspiration, and bron-
 cho-pneumonia may result from atelectasis.  " Sometimes  embolism results
 from thrombi in small veins, either near the larynx in croup, or in other parts
 from debilitated circulation, or by portions of a heart-clot torn away." Exten-
sion by contiguity, he says, is found to reach no farther than the second ramifi-
 cations of the bronchial tubes. 
CATARRHAL PNEUMONIA.
17
aged, though it is well to bear in mind the possibility of its oc-
curring in  infants, who are the chief  victims of catarrhal pneu-
monia.  This is said to occur both in the upper and lower lobes.
The bronchi, even in their earlier ramifications, become cylindri-
cal and varicose, with rapidly succeeding dilatations.   The  mu-
cous membrane remains intact.  The alveolar structure  has dis
appeared ; emphysema supervenes.   The alveolar epithelium is
either fattily degenerated, or has entirely  disappeared;  obliter-
ated capillaries and lymphatics take their place  This latter fact
demonstrates that the original process was one of obliteration
(by pressure) of the capillaries.   Therefore, this is true atrophy.
    Alveolar atrophy does not lead to phthisis, since it may prop-
erly be called a curative process—an attempt to repair, and, when
acquired in childhood, often carried to a green old age.
            2 
18             CONSUMPTION AND TUBERCULOSIS.
                CROUPOUS  PNEUMONIA.

    The term " croupous," as you know, is used in connection with
a number of diseases, as of the larynx, lungs, and kidneys.  Flint
describes  all  croupous affections  as  being characterized by  an
exudation of lymph.   It is well to have in mind that this exuda-
tion is upon the surface of membranes in contradistinction to
diphtheritic exudation which takes place within the tissue itself.
German authorities,  therefore, invaribly define  croupous  inflam-
mations as characterized by an exudation, wThich is rich in fibrine,
upon  the  surface of mucous membrane.  Latterly the identity
between croupous and diphtheritic exudations has been sought to
be established, at least so far as laryngeal troubles are concerned.
But to dwell upon this  point would take us too far from our real
subject.
   Again, one of the pregnant questions of the day  is, whether or
not croupous pneumonia is an acute infectious disease, running as
it does a decidedly typical course.
    Juergensen makes  the  following declaration:  " Croupous
pneumonia is a disease affecting the system generally, not a par-
ticular locality.  Inflammation of the lung is merely a prominent
symptom.  The  phenomena of  the  disease cannot  be accounted
for by the local conditions."
   Briefly let me give  the  evidence in favor  of  the above, as
gathered  from this  and other  sources, and  from the etiology,
anatomy, and pathology  of the disease :
   1st. The seasons at which pneumonia occurs, differ from those
of inflammatory conditions of the lung.  It ranks fairly as an en-
demic, occurring with a certain regularity at certain seasons of
the year.
   2d. During the whole course of  the disease there is no con-
stant relation between the. degrees of fever and the local  symp-
toms ; consequently the length of the fever is not to be credited
to the local conditions.
   3d. The decidedly typical course.
   4th. Inflammation of the lung accompanying typhoid fever
and other infectious diseases is not croupous  pneumonia ; there- 
CROUPOUS PNEUMONIA.
19
fore croupous  pneumonia is never a secondary, a consecutive in-
flammation.
    5th. Death is often due to paralysis of the heart, as it occurs
in other acute infectious diseases, where the quantity of infection
can be estimated in a measure by its effect upon the innervation
of the heart.
    6th. Attempts to abort, to  cut  short  the course of croupous
pneumonia, have tended  only  to  enfeeble  the  already weak
powers of resistance of the patient.   In view of the numerous dis-
cussions of  late  in regard to  this point, I regret that  we cannot
now go further into this.
    The inflammatory process itself is  one  affecting the alveoli
and bronchi, in  the course of which an exudation rich in fibrine
is poured out  upon the surface of the mucous membrane and then
coagulates.  No one has ever attempted to establish the existence
of  a  croupous pneumonia running a chronic  course, and I wish
this point especially to be borne  in mind, when I come to speak
of  the possible  terminations  of croupous pneumonia and their
results.
    The croupous process is a truly superficial one ; indeed, quite
as  much  as the catarrhal process.  While in catarrh we have
transudation of  serum from  the blood, in croup  there is added
an abundance of fibrine.  You will find it stated by most authori-
ties that the exudation  raises  the epithelial layer, thus doing
away with the latter. This is erroneous.  It has been established
long ago  that the fibrine passes over the epithelium, as any ordi-
nary secretion, and  the epithelial layer is lost by subsequent de-
generation.   Niemeyer had always  held  that an exudation,  rich
in fibrine and quick to coagulate, is deposited  upon the surface,
enclosing within itself the normal epithelium and newly-formed
cells.   The  fact is, the epithelial layer  covered by the fibrinous
exudation undergoes no other changes save  cedematous swelling,
opacity, and incipient fatty or mucous degeneration.
    Passing  to the pathology proper of  croupous pneumonia, we
find it almost  invariably involving the greater portion of a lung,
beginning mostly at the root,  involving the  lower  lobes,  and
thence passing to the upper lobes.  And right here is a chief dis-
tinction between  the characteristics of croupous and catarrhal
pneumonia.   Both are superficial.  In  the  catarrhal form, how-
ever {vide my second article), the process is one derived from the 
20
CONSUMPTION AND TUBERCULOSIS.
smaller bronchi, and hence only lobular, while croupous pneumo-
nia, involving the lung parenchyma proper, is diffused as well as
lobar, involving the bronchi only as a secondary process.
    Croupous  pneumonia  has  three distinct  stages.   It will be
necessary, for completeness' sake, to  dwell upon  each of these
stages, in order to arrive  at safe conclusions regarding the final
termination.
    In the first stage, that  of inflammatory determination or en-
gorgement, the lung parenchyma is of dark red  color, is heavy
and harder,  and has lost its elasticity.   On section, the  cut
surfaces present a dark appearance, and blood flows in abundance,
together with serous fluid  more or less frothy.  In  speaking of
the possibility of considering  croupous pneumonia as an  exag-
gerated catarrh, Buhl says: " When we see in catarrh serous exu-
dation, superadded  to the  normal secretion of the mucous'mem-
brane,  the same addition  is present in croup of  the pulmonary
alveoli in the shape of  gas and watery vapor, changing at once
into perfect  lymph.  Looking  at it from this standpoint, the in-
flammatory engorgement of the lungs, characterized by transu-
dation of bloody serum, is  analogous to catarrh of the bronchial
mucous membrane; and if this goes on gradually,  the exudation
contains more and more fibrine, the  process is aggravated into
croup."  I quote the above merely as  an individual opinion.  It
is neither an accepted nor  an established fact.
   The passage from the state of engorgement to  that of hepati-
zation  is always of short  duration, commonly in one  day.   The
alveoli and bronchi are now filled with coagulated fibrine, mixed
with blood (giving it the red color); the air has disappeared from
the alveoli.  Hence the  lung is solidified, and the  characteristics
of croupous pneumonia are established.  The cut surfaces present
a granular appearance, most  plainly observable  in the larger
alveoli.   These granulations are small, firm props  of  coagulated
fibrine.   Flint says they are composed of amorphous fibrine or
lymph in a granular form, epithelium, fatty granules, some blood-
disks  and leucocytes.   These coagulated  alveolar contents press
upon the  parenchyma, infiltrated with  serum (oedematous), and
this pressure is what causes the croup-props to bulge out as granu-
lar matter, and they are in  this shape true mouldings of the alveoli
and infundibula.
   In this connection it is well to point out another distinction 
CROUPOUS PNEUMONIA.
21
between croupous and catarrhal pneumonia.  As the whole lobe
of the lung has  materially increased in weight  and volume, the
pleura covering it is likewise tense and oedematous, and likewise
becomes covered with transuded  fibrine.   Serous  effusion  also
supervenes.  This form of pleuritis  is peculiar to croupous pneu-
monia, and totally wanting in the catarrhal form.
    In the further course of the disease  the red color of hepatiza-
tion gives place to a gray or yellowish  appearance, the lung tex-
ture  remaining the  same.  I  think this is due to  the  usual
changes in the hazmatin of the red blood-corpuscles, as commonly
seen in  superficial  ecchymoses, though I fail to find this stated
by any  author.  This intermediate discoloration is sometimes
denominated gray and yellow hejjatization.
    If resolution supervenes (after the seven days of hepatization),
this is effected by fatty degeneration of fibrine  and young cells,
possibly also  of  mucous  degeneration.  There is softening,  ex-
pulsion, as well as reabsorption.   Most  authorities allow that
th3se processes go  on during restitution in all parts of the dis-
eased tissue  simultaneously.  Buhl, however, very ingeniously
demonstrates  the following facts: the  alveolar epithelium  takes
the  lead in fatty degeneration, becoming  granular, and by this
pi'ocess the croupous props are detached and  raised  from the
inner alveolar walls.   The bronchial vibrillated epithelium, on
the  contrary, largely undergoes mucous degeneration; likewise
the croup-props become detached and softened.   The quantity of
mucus formed in the smaller bronchi  is always large.  Now in
order to expedite  excretion, there  is  a necessary vibratory mo-
tion,  a  narrowing  and widening  of air-passages, in inspiration
and expiration, and  sound  elasticity of the lung  parenchyma.
All  these conditions  are  rendered nugatory by  dense  hepatiza-
tion.  The first step in actual degeneration is an active cell pro-
liferation  below the detached alveolar  and bronchial epithelium.
It is  not until this condition is fulfilled,  that vibratory motion
can be possible, and this is confined to  the bronchi.   In order to
expectorate the alveolar  portion of the deposit, the factors of
forcible  contractility  of  the  air-passages, as  well as  elasticity
of the lung parenchyma, are required ; yet these forces have been
and  will remain paralyzed for some time to  come.  Moreover,
the sputa  of  pneumonia  are catarrhal  products  of  the bronchi,
mixed with fibrine and reddened by the admixture of red cor- 
22              CONSUMPTION AND TUBERCULOSIS.

puscles  (rusty colored sputa),  all derived from  the  bronchial
mucous membrane almost exclusively.  The  deduction from the
above is, that the whole of the hepatized lung  tissue proper
UNDERGOES RESOLUTION ALMOST  ENTIRELY BY REABSORPTION  OF THE
softened alveolar props on the spot.  This  fact is important in
considering further terminations of croupous  pneumonia.
   Resolution, when  it takes  place,  is always  somplete.   This
proves croupous  pneumonia to be  a superficial inflammation only,
spending  its force upon the alveolar  epithelium,  but  not pene-
trating into the lymphatics.  Keep this fact in mind.
   On the other hand, the process may pass  into the third stage
of destruction, so-called gray hepatization or purulent infiltration,
chiefly caused by lack of the general powers of resistance  and
weakness  of  the heart's action.  The pathological  anatomy of
these changes does not differ from those of resolution,  save in
that, on account  of the enfeebled powers of resistance, the regen-
erative processes do not keep pace with those of the degenerative,
or the former may  be even wanting altogether.  The  volume
and weight of the affected part remains unchanged.  The granu-
lations (croupous props) are now  readily pressed out  and  disap-
pear.  The parenchyma remains not only anaemic and devoid of
air, but is  much softened, breaking down on slight pressure. Red-
dish gray  thick pus flows freely over the cut surface, and may be
readily pressed out in large quantities.   But the minute structure
of the lung is  still unchanged, and at this stage a  late resolution
is still possible.  Death usually ensues (as late as the tenth day),
but in a few cases a small amount of surplus vitality causes the
products to be absorbed, as in the hepatized  condition.   This, of
course, is  immediatly consequent  upon the disappearance of the
croupous props.   But if absorption fails, the formation of pus (as
above stated), true purulent infiltration, will lead to' death.  An
important point in  this connection  is  the presence of  pus-cor-
puscles in the lung  structure  itself.   The pleura takes  part in
this  purulent infiltration and its effusion, consequently becomes
purulent.   Remember the point,  in the beginning of this paper,
viz.:  the  truly superficial  character of  croupous pneumonia,
wherein the parenchyma was  merely  oedematous, and now by its
purulent  infiltration  forms, as it were, a bridge to interstitial
forms of  inflammation, and  this  is in itself sufficient to lead to
the formation of abscess of the lung.   Abscess  of the lun«-  may 
CROUPOUS PNEUMONIA.
23
occur during life, but  then it may be looked upon as a decidedly
slow and localized  process, taking weeks  for its formation, since
rapid  infiltration would kill rapidly.   Moreover, in  order to
form a perfect abscess, the neighboring parts must be undergoing
resolution and must be healing.
    I find it necessary  to dwell for a few moments upon the pos-
sible ending in pulmonary gangrene.  This occurs in  croupous
pneumonia (it may occur suddenly by thrombosis, etc.), in the
stage of red hepatization.   Stagnation and numerous thrombi in
the  branches of  the bronchial arteries, which carry on the nutri-
tion of the lung, causes the flow of blood to be cut off from the
inflamed parts.   Cessation of nutrition and the constant presence
of atmospheric air are the  factors for mortification, which in-
volves both lung structure and the infiltration.   But as it may be
set down as a rule  that anaemia from thrombosis is nearly always
a localized process  in the different organs (e. g., the brain), so it is
the case with the lung.  The same condition and action of the
neighboring parts, as  just spoken of  in lung abscess, here  super-
vene.  Demarcation, granulation, and throwing off of the  morti-
fied part, and indeed in both abscess  and gangrene of the lung,
the favorable termination consists of a loss of substance—in short,
a cavern.  Only  in case of  exceptionally small loss of substance
and consequent caverns of the size of a pea or a trifle larger, may
cicatrization and complete closure occur.   This is, no doubt, the
only condition under  which cirrhosis of the  lung (induration)
occurs as a sequel  to croupous pneumonia, though some authors
mention diffuse proliferation of connective tissue and cirrhosis as
a sequel.   Of this  there is no proof.
    Lastly, I return again to the important question of the possi-
bility  of croupous  pneumonia leading  directly  to  pulmonary
phthisis.  It will be remembered  that my quotations from au-
thors, at the beginning of this paper, are  to the effect that crou-
pous pneumonia was  in itself strictly superficial.  If you have
closely followed the pathological anatomy of all possible termina-
tions, to wit: gray  hepatization, purulent infiltration, abscess  and
gangrene, it will  have become apparent  that one of two results
alone is possible, viz. : resolution and absorption, or  destruction
by pyaemia, or the  formation of a cavern (in  abscess and gan-
grene).   The formation of a cavity, it should be  remembered,  is
not primarily the effect or a product of croupous pneumonia, for 
24
CONSUMPTION AND TUBERCULOSIS.
these products have by this  time all  disappeared.  These facts
would seem to effectually remove any doubts as to the impossi-
bility of a termination in caseous pneumonia; and yet, as far as
I am able to ascertain, almost the majority of  authors state it so.
Niemeyer even mentions caseous pneumonia as of quite frequent
occurrence in this connection.  He says, that when the extrava-
sated fibrine has undergone fatty degeneration, and this mass is
not properly supplied with serum by the alveolar walls, the fatty
mass will  dry and become  changed  into  a  more or  less firm,
yellow, cheesy mass.
    Finally, let me tersely recapitulate and condense the opinions
of the  present day in regard to the possibility of products  of
croupous pneumonia  leading to phthisis, that you may not  get
confused in regard to it.
    Remember, always,  that  a rapidly destructive process, such
as fatal  terminations  of lung inflammations (gangrene, abscess),
bear no  relation to phthisis.  Bear this well-established fact in
mind: that in order that an inflammatory  process should
LEAD TO CONSUMPTION, ITS PRODUCTS MUST  HAVE A REMNANT, AND
THIS REMNANT MUST UNDERGO CHEESY DEGENERATION.
    Based upon this, the only questions to be answered in relation
to croupous pneumonia are:   1st. Do any remnants ever remain %
2d. Do these remnants undergo cheesy degeneration ?   In regard
to the first question, we have exhausted  the  subject throughout
this paper; yet, once  more,  I condense  the views  of prominent
observers.  They are  as follows:  Buhl denies all possibility of  a
remnant, and he has many supporters.  Juergensen, Rindfleisch,
and Ruehle have taken pains to oppose this view.  The views  of
all, however, coincide in this, viz.:  even if no distinct remnant
remain, the inflamed parenchyma may be, to a greater or less ex-
tent, a starting-point for limited development and contraction  of
connective tissue (cirrhosis).
    Again, a number of Buhl's cases of desquamative pneumonias
may have been croupous, or  croupous  cases of the  other authori-
ties may have been desquamative,  as  they are clinically hard to
separate.
   And, thirdly, the possibility is  held out that  a  desquamative
process might follow directly in the lead of a croupous.   Now all
acknowledge (Buhl included) that  cirrhotic conditions and des-
quamative pneumonia are prone to cheesily degenerate. 
CROUPOUS PNEUMONIA.
25
   The second  question  answers itself.   If remnants remain,
they can readily undergo cheesy degeneration,  especially while
the patient is still in a debilitated condition.
   Again: If croupous pneumonia is an acute infectious disease
and never an accompaniment of other diseases, never secondary
or consecutive, no remnant can remain for cheesy degeneration.
   If, on  the other hand, as an ordinary inflammatory disease it
runs no typical course, and if desquamative pneumonia as an in-
dependent disease is a  myth (as asserted  by Rindfleisch), or, if
existing, it may follow  in the wake  of  croupous pneumonia, the
conditions  for the  remaining  of remnants are  given and their
cheesy degeneration a natural sequence. 
26             CONSUMPTION AND TUBERCULOSIS.
             DESQUAMATIVE  PNEUMONIA.

    The name of " desquamative pneumonia " will no doubt sound
strange to you.   I will introduce it by stating that its existence, as
a separate form of lung trouble, was first mentioned by Prof. Buhl,
of Munich (see Henle  and Pfeufer's Journal, series viii., 1856).
While its existence as a distinct and separate disease has been at
times tacitly acknowledged by others, Buhl alone, as far as I can
ascertain, has furnished the literature of pathology and pathologi-
cal anatomy.  In the present paper on desquamative pneumonia,
I can only endeavor to  collect his thoughts and reproduce them
in condensed form.
    Desquamative pneumonia occurs in  two grades and  modifica-
tions, each one  of which will be separately considered.
    The first variety, and the one of lowest grade, is that which
occurs as an accompaniment to severe general diseases, and  is
therefore denominated by Buhl as " consecutive  desquamative
pneumonia y "  it is chiefly an accompaniment of acute infectious
diseases, but the introduction of any inorganic poison  into the
body, as pyaemia, etc., forms the basis of this  first variety of  des-
quamative  pneumonia.   The  pathological  changes  in other
organs, in  connection  with  general diseases, are  spoken of  as
parenchymatous inflammations, such as parenchymatous nephritis,
hepatitis ; and  it would seem rational to  allow  the existence  of
parenchymatous pneumonia, though this term is  not now  in
vogue.   In  consulting other authors, it will  be found that they
speak  merely of hyperaemia, hypostatic congestion and oedema
of  the lungs in connection with  infectious  diseases; but the
pathological  anatomy of  the process seems  to  have often been
supposed to be  that of croupous pneumonia.  I find it stated, with
strange uniformity, that pneumonia accompanying typhoid fever
is croupous, and originates under  the  same  influences as does
catarrh of  the  air-passages in measles, without any reference  to
the  existing pathological condition, which  corresponds to  our
desquamative form and  differs materially from  croupous  and
catarrhal pneumonia.
    Consecutive desquamative  pneumonia (alike  desquamative 
DESQUAMATIVE PNEUMONIA.
27
 nephritis)  occurs bilaterally, is difuse,  consequently lobar,  and
 affects  the bronchi secondarily only.   The  lungs are  enlarged,
 gorged with blood, minute  extravasations exist in the centre of
 the  parenchyma, as well as subpleural; do not  collapse when
 removed, notwithstanding they still contain air.  Foamy serum
 flows from the  cut surface, and very minute  excrescences  are
 seen.   The tissue is soft and readily torn.  The microscope here
 becomes indispensable and reveals epithelium of the lung alveoli
 in great quantity ;  they are bloated and rounded off, filled with
 fine granules.  This is proof positive of the changed cells raising
 themselves from their  stratum and from each other;  in other
 words,  desquamating,  analogous  to  parenchymatous  nephritis.
 Hence  the name.
    Catarrhal and  croupous  pneumonia  are characterized by
 changes in  secretions, while here serous  infiltration  of  the
 PARENCHYMA IS  THE CAUSE OF  THE DESQUAMATION OF THE  EPITHE-
 LIUM.
    Pus-corpuscles are not present.  Pleurisy is wanting.  Where
 death  does not ensue in consequence of the acute infectious dis-
 order and the accompanying  desquamative  pneumonia has not
 reached too  high  a grade, resolution  takes  place by transitory
 fatty degeneration of the detached epithelium and regeneration
 of  the  same, as hyperaemia and  swelling  disappear.   This is
 analogous  to what occurs in the liver and kidneys.
    Death, however, may not be caused  by the general disease,
 and disease of the lung may have been of so high  a grade as to
 require time for the  ultimate removal  of its product.  In  such
 cases we are dealing with a chronic fatty degeneration,  of which
 more will be mentioned hereafter.
    Buhl insists (see Virchow's  Archives, XII., 1857) that another
 termination of  consecutive desquamative pneumonia  is in acute
 atrophy of the lung, formally disposed of as a result of hypostatic
 or catarrhal pneumonia.  It would take us too far  away from
 the  subject-matter  proper to dwell  upon this  condition  further
 than to say  that he  refers to  the lung  in an atelectatic condi-
 tion.
   The second form of this disease is that which is denominated
genuine desquamative pneumonia.   It holds the same relation to
the foregoing consecutive form as does  Bright's disease  to  the
kidney  affection accompanying general diseases—albuminuria. 
28
CONSUMPTION AND TUBERCULOSIS.
It is therefore to be regarded  as  an independent, a primitive in-
flammation, or, in  other words, the localized expression in  the
lungs of a general  disease.
   When  confined to one  lobe, it is usually  the upper  one.
Again, it may involve the whole lung, when the upper lobe will
prove to be the one most affected.  The inflammatory process is
almost invariably further developed in the upper portions and its
downward course can  be readily noted.
   The pathological anatomy of such a lung presents the follow-
ing picture in cases  which have lasted from six to eight weeks :
volume and  weight of  the  diseased lung are  augmented;  the
surface is smooth, of dull lustre.   The pleura is oedematous, with
sparse ecchymotic  spots.   The lung  does not collapse either by
opening the thorax or upon incision ;  its elasticity appears  to be
entirely wanting.  Nevertheless, it is quite frangible.   On section
we readily discover the lobar (diffused) character of the inflam-
mation.  There is also a granular surface, as in croupous pneu-
monia.  In croupous  pneumonia, however, the  granulations  are
filamentous plugs partly passed out of the alveolar spaces.  Here,
on the contrary, we have the granulations formed  by the  thick-
ened  interalveolar parenchyma, rendered  firm   by the  great
oedema  and  bound down  by newly-formed connective  tissue.
The parts are rich in blood, and pigment in granular form is
present in quantity corresponding to the duration of the disease.
On  account of the parenchyma  being firmly bound down, only
small quantities of gelatinous fluid can be scraped off from  the
surface; this fluid is freely mixed with cellular elements.   The
cellular elements serve to distinguish this form from  consecutive
desquamative pneumonia, in which oedema alone is present.
    The exudation of genuine desquamative pneumonia is a plastic
exudation.
   The microscope reveals  detached  epithelium  in  profusion;
these  are from the  alveoli as well as the finer bronchi, which they
fill.   These  epithelial cells are undergoing  the process of fatty
degeneration  ; neither pus nor mucus is present.  Let me repeat:
the plastic exudation  consists of epithelium  in profusion,  filling
alveoli and  finer  bronchi and  undergoing fatty degeneration.
This  exudation  is bound down  by newly-formed  connective
tissue.
   Clinically, this  is of great importance in connection  with the 
DESQUAMATIVE PNEUMONIA.
29
sputa,  which  contain  alveolar  epithelium  in large quantities,
something not occurring in catarrhal or croupous pneumonia.
   Another characteristic of the epithelium is the  proliferation
of nuclei and younger  cells, denoting  active regeneration  and
plastic activity from the beginning of the disease.  In croupous
pneumonia, it will be remembered, regeneration is the  closing
act.
   The four chief characteristics, viz.: firmness of  parenchyma,
pigmentation, proliferation of connective tissue, and a profusion
of epithelium, serve to stamp genuine desquamative pneumonia
as a parenchymatous  inflammation, far in excess of the con-
secutive form.
   Buhl points out (page 53) that genuine desquamative pneu-
monia serves  to  show the connection  and analogy between con-
nective-tissue  corpuscles, lymph-endothelium and  alveolar  epi-
thelium, since the desquamation of alveolar epithelium cannot be
traced to oedema of the alveolar walls alone, but must be regarded
as proliferation and degeneration of tissue elements of one species.
   Though likely to end in death, complete recovery is possible,
at least as often  as in Bright's disease.  The great majority of
cases, however, are  subject to  frequent recurrence and gradual
continuance of the  same processes, thus bringing about perma-
nent and irremediable conditions.  And this brings us to our
chief  point,  namely:  its termination into consumption.   The
form in which this is accomplished is that of chronic fatty degen-
eration, and the process is simply the  continuation of the acute
form:  proliferation  and fatty degeneration of epithelium becom-
ing chronic.  The clinical appearances are from  thence those of
phthisis.
   In  such cases general anaemia  of course supervenes, which
accounts for the lung being found quite pale.  It  is of light slate
color,  owing  to  absorption of the pigment, and dotted with
minute white  specks—alveolar spaces filled with fattily degen-
erated  epithelium.
   I now wish to draw attention  to certain conditions and facts
which  to  my  mind are of the greatest clinical  importance.  I
refer to the pathological anatomy  of  incipient phthisis, as  that
terra is understood, or what is still oftener designated as catarrh
of the apex.  It was my intention  to enlarge upon physical signs
and  their significance at this stage of lung trouble.  But let it 
30
CONSUMPTION AND TUBERCULOSIS.
suffice to  say this:  if we accept Buhl's observations of the dis-
appearance of the products of croupous and catarrhal pneumonia,
we are forced to this conclusion, viz.: With the rare exception
OF CASES OF ACUTE MILIARY TUBERCLE, NEARLY ALL CASES OF CATARRH
OF THE APEX, IN PERSONS PREVIOUSLY HEALTHY, ARE CASES OF SUB-
ACUTE GENUINE DESQUAMATIVE PNEUMONIA.
   I say " if " advisedly, as in a future paper on  phthisis itself
the summing up of  other authorities against Buhl  is very strong.
The  bulk of evidence would  show that his  desquamative  pneu-
monia  is not entitled to be classed as a new picture of disease,
but as the  result of combination of the other pathological changes.
   Still, as above stated, if the products of catarrhal and croupous
pneumonia are always disposed of, we must allow that catarrh of
the apex fits into the frame of desquamative pneumonia.
   It will be remembered that  chronic fatty degeneration is
merely  a  prolonged desquamative  process.  The  same process
can scarcely exist in a subacute form.   While elimination takes
place, there is regeneration at the same time ;  and this fact is one
of the chief factors in my hope  of the successful treatment of
consumption.  Again, the  rales heard in catarrh of the apex are
fine crepitant ones,  pointing to the alveoli as their seat; and sec-
ondly, the sputa are chiefly the same as in genuine desquamative
pneumonia, large quantities of cast-off alveolar  epithelium being
the principal ingredient.
a   As before stated, I will, in my final summing up, once more
recur to this subject. 
LNTERSTITIAL PNEUMONIA.
31
                INTERSTITIAL PNEUMONIA.

    The healthy lung contains but little connective tissue, which,
 together with numerous elastic fibres, contributes  to the forma-
 tion of the lung-cells.   This connective tissue also serves to con-
 nect  the different lobules with each other, as well as to accom-
 pany the walls of vessels and of the bronchi.
    In a comparatively large number of  cases of lung trouble,
 we find, in the place of these traces of connective tissue, exten-
 sive sections of the lung converted  into a tough, knotty, fibrous
 tissue.  This is the result of chronic interstitial pneumonia.
    Whether or not interstitial pneumonia ever occurs as a pri-
 mary disease, is  a mooted  question.  This would  at first  glance
 seem strange;  but the fact is, that here  we are dealing with a
 question of time.  It is difficult, nay, almost impossible, to ascer-
 tain the original condition of  lung trouble in a patient afflicted
 with the chronic interstitial form.   But when you consider that
 there exists such a thing as an intensely acute interlobular  pneu-
 monia, it is  not  difficult  to imagine cases primarily running a
 subacute course.  Niemeyer, Notlmagel and others state that it
 " rarely ever occurs as an independent disease," and further that
 this  is  only the case  where  the long-continued inhalation  of
 coal-dust and iron particles is the exciting factor.  Even then,
 it is said, the cirrhotic  condition is not primary, but the  result of
 bronchitis.
    Our  subject  is to  be  considered under two  heads: 1st,  as
 an acute process, running a rapid course, and leading to the
formation of pus ;  2d,  as a chronic proliferation  and con-
 traction of connective tissue, the result of a variety of processes.
    It will doubtless astonish you  to learn that there exists such
 a thing as a  separate and anatomically well-defined acute inflam-
 mation of connective  tissue of the lung.  If there is anything
 found in regard to it in medical literature, it is only hinted at as
 a possibility ; this is owing to the well-nigh impossibility of clin-
 ically distinguishing  it from  other inflammations.  In  other
 words, a differential diagnosis is  rendered impracticable  by the
 sameness of  the symptoms.  The  chill, the fever, the rales, and 
32
CONSUMPTION AND TUBERCULOSIS.
 the locality of the process are not pathognomonic ;  nay, not even
 the  sputa would necessarily  settle  the  question.  Still  a  close
 study of the history of a case  which might be  luckily seen in its
 inception,  the inflammatory character of the temperature, and
 above all  the subsequent course,  differing in regard  to  time
 from that of croupous pneumonia, ought to elevate acute intersti-
 tial  pneumonia to the  dignity of an  independent  and separate
 picture of disease.
   From the sparse material on  this subject, we gather that this
 form of lung trouble occurs only as a consecutive one, by  absorp-
 tion  of  septic  material.  Its existence presupposes a centre for
 pyaemic infection.  This centre may be only a cheesy mass.   We
 do not know what are the immediate changes which would cause
 a cheesy mass to undergo suppuration.  We do know that  such
 changes are most likely to occur in  broken-down constitutions
 (alcoholism), when the absorbed  purulent matter would rapidly
 follow the course of the  lymphatic vessels, which spread out in
 the interlobular and subpleural tissue.  Again, the original cheesy
 centre may  escape detection by its small size, though I am satis-
 fied that its absorption is never total.   But if, on the one hand, the
 original centre is not always demonstrable, and, on the other, the
 likelihood that a phlegmonous inflammation may as readily exist
 primarily in the lung as  any other  tissue, the question may be
 looked upon as an open one.
   The chief anatomical characteristics of suppurative interstitial
 pneumonia  are: turbid,  dirty yellowish  swelling  of the con-
 nective  tissue  forming the  support  for  the  lung, infiltration of
 pus,  that is, copious exit of white blood-corpuscles or hindered
 progress of lymph-corpuscles, and rapid  breaking-down  of the
 same.   I beg you to remember that  this process takes place in
 the interstices  of the lung-lobules  themselves, and not in the bron-
 chial walls.
   This disease  occurs most frequently in newly-born  children,
 whose pyaemic infection is then traceable to the puerperal infec-
 tion of the mother.  It may, however, also occur in adult  life, in
case of  death by pyaemia.   Indeed, we may say that all pyaemic
infections involving the pleura and the adjacent connective tis-
sue of the parenchyma, which are not caused by an embolic in-
farct, are lymphatic interstitial pneumonia.  Or, to state  it still
 more clearly:   the embolus  plays its part  in 'the  pulmonary 
INTERSTITIAL PNEUMONIA.
33
artery and its branches, spread out upon  the lung-tissue  proper,
and the results consequent upon its presence are seen in the same
tissue.  The pyaemic infection is carried  on by the blood-vessels.
Infection from a cheesy centre  (oftenest a lymphatic gland) is
carried on by the lymphatics, which play their part in the tissue
to which  they are distributed—in our case the  connective-tissue
support of  the lung.   Hence, I repeat that, both  for fact and
simplicity,  this process should properly  be denominated lym-
phatic in terstitial pneumo nia.
    The termination is probably always in  death by suppuration
and its consequences,  which, as  is known, is  the most likely
course in loose connective tissue (phlegmonous processes).

    In passing to the  second form of  interstitial  pneumonia,
chronic proliferation and contraction of  connective tissue, we at
once find  ourselves face to face with decidedly different views of
different authors.  One theory is supported by a single authority
(Buhl), while  all others  (Rindfleisch, Ruehle, Stokes, Virchow,
etc.) substantially agree.  Buhl's position may be stated in a few
words.   The following are his claims, verbatim : " The name  of
chronic interstitial pneumonia signifies nothing  else but the ter-
mination  of genuine  desquamative pneumonia."   Having dis-
posed of  chronic fatty degeneration as one termination, he makes
chronic interstitial pneumonia another, byr the following reason-
ing :  in consecutive  desquamative pneumonia we have parenchy-
matous oedema,  due  to  serous  transudation only; in  genuine
desquamative a more plastic exudation, characterized by prolif-
eration of alveolar  epithelium and connective-tissue corpuscles.
Where genuine desquamative pneumonia terminates in  the  cir-
rhotic condition, proliferation of connective-tissue cells predomi-
nates over the more superficial epithelial changes.   The beginning
of this proliferation takes place, in the acute stage, by the forma-
tion of spindle shaped and stellated cells (see last article), the first
indication of embryonic hyperplasia of connective tissue.  Cir-
rhosis of  the lung proper, however, can only be  spoken of when
connective-tissue proliferation is  enormous  and  appears as  a
fibrous cicatrix, in which the alveolar parenchyma and the finest
bronchi are enclosed, obliterated, and have disappeared.
    In order to simplify the question, I  will add that, except by a
few personal adherents, Buhl's proposition has been abandoned.
            3 
34
CONSUMPTION AND TUBERCULOSIS.
Other authorities,  including such  pathological  histologists  as
Colberg, Rindfleisch, and Nothnagel, teach that chronic interstitial
pneumonia is  a termination of all forms of lung  inflammations.
At the same time, the  existence of desquamative pneumonia is
denied, of which Rindfleisch recently said that no one had ever
diagnosticated a case but Buhl himself.
   The objections  to  Buhl's desquamative pneumonia may be
summed up  thus: other observers have  found and described in
detail the same pathological  changes, speaking of desquamation
of epithelium of the  alveoli.  But they hold  that this process is
part of every acute lung or bronchial trouble, and not one which
occurs as an independent disease.
   In chronic interstitial pneumonia the inter-alveolar and inter-
lobular connective tissue become the seat of inflammatory, nutri-
tive changes, consisting of hyperplasia of the connective  tissue,
thereby causing an increase  of  the supporting structure  at the
expense of the tissues containing air.  In the further progress of
its proliferation,  the  newly-formed  connective tissue undergoes
the same changes as the connective tissue formed by inflamma-
tory hyperplasia.   At first  soft and vascular, it gradually  under-
goes a process of contraction, converting it into  a hard,  blood-
less tissue,  occupying far less space than did the healthy  paren-
chyma.
   On section, the lung is found to be  of one-half to one-third of
its original  normal size.  It  is firm, even  to  the  consistency of
cartilage, devoid  of  blood-vessels, and anaemic.   Instead  of the
white color of connective tissue, we have a gray, slate color, due
to pigmentation, for which the lung seems to have a predisposition,
and more especially so in  chronic  interstitial pneumonia,   Rind-
fleisch calls  this " slate-colored induration."
   In the midst of  this hardened tissue, and throughout various
parts  of it, we find dilated bronchi and sacculated caverns, the
latter an exaggerated dilatation.  Excessive pigmentation is also
characteristic  of  desquamative  pneumonia;  and hence Bubl
dwells upon this as one of  his reasons for makino- cirrhosis a ter-
mination of  this disease only.
   The next point to claim our attention is the  important role
played by the pleura.  An autopsy of diffused cirrhosis  of the
lung always shows the  pleura to  be much involved.  The two
layers  are adherent and transformed into a hard  thick  fibrous 
INTERSTITIAL PNEUMONIA.
35
 sward, often one centimetre in thickness.  Through this the lung
 is attached to the inner wall of the thorax.  The thickest, densest
 portion  is mostly at the apex of the lung, while farther down
 the adhesions get to look more like a cobweb.
    By far the greater number  of cases of cirrhosis of the lung
 have their origin in pleurisy, whether uncomplicated or as a con-
 comitant of other acute processes.   Corrigan (whose investigations
 j ustify the oft-applied name of  Corrigan's cirrhosis of the lung)
 has shown that the process of chronic proliferation of connective
 tissue passes from the pleura to  the lungs.   This raises the ques-
 tion, whether all pleuritic processes (pleuritis sicca, serous effu-
 sion, empyema) lead to  cirrhosis.  In  pleuritis sicca it  is less
 likely, on account of the usually rapid absorption of fibrine.
    There can  be no  doubt that cases in which  absorption of the
 exudation has required a  considerable length of time,  lead to
 cirrhosis, as  they likewise do to retrecissement de la poitrine.
 Laennec believed that hemorrhagic pleuritis was most apt to lead
 to retraction.  The true  solution seems to me  to  be this: Any
 PLEURISY (WHETHER  SICCA, WITH SEROUS EFFUSION, HEMORRHAGIC,
 EMPYEMA, OR IN CONNECTION WITH CROUPOUS PNEUMONIA) MAY EITHER
 PRIMARILY PASS OVER INTO THE LUNG BY MEANS OF THE SUBPLEURAL
 CONNECTIVE TISSUE, AND CONTINUE AS SUBACUTE INTERSTITIAL PNEU-
 MONIA ;  OR CIRRHOSIS OF THE LUNG  MAY BE PRIMARILY CAUSED BY
 RETRECISSEMENT DE LA POITRINE, FOLLOWING  THE  ABSORPTION OF A
 PLEURITIC EXUDATION.

    That is, primarily, only so far as the lung itself is concerned,
 since it  presupposes a pleuritic  trouble.  This is the  only form
 in which chronic  interstitial pneumonia can lay a claim to being
 an  independent disease.   It  is  evident that the claim is but a
 slight one.   Let me add that in croupous pneumonia it is not so
 likely to occur, on account  of the usual restitution of the pleura
 too-ether with the  lung exudation.
    Besides pleuritis, other primary  diseases of the lung may lead
 to cirrhosis.    Bear  in mind, however, that the inflammatory
 products (exudations,  secretions)  do  not  themselves  undergo
such change, but are subject to cheesy degeneration.  You may
imagine  the  process as one  which, in  consequence of the pul-
monary  affection,  manifests  itself as  an  extensive  interstitial
 pneumonia,  starting from the  original seat of trouble.  The 
36
CONSUMPTION AND TUBERCULOSIS.
question as to whether cirrhosis will supervene in  any given
case, is altogether a question of time, the same as in pleurisy.
An exudation  which  does not  begin to be absorbed directly
upon the subsidence of the active  process, or is not absorbed  at
all, acts as sufficient irritation of a  subacute character.  Now, to
any subacute irritation sufficient to give rise to renewed inflam-
matory exudation, the tissues respond by a development of con-
nective tissue.  Chronic interstitial pneumonia, then, may occur
as a sequel to or in connection with:
    1st. Croupous pneumonia, for which we have the authority of
Stokes, who quotes a number of cases uncomplicated by pleuritis,
where, after the absorption of the croupous exudation, the cirrhotic
condition existed  and continued.  The co-existence of  a subacute
pleurisy might in these cases have readily escaped the best observer.
   2d. As a result of  catarrhal pneumonia, Bartels found, in a
number of  cases  which had run a chronic course, the lower lobes
in a cirrhotic condition.
   3d. As a result of  collapse of the lung, either primarily or  as
a sequel to catarrhal pneumonia consequent upon the collapse.
   4th. Consequent upon gangrene  and abscess of the lung.  You
know that in the healing process the  destroyed part is bordered
by connective tissue.   From  this cicatrix the process  of shrink-
ing may extend to the  rest of the lung.
   5th. Interstitial pneumonia is said  to occur as a complication
of chronic bronchitis,  the discussion of  which we leave  for the
chapter on  peribronchitis.
    6th. The development of cancer, the  presence of hemorrhagic
infarct, and apoj)lexy of the fom^lead to incapsulation by connec-
tive tissue, a sort of local  cirrhosis.   It is doubtful  whether a
whole  lung can  become involved  in  the  process in  such cases.
In  embolism (embolic  pneumonia, so called) the pleura is second-
arily involved.   This is to  be  accounted for thus:  the embolus
originates in the right side of the heart or is carried to it by the
peripheral  circulation, and  entering the pulmonary artery clogs
up sections of  lung circulation; but  this is speedily made  up
by other branches of  the  pulmonary, whose  compensating dis-
tention is assisted by the elastic yellow  fibrous tissue.  Hyrtl
has lately established the fact that the branches of the pulmonary
artery pass directly into the pleura. The pleural vessels are not
in intimate relation with the bronchial arteries. 
INTERSTITIAL PNEUMONIA.
37
   In a certain  sense  the deposit of tubercle, and more particu-
larly the softening of tubercular masses, gives rise to interstitial
pneumonia, "with nutritive exudation."  (\Tirchow.)  But  this
process is decidedly a  local one, not extensive enough to be  dig-
nified by the designation of interstitial  pneumonia.   Through  it
originate  the  connective-tissue capsules, which serve to  separate
tubercular products from normal lung-tissue.  When we come  to
speak of  tuberculosis, I will endeavor to show  that tubercular
invasion is  apt  to supervene during the progress of chronic in-
terstitial pneumonia, and often causes rapid death.
   These  articles do not  concern  themselves  with diagnosis.
1l et it may not  be amiss  to speak of the importance of the pa-
tient's previous  history of the trouble;  its inception ; of the em-
physema accompanying its  further  progress,  and the consequent
displacement of the liver, spleen, diaphragm, and heart, as well  as
to mention  bronchiectatic caverns, which are  often dry.
   Two diagnostic points  are of great value in this connection.
They are: 1st, Almost total absence of fever during the prog-
ress  of chronic  interstitial  pneumonia  and until tubercular infil-
tration  supervenes;  and 2d,  The  character  of the cough  and
sputa, of which  Niemeyer says: " Hard attacks of cough, repeat-
ing  themselves  at long intervals, by the force  of which large
quantities of stinking sputa are expectorated,  are pathognomonic
of bronchiectatic caverns." 
38
CONSUMPTION AND TUBERCULOSIS.
                 CASEOUS PNEUMONIA.

    Having now  considered the primary affections  of the lung,
 acute and chronic, wTith their terminations, we pass to that condi-
 tion,,which even more  than cirrhosis  is the result, the frequent
 fate of  their products.  While in  the  event of resolution of the
 inflammatory product in pneumonia this product  undergoes fatty
 degeneration, liquefies, and is absorbed, fatty metamorphosis may,
 on the other hand, be incomplete, the infiltration  dry up, the  cel-
 lular elements becoming atrophied and shrinking from  loss of
 their watery contents.
    There is no question that " every form of pneumonia may,
 UNDER GIVEN CONDITIONS, TERMINATE IN CASEOUS PNEUMONIA;  BUT
 IN NO FORM OF PNEUMONIA IS CASEOUS  METAMORPHOSIS THE CON-
 STANT AND ONLY  TERMINATION."
    This doctrine naturally  suggests the question : which forms
 of pneumonia are the  most liable to  terminate  in cheesy pneu-
monia ?
    We  find that for the picture of pathological conditions, which
Buhl calls  desquamative pneumonia, he  claims the  parentage of
each and every caseous pneumonia, to the total exclusion of crou-
pous and catarrhal pneumonia.   I will  tersely state his  reasons
therefor:   cheesy degeneration  is fatty  degeneration,  distin-
guished from the fatty metamorphosis by absolute  anaemia  and
constant absorption  of  wTater, begetting  paleness and dryness;
while in fatty degeneration the parts  are even more than nor-
mally moistened by constant flow of blood.  The conditions for
cheesy  degeneration  are  found  in  desquamative  pneumonia.
Cheesy  degeneration  supervenes where  a part supplied by a capil-
lary trunk is suddenly cut off from its source of circulation, caus-
 ing anamic necrosis.  It is this  necrotic  tissue  which becomes
 caseous. Thus we have in cheesy degeneration various stages of
 pathological changes, an acute as well as a chronic one.
    In the  acute  stage  the lung  presents  the following  appear-
 ances : it is augmented in volume as well as weight; the cut  sur-
 face is of the color of porphyry red, displaying upon its face yel-
 lowish-wlnte granules of  various  sizes,  isolated  or  con cremated 
CASEOUS PNEUMONIA.
39
The red color is due to hyperaemia.  The lung does not contain
much air.   From the cut surface a large quantity of  transparent,
jelly-like fluid can  be  scraped off, in which  are found, besides
red  blood-corpuscles, bullet-shaped or flattened,  sharply-defined
transparent cells, having one or  more  nuclei.   These  are  the
gelatinous,  desquamating, and self-regenerating  epithelia of  the
alveoli.
    The yellowish-white deposits are dry, friable parts of tissue,
void of air and blood.   Their various sizes correspond to single
alveoli, or more frequently whole alveolar spaces, or even a convo-
lution of several.  Microscopically they consist of shrunken alve-
olar endothelium and necrotic connective tissue.
    According to Buhl, the red groundwork is the same as in gen-
uine desquamative pneumonia, and the yellowish deposits merely
anaemically necrotic parts.
    It will not be amiss here to quote Niemeyer,  in order to show
that, as regards the  pathological anatomy of what is called cheesy
pneumonia, there is no great diversity of  opinion.  He says: " A
PNEUMONIA  WILL LEAD THE  SOONER  TO  CONSUMPTION,  THE MORE
ABUNDANT IS  THE AGGREGATION  OF CELLULAR ELEMENTS  IN THE
ALYEOLI AND  THE  LONGER THE INFLAMMATION  LINGERS, AS THESE
TWO FACTORS  TEND  TO ENCOURAGE  CHEESY DEGENERATION OF THE
INFLAMMATORY INFILTRATION."
    Passing to the  pathological  anatomy of cheesy degeneration
in its subacute and  chronic state, we find several possibilities of
final termination of  the acute stage.
    One termination is restitution to the normal  condition. This
is accomplished by  transitory fatty degeneration of the hyperae-
mic (red) groundwork, while the yellowish-white  anaemic necroses
shrink more and more by the continued absorption of  their watery
contents, that is, they become cheesy.   This termination is likely
to occur where the yellow masses are not very numerous, and at
a tolerable  distance from each other.  Even then the  lung con-
tains cheesy tissue in various  parts, always  closely surrounding a
minute bronchus.
   The  second termination is one likely to occur when cell-pro-
liferation has not been so copious as  to seriously compress  the
alveolor walls, and thereby cut off the circulation of  those parts.
The cheesy mass  then becomes more and more  inspissated, and
the  shrunken  atrophic  cells  remain  as mere  detritus.   The 
40
CONSUMPTION AND TUBERCULOSIS.
 organic substances gradually disappear, while calcareous deposit
 takes place, leaving at length a chalky concrement.
    It is during these changes that the important act of  copious
 proliferation of connective tissue takes place, as described in my
 letter on cirrhosis.
   The chalky concrements  are thus incapsulated, and then  may
 undergo  slow fatty degeneration.  The spaces, out of which  the
 fattily degenerated cells have vanished by liquefaction and absorp-
 tion, are filled by connective tissue.  Here, then, as elsewhere,
 the caseous mass is the  remnant of the  original  inflammatory
 infiltration and the newly-formed connective tissue its capsule.
    It is well to remember that all these conditions may \o found
 in the same lung at the  same time, to  wit: normal  integrity,
 fatty degeneration, and cirrhosis.   This is due to the uneven dis-
 tribution of the cell-infiltration, giving rise here  to anaemic ne-
 crosis, there to cirrhotic induration alone, and again to fatty degen-
 eration.
   Remember that I stated, in my letter on desquamative pneu-
 monia, that all authors substantially agreed as to the pathological
finding in  inflammations of the  lung accompanying  infectious
diseases, the name alone not being universally recognized.
   The question  is merely, whether  or  not these appearances
present such a well-defined, distinct picture of  disease as to raise
it to the dignity of a separate designation.   Once more  touching
upon this subject, we may sum up the negation to Buhl's dictum
as follows: besides  the processes which  Buhl  calls consecutive
desquamative  pneumonia, other forms of  inflammation  occur in
connection with acute infectious diseases, from simple hypostatic
hyperaemia to lobular and lobar croupous pneumonia, which latter
are not found at the most dependent portion of the lung, and not
dependent  upon  hypostasis, and are  said to occur during the
height  of  the  infection.  This too  can  be explained.   Careful
observation in dissections will show the characteristic changes of
organs m  infectious  diseases (for instance, the  infiltration of
Peyers patches)  to have come to a stand-still at the time when
 croupous or catarrhal pneumonia commenced.  I think we are
 safe in setting up this doctrine: inflammations of the lungs ac-
 companying infectious diseases are of the hypostatic hypLmic
 or  oedematous  Und  {consecutive  desquamative  pneumonia).
 Croupous and catarrhal pneumonia and cirrhotic processes occur 
CASEOUS PNEUMONIA.
41
in debilitated persons after the infection has  run its  course;
where they begin before the legitimate termination, the pathologi-
cal changes characteristic of the original infection will be found
to have reached their acme.
   Applying this doctrine to the residuary products of a lung
trouble accompanying infectious diseases, which products are all
the more apt to undergo cheesy  degeneration, because of the de-
bilitated condition of the convalescent patient, we are safe in
pronouncing:  if (according  to  Buhl)  all  inflammations  accom-
panying infectious diseases, at any stage, were desquamative, then
the  subsequent cheesy  degeneration  cannot have  been a  crou-
pous or catarrhal product. But since croupous and catarrhal pneu-
monia and cirrhotic processes occur during the disease as well as
after, their products are  present and subject to  cheesy degenera-
tion.
    That products of inflammations accompanying infectious dis-
eases should  be eminently prone to cheesy degeneration is not
astonishing, when we consider that it requires an infection of no
mean intensity to give rise to an accompanying pneumonia.   The
intensity of the invasion leaves the convalescing patient in a very
debilitated condition.
    From this we are justified in  making this  deduction : in-
flammatory PRODUCTS  OF LUNG TROUBLE IN CONNECTION WITH IN-
FECTIOUS DISEASES WILL TEND TO CHEESY DEGENERATION IN CASES
WHERE  CONVALESCENCE  IS SLOW  AND THE EXUDATION LINGERS FOR
MORE THAN A VERY LIMITED PERIOD.
   NExt in frequency in the tendency of its products to cheesify,
is true croupous pneumonia.  Clinically it is so often impossible
to distinguish  croupous  from " desquamative "  pneumonia,  that
we are  not  able  to establish from  experience,  at  the  bedside,
whether croupous exudation, as  such, often undergoes cheesy
degeneration.  Jnergensen hints at  the possibility of a desqua-
mative  process  following croupous  pneumonia (if  we  place it
among infectious  diseases) and  leading to  contraction, formation
of cavities, etc.  According to  Ruehle, cheesy degeneration is
most apt to supervene, where  the upper lobe has been involved,
since it has been  shown that in such cases the  disease  drags on
for a longer period than is common in the  lower lobes.
   The products of  catarrhal pneumonia next  claim our atten-
tion.   In  all cases of exquisite catarrhal pneumonia  the  same 
42              CONSUMPTION AND TUBERCULOSIS.
sequel occurs as mentioned  in connection  with croupous pneu-
monia.   The seat of catarrhal pneumonia is always in the lower
lobes, less accessible to atmospheric  influences.   Besides, as you
will remember, I have stated that both Bartels and Ziemssen have
found only two cases, each of well-proven cheesy degeneration of
products of catarrhal pneumonia.
    In regard to bronchial catarrhs, pleurisy,  and hemorrhages,
let  me  tersely state that  there  is now, as  there has ever been,
great diversity of opinion regarding the caseation of their prod-
ucts, as  well as of their leading more or less  directly to con-
sumption.  The difficulty here lies in the well-nigh impossibility
of positive clinical proof, of which  I have spoken before.   No
doubt, you have often asked yourself  the question : does bronchitis
lead directly to consumption?   Let me give you a few points in
reference thereto:  1st.  Catarrhal  pneumonia (capillary bronchi-
tis)  does so rarely, and yet  the bronchioles are nearest the par-
enchyma.  2d.  Where it  does occur, it is  of  the form which is
consecutive upon general  diseases  and where the patient is much
reduced.  3d.  Bronchitis  of  specific tendency, born  of scrofulo-
sis,  alone paves the way to caseation and consumption  directly.
Of  this more in  a subseqent  letter on the relation of scrofula to
consumption.  The products of pleurisy, when slow to be absorbed
and lingering, are  the indirect  cause of cheesy degeneration of
such products in the lung tissue, which  coexisted with  the pleu-
ritic ones.   Remnants of  pus  in  the pleural  cavity,  especially
when incapsulated, may dry to the consistency of  mortar, and
thence become cheesy centres.  I  refer you to the letter on inter-
stitial pneumonia, and repeat, what  has been stated once before:
the  inflammatory products existing at the termination of a lung
trouble  are subject to  caseous degeneration.   Interstitial pneu
monia {cirrhosis) may begin at any  time after the acme has been
reached, and then tends to enclose, to encapsulate these products
by proliferation and subsequent contraction.
    Hemorrhages, haemoptysis, as well as bronchial hemorrhages,
from any cause, are by no means  only evidences of progressive
phthisis.    On the  contrary, hemorrhage  from any fulness  of
blood-vessels, by stagnation, may furnish the material for cheesy
degeneration.   Indeed,  the rapidity with which this  occurs
second only to its rapid decomposition by contact with atmospheric
air  and  expectoration or  its  partial  reabsorption,  and may  be 
CASEOUS PNEUMONIA.
43
looked for when  lingering for more than a very limited  period.
You are aware that caseous products were formerly called yellow
tubercle.   Niemeyer, following the  teachings  of  Virchow, first
drew attention to their being products of various forms of pneu-
monia.  Still he held, and  in  this is  supported by more recent
authorities, that  tubercles proper are  present in  these  cheesy
masses.  In  a future letter, on tuberculosis, I will endeavor to
demonstrate tha.t both in primary chronic interstitial jxneumonia,
as well as in cheesy degenerated products of pneumonia, miliary
tubercle may supervene.
    Other  important  points, touching upon  the ultimate  fate of
cheesy pneumonia and its relation to consumption, acute tuber-
culosis, and scrofulosis, will be treated of in future  letters.
    A  fourth termination, and one which may supervene during
the active stage of pneumonic processes, is that of the formation
of caverns, cavities.   Great intensity of the inflammatory  process
and rapid degeneration (passing, as it wrere, over the acute stage of
cheesy transformation) may lead by demarcation to the  detach-
ment of a slough.  This process depends upon  an augmented cell
proliferation, surrounding and cutting off the capillary arteries;
or it may be caused by embolism of minute arteries, a pyaemic
infarct.
    Caverns in close proximity may burst into one another, form-
ing extensive caverns.   Superficial ones may perforate the pleura,
and produce pneumothorax.
    Demarcating suppuration,  the gradually developing granula-
tions with continued suppuration (the pyogenic membrane), are
factors too well  known  to dwell upon.   Suffice it to sayT, the
granulations may become a fibrous wall, with subsequent slight
contraction of the original connective tissue zone.
    These  same granulations,  however, may continue to  furnish
pus, which, decomposed  by  contact with atmospheric air, fur-
nishes a fresh incentive for sloughing.  By sloughing, layer upon
layer of the cirrhotic wall  is  detached, the cavity  enlarged, and
previously dilated blood-vessels opened, causing a hemorrhage.
    It is for these reasons that cavities, not exceeding the size of a
pea, are the only ones where we may hope for a permanent heal-
ing process, by a contracting zone of connective tissue, and the
subsequent slow fatty degeneration or calcification  {chalky trans-
formation) of the limited contents.   And  this favorable result 
44
CONSUMPTION AND TUBERCULOSIS.
even is largely dependent upon the number of such smal cavi ies
and their proximity to each other, since, where small cavities are
numerous, the breaking-down process may supervene before time
sufficient has elapsed for the slowly progressing indurative pro-
cesses ; while their close proximity is a factor in favor of enlarge-
ment, by breaking down  of walls and the  union of one or more
small cavities.   Another  method of  enlargement is  the junction
of a cavity and a bronchus.  In  fully-formed  cavities, in which
cheesy masses  develop slowly, the pleurae have time to form ad-
hesions.  If rapidly, air  may escape into the pleural cavity, and
lead to pneumothorax and suppurative pleuritis.
   Where shrinkage of connective tissue takes place to any great
extent, blood-vessels will be formed, chiefly in connection with the
pleura, a fact  to which reference has been made before.  These
newly-formed vessels do not penetrate deeply into the infiltration^
but surround and supply it with constant though scanty nourish-
ment.  This is similar to the relation between perichondrium and
cartilage.  The dense connective tissue surrounding old  lesions
is  continuous on  the  outside with the thickened pleura, inside
with the peribronchial connective tissue.
   Large cheesy masses,  therefore, are held in their periphery by
cirrhotic  contraction outside;  they are moistened continually by
the  newly-formed  circulation  above mentioned, and thus the
fibrous capsule encloses  a  chronic  cavern, wdiose chances of en-
largement are second  only7 to those of a newly-formed cavity. 
PERIBRONCHITIS.
45
                     PERIBRONCHITIS.

    No treatise on consumption, the conditions leading thereto,
 and the possible complications of these  conditions, can be  com-
 plete without  a full  understanding of  such processes  which,
 mostly as secondary consecutive  forms of inflammation, playT an
 important part.
    Certain forms of peribronchitis are primary, independent,
'totally unmixed diseases from the beginning.  Now, you will want
 to know why they are not enumerated as such in  text-books, and
 a clinical picture drawn of them  for  our guidance.  Distinct
 symptoms, capable of being detected by physical exploration, do
 not exist to such  an extent or sufficiently different from  other
-forms of chest trouble  that a clinical picture can be made out,
 even with the  assistance of an exact history of the case.  As a
^rule,  it may also be said that the subjective symptoms  often
 escape the patient, until .secondary  destructive  processes cause
^distinct discomfort, when we  are then dealing with a tubercu-
ijlous process leading directly to consumption.
i    Thus it is that pathological anatomy alone can establish the
(existence of such  diseases as peribronchitis, some forms of inter-
 stitial pneumonia, etc.; and it is from pathological anatomists, like
 Rindfleisch, that we derive  our facts.  But  no sooner have these
 pathological changes, as found  in the cadaver, been properly sifted
 and described, than we find a number of the same observers aver
 that these same findings compelled  them to fall back upon the
 old theory of the identity of all phthisical processes with tubercu-
 lar degeneration.   Thus Rindfleisch, who in his former work (pp.
 334 and 345) describes purulent peribronchitis as a distinct  form
 of disease, now says : " I feel  it  incumbent upon myself, on the
 strength of new observations, to widen the at present much con-
 tracted sphere of tuberculosis of the lung, and give support to the
 views  of those observers who have never ceased to look upon con-
 sumption as essentially a tuberculous affection."  Of course all
 proof in this connection properly belongs to a chapter on tubercu-
 losis ;  and it is to  this I must  once more refer you, in order to
 avoid tedious repetition. 
46              CONSUMPTION AND TUBERCULOSIS.
    I will here confine myself to the description of peribronchitis,
 as spoken of by authors, on the basis of pathological anatomy, and
 again warn yrou not to attach too much clinical importance to the
 same.
    Peribronchitis  is  an  inflammation of  the bronchial tubes,
 having its  principal  seat in the adventitia of the bronchi and
 bronchioli,  and  involving only secondarily the quality and quan-
 tity of the  secretions of  the bronchial mucous membrane.  It is
 altogether an inflammation of connective tissue, all other processes
 following in its train.  In this it resembles interstitial pneumonia,
 and,  like it, presents two possibilities: peribronchitis with and
 without the formation of pus.
    As often indicated before, let me repeat here that, as in all in
 flammations of  the same family7, these two conditions mayT co-
 exist.
    It seems natural  to begin wTith the simple  form, in which no
 pus is generated.   Simple peribronchitis  is  always   a  chronic
 inflammation.   This is all the more  easily understood when you
 consider that  an acute inflammatory process of connective tissue
 in any part  tends to rapid transfusion (oedema) and equally rapid
 migration of  white blood-corpuscles (purulent infiltration).   A
 less rapid process, on  the  other hand, will  tend to  the  formation
 of new tissue, rather  than to the production of serum, mucus, or
 pus.
   The simplest presentation of peribronchitis is where, in pneu-
 monic processes, white fibrous layers accompany the finer bronchi
 and bronchioles without necessarily obliterating them.  Such a
process may be  termed " diffused cirrhosis  of the  lung," where
obliteration  of alveoli and bronchi are accompanied by extensive
substitution  of condensed connective tissue.
   Where, on the  other  hand, multiple black fibrous  knots  are
found in otherwise healthy lung tissue, we may consider the pro-
 cess as one  of lobular cirrhosis of the lung.   We need only to
remember that connective tissue is here a continuous tissue of the
same  kind, not varying, as that of the inner aspect of the bronchi
 and alveoli.   So that  in all these peribronchitic processes we  are
 only dealing with a change in quantity, in which either the inter-
 alveolar  or  the  peribronchial connective tissue may be predomi-
 nantly7 hypertrophied.
    You will remember that, speaking of the higher  o^des  of 
PERIBRONCHITIS.
47
desquamative pneumonia, mention was made of the cellular lry-
perplasia of endothelium of the arterial coats.  This same condi-
tion supervenes in peribronchitic processes.  A bronchial tube
becomes uneven, knottily  thickened, and fibrous, with degener-
ating endothelial cells.
    This is one of the most frequent chronic disturbances, and is
very7  properly  termed  peribronchitis nodosa.   Peribronchitis
nodosa  may occur independently; indeed, the same  individual
may several times during lifetime suffer from localized processes
of  this  kind without  active symptoms, just as slight pleuritic ad-
hesions occur.
    Mostly7, peribronchitis fibrosa and nodosa occur together, and,
by continued shrinkage of the hypertrophic tissue, may  lead to
atrophic ectasia of alveoli and bronchioles as well as dilatation of
the blood-vessels contained therein.
    In very  intense, acute cases  of  course  the tense traction, by
shrinkage, upon the arterial branches and capillaries, may lead to
complete interruption of the circulation, and the natural  local
consequences, anaemic necrosis or gangrenous throwing  off of a
great portion of a bronchus.  It more frequently occurs, howr-
ever, that the relatively small section of necrosed tissue remains
in organic contact and undergoes cheesy degeneration.
    When local gangrene  occurs in  this way, it is of course an
acute or subacute  process, but as such strictly localized and not
diffused, while the universal cheesy degeneration is altogether a
chronic process.  Like diffused cheesy pneumonias, these cheesy
lobular masses  are encapsulated by black  cirrhotic tissue, and,
when quite small, may be reabsorbed. Such  multiple  lobular
pneumonias have been classified under the head of chronic tuber-
culosis, they being looked upon as a slow cheesy metamorphosis
of  existing  tubercle.  In reality they represent merely  various
stages of a connective tissue process, and the results are governed
by the length of time necessary for their development;  the acutest
form gives  rise to alveolar inflammation, the subacute  moves
towards the bronchioles, and the ch\QX\\vform (whether as a rem-
nant of an acute process or of slow progress from the beginning)
lays hold of the coarser ramifications of the bronchi.
    In conclusion I will add that a  close analogy seems to exist
between desquamative  pneumonia and peribronchitis  in this : as
desquamative pneumonia is a localized expression of some general 
48
CONSUMPTION AND TUBERCULOSIS.
 disease {i.e., being the form of pneumonia which occurs in con-
 nection  with acute infectious  diseases), so may peribronchitis,
 which plays its part in the same tissue, be a localized expression
 of general disease, possibly chronic.

    Peribronchitis purulenta.   It is my opinion that of all forms
 of respiratory affections, this one is the least understood.  In vain
 do we search the works of even  the  more recent  authors for a
 clear, well-defined picture of this disease.  This is all the iriore
 astonishing, as purulent peribronchitis occurs as an independent,
 uncomplicated disorder.  Its histological factors have  been best
 described by Rindfleisch, and it  is to his observations we will
 address ourselves.
    Purulent peribronchitis  is  characterized  by acute purulent
 infiltration of the finer bronchi (those wanting in cartilage, muscle,
 or glands), involving their whole thickness, from the cellular coat
 to the mucous  membrane.  It rapidly extends along the lobules
 and into the alveolar walls.  In its train may follow the  results
 of all rapid  purulent  infiltrations—loss of substance, abscesses,
ulcers of the bronchi, vegetable parasites of a low order.   This
purulent softening must not be confounded with anaemic necrosis,
though  the  dead  mass may become cheesily  degenerated, and,
when of  large extent, form cavities.  In the formation of cavities
a number of terminal bronchi, with lung lobules  belonging  to
 them, will be dissolved  in the pus, or  the purulent infiltration
 may proceed  towards the  bronchioles, and find its limit only
 where cartilaginous rings begin.   As in simple peribronchitis,
 there appears to  be (according to Buhl, of course) an analogy
between  desquamative pneumonia and purulent peribronchitis In
 this :  that in  desquamative  pneumonia  the parenchymatous
 swelling  is of a proliferating, productive character, while in puru-
lent peribronchitis it  is  the same process with  a destructive
 tendency7.
   In consequence  of the swelling and  removal  of  bronchial
 tisanes, the entrances to the  alveoli are  often well-nigh c.Wd.

 Ln^S1 are *," ^^ °l ah'' and' «l*»ti<£ becoming
 imponble, an acute mulUple lobidar emi>kysema s„pervenes.
   Th» .. one of the few pathognomic symptoms of purulent peri-
 bronchus and may result in pneumothorax from seve af smaU
 forced ruptures at once.                           »e\eiai smau 
PERIBRONCHITIS.
49
    In regard to diagnosis, which  you know we  do not strictly
 enter into in these letters, I cannot forbear to mention the fact that
 the chills and continued fever, as evidences of rapid formation of
 pus, are guiding-points for a differential diagnosis.
    So far  as known, purulent peribronchitis does not become
 chronic.  This may7 be  inferred from its  character as  an  acute
 purulent infiltration.   In case of any less rapid course (as, for in-
 stance, when successfully combated by treatment), the primary
 results may become circumscribed  by  cheesy induration  of the
purulent infiltration  and such  weak  condensation of  the sur-
 rounding connective tissue as to render constant repetitions almost
 certain.
    In regard to purulent peribronchitis, the same  rule holds good
 to which, in other conditions, I have so frequently drawn your
 attention, namelyr, that of combining with other forms of inflam-
 mation—in this  instance with desquamative pneumonia and
 knotty peribronchitis—frequently  forming the last stage  of  the
 series.
    Niemeyer had  a favorite aphorism, to  the  effect that " the
-greatest danger in chronic inflammatory processes of the lung is
rthe  supervention of tuberculosis."  Buhl is, no doubt,  in  the
 right when he desires to have this modified so as to  read, "the
■ danger consists in the  addition of purulent peribronchitis."  And
 he seeks to establish the importance of the occurrence of purulent
 peribronchitis in any case by the following deductions : the for-
 mation of pus in this trouble is not to be found in the migration
 and  infiltration of white blood-corpuscles, but is accomplished on
 the spot.   Migratory cells do not reach the surface of  unharmed
 mucous membranes.
    The connective  tissue corpuscles and endothelium of the lym-
phatics produce pus-corpuscles freely from their  nuclei, rapidly
 degenerating  themselves  and  leaving the  pus-globnles  free.
Though not strictly7 proven, it is  now one of  the  theories under
 investigation that the formation of lvmph and white blood-cor-
      O                             1/  J.
 puscles in the healthy7 state takes place from  the  endothelium of
~;he lymphatics, confined to certain parts of the organism, but that
"under  pathological irritation they  may be produced in  any part
where lymphatics or connective-tissue cells analogous to endothe-
lium exist,  And let me add here, that it seems plausible to  me
 ;hat  length of time as well as severity of attack  is an  element,
           4 
50              CONSUMPTION AND TUBERCULOSIS.

and that the two are the chief factors in producing destruction in
the shape of  rapidly formed endothelial and connective-tissue
cells, on the spot, in  contradistinction to more chronic ana less
severe  invasions, which give rise to slow processes m the snape ot
migration of white blood-corpuscles, etc., resulting in hyperplastic
conditions. 
TUBERCULOSIS.
51
                      TUBERCULOSIS.

    Our present conceptions of the nature of tuberculosis are to a
great extent based upon  the investigations of Virchow.  It was
Virchow  who  first  demonstrated that cheesy7 degeneration, far
from being a specifically tuberculous  process, supervened  in the
train of other  neoplasms, cancer, sarcoma, etc., nay even  quite
frequently as a sequel of chronic inflammations; he taught us to
become acquainted with the true character of lobular hepatizations
in the lung as  well  as  cheesy peribronchitis, which had been so
often confounded with tubercle, and  pronounced as the ty7pical
form of tubercle the miliary eruptions of serous membranes.
    The definition given  by Virchow  of  tubercle,  aside from  a
few modifications, holds  good  to-day: " Tubercle is  a  neoplasm
which appears in the shape of  small  nodules, always originating
from connective-tissue strata, consisting of  densely7 crowded small
round cells.  This neoplasm has  a limited  lease of life,  very soon
degeneration of its  elements sets in, always beginning in the
centre of  the nodule ;  in  most cases  the  change  is into cheesy
degeneration.  Apart  from this  local malignity, the  neoplasm
possesses  another trait, which places it in  the category  of malig-
nant tumors : a well-marked tendency to generalization over the
whole organism.''
    We  may look upon these propositions  of  Yirchow's as the
foundation for  the present views on tuberculosis and  endeavor to
amend them in accordance with newly discovered facts.
    The next development was that Langhans drew  attention to
the almost constant occurrence of giant-cells in the  interior of
tubercle.  Virchow, too, had spoken of the occasional presence of
giant-cells, but Langhans was  the first to  announce them as  a
typical occurrence.  He pointed  to the peculiarly typical nature
of tubercular giant-cells  in contradistinction  to the  well-known
giant-cells of sarcoma  and to other neoplasms; he  dwelt  upon
the peripheral  location, the uniform size, the radial arrangement
of their nuclei, and  thereby characterized them as a growth sui
generis.   The protoplasm of these giant-cells is distinguished by
uniform, rather dark nucleation,  and in superficial  observation 
52
CONSUMPTION  AND TUBERCULOSIS.
 bears some resemblance to certain  forms of  bacteriae.   Some
 observers hastened at once to pronounce the dark granula of the
 giant-cells as micrococcus; the  simple  reaction  with  a  potash
 solution, which  at once  dissolves the granules, when moderately
 warmed, dispelled this opinion.
    Further pursuit of  Langhans' discovery led Koester to find
 tubercle in a locality where up to date they had escaped all obser-
 vation, namely, in the granulations of fungous inflammations of
 joints.   Indeed, the occurrence of tubercle in this disease seems
 to be inexceptional, and their aggregation  often visible  to the
 naked eye.
    Next Schueppel found the same giant-cells in cheesy or appar-
 ently purely hyperplastic lymphatic glands.  Here they are only
 to be seen microscopically, not so much on  account of their small-
 er size—they measure from one-third to one-half of a millimetre
 —as because they are not sufficiently distinguishable from the sur-
 rounding parenchyma of the lymphatic gland.
    Again, according to the  researches of  Friedlander, a constant
 and prolific eruption of tubercle wras found in scrofulous abscesses
 and ulcers of the skin, as well as in caries.
    Thus we see that all of the most important scrofulous diseases
 are linked with the development of tubercle.
    In addition to what has been  said of the past history7 of tuber-
 cle, a rapid glance at its anatomico-histological character is neces-
 sary for a thorough comprehension of its subsequent fate.
  Tubercle is a neoplasm of microscopical  dimensions, of a diam-
 eter of  Jj-f".   Tubercle  has  within itself no  blood-vessels,
 though  surrounded  by  a network  of blood-vessels, and itself is
 found  in the connective tissue  accompanying Ivinphatics and
 other vessels, especially the  adventitia of the more  minute arte-
 ries.  Histologically, tubercle  appears  to  be analogous with all
 lymphoid structures of  the human  body (Malpighian  bodies  of
 spleen, lenticular follicles of intestines).
   Under the microscope tubercle is seen  to be a bullet-shaped
mass, commonly from  two to ten of  them  closely ao-o-reo-ated
together, so that the individual tubercle is really composed of  a
group of bullet-shaped masses.  The real histological character of
tubercle has been found by E. Wagner to consist°of : a network oj
most minute fibre (reticulum) in which we find cells which, both as
to number and size, increase from the periphery to the centre. 
TUBERCULOSIS.
53
    In regard to these cells it may be well to cite opinions as to
 their different character in connection with their location.  Ima-
 gine, therefore, the above-mentioned body of delicate fibrous tissue
 with cells, of which there are three kinds:
    1st. So-called cystoid  bodies, found chiefly in  the periphery
 of the fibrous groundwork.  Several authors contend that these
 particular elements of tubercle are migrated lymph-corpuscles or
 white blood-corpuscles.  This is gainsaid by the fact that tubercle
 are  much smaller, as also are their nuclei  smaller and  more shi-
 ning.   Again, the centre of the fibrous groundwork are giant-cells,
 so that peripheral cells would  have  to increase in size, instead
 of undergoing the well-known fate of tubercular cells to the con-
 trary.
    At the end of the chapter on tuberculosis, I will again sum-
 marize the accepted theories of the present time.   The analogy
 between tubercle-cells and lymph-cells is now under investigation.
 It may be reserved to histologists  of the future to show the anal-
 ogy between  tubercle-cells, lymph-cells, and white blood- or pus-
 corpuscles; and while it is not  requisite that tubercle-cells (any
 more  than  pus-corpuscles) should  grow after migrating, it may
 yet be shown that their condition is produced within the lymphat-
 ics and capillaries,  or during their migration through the vascu-
 lar walls, or both.
    The second form of tubercle-cells are the giant-cells, and these
 are situated in the centre  of the fibrous network.  The increase
 in size is so marked as they approach the centre, that the most
 central giant-cell is always  superior in size to  its surrounding
 neighbors.
    Schueppel (1871) endeavored to invest the giant-cell with  the
 dignity7 of a specific characteristic of tubercle, but as giant-cells
 exist on the inner surface of periosteum and elsewhere, this opinion
 does not hold good.
    3d. Besides cystoid and giant-cells, we find cells of  epithelial
 character, which as  regards size  and situation appear to  be a tran-
 sition  between  both (Buhl).   The smallest giant-cells are the
 largest of this  species.  They  fill  the meshes of the reticulum
 surrounding the giant-cells;  become smaller as they approach the
 peripheral cystoid cells, and appear to  lose  themselves  into the
 cvstoid cells on  the one hand, as they do into the giant-cells  on
the other. 
54
CONSUMPTION  AND TUBERCULOSIS.
   Where giant-cells do not exist, the epithelial cells may form
the centre, or, in their absence, the  cystoid cells have the ground
to themselves, and are then  not to be distinguished  from lymph-
follicles.
   Two things seem to me possible  in connection with the history
of tubercle-cells.   Since the peripheral  cystoid cells are not sup-
posed to be the juniors of the giant-cells, not a transition cell de-
veloping from the periphery to the centre ; since tubercular ulcer-
ation and disintegration begins in the centre, as do  all  ordinary
ulcerative conditions  leading to destruction of tissue, it might be
worth while to investigate whether the two following propositions
are not founded on fact:
   1st. That the proliferation of the various  kinds of  cells
(cystoid, epithelial,  and giant) does not take place from the
periphery, except perhaps in the beginning, but from the bottom
of the previously developed connective-tissue network.  this
would be analogous to the process of repair in varicose ulcers treat-
ed by7 cutting off the peripheral circulation, when reparative nour-
ishment of the ulcer is accomplished through tissues underneath.
   2d. That, as is the case in inflammatory7 conditions, the centre
of the existing condition produces not only more fully developed
cells (as shown in the prolific development of granulations in a
wound), but this centre is invariably7 the starting-point of suppu-
ration and disintegration.
   As long as the  tubercle  granule is still  growing, there is in-
creased activity of proliferation in the whole surrounding tissue,
which  ends rather  rapidly in fatty7 degeneration or calcification
of the central giant-cells, and in hypertrophy of connective tissue
from the cy7stoid cells of the periphery.
    It is  but natural that the origin of  tubercle has always at-
tracted  a large share of attention, and every tissue, beginning
with the circulation and ending with the cells of the immediate
surrounding of tubercle, has been charged with its paternity.  I
will give you the present views about the paternity of tubercle in
a few words:
    Remember, as above  stated, that tubercle essentially consists
of giant-cells, next epithelial, then cystoid cells.   Either of these
three maybe developed from connective-tissue corpuscles (accord-
ing to Langhans), likewise from endothelial  cells (according to
Klebs, Rindfleisch, and others).  Then Waldenburg, in his  excel- 
TUBERCULOSIS.
55
lent work on tuberculosis, endeavors to show the origin of tuber-
cle in capillary emboli caused by corpuscular elements.   For ex-
planation of  these theories, I have to refer y7ou to the works of
these respective observers.
    The limit of my7 letters will  only allow me to confine myself
to tubercle in  the lungs.  In these, as in other parts, we  find
them only where connective tissue, lymphatics, and  minute arte-
ries with endothelial (lyTmphatic) coat are found.  The part which
these tissues play in the development of tubercle, is best described
by Buhl: " Connective tissue, its  interstices and vessels  become
animated to formation, wherever tubercle is located in the alveolar
walls as well as the alveolar epithelium (as part of the continuous
lymph-endothelium);  likewise by the sub-pleural extension, the
pleural  endothelium;  when tubercle is located  in bronchial
walls, the endothelium of lymphatics and epithelium of  mucous
membranes will  take on prominent action.   But all productive
activity7 accompanying the formation of tubercle will only make
itself felt so long as the tubercular growth is  fresh  and viable,
and will cease  and become  retrogressive, as soon as the develop-
ment of tubercle ceases and its degeneration begins."
    Recent tubercle  is soft  as  jelly,  and has a grayish color.
When  it has reached full growth, which, from the fact of its
[being non-vascular, can never be considerable, fatty7 degeneration
or horny calcification begins  in the centre, and the growth looks
yellowish and  opalescent.  This  is characteristic of retrograde
action on the part of tubercle; it becomes as a fibroid-kernel,
[and may be entirely7 reabsorbed.
    In consequence of compression of  the most  minute arteries,
the whole tract  supplied  by them becomes  void  of blood and
;undergoes anazmic necrosis and rapid cheesy degeneration.  The
.whole of these together may sometimes form tuberculous caverns
of small dimensions with cheesy contents, but here the action of
tubercle proper ceases, since other processes originate from  their
ineighboring tissues.
    What has been taken for yellow tubercular masses, as spoken
of  in my introductory letter, is microscopically found to  be  a
[tubercle-lymphoma (tumor of that character, if you choose)  with
central  degeneration ; if large, as a necrotic group of alveoli,
with their desquamated epithelium  around and between them,
ready to undergo cheesy degeneration. 
56
CONSUMPTION  AND TUBERCULOSIS.
    Let us  now pass from the pathology of tubercle to the con-
sideration of the further course of  acute  tuberculosis.   Miliary
tubercle  with  the  cheesily  degenerated  alveoli,  lie  either  in
healthy lung-tissue, or the  lung-tissue will  be undergoing fatty
degeneration ; in the apices, where  tubercle  and its masses are
chiefly located, cirrhotic processes supervene, but not to any great
extent.   It is this which makes diagnosis ofttimes so difficult in
the absence of decided physical signs.
    These letters do not concern themselves with diagnosis, but I
cannot refrain from impressing upon you the following : Where
percussion  and auscultation yield almost negative results; where
the patient  himself manifests no special subjective chest symp-
toms ;  where continued high temperature, not readily affected by
quinine,  a rapid pulse and equally rapid emaciation supervene,
every careful physician should carefully inquire into the previous
history of the patient.   Nor should he neglect to search the fun-
dus of the eye,  the  choroidea for  freshly-developed tubercle.
This en passant.
    Ofttimes tubercle  may in the general mass of cheesy degene-
ration  have become obsolete and disappear, w7hen it  would be
difficult to  determine whether or not the mass  before us is the re-
sult of slow peribronchitic processes  or cheesy7 pneumonia, repre-
senting remnants of acute forms of lung trouble.  The presence
of a more recent crop of tubercle attests the character of the mass
before us.   At the same time it furnishes us with a hint as to the
probability  of a  future permanent  cure, which hope of  course
rests in  the chances of reabsorption.   Unfortunately, however,
the next  step in the development  of tubercle  is found  in  their
movement into the  bronchioles  by7 local infection, and what in
the alveoli  was a closely condensed  mass is found at greater inter-
vals to correspond to the anatomical site of the minute bronchi.
   I come now to speak of the etiology of  miliary tubercle, and
more particularly of the theory of  its being a  specific infectious
disease, a disease of absorption  of  toxic matter.  The literature
on this subject is very extensive, and it will  be mv endeavor  to
summarize the evidence upon which  this theory rests :
   1st. Miliary  tubercle  is  found  and developed  where
CHEESY DEGENERATIONS EXIST IN SOME PART OF  THE BODY.  This
fact was  known to Laennec and others, and accounts for his dis-
tinction into gray and yellow  tubercle,  yellow tubercle signify- 
TUBERCULOSIS.
57
ing with him what  are  now known  to be  existing  cheesy
deposits.
   From these centres particles are absorbed by the blood and
lymph vessels, causing the multiple eruption of tubercle in one
or several organs of the body, and nothing else.   This, therefore,
is  self-infection  pure and  simple,  resembling the invasion  by
other septic matter, as in septicaemia and pyaemia.
   This proposition naturally gives  rise to the  question :  Have
cheesy7 parent deposits invariably been present, where tubercular
eruption has taken place?  This question is affirmed by some,
negatived by others.   As far as statistics  of dissections are avail-
able,  the result appears to be that in from eight to ten per cent, of
deaths  by miliary tuberculosis, no previous deposits were found
at the autopsy.
   The results of trials of inoculation  are in accord with this.
Where  material was used which was not  of inflammatory origin,
the point of inoculation in each case first became  inflamed and
furnished products of inflammation,  which  afterwards became
cheesy, and it was from this often rapidly formed cheesy centre
that self-infecting absorption took place (Waldenburg).
   2d.  Cheesy  deposits,  leading  to miliary tubercle,  can
BE TRACED  BACK AS REMNANTS OF  FINISHED INFLAMMATORY PRO-
CESSES.   Of course in order that absorption and infection may be
accomplished, the caseous deposit must not be  incapsulated,  not
surrounded  on all sides by firm fibrous tissue.
   3d.  Another proof of the origin of  tubercle by absorption is
in infection by contiguity, probably due  to absorption by local
lymph-vessels.   " Tubercle namely appear in greatest aggrega-
tion in  the immediate neighborhood of the cheesy mass and mul-
tiply  from thence in  eccentric lines."   The oldest tubercle  are
nearest the  deposit, the youngest most remote.
   Here we would almost have a basis for believing with Rind-
fleisch,  in the existence of chronic tubercle, if  we would and
could distinguish as follows :
   As  acute  tuberculosis,  those processes which  result  from a
rapid absorption into the general circulation of  caseous material,
producing constitutional symptoms  (fever, etc.), and running a
rapid course.
   As chronic tuberculosis, those processes which are local from
the beginning, allowing only of neighboring infection  by means 
58
CONSUMPTION  AND TUBERCULOSIS.
 of local lymphatic absorption and  holding its own for a  time,
 without falling a prey to absorption into the general circulation.
    No such distinction, however, can  properly be  made, chiefly
 because localized tubercle is doomed to speedy death.
    4th.  Another proof of the specific character is the seat of mil-
 iary tubercle in connective tissue well supplied with lymphatics,
 and their analogy with the histological formation of the normal
 lymph organs of the body7.
    Having thus passed rapidly over what  is known clinically of
 actual absorption, I draw your attention to what is claimed to be
 another  mode  of transfer of virus, viz., by7 thrombosis (Pan urn,
 Waldenburg, and others).  Let me at once say, that thus far this
 is conjecture and has never yet been observed or demonstrated.
 But absorption and thrombosis are not necessarily7 irreconcilable.
 Buhl has endeavored to show that bacteriae are the  intermediate
 factors between a thrombosis and its partial absorption, by assert-
 ing that the corpuscles in the interior of giant-cells are in great
 part staff-bacteriae.
   I regret that it would  again lead too far out of our prescribed
 path, were  I to prove to you that bacteriae are present in all ne-
 crotic breaking-down tissue, markedly so in the centre of ulcera-
tive processes, just as in this case the giant-cells are  the centre of
 tubercle and the first to undergo  degeneration.
   5th. Still another  pillar  for the  support *of  the infection
theory is the transfer  as between husband and wife.  As regards
 the proof of this, I will say that  quite a number (I am sorry to
 say there are no positive statistics) of well-authenticated cases of
 transfer between man and wife have been recorded, similar to
 syphilitic infection.
   6th. It is held by most  authors  that tuberculosis never goes
 hand in hand with  other  infections.  This is  true of carcinosis
typhoid, pyaemia, etc., but I  am not sure  whether it  is equally
 true in regard to malaria, that bane of mankind, which accord-
ing to several authorities  does go intercurrent with tuberculosis.
And  I wish to impress  upon you my oft-expressed belief, that
malarial infection is the immediate cause in every new  country
of breaking down and^ absorption of caseous products, and the
occurrence of acute miliary tuberculosis.
   7th. Last but not least, the supporters of the infection theory
look upon  the  success of  the inoculation of true tubercle upon 
TUBERCULOSIS.
59
animals, as an incontrovertible proof  of  the  correctness  of  the
absorption and infection theory7 of tuberculosis.
   From  all this evidence we are justified in speaking of general
miliary7 tuberculosis as  an acute infectious  disease, in the sense
that the own body7 furnishes the virus for the infection.
   Let us now inquire  in how far tubercle may7 be said to be a
product of inflammation.   1 do not propose to engage in any  dis-
cussion or examination  of  whether we may properly speak of a
tuberculous inflammation, as  this would  amount  to a  war of
words.
    We have just seen that acute miliary tuberculosis is regarded
as an acute infectious disease.  Its  character therefore is  that of
a general disease, and  in order to be inflammatory  in the  true
sense of the word, it would have to be strictly localized and  pro-
duce local inflammatory products.
    Therefore we may conclude to speak of acute miliary tuber-
culosis as an inflammation, where simultaneously with  the ap-
pearance  of  inflammation,  tubercle-lymphoma are developed,
which remain for a short time confined to the tissue  then in-
volved.
    Now  you will  ask: Is there  a double manifestation of the
tubercle-granule %  Is there a secondary infectious miliary tuber-
culosis, taking its  material from a cheesy centre, as well as a
primary  tuberculous  eruption,  which takes place  during  the
existence of  an inflammatory process, and at  the  site  of  that
inflammation ?  In  a certain  sense, yes.   According to Rind-
fleisch  and others,  the  tubercular manifestations coexisting with
inflammation occur in scrofulous individuals, and the products of
such inflammation  are  marked by copiousness and a tendency to
lino-er.    Others again do not call products of that nature scrofu-
lous  but dwell only upon the fact that they occur in  individ-
uals of feeble resisting power and general vulnerability.  The
supposition is in any case that before tubercle is formed, the  pro-
ducts have undergone cheesy degeneration to some extent. Since
Rindfleisch  claims that the local as well as general manifesta-
tions are all based upon scrofula, I have  thought it best  to  give
his view's  unbroken in the subsequent chapter on " consumption."
   So you may look upon tuberculosis as twofold in  its mani-
festations.
    1st. As a local  neoplasm, at the site of subacute or  chronic 
 60             CONSUMPTION AND  TUBERCULOSIS.

 inflammation, where the progress is confined to infection of the
 direct neighboring parts, and,
    2d. As an acute infectious disease with all  the attributes of
 infection, taking its origin by absorption from the localized centre,
    It is to the first, to local tuberculosis, that I wish to invite your
 attention.   Tubercle may occur in almost any part of the body,
 but it may be laid down as a rule that it has a certain predilec-
 tion for serous membranes.   Favorite sites are the pleura, peri-
 cardium, pia mater, peritoneum,  the  synovial  membranes—in
 short, in those parts  where lymphatic absorption is always active
 and the communication with lymphatic glands  free  and  the
 glands themselves numerous.  Thus lying within a  territory
 where changes are rapid, where transudation and exudation as
 well as absorption are very active, the ready general  dissemina-
 tion of tubercle from a localized centre is easily understood.
    The tendency to  rapid distribution, governed by laws of which
 we know nothing, and their  well-known tendency to equally rapid
 disintegration under certain conditions, justifies us in pronouncing
 tubercle capable  of great  local  malignity.   We find it  so  in
 lupus, in the chronic inflammation of joints known as synovitis
 fungosa, and wdiat is of more interest to us just now, in the lungs.
 Here, often grouped together in a heap, they follow the course of
 the connective-tissue stratum of  the  bronchi.  The intimate re-
 lations between this  stratum and the subpleural connective tissue,
 invites the  belief that the starting-point of tubercle  in that local-
 ity is  to be sought for in the pleura.
    We find alongside of tubercle  nodes always a more or less
 copious collection  of small round  cells, indicative of inflammatory
 irritation.   The clinical  picture of local tuberculosis is  thus
 always one of a subacute or chronic  inflammation.  Thus three
 possibilities are presented:
    1st. The tubercles and the inflammation are co-effects of  the
 same  cause.
    2d. Tuberculosis calls forth a secondary inflammation.
    3d. Tuberculosis is caused directly by the inflammatory pro-
 cess, consequently  a secondary phenomenon.
    You are already aware that this last theory is based upon the
proofs furnished by Buhl, that in nearly all cases of general tuber-
culosis a cheesy parent-focus is found.   And we have the equally
well-known artificial creation of  tubercle by creation of cheesy 
TUBERCULOSIS.
61
products in animals.  That in  nearly all cases of death by gene-
ral tuberculosis some cheesy focus should  be found, is not at all
astonishing.  Few persons die, who have not carried within  their
body a cheesy product of greater or lesser dimensions during life.
And after death from general tuberculosis, it is natural  to sup-
pose that amidst a quantity of tubercle, some of the older crop will
be sure to have undergone calcareous metamorphosis.  It is thus
in a local sense that we may speak of  "chronic tuberculosis."
    We come now to dispose of Villemin's  inoculation of tubercle
in squirrels and the development of tubercle within their organs.
The trouble about it is, that the disease following the inocidation
of animals is not tuberculosis.  What has  been  produced has
neither the typical structure of tubercle,  nor are any giant-cells
present.  The  fact is that these  artificial nodules  are  lobular
pneumonias, which consist of the  appearance of multiple centres
of irritation with ready tendency to cheesy degeneration.
    In disease  caused by these  cheesy masses, we  are  dealing
with a  chronic intoxication (chronic py7aemia)  of animals,  from
wdiich we have no right to  make any deductions touching tuber-
culosis in man.
    All that has been said above, holds  good  for the relations of
the various inflammations of the lung to tubercle.  Let me repeat:
    Tubercle occurs,  1st. As a more or less independent  local
manifestation  with local malignity7,  manifested by  neighboring
infection and  rapid  disintegration.  Its favorite site are serous
membranes.  What agency primarily gives rise to the formation
of tubercle, we do not know to-day any more than formerly.  Nor
do we know why it has a great tendency  to  the breaking down
of its elements, but  we conjecture that this occurs  when a per-
son's circulation is out of order (qualitative as in malarial poison-
ing, quantitative as in anaemia) or the equilibrium of the central
nervous functions are disturbed.   For those whose  lymph organs
are  naturally  vulnerable by inheritance,  a  mere  trifling cause
may suffice, usually a gastric or bronchial catarrh.
    2d.  As  an  acute infectious disease, taking its  material  for
absorption from one  of its own  local  deposits  or an already ex-
isting cheesy deposit or chronic suppuration.  General self-infec-
tion is the result.  But let  me impress it upon you, that before
this general absorption takes  place, tubercle must be formed on
the  site  of caseation or  suppuration.  So that tubercle occurs, 
62
CONSUMPTION AND TUBERCULOSIS.
  3d. Locally again, inside of and in connection with  the cheesy
remnants of finished inflammations, and with chronic suppura-
tion.  Without further reference to other cheesy centres (scrofn-
lous glands), or to chronic suppurations (chronic inflammation of
joints, synovitis fungosa), we will address ourselves to remnants
of inflammation of  the lung and chronic suppurations of it and
the pleura.  In going over this ground, the repetition of some
things which have been spoken of in previous chapters becomes
unavoidable.
    Of possible cheesy remnants of lung trouble we have :  those
of croupous pneumonia.   This possibility  is denied by  Buhl,
while all others allow it, but specify that it is a rare occurrence;
either extreme—total and rapid restitution or equally rapid gray
hepatization being the rule.
  Those  of catarrhal pneumonia : also denied by Buhl.   Nie-
meyer  claims  for it frequent caseation.   Others, more cautious,
place it among the possibilities.
    Those of desquamative pneumonia:  to  which form of in-
flammation alone Buhl credits the caseation of products.  Rind-
fleisch and Juergensen allow for the pathological processes of this
form, but not  for the name.   Others  deny its existence,  and call
the inflammation accompanying general diseases  catarrhal pneu-
monia.
    In connection with interstitial pneumonia : in  suppurative
infiltration, as  in gray hepatization  and gangrene of the lung,
the process almost  invariably runs  such a rapid course as  to
almost  preclude the possibility  of  any other termination  than
death.  We may imagine, however, that there exists such a thing
as a subacute stage in which the formation of pus and of connec-
tive tissue go hand in hand, or, what  is more likely, that a local-
ized suppuration (if  that ever takes place in such  loose tissue)
may be followed, and more or less encapsulated by newly-formed
connective tissue.  Here, then, we have the pus of a cold abscess
drying up, thickening, and assuming a mortar-like consistence.
This too is caseation.  The  occurrence  of  tubercle in newly-
formed connective tissue, in cases where chronic interstitial pneu-
monia occurs as an independent disease of the apex, or in connec-
tion with the  cheesy remnants  of  inflammations, may be im-
agined thus:  as long as induration has not commenced, and the
process  is still one  of proliferation, the  ground  is ripe for the 
TUBERCULOSIS.
63
development of  tubercle, for we have  the authority  of most
observers to the effect that " tubercle of the lung locates itself
only where connective tissue, minute arteries, and lymphatics are
found."
    Perhaps the  most interesting connection, however, consists
between the products of pleuritis and the formation of tubercle.
We may safely  exclude  pleuritis sicca, with its fibrinous  exuda-
tion, since there absorption is the rule, or at most limited adhesions.
But in connection with the sero-fibrinous, serous, and purulent
effusions, the  proofs are  manifold of  an etiological  relation
between acute miliary tuberculosis and the absorption of pleuritic
exudations.  It  has  been found  that after the  somewhat rapid
absorption of pleuritic effusions, tubercle has been developed on
the spot as well  as that general  tuberculosis subsequently super-
vened.
    The formation of tubercle in the pleura occurs as soon as the
active symptoms have  run  their course and  the exudation is
perfect.
    As stated in the beginning of this chapter, the favorite sites of
tubercle are serous membranes.  Now, of course, a crop of tuber-
cle may  have existed in the pleura, just previous to the lighting
up of  the inflammation,  yes, may have  been the local exciting
cause.
    Upon the completion  of  the  exudative  process, the pressure
of the blood-vessels and lymphatics is very great, and the function
of the  absorbents greatly  interfered with, interrupted,  indeed, by
their thorough  soaking.   Here, then, the lymphatics are com-
pletely clogged up, and the relation between waste and  supply
entirely suspended.   Diuretics and other remedies are used, the
lymphatics  are partly freed, and rapid  absorption takes place.
Now, in  this ready absorption into the open lymphatics enters also
the tubercular virus, which in that respect has an equal chance
with the exudation.  It  is  from this point  that  general tuber-
culization begins.
    But here we are at once confronted by another question :  is the
formation of tubercle in other organs due to rapid absorption of
the pleuritic exudation?  I do not think w7e are justified  in as-
suming this.  The injection of other foreign bodies, in  short their
introduction into the circulation direct or by hypodermic injec-
tion in  animals, does not, as you now know,  produce miliary 
64
CONSUMPTION AND TUBERCULOSIS.
tubercle, but inflammatory foci, which are nothing more nor less
than multiple lobular pneumonias.   Now, a difference may exist
between foreign corpuscular  matter from without and the prod-
ucts of  disease within the body,  though the present accepted
theory  is, that while many cases of acute miliary tuberculosis
originate  from self-infection, it  does  not necessarily require a
special  specificity  of  infecting material,  but  retrogressive prod-
ucts of  inflammation  and detritus  suffice, which may be formed
by a variety of inflammatory processes.   Temperature and other
factors may play an important part here ; but of this we  do not
know anything.
   So that I think we  may, from these premises, set up the follow-
ing propositions :
   1st.  After the absorption of  a pleuritic exudation,  gen-
eral tuberculosis frequently supervenes.  This has been dem-
onstrated  by autopsies in cases of death in adults almost exclu-
sively, the age of  development being  comparatively free, which
may7 be readily accounted for by  the rapid changes in early life.
   2d. The source  of tubercle in these instances is  either
TUBERCLE  OR SOME OTHER CHEESY CENTRE ALREADY  EXISTING IN
the pleura, or both.  In addition to what has been said under
that head above, we will look upon the probable results in case of
empyema.   Rapid absorption of  pus in any quantity7 would give
rise to pyaemia and early death, and not to tuberculosis.  Let us
imagine a  purulent  remnant encapsulated  in  the  pleura and
gradually becoming inspissated, drying  up from still  slowly pro-
gressing absorption, and undergoing cheesy degeneration.   Now,
whether a general tuberculosis  would  be lighted up at some fu-
ture time, or whether a sudden recurrence of pleuritic symptoms
would  take place, we will in  both cases be  compelled to look
upon the encapsulated remnant as the direct centre of absorption.
   But  even  in cases where no traces of an older crop, of an
original stock of  tubercle, or  cheesy mass can  be found after
death, we still have an explanation  for the occurrence of general
tuberculosis so soon after reabsorption.
   The absorbed matter may pass on its way to the general circu-
lation through lymph-glands, which are already in part cheesily
degenerated, either from hereditary influences (scrofulous), or by
more recent disease, and there readily take up the detritus.   So
we may formulate: 
TUBERCULOSIS.
65
   3d. A PLEURITIC EXUDATION, BECOMING ABSORBED AND PASSING
ON ITS WAY THROUGH LYMPHATIC GLANDS ALREADY CHEESILY DE-
GENERATED, WILL  START ACUTE MILIARY TUBERCULOSIS FROM THAT
POINT.
   Right here it may not be out of place to insert another diffi-
culty, with which we have to deal when looking for the original
mother focus of cheesy degeneration after death by acute  tuber-
culosis.  The original focus may be nothing more than a corpus-
cular one (Waldenburg); and whether existing within as a rem-
nant of inflammation, or having been introduced from without, it
may7 have lain  dormant, and with its local inflammatory products
remained unabsorbed,  owing to the absence  in its  immediate
neighborhood of  a  good and unobstructed absorbent.  Circum-
scribed encapsulation  may  have taken  place.  Thus it may re-
main  innocuous  until  some general  disturbance  of  the  health
takes place rendering the patient less capable  of  resistance.  I
have mentioned before  my7 belief that, as soon as fever sets in, the
oft-mentioned " breaking-down " of the quality of the blood in such
a patient rests upon the cessation of the formation of its constit-
uents {notably red blood-corpuscles,  and perhaps fibrine), as evi-
denced by enlargement of the spleen, etc., and not so much in the
loss  of any constituents  already existing.   This, as you  know,
would relieve the absorbent lymphatics and veins from assisting
in the process of assimilation; their  whole  attention may be
turned to the absorption of  home tissues and  products.  It is  at
such a time of vascular activity and rapid  absorption  that such
an isolated  cheesy focus may readily fall a prey and  be carried
into the  general  circulation.   First, its molecules are carried  to
the right side  of the heart in constantly enlarging vessels, and,
passing into the pulmonary  circulation, reach smaller peripheral
branches, where they may become lodged or be deposited  in the
lung;  which fact would readily enough account for the predilec-
tion  of  tubercle and  the  development of consumption  in the
lung and equally as much for the pleura, when  we  recall the
fact that the " branches of the pulmonary artery pass directly into
the pleura " (Hyrtl).
   This, too, w7ould give color to the before-mentioned " embolic
theory "  of Waldenburg and others, as  yet, however, but conjec-
ture.
   Again, where such active absorption  is  going on, is it to be 
Q6
CONSUMPTION AND TUBERCULOSIS.
wondered  at  if the whole  of the cheesy  focus be absorbed, so
that on autopsy we find naught but tubercle of the same crop and
degree of development %
    In addition, I merely hint at the difficulty of searching every
nook and corner  of  every tissue of a  cadaver for remnants of a
cheesy parent focus.
    I have dwelt at such length upon the relations  of  pleurisy to
tuberculosis, as its importance cannot be overestimated.
    Lastly, there remains for our consideration the  relation  of
peribronchitic processes to tuberculosis.   Here, so  far as the cir-
rhotic conditions  are concerned, the same  holds good  in the con-
nective tissue of the bronchi, as has  been laid down for that of
the lung parenchyma.   Part of these processes are the basis for
Rindfleisch's elaborate  explanation of the progressive stages of
tuberculization.  In order to avoid confusion  and put things  as
clearly as possible, I will devote part of the chapter on  phthisis
proper to Rindfleisch's deductions. 
RELATION OF TUBERCULOSIS TO SCROFULOSIS.        67
 RELATION  OF  TUBERCULOSIS  TO SCROFULOSIS.

    For the past century there has existed a clinical premonition,
to the effect that " tuberculosis is developed from  scrofulosis."
A mathematical formula with two unknown factors, a deduction
without major or minor premise, it has stood  until, in the last
twenty years, these factors have been investigated and elucidated.
    Pathological anatomists (Virchow, Buhl, Reinhardt) as well
as clinical observers (Niemeyer,  Traube, and others) brought it
into such  shape that distinct questions could be formulated, to be
answered  by experiments on animals.  Villemin (Etudes sur  la
Tuberculose) paved the way to systematic  experimental investiga-
tion, and was followed  by Lebert,  Cohnheim, Langhans, Fraenkel,
Waldenburg, and others.  They have not  succeeded in  closely
defining either tuberculosis or scrofulosis, but have considerably
narrowed  the sphere within which both are permitted to exist.
    You have seen what tubercle is, under what conditions it is
formed, and in connection with what other conditions it is likely
to supervene.  If,  now,  I will endeavor to prescribe and limit
what constitutes scrofulosis, you will  be  prepared to understand
the relation between the two.
    Against noxious agents, which  excite  inflammatory  action,
which surround us and which we meet during life, different indi-
viduals possess very different conceptions.  The greater number
of these noxious materials  may be regarded as  being suspended
in the air; and against their absorption into the human body the
thick epithelial layers  of the skin are the physiological safeguard.
If you now imagine  such an impervious covering somewhat imper-
fectly developed, and  even defective  in  its unbroken continuity,
you are quite near the truth.  Between the epithelial and epider-
mic cells  minute porous canals are found, and  it is  especially in
the Rete  Malpighi that they are  easiest demonstrable.  Nothing
is more likely than that these canaliculi are  of varying width and
more or less  developed in different persons,  and that persons
with open, easily accessible  pores are most prone to oft-repeated
entrance of noxious matter.   Such persons are called " irritable "
and  "easily vulnerable," and are justly supposed to be likely 
68              CONSUMPTION AND TUBERCULOSIS.
victims of scrofulosis.  And we can safely place on  record, as
our first proposition, this dictum:  the predisposition to scrofu-
losis  IS SHOWN BY  THE INCREASED  VULNERABILITY AND GENERAL
IRRITABILITY  OF THE BODY, AND A  TENDENCY  TO REPETITION OF
ORDINARY INFLAMMATORY PROCESSES.
   But, since  not every  irritable person is  scrofulous, but  all
scrofulous persons vulnerable and  irritable, we  must add another
quality to such inflammations.  It is, that inflammations of thu
kind have a great tendency to extend themselves, both as to spaa
and time.
   They are  never sharply defined nor  confined  to one locality
but show  a tendency to spread sluggishly over  surfaces and into
organs, and by their sluggishness to become chronic, to extend
past the ordinary time-table of inflammatory  processes.
   We next find that these processes depend for their extension
upon the absorbents of the plasmatic circulation, upon the lym-
phatic  vessels.  The porous canaliculi  are part of the  lymph-
carrying system, and take part in carrying movable connective-
tissue cells, migrated white blood-corpuscles,  as well as any nox-
ious matter from without.  If we may imagine  the  lymphatics
proper to be  as voluminous in proportion as are the admitting
pores, the explanation for ready7 infection  would be found.  Xo
positive examination has as yet been made  regarding the com-
parative size of lymph-vessels in  different  persons.  Instead, we
recognize a great difference  between the dry connective tissue,
poor in cellular elements, of the adult, and the moist,  juicy con-
nective tissue,  very rich in cells, of  the infant,   Scrofulous chil-
dren present a " pasty," pulpy  appearance.  This is due to the
over-filling of the connective tissue with  nourishing  juices, plas-
matic fluid.  The infant, whose growth is as yet to follow, is natu-
rally supplied with an abundant plasmatic circulation, with larger
calibre of vessel.  Its growth is dependent upon rapid assimila-
tion and equally rapid retrograde absorption.   Hence  the readi-
ness with which noxious material  is absorbed in childhood.  Let
the noxious matter enter the dilated canaliculi in force, and the
lymphatic stream will quickly carry it  along to  the neighboring
glands.
  Thus  we  have  our. second  depot,  and  may formulate this
fact   as follows:  inflammation  of lymphatic  glands is the
SECOND IMMEDIATE STAGE OF  SCROFULOUS  PROCESSES.  At best all 
           RELATION OF TUBERCULOSIS TO SCROFULOSIS.         69

inflammations of lymphatics run a more or less chronic course, as
you will remember when thinking of syphilitic and other infec-
tions.  Recall to mind what I have  twice stated in previous let-
ters, that slow inflammatory processes do not tend to acute oedema,
suppuration, and destruction, but rather to the formation  of con-
nective tissue.   An  exception to this rule has been claimed  by
Virchow to exist in the formation of minute quantities of pus in
a lymphatic vessel previous to its entrance into a gland (vas effer-
ens), where the fibrillary connective  tissue is almost wanting and
cells abound.   Billroth, and  after him Hueter, holds to the be-
lief that cells and lymph or plasma are the only constituents to
enter the gland, and that at no time did the cells form part of an
abscess.
   The next step in the fate of the infiltration of the gland is
the caseous metamorphosis of  the cells.   This, for the present,
ends the cy7cle of events.  The beginning is a local inflammation
(pharyngitis, rhinitis, eczema) correctly enough called scrofulous
inflammation, if you will but keep well in mind that this  inflam-
mation in its etiology is an ordinary  inflammation excited  by the
same ordinary noxae as in common inflammation. But the differ-
ence is that they run their course in tissues  so constructed as to
permit of the inflammation becoming chronic, and of prompt
conveyance of the noxious 'matter into lymphatic glawls.
   Our third  station, then, and  for a time a  halting-point in the
course of scrofula, is this : scrofula culminates in  cheesy infil-
tration OF LYMPHATIC GLANDS.
   With this present ending of local  manifestations begins the
danger for the whole  organism.  To  understand this,  let me
relate  the  possible ultimate  fate of these cheesy degenerations.
Resolution is a bare possibility, but not probability.   The  mass is
cut off from further connection with absorbent lymphatics, and
thus might  be looked upon as  dead, were it  not for the indirect
nourishment it receives from the  circulation.  Complete  drying
up of the mortar-like mass of cells and encapsulation are possible,
but not likely sufficient to be a permanent protecting investment.
And why ? Because the same locality (skin or mucous mem-
brane) which permitted of the passage of the  infection formerly,
will  be likely to do so again, and  get into sufficiently close con-
tact with the cheesy mass to light  up a subacute suppuration in
the caseous mass.  Such pus is mostly found in the most super- 
70
CONSUMPTION AND TUBERCULOSIS.
ficial layers of the gland—an additional proof that the irritation
culminating in suppuration came from without.
    Self-infection in the course of general or local diseases may
bring toxic material within reach of the cheesy mass.   But this
need  not be dwelt upon, inasmuch as  all this will  be compre-
hended in the explanation I  am now about  to  make, of how
tuberculosis springs from scrofulosis.
    Not only does scrofulosis  beget in many this general disposi-
tion to inflammation running the  course described, but, like other
diseases, furnishes the inoculating virus for miliary tubercle.  In
the experiments on  animals, where the infecting  detritus comes
from  without,  the blood circulation must be looked  upon as
means of transportation, and  the  deposits observed in connection
therewith must have their origin in the small arteries or capil-
laries.
    In the formation of tubercle in man, it is most frequently the
lymph tract which takes up  the material  and carries  it on to
general distribution.
    In accord with this, we  surely7 enough do find tubercular for-
mation in the immediate  vicinity of cheesy deposits, along the
track of lymphatics  and in lymphatic glands, into which they
pass.
    In what manner a general infection  comes about, and acute
miliary tubercle is developed, is  not so easy to say.  Probably
something does finally pass into the blood ; but what  takes place
here,  whether merely physical or  also chemical changes occur, or
both,  is at present not settled.
    I have before touched on Rindfleisch's opinion that tubercu-
losis,  and for that matter consumption in any form, is on a scrof-
ulous basis, and will give  an  outline of  his views when  finally
reviewing phthisis pulmonalis.
    What I will quote here is part of what he says in regard to
the existing relation:  " The final disintegration of a scrofulous
infiltration is effected by chemical metamorphosis, which, aside
from  very small fat  drops  and albuminous granules, which can
be  seen  by the microscope, furnishes an indefinite quantity of
soluble  substances not visible  microscopically.  All these sub-
stances, however, not only may, but must be reabsorbed.   When
we see that they are just scrofulous persons who are the favorite
victims of tuberculosis;  that we  know no such thino- as tubercu- 
           RELATION OF TUBERCULOSIS TO SCROFULOSIS.        71

losis of non-scrofulous individuals ; when we see that all  the
various pictures of disease  constituting  tubercular phthisis  are
composed of scrofulo-inflammatory elements  on  the one hand,
and tubercle formation on the other;  when we can correctly say
that scrofulous individuals  need only to have an inflammation to
be at once in danger of tuberculosis,—every7 one will look for the
reason of these facts in  the peculiar course and termination of
the primary7 inflammation, which, in its  sluggish  cheesy infiltra-
tions  and purulent secretions of mucous membranes, generates
the poison  itself, which, taken into the  juicy parts of the body,
produce tuberculosis.  This sentence  contains all we need to
know for  the comprehension of the intimate  relations between
scrofulosis and tuberculosis."
    We may then elucidate one of  the final terminations of scrof-
ulous  products, as well as  clinch the  relation  of scrofula to
tuberculosis, by7 the following formula :
    The lingering cheesy infiltrations in lymph-glands and the
purulent secretions of mucous membranes  generate a virus,
the exact  nature of which we do  not know, which, carried
along by the efferent lymphatics, deposits as tubercle.
    How does the virus " deposit" as tubercle \
    This seems to be the proper place for referring once more to
the embolic theory  of distribution.   Thus far it has not  been
proven, but from all  observations it is likely that the granular
detritus is carried through the right side of  the heart into the
lungs  and into the  most minute vessels;  that  at length  they
become clogged  in  some  remote vessel as  emboli; that white
blood-corpuscles migrate from the blood to the surrounding tissue,
and thus miliary tubercle is formed.
    This would seem to call for emboli of respectable dimensions
to fit  the  lumen  of  capillary vessels.   The lesser granules may
pass on, partly to  the  pleura, and stagnate  only where capillary
circulation happens to  be a trifle sluggish, or, for aught we know,
they may migrate and become imbedded  in connective tissue.
   Miliary  tuberculosis would then be counted  as an embolic
disease, a "pyaemia with multiple inflammatory centres.
    Indeed,  the arranging of tubercle along the walls of capil-
laries,  most frequently at a bend  in  their course (Billroth), and
lastly the presence of one or two stellated giant-cells in the centre
of tubercle (Langhans), all point to the embolic origin of tubercle. 
 72             CONSUMPTION AND  TUBERCULOSIS.

    Of  course, in  order  to  be carried along in the  circulation,
 cheesy detritus must first be absorbed by the lymphatics ;  and this
 too is in accord with clinical observation, which teaches that sup-
 purative disintegration of the cheesy lymphatic gland as  a rule
 precedes the development of tubercle.   We have thus a reabsorp-
 tion of a cheesy mass ; and  while we may not conclude to believe,
 with Rindfleisch, that  its  disintegrated  constituents "must  be
 absorbed," the possibility and probability of a total absorption is
 given.
   As a final proposition, let  me say: not detritus  of caseous
 LYMPH-GLANDS  CARRIED  INTO THE CIRCULATION ALONE  MARKS THE
 RELATION BETWEEN SCROFULA AND TUBERCULOSIS.   LOCAL SCROFU-
 LOUS INFLAMMATIONS GIVE RISE TO THE  FORMATION OF TUBERCLE IS
 the granulating surface on the spot.  The most lucid example
 of this  local development  is found in synovitis  fungosa, where
 Koester demonstrated tubercle in the granulation tissue of a sup-
 purating inflammation of the joint.
   This  is in accord with what I have endeavored to show you
 when speaking of the formation of tubercle after pleurisy.  To
 this I refer you, and will add that another example of local tuber-
 cular infection, in which we are interested, is its  occurrence  in
 caseous pneumonia, where  miliary tubercle follows into the peri-
phery of the  pneumonic cheesy mass.   All these facts have been
dwelt upon when speaking of local  and general tuberculosis. 
PHTHISIS PULMONALIS.
73
                 PHTHISIS PULMONALIS.

   The term " consumption " comprises  all progressive destruc-
tive processes of the respiratory organs, which do not occur im-
mediately in the  train of acute inflammation.  It is accompanied
by more or less rapid  wasting and reduction in  weight of the
body, and one of  these twTo factors is likely to predominate.  We
may say that the more rapidly7 phthisis runs its course, the more
rapid is the-destruction  of  tissue;  while the slower the progress,
the stronger will it be marked by wasting and reduction of the
body7.
   Phthisis is the  collective expression, the highest potency
of  a number  of acute inflammatory processes which have
failed  to run their prescribed course.
   The termination of such processes is when, having passed into
the  chronic condition, their  products  become  caseous (cheesy
pneumonia), while the peripheral connective tissue endeavors by
proliferation to form a capsule for the cheesy mass, and, finally,
by contraction and almost total  exclusion of all nutritive mate-
rial, to  encapsulate and render it harmless.
   Where this is not accomplished, the cheesy mass may7 under-
go a subacute suppurative process; tubercle  may be formed on
the spot; and the active  neighboring lymphatics  absorb and carry
to other parts the granular matter and tubercle.
   What agency is first  concerned in the formation of tubercle
or the mortar-like, cheesy mass, we do not know  to-day, anymore
than formerly.
   Consumption, then, may be said to begin where cheesy degen-
erations in the lung are  lighted up to renewed activity.
   Referrino- again to the factors of destruction and wasting, we
may formulate the progressive processes into two principal heads,
with a few subdivisions:
   1st.  Where a  rapid course tells of the equally rapid  destruc-
tion of the respiratory organs, where, in short, the disease may be
said to be acute.
   a. Acute miliary tuberculosis,  disseminated throughout the
lung. 
74
CONSUMPTION AND TUBERCULOSIS.
     b. Inflammatory conditions, which do not lead to sudden and
 immediate death, as do gangrene  and  purulent infiltration.
 Under this head belong acute pneumonias and purulent peri-
 bronchitis.
     2d. Where a slow course  tells of equally slow destruction of
 the tissue and attempts of nature at repair.
     a. Caseous pneumonia (cheesy remnants of inflammatory pro-
 cesses, both lobar from pneumonia and lobular).
     b. Chronic interstitial pneumonia (cirrhosis, with the forma-
 tion of bronchiectatic cavities) as a one-sided, independent disease.
     c. Local  proliferation of connective  tissue  (peribronchitis
 nodosa),  or in  the  periphery of cheesy masses, endeavoring to
 form a capsule  around it.
     3d. The combination of two or more of the above conditions.
 We  find  acute  tuberculosis supervening upon the  results of
 acute inflammatory  conditions,  with  cheesy  pneumonia, with
 chronic  interstitial pneumonia, and, vice versa, see an infiltration
 of tubercle becoming cheesy, always beginning in the centre of
 its nodules, and the  development  of connective tissue  in the
 vicinity and its subsequent contraction.   The tubercular and in-
 flammatory7 elements are mixed, and pursue their course together,
 unfortunately7 rarely towards repair, but towards destruction.
    I have before intimated that several observers have recently
 fallen back  upon  the  old   tubercular  theory, not with  all its
 defects, but merely endeavoring to demonstrate that all cases of
 consumption  are tubercular, on a scrofulous basis, and that in-
 flammatory conditions only7  occurred as accompanying elements.
 Rindfleisch is the  chief  exponent of this theory; and  in giving
 an outline  of his views,  I will redeem my promise of the fore-
 going chapters:
    In scrofulous products, Ave note especially their great tendency
 to cell-development, and an equally great one to disintegration of
 this same hyperplastic cellular element.
    White blood-corpuscles,   which  in  normal  individuals pass
 from vessels of  an inflamed  tract to an adjoining surface and
 into lymphatics or lymph-glands, or else collect in  abscesses, will
 in scrofulous  persons become larger  on  their way throuo-h  the
 connective tissue, by becoming impregnated with  albuminous
substances, which substances  are the direct cause of their slow
degeneration. 
PHTHISIS PULMONALIS.
75
   In scrofulous catarrhs we note an abundance  of  cells, and the
thick, quickly-drying character of the catarrhal secretions.  Cells
likewise abound in the submucous tissue, from where they wan-
der to the surface, become granular, and at the same time fattily
degenerate, or else they pass into lymphatic vessels.  Their de-
tritus becomes mixed with lymph, which flows  off from the in-
flamed tract into the lymphatics.  Whether or not we here have
the formation and  transportation of  tubercle virus, we do not
know.
    Tuberculization of scrofulous persons.   Final disinte^ra-
tion of a  scrofulous  infiltration is accomplished by chemical met-
amorphosis,  furnishing minute  fat-globules  and   albuminous
granules, together with an  indefinite quantity of  soluble sub-
stances, the  latter  not visible  microscopically.  All these sub-
stances not only may be, but must be reabsorbed.   Thus scrofu-
losis, with its  lingering cheesy infiltrations and purulent  secre-
tions of the mucous  membranes, generates its own poison, which,
taken up  into the  juices of the body, develops tubercle.
   Those  who  look  upon tuberculosis  as a purely  independent
acute infectious disease, should remember that the tubercle virus
in question  is self-manufactured and the infection  a self-infec-
tion.   Nor has this virus ever been proved capable of inoculation
upon perfectly healthy persons.  Rindfleisch's views may7 therefore
be thus summarized :
    Tuberculosis hardly ever occurs except in  scrofulous persons.
    Tubercular phthisis is nothing but a combination of scrofulous
inflammation and  tubercle.
    In scrofulous persons any7 inflammation brings with it the risk
of tuberculosis.
    The well-known  cheesy intumescence of lymphatic glands has
always been  looked  upon as the chief product of scrofula.   And
indeed the lymphatic glands are the anatomical centre of scrofu-
lous  inflammation  and hyperplasia.  Scrofulous  glands  are
always to be looked  upon as tuberculous glands.  The swelling
and obstruction of the efferent  lymphatic may cause the disease
to remain localized for a time in the gland.
   The course pursued by scrofulo-tuberculous  troubles justifies
a division into primary, secondary, and tertiary tuberculosis, if
you will only not  apply these appellations too strictly, but only
as a o-eneralization.  In accordance with the various  " depots," of 
76
CONSUMPTION AND TUBERCULOSIS.
 which I spoke in discussing the relation of scrofulosis to tubercu
 losis, we may divide the development of  tubercle  into three
 stages also:
    By primary tuberculosis we comprehend local affections of
 the various organs of the body, which happen to be affected by
 scrofulous inflammation and development of tubercular elements
 on the spot.
    Secondary tuberculosis designates the tubercular infiltration
 of lymphatic glands.
   In tertiary tuberculosis, finally, we have the dissemination of
 tubercle throughout the organism, affecting organs not primarily
 diseased, as, for instance, the lungs, liver, kidneys, and the serous
 membranes.
   The stages, in short, are:  strictly local, whether on surface
 (skin and mucous membrane)  or in internal organs;  lymphatic
 glands; distribution throughout the whole organism.

               BEGINNING OF LUNG TROUBLE.

                  I.— Chronic Tuberculosis.

   An old maxim teaches that a lingering  catarrh gives rise to
consumption.   The truth of this is: when a case of  catarrh of
the apex  is diagnosticated, an autopsy would,  in  addition to
catarrh,  reveal genuine tubercle  upon the acini  of the lung
parenchyma   supplied by  the  affected  bronchi.  Rindfleisch
believes  that the catarrh is the earlier,  tuberculosis  the later
manifestation.  He imagines the tubercle  virus to be contained
in the cellular catarrhal  secretion of anaemic, scrofulous indi-
 viduals.  You know that other authorities hold  that the primary
presence of tubercle incites to catarrhal inflammation.   As usual
 in such  questions, the truth is most likely  in the middle, that is,
 both cases are possible, and  the history of  the  case should solve
 the question in each individual case.
   The points at  which  the  smallest bronchioles become con-
 tinuous with the acini of the  lungs are the situation of the  first
 eruption of veritable tubercle.
   1st. Tuberculous  infiltration  of  all  edges and  projec-
 tions, which exist at this point of junction, is the first pathologi-
 cal change, and leads  to the formation of circumscribed white 
PHTHISIS PULMONALIS.
77
nodules in the connective tissue.   This corresponds to Laennec's
tubercle-granulation, and is the anatomical nucleus of the disease.
With its softening particles in the centre  (if any exist), a broad
zone of cheesy infiltration and peripherally a zone of recent large
cells, it represents an infiltration of the  connective tissue of the
lung, bloodless, incapable of suppuration, reabsorption, or organi-
zation, but only of degeneration.
    Initial hemoptysis and pleurisy.  Before considering the
further progressive mission of the  lung trouble, the above  condi-
tions must again be touched upon, because it is at this stage that
their occurrence furnishes a clew for diagnosis.
    The minutest branches of the pulmonary7 artery take part in
the tubercular invasion.  A  pushing on of perivascular hyper-
plasia into the inner coats of the artery takes place, and we have a
tuberculous  degeneration  of the  middle coat as well as of the
intima.  A sudden tension by muscular action, or temporary over-
filling of  the artery, may lead to rupture and  hemorrhage.  I
have, in a previous chapter,  said that haemoptysis is likely never
the beginning of lung trouble, but the result of conditions pre-
pared some  time  beforehand.   No satisfactory dissections have
been made immediately following a haemoptysis.
    Pleurisy, you are aware, is  an accompaniment of all  stages
of consumption.   The adhesive form is  the rule.  The relations
between tuberculosis  and pleurisy have been  discussed in the
chapter on " Tuberculosis."  Rindfleisch states that while tuber-
cular pleuritis is not rare, the pleurae of a consumptive  patient
rarely shows tubercle.  On the other hand, he draws attention to
the great wealth of blood and  of  vessels in all its products.   I
have told you of the passage of small branches from the pulmonary
artery into the  pleura direct.  This would make the pleura a
sort of reservoir in case of stagnation in the lung, while the pres-
ence of a large  quantity  of blood of sluggish movement would
account for the uncommon development  of  new connective tis-
sue which takes place in the pleura.
    2d.  Secmd  Depot of  Consumption.—-Caseous   broncho-
pneumonia.  From the tubercle-granule there arises, after a time,
the larger cheesy mass,  formerly known as crude  or yellow
tubercle.   The cheesy  mass passes  from the above-mentioned
bronchial endings .into the smallest bronchi and further on into
all the branches, the shape of the  cheesy  mass corresponding to 
 7S             CONSUMPTION  AND TUBERCULOSIS.

 the course of  the involved bronchi up to bronchi with cartilage
 rings, where its progress ceases.
    From this on, the  further  progress may be looked  upon as
 consisting of three factors, each more or less independent:
    1st. Tuberculous ulceration of bronchial mucous membrane.
    2d.  A nodular tuberculous peribronchitis.
    3d.  Scrofulous  cheesy  pneumonia,  so-called  desquamative
 pneumonia.
    Observe that Rindfleisch  thus  includes all cheesy and cir-
 rhotic processes, which bw others have partly been accredited to
 remnants of acute inflammation and  by Buhl  to the products of
 desquamative  pneumonia and  connective tissue hyperplasia, and
 gives the parentage to tubercle alone.
    Third Depot.—a. Tuberculous ulcers of  mucous membrane
 have  a tendency to spread towards the periphery as well as into
 the depths of tissue.   In the periphery we have the same nodules
 of tubercular infiltration which  compose the  primary tubercle.
 In the  depths we find the eruption  of  large miliary tubercle at
 the bottom of the ulcer and at a little distance in the deeper strata
 of the  bronchial walls.  They  are  in  close  relation with the
lymphatics, being in the walls of such a vessel, or they may sur-
round the lumen of  such lymph-vessels as  lead  downward  into
the submucous and peribronchial connective tissue.
   b.  Peribronchial infiltration  consists of the  propagation
of tubercle in the peribronchial lymphatics.   Almost one-third
of an  infiltration consists of aggregated tubercle, the other two-
thirds of connective tissue in  the process of  contraction.   From
this second depot of  peribronchial invasion there is,  again, direct
continuity  between it and the third factor, cheesy7 broncho-pneu-
monia, or exquisitely7 scrofulous desquamative pneumonia.
   c.  Desquamative pneumonia. The desquamation and change
in form of  alveolar epithelium, which Buhl thinks  of sufficient
importance to present as an independent picture of disease, and
which by others  is included in the catarrhal form, is in reality a
stereotyped accident of most disturbances which befall the paren-
chyma of the lung,  and merely act as an accompaniment to the
more  important changes in the connective tissue.   This is infil-
trated with an enormous quantity of cells, so that connective
tissue, elastic fibre, and  vessels can no longer be seen.  Compres-
sion of the capillaries next begets bloodlessness, leading of course 
PHTHISIS PULMONALIS.
79
to lack or nearly total  absence of nutrition  from the anaemic
parts, and to cheesy degeneration.
    Before caseous metamorphosis becomes complete, contraction
of the accompanying  connective  tissue takes place.  The degree
to which  desquamation  of alveolar epithelium supervenes,  and
the independence of  its occurrence in connection with peribron-
chial infiltrations, varies somewhat, and by its  course justifies us
in distinguishing between a chronic and a more acute progress of
consumption.
    Fourth Depot.—Common chronic form of consumption may
be said to occur where the scrofulous infiltration of peribronchial
and perivascular connective tissue keeps on continuously to in-
vade the adjacent connective tissue .of the parenchyma, the  con-
nective tissue most  intimately connected with  the lung tissue
proper, and bearing the same relation to  the peribronchial tissue
from whence comes the invasion as does the connective tissue of
the muscles bear to the subcutaneous layers.  The desquamative
pneumonia here appears the least  independent, serving only to
assist in augmenting the fibro-cheesy mass,  and by7 uniting with
other parts similarly  infiltrated.
    The difference in the  progress of peribronchitic infiltration
and the  desquamative process is that  the  former passes upward
from bronchiole to bronchus, while the latter's invasion is lateral
into the parenchyma.  What now occurs, when the lumen of a
bronchiole is thus occluded, is that atelectasis  supervenes.  A
corresponding portion of the lung will contract by its own elasti-
city to its smallest possible compass, the air within it disappears,
and is replaced  by a certain amount of serum and largely by
capillary nets from its  own walls.  One would think  that here
local death would supervene;  but, on the contrary, the  next  step
is a  passive hyperaemia, by which the atelectatic part becomes
oedematous.   Serum  is  effused from  the dilated  vessels filling
the alveoli, and distending  them.   By gradual thickening of the
serum, the infiltration may assume  a gelatinous appearance.  To
this is added fatty degeneration of the alveolar epithelium.
   Thus,  in cases where the lesser  and most minute  branches of
the bronchial tree have fallen a prey to tuberculosis, we have in
the affected lung circumscribed  sections, with  atelectasis, invete-
rate  and more recent oedema, and fatty degeneration of the epithe-
lium. 
80
CONSUMPTION AND TUBERCULOSIS.
    A different picture will  present  itself where a  somewhat
 reduced but still open circulation encourages rather than retards
 the  development  of  the desquamative process, and  the  latter
 assumes more independence.   This may occur to  such a degree
 as to involve an entire lobe in a diffused inflammation  ; but this
 lobe must be one previously invaded by tuberculosis.
    Oftenest it occurs as a fresh onslaught, where cavities already
 exist at the apex.
    True to his scrofulous theory, Rindfleisch goes on to  say that-
    1st. The relation of desquamative  pneumonia to tuberculosis
 proves it to be of scrofulous parentage likewise ;  and,
    2d. Its independent occurrence where tubercle  already  exists
stamps  it in a  measure as an independent disease, such as Buhl
 claims it to be.
    But, according to these two factors, desquamative pneumonia
is a specific scrofulous  inflammation, and as such to be classed
with all scrofulous catarrhs—that is, common inflammation  in an
individual prone to the  development of cheesy material.
  Fifth  Depot.—Formation of cavities.   The term  "cavity"
should be restricted to all holes of larger  size which originated
in necrosis and ulceration of lung parenelryma ; " bronchiectasis,"
on the other hand, denoting  the distention of previously existing
hollow tubes.  In  bronchiectatic conditions the pressure of air,
failing to impart itself to the occluded  parenchyma  beyond,
exerts its power on the bronchial tubes.  The resisting  power of
the lesser bronchi  is none of the greatest, and many7 a bronchiec-
tasia can compete as to  size  with large cavities.
   The  earliest stage  of  formation  of true cavities may be
said to exist in the little spots of  softening, which we  occasion-
ally find in the interior  of tubercle granula, and which  spots cor-
respond to  the former lumina of  the  alveolar passages.  In the
further progress  of disease and the formation of cheesy  nodes
the lesser  bronchi likewise represent the plan of the future
cavity.
    The  softening masses  afterwards  empty into  the cavity,
through the mechanism of respiration.  The wall of  the  bron-
chus, inflamed, infiltrated,  and hyperplastic, is rendered  more
yielding, less able to withstand extensile traction by the muscles
of respiration than the surrounding  parenchyma.  Hence  the
 bronchus dilates and the parenchyma contracts. 
PHTHISIS PULMONALIS.
81
    In the process  of emptying of the contents of a cavity, the
forces of  inspiration reach the periphery of the softened mass.
Thus cavities are formed  by the air penetrating into softened
material and by creating a hollow space in forcing  its discharge,
and not by the emptying of cavity contents into a bronchus.
    Cavities are to be regarded as spaces filled with air and acted
upon by the forces  of inspiration.  The enlargement of a cavity
is finally checked  by reaching  the pleura, which becomes thick-
ened  and forms a definite limit.
    Other modes of enlargement are the  junction of two cavities
and the further drawing  in  of  dilated bronchi into the walls of
the cavity.
    Mixed and rare varieties of consumption.  We  have seen
ere this that the post-mortem appearances in consumption are
exceedingly varied, all processes sometimes  being represented in
different  stages  of  development  aud  different as  to relative
quantity.   We may find tubercle-granulation and peribronchitis,
gelatinous infiltration (as remnant of catarrhal products) and
cheesy pneumonia,  catarrh of the bronchi, atelectasis, bronchiec-
tasis,  miliary tubercle and tuberculous  ulceration,  pleuritis and
hyperplasia of connective tissue.
    Yet some one process will be found to predominate, and the
order of events may  be found out with the  aid of  the history of
the case.
    Still  Rindfleisch  and others draw attention to a few  forms
which deserve special mention.
   Of such  is the  uncommon form  in  which phthisis presents
itself  in children under five years of age.  As in  their physio-
logical condition, so in pathological processes, there is an increased
tendency to shedding of epithelium ;  in  the course of inflamma-
tions we find a predominance of desquamated  epithelium  in the
products.   This is  true of catarrhal pneumonia (capillary bron-
chitis), and all the  more  so in phthisis, which  is a compound of
scrofula and tuberculosis.  Each individual tubercle, indeed, is
found to be surrounded by a zone of desquamative pneumonia.
   In the adult, one of the modifications^ phthisis consists in the
prominent participation of the  lymphatic system.  The fact has
been  dwelt upon  before  that the lymph-vessels are a favorite
site for tubercle ; and I refer you to the chapter on Acute Inter-
stitial  Pneumonia for the facts  bearing upon  the  inflammatory
           6 
82
CONSUMPTION AND 'I UBERCULOSIS.
 part of it.  Rindfleisch  believes that this form represents syphi-
 litic tuberculosis.  It is found in the lower lobes, together with
 hyperplasia of  connective  tissue and cirrhosis {vide  chapter on
 Acute Interstitial Pneumonia), and the tubercular eruption of the
 lymphatics is likewise accompanied by the slow  desquamative
 process.

                   II.—Acute Tuberculosis.

    Referring back to  the beginning of Rindfleisch's propositions,
 we distinguished three stages : 1st. The local scrof ulo-tubercular
 primary affection.   2d.  Tuberculosis of the lymphatic  glands.
 3d.  General miliary tuberculosis.
    General miliary tubercle  is pre-eminently a  constitutional
 disease, which, in the number, size, and  distribution of the erupt-
 ing  tubercle, finds only an  imperfect expression of itself.  This
 is owing to the rapidity of its course, giving the successive tuber-
 cular eruptions barely time  to degenerate before death ensues.
    Rindfleisch consistently  looks upon this disseminated miliary
 tubercle  as  a circumscribed centre of scrofulous inflammatory
infiltration, and says that  neither giant-cells, nor the fact of
tubercle  being bound to  the minutest ramifications of the pulmo-
nary7 artery7, can change  its  character as a  minute  inflammatory
product; while  in scrofulous persons it  represents a small centre
of scrofulous inflammation.
    Thus far Rindfleisch.  I have given  his views at some length,
 as representing as nearly7 as possible the views of several authors
 who hold that consumption can only spring from  inflammatory
 products of scrofulous persons ; that tubercle is  one of these prod-
 ucts; and, finally,  that  consumption  exists only as "tubercular
 phthisis."
   My next endeavor will be  to condense the views of  such au-
thors as look upon consumption as a primarily chronic inflam-
matory PROCESS, AS WELL AS  THE FINAL  DESTRUCTIVE  PROGRESS
OF CHEESY REMNANTS  FROM INFLAMMATIONS OF THE  LUNG,  which
have gone before and run their course, with  more or less accom-
panying cirrhotic processes, and the occurrence of tubercle, either
secondarily or more rarely as an entirely independent disease. 
PHTHISIS PULMONALIS.
83
   This  review will represent the opinions of leading patholo-
gists, several of whom (Ruehle, Juergensen,  Fraenkel, Walden-
burg) have been quoted before.
   Phthisis is anatomically a chronic inflammatory disease, with
intercurrent simple forms of inflammation, which latter may heal
by cicatrization.  Such limitation and local healing is effected by
simple inflammation in the surrounding parts.
   For the sake of  a thorough  understanding of our subject, I
find  it necessary to dwell briefly on the  etiology of phthisis.
Time and  space will not permit  of  mentioning  every  possible
cause; a few salient points only will be noted.
   Everything which  tends  to diminish quality and quantity of
the  blood, which  depresses  the nervous system, all agencies by
which the  balance between waste  and supply is  destroyed, will
render an individual what is commonly called " sickly."  Now
when  the  circulation  is disturbed, whereby nutrition  is lowered
and  peripheral circulation becomes insufficient, or when, through
central or peripheral  agencies,  motion or sensation is impaired
for more than  a limited period, we may suppose  the afflicted in-
dividual  to be very vulnerable.   General vulnerability  (as you
will remember from the chapter on Scrofulosis) is closely allied to
scrofulosis, not by covering all the characteristics of the same,
but  because it may be the starting-point for scrofulous inflamma-
tion, which in an adult may not have occurred since infancy7.
    Imagine, for example, a disturbance of circulation or innerva-
tion, caused by a  gastric catarrh, to remain longer than they are
found as a rule, and we have general vulnerability, which in turn
gives rise to oft-repeated and dragging bronchial catarrhs or other
inflammations  characterized by active cell-proliferation.  From
scrofulosis to the development of tubercle is but a step.
    I have touched  upon  this cycle of  events in order  to once
more impress upon  you the importance of bronchial catarrhs as
well as inflammations of the lungs.   We have, at one end of  our
string, inflammation (generally catarrhal) and  localized cheesy
centres,  which may have lain  dormant for years,  especially7 in
lymphatic glands, and, at the other end, consumption and tuber-
culosis.  Now  whether in any  given  case the catarrh, as most
immediate product of general vulnerability, a previously  existing
cheesy centre, or a recently developed local tuberculosis,  was the
first to be in the field, is so difficult of demonstration as readily 
84
CONSUMPTION AND TUBERCULOSIS.
 to account for all differences of opinion on that point  as well as
 the absence of proper statistics.
    In this connection we should not omit to remember one cause,
 if not the chief one, of  disturbances of circulation  in  the  lung,
 For twenty years Dr. Brehmer, of the Sanitarium for Consump.
 tives  at Goerbersdorf, has  held that the phthisical habitus was
 characterized by  smallness and flaccidity  of the heart.   This
 theory was first put forth by Rokitansky in connection with other
 appearances.  Brehmer, however,  insisted upon its importance,
 and looked upon it as the chief etiological force of Consumption.
 Of late, however, he has become convinced  that he had overesti-
 mated the importance as well as the frequent occurrence of  small
 hearts.
   Any disturbance of  the  equilibrium  between waste and sup-
 ply, as you have  seen, leads to conditions favorable to that final
 collective expression of all chronic nutritive changes, to consump-
 tion.   If the waste be  too great from any cause, the blood will
 suffer in quality as well as quantity, and among the organs to suf-
 fer by this, and to become bloodless and flabby7, is the heart. The
 heart, whose contractive duties require constant and sufficient
 nutriment  to keep up  its  propulsive powers.  Given  a person
 with a naturally small heart, it may not require any great length
 of time to weaken its power of propulsion.  In  the lungs the  re-
sult  of excessive waste from any cause wrould be seen in  the
occurrence of anaemia  of its  tissue and consequent  loss of  its
elasticity,  thus giving rise  to that most important factor in con-
sumption, a paralytic lung.
   If the supply  be excessive, the primary result will be a clog-
ging  up in the lymphatic system, and  as a natural consequence
followed by stagnation in the  circulation of the blood; and
 nowhere more so than in the lung, whose capacity for blood is so
 much greater than that  of other organs.   Here, again, the effects
will be found to consist of loss of elasticity7, of dilatation (emphy-
 sema, bronchiectasis), and what is of more importance, to deposits
 (infiltrations, tubercle).   In the heart again, stagnation  acting
 backwards upon it will  not necessarily  produce hypertrophy and
 more  propulsive power, though the first effect may be such;  but
 eventually flabbiness must result.
   Taking  these  causes together, we  may briefly sum up  thus:
 Abnormal, smallness and flabbiness of  the  heart,  whetheb 
PHTHISIS PULMONALIS.
85
CONGENITAL OR AS A RESULT OF PERIPHERAL DISTURBANCES REACTING
UPON IT, IS A CONDITION FROM THE  EXISTENCE OF WHICH WE DATE
SUCH LESSENED  AND RETARDED  NUTRITIVE CHANGES LN THE LUNGS,
CAUSED  BY INSUFFICIENT SUPPLY OF BLOOD,  AND ITS CONSEQUENT
STAGNATION  FROM LACK OF CENTRAL PROPULSION AND PERIPHERAL
ELASTICITY, AS WILL MANIFEST THEMSELVES BY PRODUCTS WHICH WE
CALL RESPECTIVELY : HYPERPLASIA OF CONNECTIVE TISSUE, CHEESY
DEGENERATIONS, AND TUBERCLE.
    I regret that my plan will not permit me to go again over the
ground of the relations of various inflammations to consumption.
As it is, I refer you to each  individual  chapter, and only repeat
that, as a general thing, this dogma is still entertained:
    Inflammatory processes  of the lung which fail to come to
a  rapid resolution and which linger for  more than a very
limited period, elaborate products, which through caseation
lead to phthisis.
    You are aware that nearly all cases of incipient phthisis begin
at the apex, and oftenest indeed without  the previous occurrence
of an acute lung: trouble.   You hear and read of " catarrh of the
apex," and want to know what pathological conditions transpire
under that name.   In  the first pages of  this chapter I attempted
to lay out a schedule.   An additional one might be made out on
the general basis of etiology:
    1st. Those affections which  are the sequel to previous acute
lung trouble.
    2d.  Where the indirect cause  is general vulnerability follow-
ing previous disease other than  lung trouble, frequently mani-
fested  for a time by nothing but a gastric catarrh as  indication
of a disturbance of nutritive  changes.  As soon as rales can be
heard  at the apex, we are confronted by the  question which of
the  three  following conditions, or their composition, had first
existence:
    Local proliferation of connective tissue and induration.  (See
chapter on Chronic Interstitial Pneumonia.)
    Caseous  deposit, either in a  scrofulous gland from infancy
or  other  cheesy remnants,  which collectively we call caseous
pneumonia.
    Local tuberculosis, either in a  cheesy centre or independently,
havino-  originated from some purulent surface ; as yet, however,
strictly localized. 
86
CONSUMPTION AND TUBERCULOSIS.
    Two or all three  of  these conditions combined.  Such local
 inhabitants may,  at  first, produce  no  appreciable  symptoms.
 Catarrh of the lesser bronchi supervenes, and  now the pro-
 cess can be diagnosticated.  Observe that I make the catarrh a
 secondary process, and remember that, on the other hand, there
 is no positive proof that a bronchial  catarrh may not spread to
 the  parenchyma  and create  catarrhal pneumonia.  By far  the
 majority of catarrhs, however, does nothing of the kind.
    The further progress  of the " catarrh " is marked by copious
 desquamation of epithelium, which, together with the tough and
 equally copious secretion, forms the products,  which undergo
 cheesy degeneration and  destruction.   I lay stress upon " desqua-
 mation," as this forms a connecting link with Buhl's theory of
 desquamative pneumonia, which he insists begins at the apex, in
 contradistinction  to catarrhal pneumonia, which  begins at  the
 base.  Remember, also, that secretion  and desquamation  are
 equally as well dwelt  upon by other  authors in  connection with
 apex and other catarrhs ; but they do not acknowledge the neces-
 sity of having a separate designation  for such processes.
    What has just been said of  " catarrh of the apex " is intimately
 associated with what now remains for me to say of the pathology
 of phthisis.
   If we w7ere permitted to use words in  the ordinary meaning as
technical  terms, we could  safely say  that consumption was but
a termination of various diseases of the respiratory organs.
   Once any process  has passed its  initial stages, it  rarely re-
mains unmixed with other processes, one often passing  into and
becoming lost in the other.  Thus it  has been  my endeavor  to
present to you the chief types of chronic  lung trouble, and to
constantly remind  you that they very frequently combine in  the
same individual or follow upon one another.
    That the whole field may appear quite clear to you, I will not
condense the various processes  in any further schedule, but once
more explain the whole  range of consumptive  troubles in the
plainest terms possible.  Repetition is, of course,  unavoidable.
    Beginning with acute  miliary tuberculosis, we find in it  a
special affection, an independent infectious disease, which runs a
rapid course,  does not undergo various stages of progressive de- 
PHTHISIS PULMONALIS.
87
Btruction, nor  does it kill  by consumption.   It differs from
other acute infectious diseases by being  self-infectious, the virus
originating from some previously existing cheesy centre.   Tuber-
cle produced by inoculation from without are not identical in man
with miliary tubercle, but are  minute centres  of lobular pneu-
monia.   What the chemical or other  changes are by  which
cheesy matter, etc., becomes and is deposited as tubercle, we do
not know.  The white  blood-corpuscles, new  connective  tissue
cells, endothelial cells, these three factors of growth and repair
have been credited with  the parentage.   Likewise any " corpus-
cular matter " (Waldenburg) causing minute emboli in the capil-
laries of the pulmonary artery.
    Where tuberculosis supervenes in an  already progressing con-
sumption, it modifies the result and hastens the fatal issue.
    Chronic  tuberculosis can  no longer be accepted as being in
existence, since the elucidations concerning the origin of tubercle
have taught  that a greater part of  the small, indurated nodules
are dissolved in the broken-down inflammatory products.  Where
solitary tubercle or a  very small crop  primarily  exists with or
without  a cheesy focus, its inevitable fate is to die, thus allow-
ing  no  time for it   to  linger for  more than a very  limited
period.
    Persistent miliary tubercle must at the present day be  denied.
    Then wTe have  certain  inflammatory lesions of  the lung,
which, during the progress of the disease, are always combined,
and, according as one or the other  preponderates, we have sepa-
rate forms of consumption.  We may distinguish between those
which occur independently, and  run  a  slow course and are
" chronic " from the beginning, and such as are the remnants of
past acute inflammations of the lung.
    Of independent forms we have :
    Simple chronic indurative inflammation of the apex (chronic
interstitial  pneumonia) occurs in  the  alveolar and subpleural
connective tissue.
   Localized proliferation of peribronchial connective  tissue,
nearly always in connection with  a cheesy node, which  it en-
deavors to encapsulate.  This  form is independent only in not
being a remnant.
   Remnants of past  acute inflammatory troubles, exudations
which  have  undergone cheesy degeneration,  so-called caseous 
88
CONSUMPTION AND TUBERCULOSIS.
 pneumonia.   Croupous pneumonia likely furnishes no cheesy
 remnant, though this possibility is still believed in by some, and
 is chiefly based upon the fact that croupous pneumonia, as well
 as any of the other forms, is said to occur as an accompaniment
 to general diseases.
    Catarrhal pneumonia.   Negatived by Buhl and others ;  be-
 lieved to  be the source of  cheesy products by Juergensen,
 the late Niemeyer, and others.  The  question here turns  upon
 the products of  such  inflammations, the secretion,  and  the
 desquamated epithelium, which  do  undergo cheesy  metamor-
 phosis.   If the shedding of epithelium is so marked  (for other
 characteristics mentioned by Buhl, see chapter on  Desquamative
 Pneumonia)  as to call for  a separate picture of disease and to
 be  termed "desquamative pneumonia," then the question solves
 itself.
    I believe that the products of such inflammations of the lung
 as accompany7 general diseases are only more prone to cheesy de-
 generation, because in independent acute inflammations the  pa-
 tient does not suffer from the combined effects of  convalescence
 from a general disease and a fresh local trouble.
    In this connection, I  must again insist that, in  the absence of
 any connecting link between general diseases and the subsequent
 occurrence of consumption,  the most plausible theory to account
 for the predisposition of the patient and for his  anaemic condi-
 tion is:
    From the moment  of rise of temperature  until normal de-
 grees are  regained, the formation of red blood-corpuscles and
fibrine ceases.  The consequence is that the waste will be greater
 than the supply.
    The products of  haemoptysis, of pleurisy, of purulent peri-
 bronchitis, embolic pneumonia begetting anaemic  necrosis, local
 gangrene, and abscess.
    Now, either one  of these three great  factors—tubercle, con-
 nective tissue hyperplasia, cheesy centres—may exist in the lung of
 an  individual without causing  appreciable symptoms, thereby
 escaping diagnosis.  It is when  their constituents  begin to break
 down, and they commence  to be interwoven together, that they
 cause catarrh of the mucous membrane and rales may be heard.
    On dissection it is ofttimes possible to determine winch of the
 three conditions kept the lead during lifetime.
% 
PHTHISIS  PULMONALIS.
89
   As a rule, we may say, when considering the likelihood of tu-
bercle supervening in an existing  chronic process, that that pro-
duct  of a cicatrization  (whether of hyperplasia of  connective
tissue or  cheesy node, or both)  which has most stumps of  the
original pulmonary artery remaining in  its periphery, and is  the
most indirectly nourished, is most apt to have  tubercle  superven-
ing within it. 
90
CONSUMPTION AND TUBERCULOSIS.
                      THERAPEUTICS.

    Since you request it, and do not ask for more than " a general
 outline of therapeutics," I will add a few general hints as to what
 treatment should be  based upon.
    The two great factors in the treatment of consumption are
 individualization and strict attention to detail.
    The indications for  medical action  should be evolved  from
 the pathology, the exact knowledge of  the course any given pro-
 cess is likely to  take, which in turn implies equal exactness in
 diagnosis.  It will not suffice to establish that your  patient is a
 victim to consumption.   He likely enough knows it himself, or
 at least has a strong premonition that such is the case.
    Remember, also, that with all  modern means of diagnosis  on
 hand,  we are unable to positively diagnose  a strictly localized
 process at the apex  before  it is amenable  to auscultation, and
 the symptoms then presenting themselves are those of an actively
 progressing trouble.  No fault of ours, if we are so rarely con-
 sulted in  the earliest stages.   Nor of the patient's, whose atten-
 tion is not  called to it  until a persistent gastric catarrh, with
 more or less fever, fixes his attention.  Indeed this  is by far the
 most  frequent immediate cause of the retrograde changes which
 from thence take place in the apex.
    But I was going  to write of general therapeutics, and not of
 diagnosis, however tempting that field may be.  What I wanted
 to say was, that  the  same exactness in individualizing in  each
 separate case is stringently called for in therapeutics  as in diag-
 nosis.  It is this strict individualization, too, which will guide you
 in deciding  whether a patient should  be without delay sent to an
 appropriate  climate,  under proper directions, or whether he can
 be treated at home.   It is the  loss of valuable time, entailed by
first trying the  home  treatment, and, as a last resort, sending the
patient to Florida, Nassau, Colorado, or  Europe, which  causes
such bad results to be recorded, even where  great skill has been
exercised.
    Close  attention to detail in  the carrying-out of a plan  of
treatment has always seemed to me  to be the key-note to  final 
THERAPEUTICS.
91
 success.  It is this which of late has made the treatment of diph-
 theria  more successful.  Authorities, like Prof. Jacobi  of  this
 city, have insisted upon this, and in no small measure contributed
 to the reduction of the rate of mortality.
    The same  attention and never-lagging exactness with which
 every  detail is carried out is the secret of the success of  Lister's
 antiseptic  treatment of wounds.   The failures  are  all recorded
 on the side of  only partial adherence to a plan.  Whatever is ra-
 tional  in any given line of treatment, cannot be lightly dispensed
 with without endangering the  success of  the whole.
    The broad  indications  are  these: if anomaly of  constitution,
 hereditary  influences are at work, of which  scrofulosis  is  now
 again  claimed  to be a leading  example, our first duty is to remove
 the constitutional  tendency, anaemia, etc., in which branch  Bu-
 chanan has of late excelled.  Our best hold is no doubt appropriate
 climatic influences.   When we consider  how many localities, ex-
 tensive as well as strictly localized, exist all over this globe in the
 temperate  zone, it seems a simple  duty to spot such regions, and
 make  them accessible, as far as possible, to all classes of society.
 If  careful  search be  made, I  am satisfied there  is not a State in
 this Union which cannot boast of  some locality  where the requi-
 site conditions of temperature  exist.
    Here also I may mention the results obtained by7 Dr. Brehmer
 of Goerbersdorf in Silesia, by individualization and strict attention
 to detail.
    Dr. B.  claims  that he has  demonstrated  that reduced atmos-
 pheric pressure (lessened pressure of the air-column) and a  con-
 sequent low barometer, forms  the basis for the cure of consump-
 tion ;  not because the patient  inhales either less or more air than
 he does in the plains, but because the pressure of the atmospheric
 column is sufficiently reduced  to  allow him  to  inhale, at one in-
 spiration, the same quantity of air with less exertion of muscular
force,  an  important factor for a  person with flabby heart  and
 respiratory muscles.   And the same exertion of strength required
 for respiration in the plains will beget proportion ally far greater
 and more rapid nutritive changes, more especially as the out-door
 exercise involves  more or less climbing and calls for increased
 exertion of the respiratory forces.   Before such additional exertion
 is required of the patient, however, the other important factors of
 the  prescribed course: food, drink, cleanliness, light, absence of 
 92              CONSUMPTION AND TUBERCULOSIS.

 mental exertion, have fully prepared him for this additional task.
 I should add, what in reality is  self-evident, that  the air of  the
 mountains is  cleaner, free  from impurities, and contains  more
 ozone than the atmosphere of the plains.
    The effect of breathing under low barometrical standing is,
 1st. The pulse becomes  accelerated, whereby—a.  The  blood is
 forced through the lungs, instead of stagnating  there, as it  did
 before, and—b. Brings to an immediate standstill the proliferation
 of connective  tissue, shedding of  epithelium and the formation
 of tubercle, which were induced  and  kept  up by  the slackened
 circulation and  the consequently slow and imperfect  nutritive
 changes.
    2d. Uninterrupted  frequency  of   pulse, heart-contractions
 which  overcome peripheral  impediments in the  lung and else-
 where, begets normal hypertrophy of the ventricles, enlarges and
 strengthens the muscular element of the heart.
    The " thinned air" treatment is supported by general or local
 derivation to the skin by means of the shower-bath (with  some
 force,  not long continued), mixed food,  Hungarian wine,  etc.
    Now let  us see what is accomplished by inhalation of com-
pressed air, by means of any of the numerous pneumatic appar-
 atus, or the " pneumatic  cabinet" so-called.* Here  also  it is
 claimed that the pulse is  accelerated  and the propulsive power
 overcomes the impediments  in the peripheral circulation.  True,
 but it  is not continuous and only practised  for a limited period
 each day.   What  effects  are  produced?   The patient inhales
 under^ increased  pressure a large quantity of oxygen, in a com-
paratively short space of time and with increased muscular exer-
 tion.   But it is claimed that in the beginning it is so regulated as
 to make the exertion gradual.  Theoretically this may be supposed
 to increase the muscular  elements in proportion  to the  increase
in the pressure afterwards exercised, but practically  it is not true.
The factors against that presumption are too numerous:  twenty-
three  hours and  over of  time-out of twenty-four  in which the
patient breathes ordinary air; lives under the same conditions of
assimilation of  food and drink; the same mental strain  (sure  to

   * For a review of the different methods and apparatus for inhaling com-
pressed air, to exhale into diluted air, etc., as well as the latest publications on
this subject, I refer you to the last number of Schmidt's Jahrbucher (Jahreanir 
THERAPEUTICS.
93
exist as long  as he remains at home); less  direct action  of the
sun's rays  than he would have in the mountains ; impurities of
air, such as dust, which are  inseparable from  the atmosphere of
the common earth's surface.   But above all we will find three
strong contra-indications:
   1st. Not even the  daily breathing of compressed air for a
considerable period will suffice to increase the muscular elements
or the elasticity of the central propulsive  powers.
   2d.  It is always with greater voluntary muscular exertion
that the sittings are accomplished, and it is  this which gives rise
to temporary acceleration of the pulse.
   3d.  This increased muscular exertion  is made, then, at a time
when the patient does not feel within himself the power to exert
himself, and the effort is, to say the least, lost.
   4th. Supposing the effect of the inhalation to  be  increased
and more forcible heart's contractions, overcoming of the sluggish-
ness of the peripheral circulation, and consequent rapid nutritive
changes, these nutritive changes (even though they do not accom-
pany the inspiration of condensed air, but take place subsequently)
are brought about too suddenly and forcibly, and without that
evenness of uninterrupted continuity which alone can insure per-
manent nutritive changes.
   Attention to the mechanism of respiration,  derivation  to the
skin in loco or in the  arm, occasional use of  ice-bags, or warm
applications covered by  oiled silk, the  local  shower-bath  with
friction, injections into cavities and infiltrated tissue, inhalations,
transfusion of blood and milk, the hypophosphites, our old friend
cod-liver oil, or, what is often more easily digested, pure olive oil,
together with such alkaloids as may be dictated by an emergency,
are all therapeutic agents of great value in  the hands of a  con-
scientious physician who can rise above routine practice. 
 
 
 
MAR 1*1946 
NATIONAL LIBRARY OF MEDICINE
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