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The Pathology and Morbid 
Anatomy of Tubercle. 
REPORT TO THE 
WISCONSIN STATE MEDICAL SOCIETY, 
BY 
N. SENN, M. D.. 
•y/ OF MILWAUKEE, 
Chairman of Committee on Pathology. 
Reprint from, the Transactions of the State Medical Society of Wisconsin. 
MILWAUKEE: 
PRINTED BY THE SENTINEL COMPANY. 
1883. THE PATHOLOGY AND MORBID ANATOMY OF 
TUBERCLE. / 
By X. Sknn, M. D., Milwaukee, Chairman of Committee 
on Pathology. 
As Chairman of your Committee on Pathology, I have endeavored 
to select a subject for your consideration on this occasion, that should 
not only be of interest to us all, but should also serve the purpose of 
eliciting a general discussion, which might lead to practical results. 
With no little hesitation and misgivings as to my ability to bring the 
matter before you in a proper shape, I have concluded to call your 
attention, as briefly as possible, to a very interesting and important 
topic in pathology, the common property of the physician and the 
surgeon, viz: The Pathology and Morbid Anatomy of Tubercle. 
For many years, as the result of microscopical examinations of speci- 
mens and chemical observations, I have been firmly convinced that 
the so-called scrofulous affections of bone, joints and lymphatic 
glands are tubercular in structure and behavior, and constitute 
only a link in the chain of development of tuberculosis, as generally 
understood. When these organs are primarily involved, as is usually 
the case, it is an indication that the process has not become general, 
and that by early and well directed treatment, its extension to more 
important and vital organs might be prevented. In this sense the 
affection, although not entirely ignored by American teachers and 
authors, has not received the careful attention its importance and 
gravity demands. The identity of the disease, as it affects bone and 
lymphatic glands, no one denies, but the relation it bears to tubercu- 
losis has been a source of warm and often bitter disputes among 
pathologists. The prevailing ideas concerning this point may be 
arranged under three heads: 
1st. ft is a disease per se, entirely distinct from tuberculosis. 
2d. It furnishes the soil or material for tuberculosis. 
:td. It is identical with tuberculosis. 
To prove the correctness of the last assertion, which is the princi- 
pal aim of this report, we must be able to show that it is identical 
with well recognized forms of tuberculosis, histologically, setiologically, 
and clinically. In considering tubercle, as applied to bone and lym- 
phatic glands, it is necessary to utilize the prolific literature on general 2 
Pathology and Morbid Anatomy of Tubeirle. 
tuberculosis which has accumulated since the epoch-creating' labors 
of the distinguished Ltennec. There is, perhaps, no other disease in 
our nosology about the nature of which there have been entertained 
more diverse, and often diametrically opposed, views among observers, 
than the question regarding the true nature and significance of tuber- 
cle. Anatomical research and bedside observation have proved alike 
unsatisfactory in furnishing the desired knowledge, and it is only 
during the last few years that light is beginning to dawn by way of 
experiments, which have pointed out to us the correct method of inves- 
tigation, and have already yielded practical results, the importance of 
which it is impossible to over estimate. For a long time it was 
supposed that the lungs were the principal, if not the only primary 
seat of tuberculosis, hence the term was, and by some is still, applied 
almost exclusively to indicate the existence of tubercular phthisis. 
Post-mortem examination and inoculation experiments on animals 
have shown, however, that almost every organ and tissue in the body 
may become the seat of the disease, and in fact, that in most cases of 
pulmonary tuberculosis earlier evidences of the same disease can be 
found in the lungs or some other part of the body. 
The meduallary tissue of bone and lymphatic glands are closely 
related anatomically, physiologically and pathologically, and are con- 
sequently prone to the same affections. It is generally conceded that 
the so-called scrofulous affections of these organs exert a potent influ- 
ence in the causation of tuberculosis, but it is my purpose to argue in 
favor of the identity of the former with the latter. As tubercle of 
bone and lymphatic glands originates in the same way, and undergoes 
the same changes as when it affects other organs, it will become nec- 
essary for us to study the general subject of tuberculosis, in order to 
apply the knowledge thus obtained to a better understanding of the 
disease when it involves these particular organs. 
THE RELATION OF TUBERCLE TO INFLAMMATION. 
The post-mortem room and clinical observation have taught us 
that the presence of tubercle, wherever found, is invariably associated 
with more or less inflammation, but the relationship of the one to 
the other has given rise to various theories. The same discrepancy of 
opinion has existed as to the identity or non-identity of the gray, or 
crude, and the yellow, or cheesy tubercle. Bayle gave an accurate 
account of miliary tubercle in different organs, but, in addition, 
described another affection, under the name of miliary granulations, 
as translucent cartilaginous nodules. He also committed the error to 
ascribe to the cheesy products of other affections tuberculous proper- 
ties. Lamnee regarded the miliary granulations of Bayle as a variety 
of miliary tubercle, and published his well-known views concerning Pathology and Morbid Anatomy of Tubercle. 
3 
the transformation of the miliary tubercle into the tubercular infil- 
tration. lie accepted Bayle’s theory that every cheesy mass is the result 
of a previous deposit of tubercle, and that every pulmonary phthisis 
owes its origin to tubercle. Louis advanced the same opinion. 
Broussais and Andral regarded tuberculosis as a consequence of an 
antecedent inflammation. Andral was acquainted with the fact that 
in some instances pus is converted into cheesy matter, and he regarded 
miliary tuberculosis as a product of a pre-existing pneumonia. Bou- 
chardat attributed to pneumonia no direct influence in the causation 
of tuberculosis, but considered the general debility following it as a 
predisposing element, acting in a similar manner as debilitating 
causes from any other source. Colberg, on examining one hundred 
phthisical lungs, found that in ninety cases the destruction of tissue 
was due to cheesy pneumonia, and only ten were affected with miliary 
tuberculosis; of these, six were complicated with cheesy pneumonia, 
and in all of them other organs had also become affected. Slavjanski 
examined 139 lungs from phthisical patients, and found that 123 
belonged to the pneumonic, and only sixteen to the tubercular variety. 
Buhl was the first to call attention to the relation existing between 
cheesy inflammation and miliary tubercles, the latter of which he con- 
siders to be infectious, the result of absorption of a specific virus 
from the products of foci of caseous inflammation. Virchow regards 
cheesy inflammation, scrofula and tubercle as distinct and independent 
pathological conditions, but admits that it is difficult to maintain this 
distinction by established facts. lie taught that the tubercular meta- 
morphosis is not limited to tuberculosis, in its accepted sense, but that 
it also occurs in new inflammatory deposits and in heterologous for- 
mations. On this account he suggested the term cheesy metamorpho- 
sis, in place of tubercular metamorphosis. 
Lebert looks upon tubercle as a product of inflammation, the 
rapidity of its development depending on the degree of mal-nutrition 
of the tissues and the amount of absorption of pathological products. 
Reinhardt observed that tHe tissue changes in organs affected with 
tubercle, and undergo the same alterations as when they are the seat 
of chronic inflammation. The distinctive feature of the tubercular 
process does not consist in the formation of a specific pathological 
product, but that under its influence the affected organ becomes sub- 
jected to repeated attacks of inflammation, usually of a chronic type. 
Klebs adheres to the opinion that there must be a specific differ- 
ence in the products of cheesy inflammation from the beginning, 
inasmuch as not all cheesy material is capable of generating mili- 
ary tuberculosis, and that this difference in the virus does not depend 
on anatomical conditions, as the formation of capsules, etc. He rec- 
ognizes an intimate causative relation existing between scrofula and 
tuberculosis. To support this view, he mentions the anatomical 
condition of lymphatic glands in the immediate vicinity of miliary 4 
Pathology and Morbid Anatomy of Tubercle. 
deposits. In cases of cheesy degeneration of bronchial glands he 
has witnessed a corresponding portion of the lung infiltrated with 
miliary tubercle* while no trace of tubercle could be found in any 
other part of the body. 
Xiemeyer, as well as Virchow, affirms that the infiltrating tubercle 
of Laennec is the product of inflammation, consequent upon an 
attack of chronic pneumonia, particularly the catarrhal variety. 
Pidoux regards cheesy pneumonia and tuberculosis as manifestations 
of one and the same diathesis. 
The observations of Aufrecht on tubercle of the peritoneum have 
induced him to speak of the process as a peri-lvmphangitis. 
Max Schuller speaks of the tuberculous process as being of an 
inflammatory nature. Inflammation does not consist of simple 
migration of white and diapedesis of red blood corpuscles, but a 
change is always found to exist in the pre-existing histological ele- 
ments, as has been sufficiently proven by the researches of Virchow, 
Strieker and Itanvier: this cell abnormality, of course, Schuller attri- 
butes to the presence of micrococci. While caseous degeneration is a 
general characteristic of tuberculosis, it is, in his opinion, a later and 
secondary change, for the parts which have undergone metamorphosis, 
are the same as have been the seat of a specific tubercular inflamma- 
tion, and are. at the same time, matrix and product of this inflamma- 
tion. Inflammation necessarily precedes caseation. It is true that 
caseation often follows closely on the heels of tubercular inflamma- 
tion, but in other cases it does not take place for a long time, and 
occasionally it does not make its appearance at all. Schuller does not 
accept the theory of insufficient nutrition as the cause of ‘caseation, 
but attributes this change to the action of the tubercular virus, 
which, at an earlier period, excited the tubercular inflammation. 
M. Litten reports three cases of sero-tibrinous pleuritis, which 
were followed by acute miliary tuberculosis. In two of the cases 
there appeared to exist a hereditary taint to tuberculosis. The de- 
velopment of tubercle followed closely the resorption of the effusion. 
In most cases of acute miliary tuberculosis there can be found in 
some organ a cheesy deposit, or the products of an antecedent tuber- 
cular deposit. Litten argues further, that although auto-infection by 
means of products of simple inflammation is known to take place, it 
does not necessarily follow that the infecting material possesses 
specific qualities, as the absorption of regressive products of inflam- 
mation will produce, in some cases, similar results. Acute affections, 
as typhoid fever, and especially measles, may be the cause of tuber- 
culosis in individuals predisposed to this disease. Any irritation, if 
continued for a sufficient length of time, may become the cause of 
tuberculosis. Inflammation follows the application of irritants, and 
when the products of this inflammation necrose the absorption of the 
detritus, may be followed by tuberculosis. Tubercular nodules ex- Pathology mid Morbid, Anatomy of Tubercle. 
5 
cite inflammation in the organs in which they are deposited, hence 
tubercle may be either the cause or effect of inflammation. C. Huge 
and Waldenburg have asserted that irritation alone may produce 
tuberculosis, entirely independent of any caseation. 
Birch-Hirschfeld commits himself on this subject as follows : 
“The development of the neoplasm called tubercle is connected with 
inflammation of a definite type.” 
The existence of tubercular eruptions in the vicinity of caseous de- 
posits, gave rise to the opinion that the cheesy material elaborates a 
virus which produces a specific neoplasm—the tubercle. 
Ziegler, in commenting on the results of his experiments with 
inert substances in producing tuberculosis in animals, advances the 
following propositions : “Tubercle, with its giant cells, is a focus of 
inflammation, in which the colorless blood corpuscles accumulating at 
any point undergo a peculiar development. Tubercle might be re- 
garded as a degenerated species of inflammatory neoplasm (granula- 
tion), determined by necrobiotic processes. 
David Foulis makes use of the following plain language in ex- 
pressing his views on this subject : “Tubercle is the result of a local 
inflammation, set up in certain cells of low vitality, by irritation 
either from solid particles or from fluids of a composition unsuited to 
them.” 
Billroth, in studying the development of tubercle in the mesentery, 
was impressed with the fact that the initial lesion usually takes place 
at a point where small blood vessels take a sudden turn, an anatomi- 
cal arrangement which diminishes the rapidity and force of the 
blood current. In the tubercular process the endothelium and white 
blood corpuscles participate. The number of cases where miliary 
tuberculosis exists without cheesy deposits is growing constantly less, 
as post-mortem examinations are more carefully made. Tuberculosis 
is not hereditary, but the pre-disposition to chronic inflammation is 
inherited. Every person who has a cheesy deposit is liable to suffer 
from tuberculosis at any time. 
Treves remarks : “Tubercle is no neoplasm, but the product of a 
peculiar form of inflammation.” 
Wilson Fox claims that there exists a close relationship between 
tuberculosis and cheesy pneumonia. 
Morbid anatomy furnishes abundant proof that in most cases of 
diffuse miliary tuberculosis evidences may be found of previously 
existing local tuberculosis in the form of caseous deposits, and where 
these cannot be found they may have disappeared before the time of 
examination, or been overlooked during the examination. In the light 
of recent experiments it must be admitted that tubercle, as such, is 
never the product of simple inflammation; inflammation, however, 
may so alter the properties of the tissues as to furnish a favorable 
soil for the development of tubercle. It is also a well known fact 6 
Pathology and Morbid Anatomy of Tubercle. 
that the presence of tubercle will, unless it has become latent, excite 
inflammation of a chronic character, which is modified in its tenden- 
cies by the tubercular process. The origin and growth of tubercle is 
attended by cell proliferation within, and in the immediate vicinity 
of capillary vessels resembling ordinary inflammation; but the course 
of the process and the future fate of the exudation material is modified 
by the tubercular virus imparting to the tubercle nodule specific 
qualities found in no other product of inflammation or neoplasm. 
Only cheesy material, the result of an antecedent tubercular deposit, 
can give rise to diffuse miliary tuberculosis. All other inflammatory 
products can only serve as a fertile soil for the localization of tubercle, 
thus furnishing only one of the conditions for tuberculosis. Inflam- 
mation around the tubercle nodule favors local progression, but is 
only one of the consequences of local infection. 
INOCULATION TUBERCULOSIS. 
Inoculations with tubercular matter were made at an early day, to 
prove the infectiousness of the disease. The first experiments of this 
kind were made by Kortum in 1789, and Cruveilhier in 1826. In 1834 
Erdt succeeded in producing numerous nodules in the lungs of horses 
by inoculating them with scrofulous pus, and Klencke, in 1843, pro- 
duced tuberculosis of the lungs in rabbits, by injecting tubercular 
matter in the jugular vein. These experiments attracted but little 
attention until, in 1865, Villemin announced the results of his investi- 
gations in this direction. He succeeded in communicating tubercu- 
losis from man to animal by means of inoculation. Ilis experiments 
consisted in the subcutaneous introduction, behind the ears of rabbits, 
of fragments of tubercle or fluid from the cavity of a tuberculous 
lung recently removed from a patient who had died of pulmonary 
tuberculosis. The first animal was killed three one-half months after 
inoculation; the lungs and most of the internal organs were found 
diffusely infiltrated with miliary tubercle. His numerous experiments 
yielded similar results, and led him to the following conclusions; 
“Phthisis of the lungs (like tubercular diseases in general) is a specific 
affection. Its ;etiologv depends on an inoculable agent. It can be 
readily communicated from man to animal by inoculation. 
Tuberculosis, therefore, belongs to the class of virulent diseases, 
and deserves, nosologically, a place side by side with syphilis, but is 
perhaps more closely related to glanders.” 
Inoculations with pus from phlegmonous abscesses, discharges 
from cholera patients, and anthrax tissue, produced negative results. 
Yogel repeated the experiments of Villemin on horses, without 
success. Pathology and Morbid Anatomy of Tubercle. 
7 
Bifli, Verga and Sangalli experimented on mules, cows, sheep, 
dogs, cats, mice and chickens, with negative results. The experi- 
ments of Langhans led him to the conclusion that tubercle could not 
be communicated in the manner described by Villemin, the inocula- 
tion material only acting as a foreign body, the inflammation follow- 
ing its introduction differing in no way from the ordinary forms of 
inflammation. 
Among those who made successful experiments and adopted the 
doctrine advanced by Villemin may be mentioned: Ilevard and 
Cornil, Hoffman, Cohn, Behier, Empis, Mantegazza, Bizzozero, Lebert 
and Wyss, Klebs, Koester, Waldenburg, Bijuen, Simon, Sanderson, 
W. Fox, Papillon, Xicol and Laveran. Ilevard and Cornil were able 
to propagate tubercle when they inoculated with genuine tubercular 
matter, but failed with cheesy material. Marcet inoculated eleven 
guinea pigs with the sputa of tuberculous patients, and in ten of 
them the experiment proved successful. Lebert and Wyss made 
numerous experiments with various substances, as pus, cancer and 
sarcoma tissue, coal-dust, mercury, etc., and finally concluded that, 
although when using the products of tubercular inflammation, dis- 
seminated pneumonia, infiltrated glands, and granulation tissue, 
multiple infectious nodules are most readily produced, the same result 
may be obtained with products of inflammation and heterogeneous 
substances, only not so readily and constantly. Waldenburg’s inocu- 
lation experiments with different substances led him to the belief that 
all substances used must enter the circulation, and while there act the 
part of a foreign body, producing capillary embolism, the small 
thrombus serving as a nucleus for the miliary nodule, around which 
the white blood globules extravasate and are converted into tubercle 
corpuscles. 
Klebs is a firm advocate of the specific virulent nature of the 
tubercle as taught by Villemin. The following are his views: “ Tuber- 
culosis can be transmitted from man to animals by inoculation. By 
inoculation with tuberculous matter a form of affection of the lym- 
phatic glands can be produced which resembles perfectly the scofulous 
lymphatic affections in man. Inflammatory processes accompanying 
the inoculation of tubercle in animals takes place only in case the 
inoculating material has undergone putrefaction, or when it has been 
contaminated with mechanically irritating substances, or when the 
inoculation wound has been exposed to external irritating influences. 
The detritus of non-tuberculous tissue, as well as tine granular inor- 
ganic substances, if introduced into the body, can, under certain 
conditions, produce microscopical changes resembling tubercle, which, 
however, differ materially from tubercle anatomically, as well as in 
their future behavior.” 
It. Volkmann declares that tubercle in man readily inoculates 
in loco, but in contradistinction to experimental inoculations in ani- 8 
Pathology and Morbid Anatomy of Tubercle. 
mals, it is slow in becoming general; rapid diffusion can only take 
place under peculiarly favorable circumstances. Cohnheim is willing 
to acknowedge that as yet we are not able to give a correct anatomi- 
cal definition of tubercle or tuberculosis. Tubercle is not a definite 
anatomical entity. He believes that tubercle is the product of a 
specific virus, and that tuberculosis can only be produced by tubercu- 
lar matter. Animals infected with tubercle present the particular 
symptoms of tuberculosis in man, and none other. Like Virchow, he 
rejects the doctrine that caseation is the criterion of tuberculosis, as 
advocated by Laennec. He attributes to tubercle as high a degree 
of infectiousness as to the virus of vaccination or syphilis. In man 
infection usually takes place through the respiratory passages, and 
the disease is very apt to manifest itself primarily at the point of 
infection. He furnished a beautiful illustration of the last assertion, 
by injecting tubercular matter into the anterior chamber of the eyes 
of rabbits, which invariably produced tuberculosis of the iris. C. 
Ilueter also succeeded in producing tuberculosis of the iris by intro- 
ducing into the anterior chamber of the eye small fragments o! 
granulation tissue, taken from a joint affected with fungous synovitis. 
M. Ilippolyte Martin, in considering the identity or non-identity of 
true tubercle and the so-called pseudo-tubercle, produced by inocula- 
tion with inert substances, maintains that by the results of a series 
of inoculations a criterion is furnished which distinguishes one from 
the other. Inoculations with true tubercle were followed by diffuse 
miliary tuberculosis in the inoculated animals, and inoculations can 
be successively made without diminishing the intensity of the disease. 
Inoculations with pseudo tubercle never give rise to general tuber- 
culosis, and the infectivity of the product is lost at the second or 
third series of inoculation. 
M. Toussaint, in a communication to the Academie de Sciences de 
Paris, asserted that true tubercle, both in man and animals, repro- 
duces itself indefinitely with absolutely constant and identical proper- 
ties, and that it is capable of being transmitted from animal to animal 
without losing its virulence; in fact, its virulence increases with the 
number of re-inoculations. The first inoculation requires from four 
to five months to kill a pig or rabbit, while material taken from the 
fifth series of inoculations requires only two months to produce a 
fatal termination of the disease. Products of the cultivation of 
tubercular virus manifest the greatest virulence. The pseudo-tuber- 
culosis produced by inoculation of inert substances may resemble 
true tuberculosis in many respects, but it is incapable of being re- 
produced in the same manner. 
Some interesting experiments have been performed by M. M. 
Krishaber and Dieulafov on the artificial production of tubercle in 
monkeys. The conclusions drawn from these investigations are : 1, 
That human tubercle, when inoculated, kills a monkey in nine out of Pathology and Morbid Anatomy of Tubercle. 
9 
ten cases, with lesions analagous to those met with in man. 2, The 
effect of the inoculation varies according to the substance employed; 
the gray granulation is most, and the pulmonary parenchyma least 
infectious. 3, Two monkeys only were found to be insusceptible. 
I)r. V. Lentz has recently made experiments with blood from tuber- 
culous rabbits. The fresh blood from a tuberculous rabbit, he injected 
into the trachea of six rabbits. The animals were killed in from 02 to 
216 days, and two of them were found affected with tuberculosis. 
Blood from one of these was injected into the knee-joint of another 
rabbit, which resulted, after eighteen days, in caseous degeneration of 
the joint and pulmonary tuberculosis. 
Max Schneller’s experiments with blood from tubercular animals 
yielded similar results, and strongly tend to prove that the infectious- 
ness of tubercle does not depend on the presence of caseous material, 
but on a virus which is capable of being diffused through the medium 
of the circulating fluids of the body. 
Lippi, Schweninger and Tappeiner claimed to have produced tuber- 
culosis in rabbits, with inhalations of atomized sputa from tubercular 
patients, while Schottelius says he produced the same result with a 
single insufflation of an indifferent substance. Ziegler believes that 
the result was not tuberculosis, but miliary foci of inflammation. 
Finely divided substances, inhaled into the lungs, enter the bronchial 
tubes and alveoli, and migrate into the interstitial substance of the 
lungs, the lymphatic vessels, and finally are arrested in the lymphatic 
glands. In any of these localities these foreign bodies may excite irri- 
tation, and form a nucleus for an inflammatory nodule. 
These inhalation experiments have been lately repeated by Weich- 
selbaum, of Vienna, dogs alone being employed. Eleven experiments 
were made with tuberculous sputum. The duration of the experi- 
ments varied between two days and two and one-half months, and 
the number of inhalations between one and twenty-four. In all these 
cases, even in those in which only one inhalation had been administered 
and the animal killed one or two days afterwards, tubercles were found 
in the lungs and kidneys, many nodules in the former, one or two only 
in the latter. Moreover, the bronchial glands, and in some the mesen- 
teric glands also, were swollen, and presented tubercles under the 
microscope. Inhalations of emulsions of cheese and bullock’s spleen, 
yielded negative results. Pus from a carious rib, diluted with water 
and inhaled for seven weeks, produced only a few nodules in the lungs, 
although these had a structure similar to the tubercles of the first 
series. The same subject has been investigated in France, by M. 
Giboux, and in an aspect of more direct practical importance. The 
nocuity or innocuity of the air expired by phthisical patients, was the 
point examined. He collected daily forty or fifty litres of air expired 
by persons in the second or third stage of phthisis, and passed half this 
air into a hutch in which were two young rabbits, born of perfectly 10 
Pathology and Morbid Anatomy of Tubercle. 
healthy parents. Two other similar rabbits were confined in another 
cage of similar construction, and through this was passed daily twenty 
or twenty-five litres of the remaining air, which had been filtered by 
being passed through tow, impregnated with carbolic acid. The two 
cages were placed in separate rooms, so as to prevent any contamina- 
tion of the air of the one by the respiratory products from the other. 
The experiment lasted from January 15th to April 29th. At the end 
of this time, the two rabbits placed in the second cage were in perfect 
health, while the others suffered from loss of appetite, thirst, diarrhoea 
and emaciation. At the autopsy, tubercles were found in the princi- 
pal viscera, and the lesions in the lungs were much more advanced 
than in the other organs. On the other hand, the viscera of the two 
rabbits in the second cage, presented no trace of tubercle. 
Tuberculosis has also been produced in animals by feeding them on 
tuberculous matter. Successful experiments of this kind were made 
by Chaveau, Aufrecht and Bollinger. Bollinger found that herbivor- 
ous animals acquired the disease in this manner more readily than the 
carnivorous, and that the omnivorous, and among them probably man, 
resembled more the first class of animals in this respect. Among the 
animals infected by feeding tubercle, the following were the most 
important.changes found at the autopsy: Intestinal ulcerations, tuber- 
culosis of the mesenteric and portal glands, and in several instances 
also of the glands of the neck. 
Colin’s experiments were unsuccessful. The experiments of Klebs, 
in propagating tuberculosis by feeding animals with food containing 
tuberculous matter, would tend to show that localization of the dis- 
ease primarily takes place at the point of infection,—the intestinal 
canal, and that it becomes general through the medium of the portal 
circulation. 
Ziegler is of the opinion that inoculations and inhalations of sub- 
stances not possessing specific properties, have excited products closely 
resembling tubercle, and which cannot be distinguished from it anat- 
omically. He argues, however, that not the production of tubercle, 
but the clinical history of inoculation tuberculosis, is the most impor- 
tant element. Progressive infection is the most characteristic feature 
of tubercle. Miliary tuberculosis is an infectious disease, the course of 
which can often be traced step by step. The lymph vessels are the 
channels through which the infectious material is conveyed into the 
blood. In how far infection can take place through the lungs, is not 
well ascertained. When caseation takes place in the interior of an 
organ, infection has taken place through the medium of the blood. 
He is also inclined to believe that germs destroy the vitality of the 
cells in the nodule, acting, at the same time, as irritants to the neigh- 
boring tissues. 
Fehleisen claims that not all of the products of a tubercular inflam- 
mation are carriers of a specific virus, but the virus is diffused through Pathology and Morbid Anatomy of Tubercle. 
11 
the medium of cheesy matter, cheesy pus, in fact, the products of 
degeneration. This view is supported, from a clinical stand-point, by 
Volkman, who says: “ Wherever the tissues of the healthy body come 
in contact with softened cheesy material and pus, containing the 
tuberculous virus, and wherever this pus is conveyed, there arise 
eruptions of specific miliary formations, and numerous miliary erup- 
tions mark the way where the specific products have taken their 
course. These eruptions yield again new infectious and inoculation 
material, as soon as they have become degenerated into cheesy 
material.” Fehleisen inoculated the peritoneal cavity of rabbits with 
granulation tissue, from a case of fungous arthritis, also with small 
pieces of the lining membrane of a cold abscess, taking the precau- 
tion to avoid the introduction of cheesy material. The peritoneal 
cavity was selected on account of its well-known property of afford- 
ing the most favorable surface for rapid absorption. Twenty experi- 
ments were made. Two of the animals died, one on the forty-first, 
the other on the sixty-fourth day after the operation. A post-mortem 
examination revealed that in both animals the peritoneum and 
pleura costalis and pulmonalis were thickly studded with miliary 
tubercles, and scattered nodules wrere found in most of the organs. 
The remaining animals, eighteen in number, were killed from the 
fiftieth to the ninetieth day after the inocidation, and all of them 
were found to be perfectly healthy, and no trace of tubercle could be 
found in the peritoneum or any other organs. These facts induced 
the experimenter to conclude that in the two fatal cases infection was 
probably produced by cheesy pus, which may have been adherent to or 
contained within the inoculating tissue. 
J. Orth belongs to the class of pathologists wrho believe that ani- 
mals can be successfully inoculated with tubercle, and that the 
artificial product is identical with tubercle as found in man. 
Baumgarten, in opening a discussion on tuberculosis, in the Medi- 
cal Society of Koenigsberg, made the assertion that not all cheesy 
deposits are capable of giving rise to tuberculosis. To prove this 
statement, he said that animals prone to cheesy inflammation rarely 
suffer from spontaneous tuberculosis, and .that in man, cheesy deposits 
in cutaneous and syphilitic growths seldom provoke the disease. 
According to his views, only tubercular caseous deposits can infect 
the organism with tubercular eruptions. 
During a discussion on Inocidation Tuberculosis, in the Berlin 
Medical Society, Friedlander asserted that although an affection 
resembling tuberculosis has been artificially produced in animals, by 
the introduction of tuberculous or cheesy matter, or even inert sub- 
stances, the clinical behavior was at variance with the genuine disease. 
He injected from twenty to forty C. C. of an emulsion of cheesy 
material, taken from a human cadaver, into the small veins of the neck 
of a dog. Of twelve animals inoculated in this manner, only one 12 
Pathology and Morbid Anatomy of Tubercle. 
died, and in this case from an accidental disease. The remaining 
eleven dogs were killed in from three to four weeks after the opera- 
tion. In ten of the animals, nodules the size of a pin-head were 
found in the liver and spleen, less constantly in the lungs and kid- 
neys, and never in the pleura, eye or pia mater, and only in one 
instance in the peritoneum. The animals never suffered from local 
or constitutional symptoms. In the lungs, the nodules consisted of 
alveoli, filled with epithelial cells. The microscopical appearances cor- 
responded closely with the lobular desquamative pneumonia of Buhl. 
The giant cells, which are almost constantly found in tubercle of man, 
were never found. In reply, Walden burg stated that Friedlander’s 
description of the artificial disease in animals corresponded with the 
affection as found in man, with the exception of the absence of giant 
cells, and, according to Virchow, these cells do not constitute a 
specific element of tubercle. Waldenburg, Klebs and Bering have 
found the giant cells in the nodules of inoculation tuberculosis, and 
Friedlander was ready to admit that they were not uniformly present 
in tubercle of man. Waldenburg has observed the same clinical his- 
tory in the infected animals, as in tuberculosis of man. The diffusion 
of tubercle depends on the place and manner of inoculation. 
Friedreich regards the anatomico-pathological stand-point as 
insufficient to explain the nature of tuberculosis. Clinical observa- 
tion and setiological influences must be added to arrive at correct 
conclusions. He has found giant cells in typhoid products and in 
leukaunic nodules. 
Zenker considers experimental pathology of great importance in 
ascertaining the nature of disease. He was surprised at the results of 
his experiments on animals, which were made in accordance with the 
method practiced by Villemin. lie is satisfied that tubercle is trans- 
missible from man to the lower animals by inoculation. Inoculation 
can be practiced successfully by introducing the tuberculous material 
under the skin, into the peritoneal cavity, the veins, anterior chamber 
of the eye, or any other place that can furnish an absorbing surface. 
The period of incubation varies from two to four weeks. 
GERM THEORY OF TUBERCULOSIS. 
The results obtained by the simple inoculation of gray tubercle or 
cheesy material, have been so widely at variance, that experimenters 
were divided into believers and non-believers in the infectiousness of 
tuberculosis. The large class of pathologists, who maintained the 
theory of its infectiousness, were therefore anxious to isolate the virus 
giving rise to infection. These efforts resulted in the germ theory of 
tuberculosis, which has recently attracted so much attention among 
physicians and scientists. Moretto had already suspected that scrofu- Pathology and Morbid Anatomy of Tubercle. 
13 
lous diseases depended on the presence of low organisms, and C. 
Tiueter ascribed to them an essential part in the genesis of scrofula. 
The first experiments with isolated cultivation germs, were made by 
Klebs, in 1877. He found, by examining fresh specimens of tubercle 
of human lungs, that they invariably contained a species of bacteria, 
small granules, about one-thousandth part of a millemetre in diameter, 
and twice as long, possessing spontaneous motion. Transferring these 
germs through a series of cultivation fluids, composed of albumen of 
eggs or Bergmann’s cultivation fluid, he found that they retained 
their vitality and infectious properties. The third cultivation product 
proved to be pure and reliable. Injections of these germ-containing 
cultivation fluids were made under the skin, into muscles, lungs, 
pleural and peritoneal cavities, and if the animals survived the opera- 
tion for any length of time, they soon became tubercular. Injections 
of cultivation fluids, containing the germs of tissue from scrofulous 
glands and lupus tissue, were also promptly followed by tubercu- 
losis. 
Max Sehueller repeated the experiments of Klebs with the same 
results. He described the specific germs as round and rod-like bacteria, 
the rods presenting bulbous extremities, which are not infrequently 
bent to one side, and are composed of two, seldom more, spherical 
bodies. They are found most numerously in the tissues of diseased 
joints, where large colonies may be seen in the synovial membranes 
of contused joints in animals which had been infected with tubercle 
a few days previously. They are first noticed in the extravasated 
blood in contused joints ; the blood appears to serve the purpose of a 
cultivation fluid. They become more distinct on the application of 
ether and a solution of caustic potassa; a blue color is imparted to 
them by methyl violet. From the infected joints the micrococci 
enter the juice canals of cartilage, which become dilated. When they 
reach the bone, they infiltrate the cancell i; large colonies can be seen 
on the margins of osteomyelitic deposits. In the small 1 flood and 
lymphatic vessels the micrococci adhere to the tunica intirna ; their 
presence excites irritation, which manifests itself by an increase in 
the size of the preexisting cells, rapid reproduction of tissue elements, 
migration of blood corpuscles, stasis, coagulation of blood and lymph, 
and finally complete obstruction of the vessels. Transverse sections 
of such vessels present the appearance of giant cells. Micrococci 
affect the white corpuscles more than the red. The former under 
their influence appear larger, and adhere to each other, forming masses, 
thus contributing largely to the rapid occlusion of minute vessels. 
The infected district furnishes a favorable soil for reproduction of the 
germs, hence the process of infection is progressive, and continues 
indefinitely. Caseation is the result of the deleterious effect of the 
micrococci upon the newly formed tissues. The infection may remain 
local for an indefinite period, provided the local conditions are un- 14 
Pathology and Morbid Anatomy of Tubercle. 
favorable for diffusion or multiplication of germs, or when these are 
rendered innocuous or are exerted. 
In a discussion on tuberculosis, at a meeting of the Vienna Medi- 
cal Society, Billroth said that the theory of the parasitic nature of 
tuberculosis is not to be cast aside, because the investigation of the 
parasitic element is a matter of great difficulty, while acknowledging 
that in regard to the heredity of tuberculosis in the same sense as the 
heredity of syphilis, nothing is known, he believes that the parasitic 
hypothesis must suppose a special predisposition to tuberculosis in cer- 
tain individuals, and he agrees with Niemeyer’s well-known view 
that the scrofulous diathesis predisposes to tuberculosis. Neoplasms 
become more rapidly disseminated, when the local and general con- 
dition is one of debility. We also know how rapidly the organism 
will eliminate certain kinds of parasitic germs, as hyphomycites; 
when, however, the conditions of life of these germs are changed by 
cultivation in alkaline fluids kept at the temperature of the body, then 
their introduction into the body is followed by the most disastrous 
results, a fact which has been most conclusively demonstrated by the 
experiments of Grawitz. The germs under these conditions multiply 
with such great rapidity, that all efforts on the part of the white blood 
globules to eliminate them are futile, and they literally inundate and 
overpower the organism. 
In speaking of the parasitic origin of tuberculosis, Ziegler asserts 
that not all cheesy deposits give rise to infection, but that their infec- 
tious property depends on the presence of specific micro-organisms, 
the caseous material only furnishing a favorable soil for their devel- 
opment. Naegeli has called these germs Schistomycites, and Ziegler 
adopts this term. Naegeli has ascertained that these germs are ren- 
dered innocuous by the acid secretions of the stomach, but that they 
again become active when in contact with the alkaline fluids of the 
intestinal canal, hence the stomach is never, the intestinal tract on 
the other hand frequently, the seat of tubercular ulceration. The 
germs are miasmatic in the air, but acquire contagious qualities in the 
organism. The virulent germs from phthisical patients may be con- 
veyed directly to other persons, or through the medium of the air or 
soil. Ziegler is so firmly convinced of the parastic origin of tubercu- 
losis, that he adopts the phrase, “No phthisis without noxae,” as one 
of the closing arguments of his excellent paper. 
Perhaps no subject in medicine ever excited more universal and 
intense interest, than the recent announcement by Robert Koch of his 
discovery of the specific germ of tuberculosis, the bacillus tuberculosis. 
Not long ago, Cohnheim, an enthusiastic advocate of the infection 
theory of tuberculosis, made the assertion that “the direct demonstra- 
tion of the tubercular virus must to this day be considered an un- 
solved problem.” Experimental pathology and improved methods of 
microscopical examination, have at last enabled Koch to isolate, cul- Pathology and Morbid Anatomy of Tubercle. 
15 
tivate and demonstrate a germ, which he has found invariably pres- 
ent in all recent tubercular products, and which he considers to be the 
specific agent in the production of the disease. By his process of 
staining the objects for examination, the bacilli appear of a delicate 
blue, and the organic tissues of a brown color. The bacteria are rod- 
shaped, and belong to the family of bacilli. They are very narrow, 
and in length about one-fourth to one-half the diameter of a red blood 
corpuscle. They resemble the bacilli of lepra, but are more slender 
and pointed at each extremity. These bacilli are present in clusters 
in great numbers in fresh tubercular deposits, and they may often be 
seen in the interior of cells. On the border of cheesy foci they are 
usually found isolated; when softening takes place, they disappear. 
When giant cells are present, they always contain bacilli, even if they 
are not found anywhere else. From the fact that they are found 
present in these cells without exception, it must be assumed that they 
are active in their production, as they disappear as soon as degenera- 
tion takes place. In 11 cases of acute miliary tuberculosis, Koch 
found the bacilli in all of them. In 12 cases of caseous bronchitis and 
pneumonia, he found them along the border of cheesy deposits, and 
very numerous in cavities. From other kinds of bacilli, they may be 
distinguished by their blue color on staining, while other forms of 
bacilli are stained brown by the same process. He found them also 
present in one case of primary tuberculosis of brain, the deposits 
having assumed the size of a hazel-nut, also in two cases of intestinal 
tuberculosis, in two cases out of three of extirpated scrofulous glands, 
and in two cases out of four of fungous synovitis. 'They were found 
constantly in cases of spontaneous and inoculation tuberculosis of 
animals. Inoculation tuberculosis was observed in 172 guinea pigs, 
32 rabbits and 5 cats, and in all of them the bacillus was found. That 
the bacillus is the cause of the tuberculous process is evident from the 
fact that the germ is always found in places where the process is 
most active, and always disappears as soon as retrograde metamor- 
phosis has taken place. 
In order to prove that these germs were the essential cause of the 
disease, he isolated them from the tissues, and submitted them to a 
series of fractional cultivation. As a cultivation material he took 
serum from the blood of an ox or sheep, which was solidified and 
sterilized by exposing it to a temperature of 58°—65° C. for a sufficient 
length of time. Under strict antiseptic precautions tubercle tissue 
from lung, or caseous lymphatic glands from recently deceased 
animals, was conveyed to test tubes containing the sterile soil, and 
kept at the temperature of the body, great care being exercised to 
prevent the ingress of any additional atmospheric germs. After ten 
days colonies of bacilli were seen on the surface of the soil, and as they 
do not possess spontaneous motion, they did not penetrate into its 
interior. Some of these germs were carefully removed to another 16 
Pathology and Morbid Anatomy of Tubercle- 
test tube, when the same process repeated itself ; thus it was possible 
to generate the germs through a series of cultivation, without losing 
their virulence or capacity for reproduction. Under antiseptic pre- 
cautions, guinea pigs were inoculated in the groin with the products 
of the cultivation. The day after the operation the wound was usually 
found healed; on the eighth day a nodule appeared at the point of 
operation, which usually ulcerated. After two weeks, swelling of 
inguinal and sometimes of axillary glands appeared, followed by rapid 
emaciation, and death after the expiration of the fourth to the sixth 
week. At the autopsy tubercles were found in almost all of the 
organs, but most numerous in the spleen and liver. 
Inoculation of the anterior chamber of the eye produced promptly 
local tuberculosis, followed by general infection. Injections into the 
peritoneal cavity and veins of the ear, were followed by the same con- 
sequences. The microscopical examination of products of inoculation 
tuberculosis presented the same histological elements as the spontane- 
ous form. These facts go to show, that the bacilli are not accidental 
companions of the tubercular process, but that they are the essential 
muse, noxae or agens of the disease. Not the presence or peculiar 
arrangement of cells, not the non-vascularity of the product, but the 
presence of bacilli, is the diagnostic feature of the disease. The ma- 
jority of cases of scrofulous affections of bone and lymphatic glands, 
reveal the presence of bacilli, and are consequently identical with 
tuberculosis. If tuberculosis is a parasitic disease, we must endeavor 
to show where the germs came from. The germs develop only when 
kept in a temperature of from 30°—41° C., hence their vital or active 
existence is limited to the animal organism. In man tubercle is found 
most frequently in the bronchial tubes and the lungs, from inhalation 
of air contaminated with the bacillus. All conditions which favor 
the developement of the germs are in direct relation to 
the disease. Although Dr. Koch was not the first to conceive the 
brilliant idea of isolating the tubercular virus from the crude products 
of tubercle, and cultivating the same artificially outside of the body, 
he has nevertheless immortalized himself by his zeal in investigating 
the aetiology of tuberculosis, and in improving the methods of investi- 
gation. Using solid or semi-solid substances as a “Ncihrboden,” con- 
tamination is avoided with greater accuracy, and the process of germ 
development can be watched with greater ease. The results of his 
experiments are so striking, that the most incredulous must soon be 
convinced that we are on the verge of the greatest discovery in medi- 
cine—the isolation and artificial production of the tuberculosis virus. 
Telluric influences undoubtedly either favor or retard the develop- 
ment of the specific germs of tuberculosis, as it is well known that 
the arctic regions offer a certain degree of immunity against tuber- 
culosis, while the tropical countries furnish the greatest number and 
the most acute cases. An altitude of 2000 feet above the level of the Pathology and Morbid Anatomy of Tubercle. 
17 
sea, may be considered the boundary line tor the freqhent occurrence 
of tuberculosis; a dry, sandy soil and a dry atmosphere are also unfa- 
vorable for the growth of the germs, and clinical experience has 
sufficiently demonstrated that these conditions exert a favorable 
influence towards the prevention, arrest and cure of tuberculosis. 
In a communication to the Medical Society of Berlin, Dr. Ehrlich 
describes a new method for detecting the bacilli of tubercle in the 
sputa of tubercular patients, which, on account of its excellence, is 
destined to supercede that of Koch. He extracts, with a pair of 
needles, a small particle of sputum, and presses it bet ween two cover- 
glasses. He then separates the cover-glasses and has a thin layer of 
sputum on each. The cover-glasses are allowed to dry in the air, and 
in order to flx the albumen, they are either kept for an hour at a tem- 
perature of 100° 0.-110° 0., or they are passed two or three times 
through the flame of a Bunsen’s burner. The staining fluid is then 
prepared. Water is shaken up with an excess of aniline oil, and 
Altered through moistened filter-paper. To the clear fluid so obtained, 
an alcoholic solution of methyl-violet, or of fuchsin is added, drop by 
drop, until the fluid becomes opalescent. The cover-glasses, with the 
dried sputum, are then set swimming in this fluid, and in fifteen or 
thirty minutes they will be stained an intense blue or red, according 
as the violet or fuchsin has been used. Dr. Ehrlich now departs 
further from Koch’s method; he does not color the substance in gen- 
eral with vesuvin, but decolorizes it with strong acids, the bacilli 
retaining the blue color. One volume of officinal nitric acid is mixed 
with two of water, and the blue-stained preparations are placed in 
this strong acid. In the course of a few seconds the color fades, a 
yellowish cloud passes across the preparation and leaves it white. 
Everything in the preparation of the sputum is now decolorized, 
except the bacilli, which are intensely blue. But the technical diffi- 
culties of seeing them are still considerable, and it is further desirable 
to color the ground substance yellow, in the case of a methyl-violet, 
and blue in case of a fuchsin preparation. In the specimen of phthisi- 
cal sputum prepared by Dr. Ehrlich, as above, and exhibited at a 
meeting of the Royal Medical and Chirurgical Society of London, the 
bacilli were very numerous, very uniform in size and form, and very 
distinct, the magnifying powers about 900 diameters, and the illumi- 
nation strong. Dr. Ehrlich has examined the sputa from twenty-six 
pronounced cases of phthisis, and he has found bacilli in all of them, 
and most abundantly in acute cases. 
Baumgarten gives the following method of staining tubercle 
bacilli, as easier and more expeditious than those recommended by 
Koch and Ehrlich: Dry preparations of tubercular sputa are made 
according to Koch’s or Ehrlich’s method, and moistened with a very 
dilute solution of potash. The bacteria can then, without further 
treatment, be readily detected with a power of 400-500 diam. Light 18 
Pathology and Morbid Anatomy of Tubercle. 
pressure on the cover-slip will serve to bring them out more clearly. 
In order to distinguish the bacilli of tubercle from other species, the 
cover-slip is removed from the slide and laid to one side, until the 
moisture on its under surface has dried off; it is then passed two or 
three times through the gas flame, and moistened with a drop of 
dilute aniline violet, or other nuclei-staining aniline color. Now 
under the microscope, the putrefactive bacteria are stained a deep 
blue, while the tubercle bacilli remain perfectly colorless, as when in 
the potash solution. The entire process need only require ten minutes, 
and is therefore recommended for general use. 
It now seems certain that the inoculation experiments of Villemin 
and his followers, and more recently the inoculation of isolated germs, 
obtained from cultivation fluids, have at last succeeded in establishing, 
beyond all doubt, the infective nature of tuberculosis on a scientific 
basis. Experimental pathology has been the means of unraveling the 
mysteries of one of the most frequent and destructive of all diseases, 
and is now inviting the therapeutist to pursue a similar course to dis- 
cover a rational and effective course of treatment. It is to be hoped 
that these investigations will be continued until we shall be perfectly 
familiar with the mode of introduction, the conditions of life and the 
diffusion of these germs, and then the time will not be distant when 
we shall be able not only to arrest, but also to prevent the ravages of 
this, the most frequent and hopeless of all diseases—tuberculosis. 
HISTOLOGY OF TUBERCLE. 
The anatomico-pathological basis of tubercle was created by 
Virchow, and has been firmly established through the laborious 
researches of Langhans, Wagner, Klebs, Schueppel, Bindfleisch, 
Koester, Friedlander, Fox, and many others. The specific cell theory 
has had many able advocates, and has been the topic of many ani- 
mated discussions, but it has at last been abandoned as fallacious and 
unscientific. There are no specific tubercle or scrofula cells. When 
we speak of tubercle, we mean a nodule or granule, which is com- 
posed of certain histological elements. The anatomical character of 
the nodule consists, not in the presence of any one particular element, 
but in the peculiar arrangement of the cells, and this is the only relia- 
ble anatomical guide in making a diagnosis. 
Virchow defines tubercle as a nodule representing a heterogeneous 
growth, a production originally necessarily of a cellular nature, tak- 
ing its starting point from the connective tissue, or from some anal- 
agous tissue, as marrow, fat, bone. These nodules (miliary) when 
mature are often so small that they cannot be recognized with the 
naked eye, but usually they are as large as a millet seed, or even larger. 
When the nodules become confluent, they may form masses the size Pathology and Morbid. Anatomy of Tubercle. 
19 
of a walnut, surrounded by a common zone of embryonal tissue. The 
primary nodules are quite firm and of a gray translucent color. Vir- 
chow has subdivided the miliary into submiliary granules, each of 
which contain the essential element of tubercle, and by aggregation, 
constitute the ordinary miliary nodule. The yellow tubercle is a more 
advanced stage of the gray, the histological elements of the latter 
having undergone caseation. 
Colberg has shown that tubercles in the lungs originate from the 
nuclei of the capillary vessels, the connective tissue and alveolar 
cells never being primarily affected. The transition from miliary to 
yellow tubercle, he attributes to a blocking up of the interior of the 
capillary vessels by the new product, and a consequent arrest of the 
circulation, thus diminishing the supply of nutritive material. 
Edward Smith believes in the epithelial origin of tubercle. 
Bastian observed tubercle nodules upon the small vessels in cases 
of basilar meningitis, but refers their origin not to the nuclei of the 
endothelial lining of the vessels, but to the endothelial lining of the 
perivascular lymphatic sheaths through which the vessels of the 
meninges of the brain take their course. Virchow credited the 
endothelial cells in the lymphatic vessels with taking an active part 
in the production of tubercle before Bastian published the result of 
his observations, but was unable to convince himself of the fact. 
Julius Klebs holds that the endothelial cells of lymphatic vessels 
are the primary seat of tubercle. He observed that in cases of tuber- 
cular ulceration of the bowels, the peritoneum is reached through the 
lymphatic vessels, the latter containing tubercle corpuscles in their 
interior. Silver stained preparations of inoculation tuberculosis from 
rabbits showed that the finest points of tubercular material were 
deposited in the interior of the lymphatic vessels at their points of 
intersection. At some points the nodules extended into the tissues 
between the lymphatic vessels, but their center always corresponded 
to the location of a lymphatic vessel. In some places the nodules 
were seen to send out projections, but the projections in reality were 
within the lymphatic vessels, as the network of lymphatic endo- 
thelium could be seen above and beneath the tubercle corpuscles. 
Towards the center of the nodule no endothelial cells could be dis- 
tinguished, and this fact led him to the inference that the normal 
endothelial cells are directly concerned in the production of tubercle. 
In the mesentery he saw the tubercles adhere to the outer wall of the 
capillary vessels, and as the spindle-shaped cells of the outer coat 
appeared to be pushed apart, he looked upon the adventitia as a genu- 
ine lymphoid structure. 
Knauif demonstrated the lymphoid character of the adventitia 
by examining the capillary vessels of the pulmonary pleura of dogs 
which had been exposed for a long time in an atmosphere impregnated 
with coal-dust. He found the pigment lodged in small masses close 20 
Pathology and Morbid Anatomy of Tubercle. 
to the walls of small arteries and veins. Examining the same locality 
in healthy dogs, he found it occupied by opaque whitish-gray nodules, 
surrounded by round and oval cells, containing nuclei and a few 
lymph corpuscles. The same structures, which he called lymph- 
nodules, are also found around the small vessels of the human pleura, 
and by an abnormal increase of lymphatic elements they become the 
primary seat of tubercle. 
Manz has studied the development of tubercle in the choroidea in 
patients suffering from general miliary tuberculosis. So constantly 
does this disease show itself in this structure that v. Graefe, Cohn- 
heim, Fraenkel and Bouchut recommend ophthalmoscopic examina- 
tion as a diagnostic measure. Manz traces the origin of the disease 
in the choroid to a multiplication of the cells of the tunica adventitia 
of the small vessels. The process is, however, not limited to this 
structure; the non-pigmented stroma cells may also assist in furnish- 
ing material for the new product. 
Bush, on the other hand, asserts that the vessels in cases of tuber- 
culosis of the choroid are not primarily affected; the process depends 
entirely on a degeneration of the stroma cells, as the remaining tis- 
sues presented a normal appearance. Cohnheim refers the origin of 
tubercle in these cases to small, pale, finely granular cells resembling 
lymph and pus corpuscles—the contractile migrating cells of Reck- 
linghausen, which may be seen between the pigmented and non- 
pigmented stroma cells. 
Rindfleisch traces the beginning of the process in miliary tuber- 
culosis of the lungs to a proliferation of the endothelium and the 
external connective tissue layer of the capillary lymphatic vessels. 
In contra-distinction to the ordinary or lymphoid form of tubercle, 
there has recently been described the fibrous tubercle, distinguished 
by its pearl-like, light gray appearance, but possessing the same in- 
herent tendency to caseous, fatty degeneration. It is said to be found 
most frequently in dense fibrous tissue, and quite often in newly- 
formed connective tissue. It is composed of nodules of dense con- 
nective tissue, the cells of which have undergone rapid growth, con- 
taining frequently a number of nuclei. A farther development only 
takes place in the interior of the nodule, later no trace of round cells 
is found, the interior undergoing a retrograde metamorphosis into a 
fatty granular mass, somewhat striped, surrounded by a capsule of 
connective tissue. 
The description of fibrous tubercle by Langhans differs materially 
from the above. According to his observations, its favorite location 
is in the so-called parenchymatous organs, as the lungs, liver, spleen- 
kidneys, testicles, epididymis, and brain. The larger nodules are com- 
posed of three zones. The interior consists of a few connective tissue 
fibres, free oil-globules, and cells infiltrated with fat granules. The 
middle zone is composed of all the elements of a fibrous groundwork, Pathology and Morbid Anatomy of Tubercle. 
21 
the fibres of which are placed in a parallel direction to the tubercle. 
As the cells of this zone are not numerous, it presents the appearance 
of a capsule; in reality, however, it is not a capsule for the purpose of 
constituting a barrier to the further extension of the nodule, but it is 
the essential matrix of the internal tubercle tissue. He considers 
this form of tubercle not as a distinct special form, but as a more 
advanced stage of development of the ordinary variety. 
Schueppel is also of the opinion that the fibrous tubercle is only a 
variety of the common tubercle. 
1 believe it must be generally conceded that the fibrous tubercle dif- 
fers from the ordinary cellular variety only in so far that it contains a 
larger amount of connective tissue, which may lie due either to an ex- 
cess of pre-existing connective tissue in the organ which has become 
the seat of tuberculosis, or to an active proliferation of the reticulum of 
the tubercle. Shakespeare and Simes claim that the fibrous tubercle is 
most frequently met with in sypilitics, and that the granulation or 
lymphadenoid tubercle occurs most frequently in the scrofulous. 
In a clinical lecture on miliary tuberculosis, given before the 
Vienna Medical Society, Dr. Hans Chiari called attention to another 
variety of tubercle—the hyaline tubercle. It was first observed by 
Chiari in the miliary tubercle from the liver of a child aged four years 
and a half. The tubercles in the brain, lungs and bronchial glands 
in the same case presented the ordinary aspect of lymphoid tubercle. 
The clear hyaline aspect of those in the liver gave them a very pecu- 
liar appearance. The change is believed to depend on a hyaline de- 
generation of the reticulum, and resembles most closely the hyaline 
degeneration of the capillaries of the brain. Dr. Chiari conjectures 
that it may be regarded as a benign change opposed to the caseation 
which tends to infection. 
Microscopists have made diligent search for a morphological ele- 
ment, which, when found present, should be diagnostic of tubercle. 
Lebert’s tubercle corpxiscle is a thing of the past, and is only 
referred to, to indicate a landmark in the history of tuberculosis. 
Reinhart soon showed that these elements, regarded by Lebert as 
characteristic and diagnostic of tubercle, were present in all products 
of inflammation, and that their product was only an evidence that a 
certain amount of inflammation or degeneration of the tubercular 
nodule had taken place. 
A great deal has been said and written, pro and con, as to the ori- 
gin and diagnostic value of the giant cell in the tubercular nodule. 
Langhans discovered it in tubercular tissue, and as he found it 
uniformly present, he regarded it as an essential anatomical element 
of the tubercular nodule. In his description of the cell, he placed 
great stress upon its uniform size and the peripheral location of the 
nuclei. The giant cell, as described by Friedlander, consists of a mass 
of protoplasm, containing a number of nuclei. It was first discovered 22 
Pathology and Morbid Anatomy of Tubercle- 
in normal tissue by Robin, and subsequently accurately described by 
Virchow. In a normal condition it is constantly found in bone and 
the placenta. According to Koelliker, giant cells are found in such 
parts of bone where resorption is most active during the growth of 
bone. These cells are also found in fat tissue, especially in cases of 
rapid emaciation. Kundrat has observed them in inflamed serous 
membranes, and Strieker and Heitzman in the inflamed cornea. They 
are usually also found around encysted foreign bodies in the periton- 
eal cavity and subcutaneous tissue. Langhans found them around 
blood-clots, after injecting fresh blood under the skin of animals. 
Friedlander found them present in air cells of the lungs, when in a 
state of chronic inflammation. For a long time it has been well- 
known that they are frequently found in the interior of the alveoli of 
cancer. The protoplasm is composed of a coarsely granular albumin- 
ous substance, often containing granules, and the nuclei are usually 
arranged towards the margin of the cell. In regard to the function 
of these cells but little is known. They are supposed to be the active 
agents in processes of absorption, more especially that of bone (Koelli- 
ker). The origin of cells is traced to epithelial cells (Zielonko, 
Weigert), to endothelial cells (Kundrat, Herrenkohl, Zielonko), or to 
atrophic growth of nuclei of fat cells, endothelial cells or connective 
tissue (Virchow, Flemming, Ziegler). Ziegler saw giant cells develop 
from white blood-corpuscles, while Schueppel and Rindfleisch believe 
that they invariably originate within blood-vessels or lymphatics, 
where they constitute the first step towards the development of tuber- 
cle nodules. Around this cell the other elements are arranged succes- 
sively. 
Tiering, Aufrecht, Woodward, Schueller and Treves hold that these 
giant cells are not true cells, but that they only represent spaces, cor- 
responding to transverse sections of lymphatic vessels, the protoplasm 
being the coagulated lymph within these vessels, and the nuclei 
enlarged swollen endothelial cells. These cells have been studied with 
such great care in connection with tubercle, by Virchowr and Fried- 
lander, and their opinions regarding their cellular structure are so 
conclusive and positive, that we can hardly fail to be convinced of the 
correctness of their observations. In tubercle the source of giant 
cells remains unknown; it is rational, however, to assume that they 
are developed from preexisting cell elements, or that they are the 
result of a confluence of several cells. They have been observed to 
exhibit amoeboid movements. They are capable of absorbing smaller 
elements, as blood-corpuscles and pigment molecules. Their existence 
does not necessarily indicate the presence of tubercle, as they are 
found in other pathological products, and form a part of some of the 
normal tissues of the body. They constitute an almost constant and 
important element in tubercle, and from their central location in the 
nodule and the peculiar arrangement of the remaining cellular Pathology and Morbid Anatomy of Tubercle. 
elements around them, valuable diagnostic information is obtained. 
The presence of the giant cell is, therefore, only one of the require- 
ments for a positive diagnosis. 
In every tubercle nodule we find the epithelioid cells first described 
by Rindfteisch and so called from their resemblance to epithelial or 
endothelial cells. They are about two or three times the size of a 
white blood corpuscle, finely granular, and contain one large and a 
number of small nuclei. They may be seen aggregated around the 
giant cells, occupying the space between them and the peripheral zone 
of embryonal tissue. They are supposed to originate from white 
blood corpuscles (Schueppel, Ziegler, Treves), endothelial cells of 
lymph spaces (Aufrecht, Hering, Woodward), or from the endothelial 
cells of the blood vessels and lymphatics or connective tissue cells 
as described by Rindfieisch and nearly every other writer. The re- 
maining cellular element in tubercle is the lymphoid or white blood 
corpuscle found in great numbers between the giant cells and the 
epithelioid cells, and forming a complete and compact peripheral zone 
around these cells. 
The reticulum, according to most authors, consists of the pre- 
existing connective tissue pushed asunder by the cellular elements. 
According to Wagner, Schueppel, Brodowski, Thaon and Ziegler, it 
is made up of protoplasm. According to Buhl, the giant cells and 
epithelioid cells secrete a substance at their periphery which, on be- 
coming hard, is formed into a mass resembling connective tissue; 
only the marginal zone is supplied with the loose ready formed con- 
nective tissue of the organ. According to Wahlberg the principal 
reticulum consists of protoplasm which is traversed by a network of 
connective tissue. 
A mature typical tubercular nodule consists, then, of a delicate 
tissue, densely packed with one or a number of giant cells in the 
center, a large number of epithelioid cells near the center, and lymphoid 
elements disseminated throughout the nodule and forming a dense 
marginal zone. The blood vessels and lymphatics in the nodule from 
intra and inter-vascular cell proliferation become blocked during the 
early stages of the development of the tubercle, rendering the neo- 
plasm non-vascular, a condition which necessarily leads to early 
retrograde metamorphosis of the new product. .No single element of 
tubercle can be regarded as characteristic, but a combination of the 
different elements and their peculiar relations to each other, associ- 
ated with the non-vascularitv of the product, can and must be con- 
sidered as diagnostic. 
LOCAL ANT) GENERAL INFECTION OF TUBERCLE. 
The clinical behavior of tubercle is characteristic and diagnostic. 
The anatomical peculiarity of each tubercle nodule is such that of 24 
Pathology and Morbid Anatomy of Tubercle. 
necessity it must speedily undergo caseation; to this rule there is no 
exception. The circulation in the vessels has become completely ar- 
rested by intra and peri-vascular cell proliferation almost from the 
beginning of the process, thus arresting further supply of nutritive 
material, and in addition the cell elements composing the nodule are 
possessed of such a low degree of vitality, that they are incapable of 
being transformed into living tissue, hence they undergo fatty degen- 
eration. The process of breaking down begins in the interior of the 
nodule and proceeds towards the periphery. When caseation has 
taken place, if from any cause the infectiousness of the local deposit 
has ceased, a favorable termination may take place by a complete or 
partial absorption of the product, the former being possible only 
when the nodules are very small, or, what is more frequent, by calci- 
fication or cretafication, a result which is frequently observed in the 
lungs. Softening and suppuration may afford a complete outlet to 
all tubercular material, as in the case of tuberculosis of the lymphatic 
glands, and thus lead to a permanent recovery. If the tubercular 
deposit is located in the skin or any of the mucous membranes, and 
softening and suppuration take place, it results in the formation of 
obstinate tubercular ulcerations, or fistulous tracts, which very sel- 
dom terminate in complete repair. 
In some organs, more especially in the lymphatic glands, the prog- 
ress of the disease is sometimes arrested by the formation of a firm 
capsule around the caseous mass; in this manner the infectious mate- 
rial is isolated and prevented from invading the neighboring tissues. 
These favorable terminations are the exception, the growth of the 
tubercle, local and general infection, the rule. The growth of the 
tubercle nodule takes place partly by segmentation of the nuclei of 
the newly formed elements, but mostly by conversion of the normal 
cells in the vicinity of the nodule under the influence of a moderately 
active or passive hypersemia. By the growth of a number of such 
nodules, confluence takes place, which results in the formation of 
masses of considerable size. The local infection takes place through 
the medium of the cellular elements charged with the infectious 
germs. The white blood corpuscles possessing, as they do, active 
amoeboid movements, readily insinuate themselves into the surround- 
ing lymph spaces and thus become active carriers of the tubercular 
virus, establishing new foci of disease wherever they become lodged. 
The growth of the nodule is progressive; its extent corresponds to 
the area of the infected district. The tubercular process knows no 
anatomical boundary line, its onward march is slow but sure, it at- 
tacks vessels, connective tissue, glands, membranes, skin, cartilage, 
bone, etc., alike, and converts or displaces any and all of them. 
It has been supposed by many that the presence of a caseous de- 
posit is necessary to give rise to miliary eruptions of tubercle, inas- 
much as the gray tubercle is usually found around the margins of Pathology and Morbid Anatomy of Tubercle. 
25 
caseous masses. It is, however, more than probable that these case- 
ous loci are the product of a previous tubercular deposit, and that the 
gray granulations constitute the starting point of the disease, casea- 
tion following step by step the onward march of tubercle. When 
tubercle has resulted in the formation of an abscess, the lining mem- 
brane of such abscess is invariably infiltrated with miliary tubercle 
and the process of infection follows the course of the abscess. This 
explains why the so-called scrofulous abscesses have always proved 
so rebellious to the usual methods of treatment, and why so many of 
these cases have been followed by diffuse miliary tuberculosis. 
Tubercle manifests also an inherent tendency to general infection. 
The local infection is usually a slow process, and may give rise to 
great destruction of tissue, but is seldom the direct cause of death, 
unless it interferes with the function of some vital organ, while gen- 
eral infection, on the other hand, usually assumes a rapid course and 
almost invariably leads to a fatal termination. The manner of infec- 
tion is the same as in local infection, only that the histological ele- 
ments which carry the specific germs are conveyed along the lymph 
or blood current to distant organs, where they establish numerous 
new foci of the disease. The lymphatic current is usually the medium 
of communication where the primary depot is located in the skin, in 
a mucous or serous membrane, or in a lymphatic gland; on the other 
hand, when the disease is primarily located in a joint or bone, it 
reaches the internal organs through the blood current leading to 
metastatic or embolic tuberculosis. I will illustrate this by reporting 
two cases: 
Case I.—Primary Tuberculosis of Lymphatic Glands of Neck, fol- 
lowed by Miliary Tuberculosis of Lungs. — Francis Schuhmacher, 
aged 18 years, was admitted into the Milwaukee Hospital April 
fith, 1882. The history of the case does not show any hered- 
itary taint in her family. She has always been a strong, healthy 
girl until about a year ago, when she noticed a glandular enlarge- 
ment on the right side of the neck, just beneath the angle of the 
jaw. Menstruation has been regular, but scanty. The parents 
of the patient noticed that soon after the glandular enlargement 
made its appearance she became paler than usual, and complained of 
lassitude and loss of appetite. The primary swelling was soon fol- 
lowed by a whole chain of enlarged glands, extending from the ear 
to the clavicle on the affected side. The family physician instituted 
the usual course of treatment advised in such cases, but without 
signal success. The patient passed into the hands of another prac- 
titioner, who applied poultices to favor suppuration. He punctured 
two of the largest glands, but no pus escaped. From this time the 
patient rapidly became worse; redness and tumefaction around the 
punctures followed. At the time of admission the patient presented 
an extremely anaemic appearance, but little, if any, emaciation. The 26 
Pathology and Morbid, A natomy of Tubercle. 
whole right side of the neck from the ear to the clavicle presented 
one large mass of enlarged glands. At the points of puncture I 
found two large ulcerations from which protruded masses of cheesy 
material, the source of an extremely offensive odor. The skin over 
the cheesy masses was reddened and undermined for a considerable 
distance from the margins of the ulcerated excavations. The glands 
which were not ulcerated varied in size from a small orange to that 
of a hemp seed. It was evident that local infection had spread 
beyond the reach of the knife, still I was anxious to extirpate the 
glands which communicated with the air and thus remove a great 
source of irritation and suffering. The patient was etherized, and, 
with the assistance of Drs. Naum arm and Marston, a mass of lym- 
phatic glands, and among them the ulcerated glands, were removed. 
The superficial and deep glands were affected. The capsule around 
the largest glands was very thick and firm, and all the glands pre- 
sented a greater or less amount of caseous degeneration. The wound 
healed kindly, and the patient was permitted to leave the hospital a 
week after the operation. 
July 6th, 1882, the patient called at my office. The wound had 
nearly healed. The remaining glands had not enlarged much since 
the operation. About four weeks after the operation she began to 
suffer from a dry, harassing cough, fever and night sweats. Tem- 
perature 103°, pulse 140; she had become greatly emaciated, and an 
examination of the chest revealed the existence of miliary tubercu- 
losis, affecting principally the right lung. At the time of writing 
(August 3d) I hear that the patient is very feeble and is not expected 
to live more than a few weeks. This case is of great interest, as it 
illustrates the progress of the disease step by step along the lymphatic 
channels until it reached the lungs. It also teaches an important 
lesson, not to tamper with tubercular lymphatic glands, but to resort 
at once to radical treatment by early and thorough removal of the 
local deposits. 
Case II. — Synovitis Hyperplastica Granulosa of Ankle-joint, 
Evidement. Death from Metastatic or Embolic Tuberculosis.—L. 
McKennon, aged twenty-three years, laborer, was admitted into 
Milwaukee Hospital Dec. 25, 1881. No disposition to scrofula or 
phthisis present in his family, and he has always enjoyed good 
health until about a year ago, when, while working in the pineries, he 
sprained his left ankle. The joint remained painful, but he was able 
to walk without crutches until two months ago. At the time of 
admission, he suffered great pain with nocturnal exacerbations. The 
joint was swollen and a sense of fluctuation could be felt below each 
of the malleoli; superficial veins enlarged and leg atrophied. The 
patient was considerably emaciated and his appetite impaired. No 
signs of pulmonary or renal difficulty could be ascertained at this 
time. As the patient objected to an amputation, it was decided to Pathology and Morbid Anatomy of Tubercle. 
27 
open the ankle-joint and remove the diseased tissues as thoroughly as 
possible. The operation was performed under strict antiseptic precau- 
tions, Feb. 22, 1882, with the assistance of I)rs. Xaumann, Lang, 
Mendel, Mueller, Massmann and Martin. The ankle-joint was opened 
freely on the inner and outer side, when a mass of fungous granula- 
tions made its appearance, and a small quantity of sanious llocculent 
fluid escaped. The articular cartilage was completely destroyed, pieces 
of considerable size lying loose in the joint. The articular ends of 
the bones were rough, presenting a honey-comb appearance, and con- 
siderably softened. All diseased structures were thoroughly removed 
with a sharp spoon and gouge, 'the joint was well drained and immo- 
bilized. Xo inflammation or fever followed the operation. Suppura- 
ation was slight, but the wound at no time manifested a tendency to 
repair. The patient’s general condition did not improve, and about 
four weeks after the operation a slight cough and rise of temperature 
induced me to examine his chest again. Fine crepitation could be 
heard all over the chest, and the patient began to fail rapidly and 
died April 16th, 1882. Two days before his death he complained of 
intense headache, and soon became delirious. 
At the autopsy it was ascertained that the scraped ends of the 
bones were rough, having shown no tendency to reparative action. 
The lungs were studded with miliary tubercles throughout, the larg- 
est number being found at the base and margin. Smaller and less 
numerous nodules were found in the liver, spleen, kidneys and 
meninges at the base of the brain. 
In this case we must take it for granted that at the time of opera- 
tion secondary deposits had already taken place in the lungs, or that 
the local product in the joint was not completely removed. The 
practical lesson to be learned from this case is to operate early in 
similar cases, and to secure a complete removal of the infected tissues 
either by complete excision or amputation. The arrangement of 
the vessels in bone is such that infected elements readily enter the 
blood vessels and then And their way into the pulmonary capillaries and 
from them into the general circulation. When the infecting agents 
are carried along the lymph current, they generally are arrested in 
the nearest lymphatic gland, thus preventing a rapid general inva- 
sion. The infected lymphatic gland serves the purpose of a cultiva- 
tion fluid for the development of the germs, and soon sends along the 
lymph current new infecting elements, which invade a neighboring 
gland, and thus the process is repeated until the disease reaches a 
vital organ, or the germ-laden elements reach the general circulation 
and initiate an embolic or metastatic tuberculosis. 
When the germ-holding elements take a more direct route by 
entering the general circulation at once, they reach the lungs, where 
they are usually arrested in the capillaries, giving rise to diffuse mili- 
ary tuberculosis of the lungs. Some of the germ carriers may pass 28 
Pathology and, Morbid Anatomy of Tubercle. 
directly through the capillaries, or may issue from one of the new 
nodules in the lungs, and again enter the circulation and become 
deposited in a more distant organ, in preference in the spleen, liver, 
kidneys and brain, thus giving rise to general diffuse miliary tuber- 
culosis. As a rule such organs or parts of the body are most prone to 
become the seat of infection which offer the greatest amount of 
mechanical difficulties to the circulation, or where the rapidity of the 
current has become impeded by some antecedent pathological condi- 
tion; in other words, stasis predisposes to the localization of tubercle. 
HEREDITY OF TUBERCULOSIS. 
Almost all text books insist that tuberculosis is an hereditary 
disease, being, in the majority of cases, transmitted from parent to 
offspring. So firmly is the profession impressed with the correctness 
of this assertion, that in every case of suspected tuberculosis, diligent 
search is made to ascertain who is responsible for the disease. If by 
chance it is ascertained that one of the relatives of the patient was 
afflicted with a cough, and died at a premature age, then the diagnosis 
is considered as settled. It is not difficult to conceive how unreliable 
in many instances such information may be; but it is difficult to 
understand in what manner a great-grandfather, an uncle, an aunt or 
a cousin could transmit the disease, without being able to trace a 
direct continuation through the parents of the patient. The so-called 
scrofulous affections have always been recognized as being frequently 
the cause of tuberculosis; recent anatomical and experimental re- 
search, as well as clinical observation, however, tend to establish their 
identity; hence any facts bearing on the question of the heredity or 
non-heredity of scrofula will assist in proving or disproving the 
hereditary nature of tuberculosis. 
A weakness of lymphatic vessels in scrofulosis was recognized by 
Sylvius as early as 1695, by Portal in 1809, and still later by Bell, Per- 
cival Pott, Hufeland and Broussais. Pox is of the opinion that a 
disposition to tuberculosis may be found in certain anatomical or 
physiological defects in the lymphatic system. Virchow ascribes the 
cause of scrofula to a weakness or imperfection in the arrangement 
of the lymphatic apparatus, C. Hueter to a dilation of lymph spaces; 
and Billroth to a constitutional anomaly. 
Byford, in speaking of the exciting causes of scrofula, says : 
“ They are abuses which, in an ordinary condition of the system, 
would lead to common local inflammation or congestion.” 
Mordhorst regards a sluggish circulation, the consequence of super- 
ficial, imperfect respiration, by causing capillary stasis, and favoring 
diapedesis, a potent factor in producing the peculiar vulnerability of Pathology and Morbid Anatomy of Tubercle. 
29 
the tissues in scrofulous subjects. The capillaries of lymph vessels 
are composed of a delicate, structureless membrane, lined on the inner 
side by endothelial cells, and these vessels surround like a sheath the 
capillary blood vessels and small veins. In scrofula patients, these 
lymph channels are filled and become blocked with white blood cor- 
puscles, which elements, under certain conditions, are transformed 
into tubercular structures and invade lymphatic glands. Tuberculosis 
of the lungs follows when thes*e metamorphosed blood corpuscles 
reach the subclavian vein and are conveyed into the pulmonary capil- 
laries. 
Rokitansky placed great stress on the importance of an imperfect 
circulatory and respiratory apparatus as a predisposing cause to 
tuberculosis. By removing venous stasis, the rapidity of the lymph 
current is increased, and the tendency to glandular swelling dimin- 
ished. 
In 1871 Friedlander suggested that in cases of tuberculosis there 
might be present, and active, a fusion of the scrofulous and tuber- 
cular diathesis, a view which was endorsed by Charcot in 1877. 
Aufrecht claims that the disposition to the origin of tubercle may 
be found in the lymphatic vessels. Riedel defines the hereditary predis- 
position to tuberculosis, as consisting in a peculiar anatomical arrange- 
ment of the tissues, especially of the lymphatic glands, which furnish 
a favorable soil for infection. According to Max Schuller, the 
heredity of tuberculosis is greatly overrated. The germs which are 
supposed to be the specific agents in the production of tubercle, exert 
a direct effect on the tissues, exciting a slow form of inflammation, 
with a tendency to speedy retrogade metamorphosis of the new 
material. Quincke recognizes a close relationship between scrofula 
and tuberculosis, when he says: “Scrofulous persons are especially 
predisposed to tuberculosis; tuberculosis hardly ever occurs except in 
scrofulous persons.” 
Ziegler was aware that pulmonary phthisis is the most frequent 
cause of death in scrofulous patients. James T. Whittaker, in com- 
paring the aetiology of tuberculosis with syphilis, makes use of the 
following positive common-sense lauguage: “ There is no such a thing 
as a predisposition to either disease. Either a man has syphilis or he 
has it not. One man is not more predisposed to either disease than 
another. Syphilis affects one individual more than another because 
its virus finds a better lodgment upon mucous membrane. Tubercu- 
losis finds also, fortuitously, a better nidus in one case than another. 
The virus of tuberculosis is lodged in one case and not coughed up, 
just as in syphilis the virus is secreted and not washed off.” And 
again: “From any chancre, plague, gumma, or other deposit of 
syphilis, reabsorption may take place at any time, and reinfection 
with syphilis, or better, reappearance of external signs. So, from any 
caseous nodule, wherein the tuberculous virus is locked up in tempo- 30 
Pathology and Morbid, Anatomy of Tubercle- 
rary innocence, absorption may take place under favoring circum- 
stances, and a new outbreak of tuberculous symptoms appear, the 
quantity of virus thus set free determining, to a great extent, perhaps, 
the virulence of the symptoms. While the virus is thus locked up 
the disease is latent, when set free it is manifest.” Wynne Toot says: 
“Tubercles are small-celled overgrowths of lymphatic tissue (as in 
acute miliary tubercle) that have preserved such uniformity of size, 
color and shape, as to have long suggested the probability of their 
lymphatic origin.” Wilson Fox describes tubercle as “ an overgrowth, 
or hyperplasia of lymphatic tissue, resulting from irritation of the 
lymphatic elements.” 
W. S. Savory, in speaking of the relation of scrofula to tubercle, 
remarks as follows: “ It appears to me that there is nothing sufficient 
to warrant the pathological distinction which it is now the fashion to 
make between scrofula and tubercle.” And further: “ Tubercle may 
be said to be the essential element of scrofula.” According to Roki- 
tansky, the most frequent seat of tubercle in children is in the 
lymphatic glands. 
Virchow holds that scrofula constitutes the basis of tubercle, and 
that in man tuberculosis depends in general on scrofula. He says 
further: “On account of the histological identity of the scrofulous 
and tubercular new growths, it is often impossible in a given tuber- 
cular lesion, to determine how much is inflammatory and how much 
is tubercular.” 
From above quotations it becomes apparent that nearly all authors 
recognize, if not the identity, at least a close relationship between 
scrofula and tuberculosis, consequently any facts bearing on the 
heredity of the former, will apply with equal force to the latter. 
So-called scrofula implies a diminution of the relative amount of 
blood to the solid tissues (Rindfleisch), and an anatomical and physio- 
logical defect in the capillary blood-vessels or the lymphatic system, 
conditions highly favorable to the occurrence of stasis and a low 
grade of inflammation. The scrofulous habitus, then, may be looked 
upon as furnishing one kind of soil favorable for the development of 
tubercle, and in this sense the hereditary predisposition to tuberculo- 
sis must be considered as established. It is only reasonable to assume 
that congenital defects in the composition of the blood, the blood-ves- 
sels, the lymphatic apparatus and the lymph-spaces may occur as fre- 
quently and regularly as many other well-known anatomical peculiari- 
ties, the heredity of which has long been known and classed among 
undoubted facts. But this does not establish the heredity of tuber- 
culosis. Hereditary tuberculosis would imply that the specific germs 
were transmitted from parent to offspring through the medium of the 
semen or ovum. A person with an inherited disposition to scrofula, 
will enjoy immunity from any active manifestations of the disease, 
just so long as he can be kept free from infection with the specific Pathology and Morbid Anatomy of Tubercle. 
31 
germs of tuberculosis. Let such a person be exposed and he will be 
in constant danger of becoming a victim of tuberculosis. After infec- 
tion has taken place, localization of the tubercle process will occur in 
that organ which presents the least amount of resistance to infection, 
on account of congenital or acquired defects. 
The reputed hereditary tendency of tuberculosis owes its origin to 
the fact that children of tubercular parents, born, perhaps, with a 
defective body, have been exposed, more or less, either directly or 
indirectly, to infection with specific germs from the sputa of phthisical 
parents, which may be communicated through the medium of the air, 
water, food, clothing, etc., and finding a favorable soil, propagate the 
disease. Place children of tubercular parents under the most favor- 
able hygienic conditions, prevent infection by isolation or a thorough 
and well-directed system of disinfection, and tuberculosis will become 
a preventable non-hereditary disease. 
I will close by submitting to your further consideration and dis- 
cussion, the following conclusions : 
I. Tuberculosis is an infective, specific, parasitic disease. 
II. Scrofula and tuberculosis are identical', pathologically, setio- 
logically, anatomically and clinically. 
III. Tubercle is the product of a chronic, specific type of inflam- 
mation. 
IY. Xo single histological element of the tubercle nodule can be 
considered as diagnostic, but the non-vascularity of the nodule, and 
the peculiar arrangement of the cells, furnish the necessary require- 
ments for rendering a correct diagnosis on an anatomical basis. 
V. The prominent clinical feature of tubercle consists in its 
tendency to local and general infection. 
YI. Xo organ or pathological product can become the seat of 
tubercle independently of the action of the specific germs of tubercu- 
losis. 
YI1. Tuberculosis is not a hereditary disease, but a predisposition 
to it may be, and then consists in an anatomical defect of the lym- 
phatic apparatus, or the capillary vessels, combined with a diminution 
in the relative amount of blood to the solid tissues of the body 
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