expressed by the terms progressive and non-progressive. The disease is
progressive when the local and the general symptoms denote more or less
activity in the tuberculous process, the physical signs generally
showing progressive extension of the pulmonary affection. It is
non-progressive when symptoms and signs having the significance just
stated are wanting. The disease may become non-progressive early or
late, and at any period during its continuance. A stationary condition
may continue indefinitely. The symptoms and signs may show processes of
restoration--namely, disappearance of the tuberculous product,
diminution in size, and the cicatrization of cavities. The disease is
then said to be regressive. A regressive course is not extremely
infrequent. It is more or less slow and may or may not end in recovery.
A stationary condition, regression having taken place to a greater or
less extent, is not infrequently observed. This condition may remain
because the pulmonary lesions are too great to admit of restoration. In
most cases the disease is not steadily progressive. It ceases from time
to time to progress, the periods of non-progression varying much in
duration. With each renewal of progress the physical signs generally
show an addition to the tuberculous product. As a rule, this product
does not increase continuously, but, as it were, by successive
eruptions after intervals of time which may be either short or long.
Pulmonary phthisis in some cases ceases to progress, and regression
continues, recovery taking place from an intrinsic tendency--that is,
irrespective of any measures of treatment. This highly important fact
has not hitherto been distinctly recognized by medical writers and
practitioners. I have established it by having recorded a series of
cases in which recovery took place without medicinal or other treatment
and without any material change in habits of life.[1] In these cases
the disease may be said with propriety to be self-limited.[2] The
weight of this fact in its bearing on prognosis and treatment is
obvious. That non-progression and regression ending in recovery may be
brought about by judicious measures of management cannot be doubted; in
other words, the disease may be arrested in a certain proportion of
cases when non-progression and recovery would not have resulted from an
intrinsic tendency or self-limitation.
[Footnote 1: _Phthisis, in a Series of Clinical Studies_, by Austin
Flint, M.D., 1875.]
[Footnote 2: Vide "Self-limitation in Cases of Phthisis," by Austin
Flint, M.D., N.Y., _Archives of Medicine_, June, 1879.]
Pulmonary phthisis proves fatal by undermining more or less slowly the
powers of life. The appetite and digestion fail. There is progressive
loss of weight and of muscular strength. A greater or less degree of
pyrexia is persistent, with diurnal exacerbations and night
perspirations, forming what is known as hectic fever. Muco-purulent
matter is expectorated in abundance, with fatiguing cough. The
respirations are accelerated, and there is often suffering from
dyspnoea. The pulse becomes more and more frequent and weak. Oedema of
the lower limbs is of frequent occurrence. The patient dies by slow
asthenia, the mental faculties usually remaining intact and the patient
hopeful of recovery to the last.
The history of the disease in many cases embraces tuberculous
affections elsewhere than in the lungs, and other complications. The
duration is often {394} shortened by some of these. The more important
are tuberculosis of the intestines, tuberculous peritonitis,
perforation of lung giving rise to pneumo-hydrothorax, pneumorrhagia,
pulmonary gangrene, tuberculous meningitis, and chronic laryngitis
affecting deglutition. The less important affections are pleurisy with
effusion, thrombosis of the femoral or the iliac vein, a circumscribed
non-tuberculous acute pneumonia, chronic laryngitis not affecting
deglutition, intercostal neuralgia, and perineal fistula. Profuse
hæmoptysis is sometimes a grave event, and may prove the immediate
cause of death.
It is impossible to divide the course of pulmonary phthisis into
sharply-defined stages based on anatomical changes. Often after death
the lungs present in different situations all the changes which
intervene between a fresh tuberculous product and cavities. The
division into a stage of crudity of the product and a stage of
softening is of no practical utility. There are no symptoms nor signs
which are reliable for determining when softening has taken place. The
existence of cavities can generally be determined by means of the
cavernous physical signs, and the disease may be considered as advanced
phthisis when cavities are discovered. The term incipient phthisis is
used to designate an early period of the disease. Having passed the
incipient or early period, and before reaching the advanced stage or
stage of excavation, cases may be conveniently grouped according to the
amount of the tuberculous affection. In different cases and at
different periods in the same case the affection is either small,
moderate, considerable, or large. Exact chronological divisions are
impracticable.
ETIOLOGY.--Pulmonary phthisis, as a rule, is developed irrespective of
any antecedent affection of the lungs. The researches of Louis
established the fact that the phthisical affection is very rarely
preceded by bronchitis, either acute or chronic.[3] My clinical studies
have led to the same result.[4] That a neglected cold may eventuate in
phthisis is a traditional popular error, unfortunately held also by
some medical writers and practitioners. The error is to be regretted
because it often interferes with hygienic management in cases of
phthisis. The name chronic catarrhal phthisis proposed by Niemeyer was
based upon this etiological error. It is a matter of common clinical
observation that persistent bronchial inflammation leading to pulmonary
emphysema, and often accompanied by asthma, involves no liability to
phthisis. The long-continued inhalation of coal- and stone-dust, of the
oxide of iron, and particles of other substances gives rise to
bronchitis and interstitial pneumonia (pneumonokoniosis, anthracosis,
siderosis, etc.), but is rarely followed by the common form of
pulmonary phthisis. It is common for phthisical patients to suppose, as
a matter of course, that their disease originated in a cold. In giving
the previous history they often say that they took cold at a certain
time. The analysis of carefully-recorded cases shows that very rarely
does the disease follow directly upon an attack of bronchitis,
notwithstanding that the frequency of the latter, from the law of
chances, would involve an accidental concurrence in a certain
proportion of cases. Acute lobar pneumonia or pneumonic fever has
little or no tendency to eventuate in phthisis. This statement is
sustained by the researches of Louis and by my clinical studies. In the
rare instances in which phthisis follows either acute pneumonia or
bronchitis, the latter diseases act only as auxiliary causes of the
phthisical affection if the sequence be more than an accidental
connection. This statement applies also to pleurisy with effusion. In
certain of the few instances of phthisis apparently having been
preceded by pleurisy it is probable that the former was the antecedent
disease, occurring early in the history of the phthisical affection and
retarding or arresting the progress of the latter. It may be added that
there is no ground for supposing that phthisis is ever produced solely
by traumatic causes acting upon the chest.
[Footnote 3: _Recherches sur la Phthisie_, 1825.]
[Footnote 4: _Phthisis, in a Series of Clinical Studies_.]
{395} It is an old doctrine that bronchial hemorrhage may be causative
of phthisis. This doctrine has been recently revived by Niemeyer and
some others. It is disproved by the following clinical facts: in
two-thirds of the cases in which hæmoptysis antedates phthisis the
development of the latter is after the lapse of a considerable
period--weeks, months, or years. The instances are few in which
phthisis immediately follows the hemorrhage. The occurrence of
hæmoptysis during the course of phthisis, as a rule, is not followed by
any increase of the phthisical affection. On the contrary, the local
symptoms are not infrequently relieved by the hemorrhage. It is,
however, to be remarked that hæmoptysis as a forerunner of phthisis is
of much significance. In the larger proportion of cases phthisis
follows its occurrence sooner or later. It is to be added, in view of
the recent discovery by Koch, that bronchial hemorrhage may proceed
from the same local cause which afterward leads to the development of
phthisis--namely, the presence of a special micro-organism.
The etiology of pulmonary phthisis not involving any antecedent
affections of the lungs nor any appreciable local causes, it would seem
to follow that the disease involves either a predisposing or a
causative agency elsewhere within the organism; and as, with our
present knowledge, the source of this intrinsic agency cannot be
localized, it is customary to say that the disease has a constitutional
origin. This use of the term constitutional here, as in other
instances, expresses an important fact--namely, that the disease is not
purely local; that is, attributable solely to extrinsic or any
appreciable causes acting on the affected part. At the same time, the
term is a confession of the imperfection of our knowledge, inasmuch as
it does not specify the nature of the causative or predisposing agency,
nor its origin, beyond the statement that it is not local. That the
constitutional agency has a special character is a logical inference
from the fact that the disease may be said to have such a character.
The term vulnerability does not fully express the special character of
the constitutional agency. The condition of the constitution which
stands in a causative relation to the disease is something more than an
undue susceptibility to morbific influences of any kind--a
susceptibility giving rise to diseases the nature and seat of which are
accidental. The condition is one which has relation both to the
character and the situation of the pulmonary affection. Such a
condition is expressed by the term cachexia.
It remains to inquire whence arises this phthisical or tuberculous
cachexia.
A congenital predisposition or diathesis exists in a certain proportion
of cases. This is to be inferred from the number of instances in which
several or many members of a household, brothers and sisters, become
affected with phthisis. There may or may not be evidence that this
predisposition is inherited. An inherited predisposition is to be
inferred from the number of the cases in which parents or grandparents
were phthisical. While statistical facts show undoubtedly heredity as
involving a causative agency, making due allowance for the law of
chances, it is important for the physician to bear in mind that a
tuberculous parentage involves only a certain measure of liability to
phthisis in the offspring. The progenitors of many healthy men and
women have been phthisical. There are instances of large families of
children in which many have died with phthisis, leaving, however, some
who escape this disease and are in all respects healthy.[5] The
question arises whether in cases of phthisis where there is lack of
evidence of a congenital predisposition the diathesis may not be
innate. The affirmative answer seems probable in view of the inability
oftentimes to find any rational explanation on the supposition that the
diathesis has been acquired. Positive data bearing on this question are
of course not available.
[Footnote 5: For data on which these statements are based, vide
_Phthisis, in a Series of Clinical Studies_, by the author.]
{396} Age has a decided influence on the development of phthisis. Cases
in which the ages of patients are between twenty and thirty years
greatly preponderate over the number in any other decade of life. Next
in order as to the number of cases are the ages between thirty and
forty years. The form of tuberculous disease under present
consideration is rare under ten years and also in advanced life. All
that can be said with our present knowledge in explanation of the
influence of age is, that either an existing diathetic condition tends
intrinsically to the development of the disease or that the diathesis
is likely to be acquired at certain periods of life more than at other
periods. Of these two explanations the former is the more rational.
Statistics show that occupations which involve sedentary habits,
confinement within doors, especially in small, illy-ventilated rooms,
poor or insufficient food, and prolonged mental depression, increase
the liability to phthisis. The disease is developed either during or
shortly after gestation in a sufficient number of cases to show that
pregnancy has a causative agency. Facts appear to show a less degree of
prevalence of the disease in most cold and tropical climates than
within the temperate zone. It is, however, true, as stated by Ruehle,
that "there are regions in all zones which are free from the disease,
and, on the other hand, there is no zone in which it is not very
prevalent." The prevalence is less in high than in low altitudes.
Humidity of the soil has been shown by Bowditch, Buchanan, and others
to enter into the etiology. In order to determine how far purely
climatic agencies exert an influence either for or against the
prevalence of the disease, it is necessary to take into account other
associated agencies, together with an innate predisposition; and the
latter especially does not admit an exact estimation.
Certain general diseases seem to involve a liability to phthisis as a
sequel. This is true of rubeola and pertussis. In cases of diabetes
mellitus, phthisis is considered as occurring sufficiently often to
show a causative connection. In my own clinical experience, however,
phthisis has not been of frequent occurrence in that disease. Typhoid
fever in some cases appears to favor the development of phthisis. Some,
however, have contended for the reverse of this statement. Certain
affections are apparently antagonistic in their influence. In this
category are pulmonary emphysema and obstructive or regurgitant
valvular lesions at the mitral orifice of the heart. The disease is
rarely developed in chlorotic patients. Facts go to show that
alcoholism opposes its development. In opposition to current belief, my
clinical studies lead me to conclude that they who have had scrofulous
disease of the cervical glands in early life are not likely to become
phthisical in after years. Contraction of the chest from deformity
diminishes the liability to the disease.
The communicability of phthisis is a doctrine dating as far backward as
the history of medicine extends. Distinguished physicians in every age
have held that the disease may be communicated under circumstances
which involve close proximity, as from husband to wife or vice versâ,
and from patients to nurses or attendants. The contagion is supposed to
be contained in the expired breath. The clinical evidence in behalf of
this doctrine is the number of instances which seem to be striking
examples of communicability. It is easy to collect a considerable
number of such examples. But in order to constitute clinical proof of
the doctrine of communicability the number must be so large as not to
be accounted for on the ground of mere coincidence. A collection of
isolated instances gathered from medical literature or reports from
different physicians does not establish the doctrine. Owing to the
great frequency of phthisis, mere coincidence suffices to account for a
certain number of instances. Moreover, long-continued proximity to
cases of phthisis generally involves causative agencies other than a
contagium--namely, confinement within doors and mental anxiety. In my
collection of 670 recorded cases of phthisis, the number of instances
in which there was {397} room for the suspicion of the disease having
been communicated either from the husband to the wife or from the wife
to the husband amounted only to 5. In one of these instances, a wife,
who became phthisical after her husband, had lost two sisters, one of
whom was a twin sister, by the disease. It must be admitted that the
analysis of these cases, without disproving the doctrine of
communicability, fails to lend to it support, for the reason that in
such a large collection of cases the number of examples of apparent
communicability are so few.
A new and strong impetus was given to the discussion of the doctrine by
the discovery of the inoculability of tuberculous disease. Villemin in
1865 demonstrated the fact that this disease could be communicated to
rabbits and guinea-pigs by inserting beneath the skin portions of the
tuberculous product. The experiments of Villemin and many others have
shown conclusively that the insertion of fresh undecomposed tuberculous
matter beneath the skin or within the pleural and the peritoneal
cavity, or in the anterior chamber of the eye, is followed by an
eruption of tubercles in these animals within two or three weeks. If
tuberculous matter taken from an animal in which the disease has been
produced by inoculation be inserted in another animal, the disease is
transmitted to the latter. These results of inoculation, which have
been abundantly confirmed in all countries, prove indisputably the
communicability, by that mode, of tuberculous disease in certain
animals which have a peculiar susceptibility thereto. The fact that the
disease is not readily communicated to dogs, cats, and other animals
shows a peculiar susceptibility to be an important factor in the
successful results of inoculation. The conclusion drawn by Villemin and
others from these experiments is that the disease is communicated by
means of a specific virus, a term implying the existence of a
contagium.
Opposed to this conclusion are experiments which appear to prove that
tubercles may be produced in rabbits by inoculating them with various
kinds of non-tuberculous matter. By those who adopt the doctrine of a
specific virus it is contended either that true tubercles are not
produced in these experiments, or that, if followed by the development
of true tubercles, the production of the latter is attributable to the
derivation of the virus from the laboratories in which tuberculous
animals had been confined or to a contagium received directly from
these animals. The introduction of non-tuberculous matter was found by
Cohnheim and Fraenkel never to be followed by tuberculous disease when
the experiments were repeated in places where tuberculous animals had
not been confined and the animals on whom the experiments were made
were isolated from those affected with tuberculosis. Cohnheim states
that inoculation with portions of indurated lung, or of the nodules
resulting from peribronchitis, or of the contents of bronchiectasic
cavities, will not give rise to true tubercles, for the reason that,
although taken from phthisical lungs, they do not contain the
tuberculous virus. This distinguished pathologist, at first an opponent
of the doctrine of a specific virus, afterward became a strong advocate
therefor. He was led to regard a successful inoculation as affording
the only criterion and reliable test of tuberculous disease; that the
etiology of tuberculous disease invariably involves the presence in the
system of this virus; that it exists in a latent form whenever there is
an innate predisposition to phthisis; and that it may enter the system
in different directions--namely, with the inspired air into the lungs,
and even within the skull through the foramen of the ethmoid bone, into
the small intestine by deglutition, and into the uterus with the semen.
Becoming developed in any situation, the virus may remain localized, or
it may be disseminated more or less extensively by means of the lymph
and blood. The behavior of the tuberculous virus, according to
Cohnheim, corresponds closely to that of syphilis.
Experiments made by Gerlach, Bollinger, Aufrecht, Chaveau, Leisering,
{398} Harms, Gunthern and others, have shown that the disease may be
communicated by incorporating tuberculous matter with food. Rabbits,
guinea-pigs, dogs, calves, swine, sheep, and goats have been rendered
tuberculous by these experiments. Klebs, Tappeiner, Parrot, and Puech
claim to have communicated the disease by combining with the food the
matter of expectoration from phthisical patients. Gerlach and Klebs
have seen the disease in animals fed with milk from cows affected with
the so-called pearl disease (perlsucht), which is considered to be
identical with phthisis. Finally, the disease appears to have been
produced by exposing animals to an atmosphere impregnated with fine
particles of tuberculous matter by means of an atomizer, and by blowing
into the trachea this matter reduced to a fine powder.[6]
[Footnote 6: For a summary of the experiments relating to the
communicability of tuberculous disease by inoculation, by the ingestion
of tuberculous matter, and by its inhalation, and for reference, the
reader is referred to an article by Wm. P. Whitney in the _Boston
Medical and Surgical Journal_, July 28, 1881; to the article on
"Tuberculosis" by Frederick C. Shattuck in supplement to _Ziemssen's
Cyclopædia of the Practice of Medicine_, 1881; to the "Cartwright
Lectures," by William T. Belfield, M.D., published in the _New York
Medical Record_ in February and March, 1883; and to an article by
Surgeon George M. Stemberg, U. S. Army, in the _American Journal of
Medical Sciences_, January, 1885.]
It is noteworthy that tuberculous disease may be produced by
inoculating with the infiltrated product, with matter from miliary
tubercles, or from scrofulous glands in the neck. The identity of these
morbid products is thus made evident, assuming that the fact of
communicability involves the existence of a specific virus.
The practical importance of the facts already ascertained respecting
the communicability of phthisis is obvious. They constitute the
foundation for a reasonable supposition that the disease may be
communicated to man by means of the meat of tuberculous animals, by
milk, and by breathing an atmosphere charged with particles of
tubercle. That the instances in which the disease is communicated,
however, are rare seems to be a rational inference from the difficulty
of obtaining clinical proof of communicability. That susceptibility is
an essential factor is made evident by the well-known predisposition
pertaining to certain periods of life. It is to be considered that
while the communicability of the disease to certain animals is
abundantly shown by the experiments to which reference has been made,
the existence of a special virus or a contagium is not as certainly
established by these experiments. They leave to be settled, by further
investigation, the question whether or not the communicability of the
disease involves only the agency of a septic matter devoid of the
special character expressed by the terms virus and contagium. Without
waiting for data sufficient to settle this important question, prudence
would dictate the propriety of all practicable precautionary measures.
Still more recently, and since the foregoing remarks on the
communicability of phthisis were written, have appeared the remarkable
experimental researches of Koch of Berlin. Koch claims to have
demonstrated the constant presence in tuberculous products of a
specific organism which he calls the bacillus tuberculosis, and that it
is not found in non-tuberculous products. This parasite he has
isolated, and by cultivation carried through several successive
generations. By its introduction, after, as well as before,
cultivation, into the pleural cavity, the peritoneal cavity, the
anterior chamber of the eye, and in other situations, he produced
tuberculous disease, not only in rabbits and guinea-pigs, but in dogs
and rats, the latter animals being less susceptible than the former to
tuberculous infection. In his experimental observations, animals not
inoculated, placed under the same external conditions as those
inoculated, did not become tuberculous. The same parasite, alike
capable of infecting healthy animals, he found in miliary tubercles, in
the cheesy tuberculous deposit, in scrofulous glands, and in the sputa
from {399} tuberculous patients. The parasite was found not to have
lost its vitality in dried sputa.[7]
[Footnote 7: For the details of Koch's researches vide his report in
the _Berliner klinische Wochenschrift_, April 10, 1882; vide, also,
_Verhandlungen des Congresses für Innere Medicin_, Erster Congress
gehalten zu Weisbaden, 20-22 April, 1882.]