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in the whole range of literature ten cases have been collected up to the present time. Baumgarten was himself able to demonstrate a caseous mass in a cervical vertebra in a still-born child. He further cites the cases of tuberculosis in children in the first months and years of life. Here of course a positive demonstration of congenital presence of tubercle bacilli cannot be adduced. The author thinks, however, that no good ground can be cited against this view, as the disease is accustomed to show itself only very slowly. In fact, Baumgarten invented a period of latency to account for the new growth. The predominating frequency of primary lymph gland, and bone, and joint tuberculosis speaks again for congenital transmission. Further support is furnished by experimental investigation. Baumgarten got from two tuberculous rabbits, two young which were isolated and protected against infection immediately after birth. They lived three-fourths of a year. In one there was no disease, in the other a caseous nodule of the size of a cherry developed in the liver with the histology of a solitary tubercle, in which, however, bacilli were not found-rather dubious proof.

Better results were obtained by de Renzi and Gartner. De Renzi selected for his experiments guinea-pigs, which have a longer pregnancy than rabbits. Of eighteen experiments, five furnished a positive result. In the case of three newborn killed at once, this author saw tuberculosis of the lungs, of the bronchial or tracheal lymph glands. Four animals born at the same time lived two months, two lived thirteen days longer. They all showed extensive tuberculosis of the lymph glands. The importance of the longer pregnancy is shown by the fact that only such mothers cast tuberculous young which had been infected thirty days before, longer thus than the whole period of pregnancy of rabbits.

Gartner rubbed up the newly born young of tuberculous white mice, and injected the mush into the peritoneal sac of guinea-pigs. He got from ninety-six young, out of nineteen casts, three cases of pronounced abdominal tuberculosis.

Further, he injected into the blood of ten pregnant rabbits culture solutions, and three of the fetuses extracted from the uterus showed bacilli.

White mice and canary birds were further used. These animals, while they are susceptible to the disease, do not succumb for at least three months after the injection of considerable numbers of tubercle bacilli. Of 110 young mice, the offspring of 24 tuberculous (inoculated) mothers, two were found to be tuberculous. Of nine eggs from two tuberculous canary birds, two contained tubercle bacilli. Mafucci had already shown that infected hen's eggs need not perish but may continue to develop, while the issuing fowl may show signs of general infection without local lesion. The possibility of fetal infection is, therefore, established.

And infection of the human fetus by the mother has been proven also. It was in the year 1891 that Schmorl and Birch-Hirschfeld published the first case in which they were able to demonstrate with certainty the transmission of the tubercle bacillus from the mother to the fetus. It was the case of a young woman who died with miliary tuberculosis in the seventh month of pregnancy. These observers found in the placenta in the inter-villous tissue, also on and between the epithelium of the villi, in the lumen of divided chorion vessels, in the lumen of capillary vessels, in the fetal liver, tubercle bacilli which could be colored with characteristic reaction. Moreover, three guinea pigs which had been inoculated with parts of fetal organs became tuberculous. As these authors urged, there was in this case clearly a congenital tuberculosis, since all tubercular tissue changes were absent. The direct transmission of tubercle bacilli from the mother to the fetus was thus assured for the first time. Lehmann subsequently confirmed this report with another case.

In reviewing these various observations, Ribbert concludes: We must admit that a large number of interesting studies may be utilized as points of support for the possibility of congenital transmission of bacilli, but that strict proof has been brought only for placental infection to account for congenital human tuberculosis.

Infection in this way is, however, only a possibility, and that it does not thus occur as a rule is proven by the fact that the offspring of tuberculous mothers is born as a rule sound and free. Epstein observed that tuberculous mothers, notwithstanding an emaciation of high degree, bring forth, as a rule, healthy and sound children, which develop in every way normally, and in the exceptional case of feebleness at birth the emaciated children of such mothers recover perfectly when properly fed. Of 200 cases of this kind, tuberculosis was found upon autopsy only once, and then in a child aged ten weeks. The fact is, as Klebs has shown, that an intra-uterine transmission of tuberculosis from an infected mother belongs to the rarest occurrences. Long before the discovery of the bacillus, Bockendahl declared: “We may not conceal the fact that pathological experiment has compelled us to recognize in tuberculosis an infectious disease, and to surrender the view of inheritance even in individual cases.” Is it not safe to say that no one here has ever seen a case of congenital tuberculosis?

As to transmission from the father, which alone can stitute indisputable heredity, there is no proof at all. Gartner inoculated twenty-two rabbits in the testicle, and observed that although the semen contained bacilli, it failed in all cases to produce tuberculous young. The reason was obvious with the observation that in these inoculations only one bacillus would be present to fourteen million spermatozoids, so that the chances for infection in this way are reduced to a minimum. It could not further be shown that spermatozoids ever incorporate bacilli. In fact they could not be forced to take them up. With any increase in the number of bacilli, it was impossible to infect the fetus, and only rarely did there occur a local infection of the female. When it is considered that on the one hand the tubercle bacilli are so rarely found in the semen, and on the other hand primary congenital tuberculosis is itself so rare, it may be concluded that tuberculosis is never conveyed to the fetus by the spermatozoid. Thus practically tuberculosis is not an inherited disease.

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It is universally admitted that tuberculosis is extremely rare in the first months of life. Thus it is almost never seen in foundling-houses. In the foundling-house at Prague, Epstein saw in 200 post-mortems, only nine cases of tuberculosis. Two of these children had been brought into the institution from an outside nursery, where one of the nurses had been affected with the disease. The history of the other was unfortunately not examined in this direction. But in the case of the other seven of the sucklings, the mothers had been brought to the hospital to be themselves treated for phthisis. In the St. Petersburg foundling institute, according to Froebelius, of 71,370 foundlings, deaths from tuberculosis were 0.4 per cent., while the whole number of deaths was 21.7 per cent.

As now direct germinative transmission of the bacillus cannot be proven in man, and placental infection is extraordinarily rare, retreat is had to the transmission of a tendency whereby it is said that the children of tuberculous parents inherit a weaker constitution, or some other peculiarity which constitutes a predisposition of tuberculosis, which in turn makes these children therefore more ready victims to the disease. Why may not be inherited weak lungs as well as weak brains, weak stomachs, weak eyes, etc?

Mention has been made already of the paralytic thorax. the elongated, flattened thorax, which is usually found in conneciion with a long, narrow neck, a thin skin with apparent blue veins, an enfeebled musculature, etc. This condition is declared to constitute the phthisical habitus. The truth is, these individuals are often already the hosts of the tubercle bacillus, and are not infrequently the victims of manifest disease. Deutsch has shown by abundant measurements and comparisons that there is no predisposition in the configuration of the thorax, and that broad-chested men contract the disease as readily as those with narrow chests.

It is claimed that certain catarrhal conditions of the mucous membrane predispose to the disease. This may be, but the fact has not been demonstrated. Brehmer says that

a chief source of phthisis is its tendency to catarrh, and prevention of the disease consists in exercise in the open air with protection of the skin with woolen, but not too warm, clothing, etc. The truth is often here, too, the reverse of this relation. It is the individual infected with phthisis who is especially disposed to catarrh. As a sign of incipient phthisis Cullen said a century ago: “The patient takes cold with every exposure, and often without any exposure at all."

Conditions which markedly interfere with the nutrition of the lungs are declared to favor the retention and growth of microorganisms. Thus it has been noticed that individuals in whom the pulmonary artery is small, easily become victims to this disease. Congenital stenosis of the pulmonary artery is nearly always attended with, or followed by, tuberculosis. On the other hand, certain anatomical conditions render an individual less liable to be attacked. Such conditions as favor venous stasis or hyperemia offer obstacle to the development of tuberculosis. Thus tuberculosis does not occur, as a rule, in cases of valvular disease of the heart, asthma or emphysema. Beer claims to have cured a number of cases of tuberculous bone and joint disease by a passive hyperemia of artificial induction. Exceptional cases sometimes admit of explanation. Thus clinicians differ as to the effect of aneurism of the aorta. Aneurism of the aorta, so long as it causes a venous stasis, interferes with the development of tuberculosis. When it, however, attains such size or disposition as to encroach upon the pulmonary artery, it will favor tuberculosis. Schottelius finds a difference in the configuration of the bronchial tree. Formad accuses the construction of the connective tissues. Veraguth holds responsible the lymph vessels. Weber finds a deficiency of carbonic acid. Ruehle generalizes in a lighter vulnerability, etc. Defective ciliary action has been invoked in the same way. Appeal is made to hypoplasia of the heart, and to chlorosis, both of which are effects of the disease. Finally, Brehmer, in what might be called a frantic appeal for predisposition, lays the blame

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