The expression hereditary transmission of tuberculosis, or rather, of tubercle bacilli, may be construed in several different ways. It may mean the hereditary transmission from father or mother, or from grandfather or grandmother, or from ancestors still further back. If we designate the parental transmission as congenital heredity, transmission from further back as pregenital heredity, then in my view of the origin of pulmonary consumption, generally neither congenital nor pregenital heredity comes into play. And, looking at the matter as I do, if one is still desirous of speaking of the hereditary influences of relatives, one ought to use the term postgenital. It is now almost everywhere conceded that human tuberculosis as a rule is actually of postgenital origin.
Experience has taught me that if, in scientific investigation, one wishes to discover something new, one should study the exceptions to the rule. In actual practice, on the other hand, it is well to keep to the rule. We may therefore safely ignore the cases of congenital tuberculosis, but must all the more thoroughly study the circumstances which in extra-uterine life govern the tubercular infections which lead to consumption. And here I believe I have discovered a new principle which may be expressed thus:
“The milk fed to infants is the chief cause of consumption.”
This assertion will at first sight be surprising, for it has long been maintained that the suckling infant receives milk free or almost free from germs. Mother’s or nurse’s milk is taken by the child in this condition, and the cow’s milk for artificially nourished children is usually first boiled or scalded. In later life, to be sure, much less attention is paid to securing a milk as sterile as possible. How, then, is this to be reconciled with the above statement, that it is especially the milk fed to infants which constitutes the chief danger in causing tuberculosis?
And yet this statement is true, not because the milk fed to infants is at all worse than other milk, but because the human infant, like the young of all other mammals, is destitute of the protective agencies in his alimentary system which at a later period of life prevent the entrance of disease germs into his tissues. It has taken many years of experimental work to demonstrate this fact conclusively. At present, however, the chain of evidence is so strong that I have not the least hesitancy in building on it my entire plan for the suppression of tuberculosis.
In this lecture I can do no more than summarize the main proofs for my assertion regarding the ready penetrability of the infantile alimentary tract for all disease germs, but especially for tubercle bacilli.
I began with a very interesting fact discovered by my fellow-worker, Dr. Römer. He showed that true albumins penetrate unchanged the intestinal mucous membrane of new-born foals, calves, and smaller laboratory animals, and that they produce the same action on the organism as when they are injected directly into the circulation. In adult animals of all species, on the contrary, the true albumins must first be digested into peptones before they can pass through the mucous membrane. The anti-diphtheria serum and the anti-tetanus serum contain curative substances in the form of true albumins. If such a serum be introduced into the stomach of a healthy, full-grown animal or man, not a trace of these bodies passes into the blood. On introducing the serum, however, into the stomach of the new-born, the unchanged antitoxic albumin can almost entirely be demonstrated in the blood. This discovery indicates that the mucous membrane of adults, acting as a dialyzing membrane, does not allow the large molecules of true albumins to pass through unchanged, whereas the mucous membrane of sucklings behaves more like a very porous filter.
It was but a step from this discovery to the assumption that the mucous membrane of infants might behave similarly toward bacteria. For my first experiments I selected anthrax bacilli, which, when free from spores and given in milk per stomach, do not affect adult guinea pigs at all. They are quite rapidly thrown off with the excreta, remaining, however, a little longer in the cæcum. When the same dose of bacilli was administered in this way to guinea-pigs less than eight days old, they died just as rapidly of anthrax as by the customary method of infection. Next I tried anthrax bacilli whose virulence had been reduced. These are harmless when injected subcutaneously into guinea-pigs. After feeding these weakened bacilli to new-born guinea-pigs, the blood of the animals contained anthrax bacilli, though the animals did not die. Incidentally, a fact of considerable theoretical importance was discovered: that the anthrax bacilli possess a very intimate affinity for the endothelium of the heart and blood vessels.
Having thus studied the fate of anthrax bacilli introduced into the stomach of new-born and adult guinea-pigs, I now turned to a similar study of tubercle bacilli. Together with Dr. Römer I studied the behavior of guinea-pigs toward a definitely weighed quantity of tubercle bacilli given in one single feeding. And here also, as in the case of anthrax bacilli, it was found that when the tubercle bacilli could be demonstrated microscopically nowhere else in the alimentary tract, they were often present in the cæcum. After a single feeding of a small quantity of tubercle bacilli, only the new-born or the few-days-old guinea-pigs became tuberculous. When larger doses were administered it happened that older animals also became tuberculous. At the post-mortem examination of the new-born, a few days later, there were found submiliary thickenings, with tubercle bacilli in the great and the lesser omentum. There were also little nodules at a point on the root of the mesentery, not far from the cæcum. Of especial interest is the further development of this alimentary tuberculosis in the guinea-pigs which survived. In these animals, even while their general health remains good, it is always possible to demonstrate a tuberculosis of the glands of the neck, a type of disease which may be said to correspond to scrofula in man. Not infrequently there is later on developed that type of guinea-pig tuberculosis which has heretofore been regarded as the expression of an inhalation tuberculosis.
In the results of all these investigations I see experimental support for the view I have for some time maintained, namely, that the origin of the epidemiological pulmonary tuberculosis in man and that of the epizootic pulmonary tuberculosis in cattle is a primary intestinal infection occurring in very early infancy. In this I leave undecided whether the bacilli gain access to the body through feeding or through inspiration.