The results of all these scientific investigations lead us back to the old folk belief in family tuberculosis and hereditary consumption, with this difference, however, that now we believe the germs of consumption to be transmitted postgenitally from parents, relatives, or house-companions. If a coughing consumptive lives together with a new-born child, especially if cleanliness leaves much to be desired, it is impossible for this child to avoid infection with tubercle bacilli. They are present in the particles of sputum which are scattered about everywhere, and they thus gain access to the mouth and nose of the infant. From there they reach the intestinal mucous membrane, which they penetrate, and so they invade the body juices. Not alone infants, but older persons as well, are endangered in the home of the consumptive. In these, however, there must previously have been pathological changes in the alimentary tract, or an overwhelming dose of the infectious agent, in order to effect an intestinal infection. Pathological changes, accompanied by the shedding of epithelium, occur especially in the exanthemata, and particularly after measles. The laity has long noticed this close relation between measles and tuberculosis. In the infant, the disposition to intestinal tubercular infection is entirely physiological and normal. The healthiest and strongest infant is exposed fully as much as the weak, sickly one, and perhaps more so, for in the latter other parasites are contending for the cells on which they feed.

I have now given you a general idea of the origin and spread of the tubercular infections ending disastrously. This brings us at once to certain practical points in dietetic hygiene which, though never entirely neglected, are now brought into prominence.

It is unnecessary for me to further emphasize the necessity, in infant feeding, to insist under all circumstances on milk absolutely free from tubercle bacilli; nor, what is equally obvious, that it is absolutely necessary to keep coughing consumptives away from infants. But I should like to observe that not only infants but also older persons should be protected against the possibility of infection, if we have any reason to fear that the alimentary tract is anywhere deficient in its protective epithelial covering. I have already pointed out the importance of the exanthemata in this respect, and I need only remind you of the many other disturbances associated with the shedding of epithelium, disturbances due to catching cold, to indigestion, or the after-effects of certain diseases associated with intestinal ulceration, etc. There is one other condition which I must not fail to mention, namely, the temporary exacerbations of a tubercular process, in which one cannot be too careful in ordering the diet. For that large class of individuals threatened with consumption, I believe we have a valuable healing agent in the dietetic therapy made prominent during the past decade, especially by von Leyden and his pupils. In the same sense we must regard the temporary residence of tuberculous individuals in sanitaria as most valuable, for even if the lesions do not heal there, the progressive downward course of the disease is checked and the patients learn for the rest of their lives to appreciate what will benefit and what will harm them. In many cases, therefore, these sanitaria will prove themselves homes for the prevention of consumption, even if they are not homes for the cure of tuberculosis.

My own efforts in the field of tubercular therapeutics do not, to be sure, concern themselves with sanitarium treatment. Their last aim is to make all homes for the prevention of consumption, all sanitaria, etc., unnecessary by means of a protective agent similar to that by which Jenner made smallpox pest-houses unnecessary. Institutions for persons bodily wrecked are like those for persons morally wrecked; they are products of our civilization, but not desirable products. At best they are necessary evils.

OBSERVATIONS CONCERNING THE STUDY OF PHTHISIOGENESIS IN MAN AND IN ANIMALS.

1. It is possible in experiments on guinea-pigs to produce pulmonary phthisis by infecting these animals from the oral cavity in such a manner that every direct infection of the lungs (alveolar infection through the trachea = aerogenous infection of the lung) is excluded.

(a) Infection through the parenchyma of the tongue.

(b) Feeding of tubercle bacilli with milk.

2. Ascribing the pulmonary phthisis which I succeeded in producing experimentally to a lymphogenous or hæmatogenous infection of the lung following previous scrofulous disease. Definition of the term “scrofula”: multiple, caseating areas of disease in lymph-glands and in other organs, caused by Tb. infection. Concerning the etymology of the word “scrofula” (Greek = choeraden), see Virchow’s “Geschwülste,” Vol. II, p. 558.

3. Other varieties of experimental phthisiogenesis;