(a) v. Baumgarten’s experimental method of causing pulmonary phthisis by means of primary infection of the urogenital apparatus.
(b) The experiments of Troje and Tangl with tubercle bacilli artificially weakened in virulence.
4. Critical analysis of the so-called “Inhalation Tuberculosis” of guinea-pigs and rabbits.
(a) My own experiments, in which the typical picture heretofore regarded as that of an inhalation tuberculosis, in the sense of an aerogenous alveolar infection, was produced by lymphogenous or hæmatogenous introduction of tubercle bacilli, with the complete exclusion of a primary alveolar or bronchial infection.
(b) The experiments of Weleminsky (Hüppe).
(c) Signs distinguishing tubercular pulmonary consumption from so-called inhalation tuberculosis.
5. Improbability, so far as importance as a phthisiogenetic factor is concerned, of a primary bronchial, or even primary alveolar Tb. infection following aerogenous introduction of Tb. into the mouth and nose, through the inhalation of dust or droplets containing tubercle bacilli.
6. Proof for my assumptions,
(a) That inhaled tubercle bacilli under circumstances occurring in nature are taken up by the lymphatic receptive apparatus without exciting, at the point of entry into the lymph-channels, any tubercular disease.
(b) That inhaled tubercle bacilli, after they have entered the lymph-channels of the throat, take the following courses: some find lodgment in the submental glands and glands of the neck; some are transported to the mediastinal (bronchial?) glands; some gain the circulation and thus cause hæmatogenous infections, especially at the peripheral (sub-pleural) endings of the pulmonary artery, from which then the lung parenchyma can be infected; finally, some are carried through the stomach to the lowest portions of the intestines, from where they can reach the mesenteric lymph-glands, the portal vein, and the peritoneum.