In 1856, Buhl[50] first published his view, although he had for several years been impressed with the idea, that miliary tuberculosis was an infective disease resulting from the absorption of a specific virus. He based his theory upon the almost constant coexistence of one or several cheesy collections and miliary tubercles. The former were recognized as the remains of previous inflammatory processes, and the tubercles were looked upon as the immediate result of the absorption of this cheesy material. The individual thus infected himself. Buhl[51] claimed that the simultaneous occurrence of tubercles and inflammatory products was the co-effect of the same cause, and that the acute miliary tuberculosis, as a localized process, was merely an inflammation with the development of tubercles. He restricted the term tuberculous inflammation, however, to those forms which necessarily and from the beginning, produced tubercles whose presence was limited to the tissue inflamed. The tuberculous inflammation was regarded as a primary condition, while the acute miliary tuberculosis was a secondary process resulting from infection. [Footnote 50: _Lungenentzündung, Tuberkulose und Schwindsucht_, 1872, iii.] [Footnote 51: _Op. cit._, 123.] The tuberculous inflammation of this author was largely characterized by those features which, with the exception of the constant presence of tubercles, were recognized by others as attributes of a scrofulous inflammation. At the same time, he objected to the latter term as a substitute, since its use would imply that no other cheesy product than that from a tuberculous inflammation would serve as the origin of tubercles. Buhl strictly maintained that the absorption of any cheesy material, whatsoever its source, might give rise to a general growth of tubercle in the body. The views of this author were popularized mainly through the teachings of Niemeyer[52] concerning pulmonary consumption. The latter adhered to Virchow's views relating to scrofulous inflammation, but maintained that most consumptives were in imminent danger of becoming tuberculous in accordance with the doctrines of Buhl. [Footnote 52: _Klinische Vorträge über die Lungenschwindsucht_, 1867.] The theory of an infectious origin of tuberculosis, advanced from time to time by others, but most forcibly presented and maintained by Buhl, was first demonstrated by Villemin[53] in 1865. This observer showed that certain animals, especially rabbits and guinea-pigs, might be successfully inoculated, beneath the skin, with fragments of gray tubercle, cheesy products, sputum, and blood from cases of phthisis. The development of tubercles took place within three weeks after the {98} inoculation, and became general within four weeks. He also demonstrated that rabbits became tuberculous when inoculated with bits of the tumors occurring in the pearly distemper of cattle. [Footnote 53: _Etudes sur la Tuberculose_, Paris, 1868, 528.]