There is another argument against the common assumption that primary infection by way of the respiratory organs is the cause of consumption, and this is furnished by an analysis of the anatomical findings. If we allow an individual, entirely free from tuberculosis, to breathe tubercle bacilli, the opportunity for an intestinal[4] infection is surely presented; on the other hand, that any bacilli whatever reach the lungs directly cannot be positively affirmed. Infection of the organs of the pharynx and larynx in these cases always corresponds to disease of the lymph-vessels and glands in the neck, and gives the individual the scrofulous habitus. Now let us recall the neck of consumptives. It appears almost as if, at the time when an individual may be designated as being a candidate for consumption, the organs of the neck were already quite immune against a vulgar tubercular infection. I could multiply the arguments in favor of my assertion that, in order to have pulmonary consumption follow infection with inspired tubercle bacilli, it is necessary to have constitutional changes in the organism due to an early previous infection. I hope, however, to have sufficiently established my reasons for rejecting the current theory of the origin of consumption, a theory due mainly to the valuable and detailed researches of Cornet. I must decline to accept another wide-spread view, namely, that hereditary influences are deciding factors. Theoretically an intra-uterine infection with tuberculosis is certainly possible, and in a few cases such an infection has actually been proven. But neither the parental nor the pre-parental transmission of tubercle bacilli, nor the hypothetical transmission of a body predisposition to tuberculosis, is of any practical importance. Nevertheless, according to my researches, the view prevalent among the laity regarding the important influence of parents, grandparents, and other near relatives, in the etiology of consumption, is entirely justified and proper. I, too, am of the opinion that one can properly speak of the bad prognosis in cases of _family tuberculosis_. If, in taking the history of a patient, I should elicit the fact that several near relatives had died of consumption, and if, then, by means of the tuberculin reaction or of inoscopy, I made the clinical diagnosis of a tubercular infection, I should be very pessimistic in my prognosis, even though the infection were not otherwise manifest. I may very properly be asked how I can deny hereditary transmission and yet place so high a rating on the influence of the ancestors, cognates, and house-fellows, in the production of pulmonary consumption. A little explanation regarding the meaning of certain terms will make my ideas perfectly clear.