It is obvious, as stated in the beginning, that these experiments have failed to reproduce a chronic pulmonary tuberculosis. Acute pneumonic processes of tubercular origin are, however, not infrequent as a complicating or terminal process in pulmonary phthisis, and there have been several cases described in which individuals have died with the symptom complex of acute lobar pneumonia, in which it developed at post-mortem examination that the disease was tuberculosis. Our experiments throw some light on debated questions in connection with these acute pneumonic forms of phthisis.

In our experiments we believe that we have effectively reproduced this exudative type of tuberculosis of the lungs. This type of lesion may, in the light of our experiments, result from the sudden bronchogenic invasion of large numbers of virulent tubercle bacilli in a relatively resistant animal.

The large mononuclear cells so frequently encountered in the exudate seem to be brought there chiefly from outside.1 As Orth found when studying human material, it is difficult here also, to exclude the possibility that similar cells may result from the desquamation of alveolar epithelium.

The tubercle bacillus alone, without the aid of secondary infection, is competent to produce a type of lesion which leads to necrosis of the bronchi, and by discharge of the necrotic material to cavity formation. As judged by our experiments the bronchi are less resistant to involvement in the necrosis than are the blood vessels or pleural surfaces.

The fact that by the method of bronchial insufflation of Lamar and Meltzer a characteristic tuberculous pneumonia may be produced makes it probable that the lobar pneumonias generally are of bronchogenic origin.

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