of their etiologic unity, these processes were looked upon as a series of distinct diseases (phthisis, caseous pneumonia, cirrhosis, etc.).

The localization, distribution, and course of the tuberculous diseases of the lungs are so manifold that it becomes well nigh impossible to consider these processes from a common histologic standpoint. All the forms of inflammation and their several terminations, which were referred to previously, may run their course side by side with the specific tuberculous processes; no organ in the body undergoes so many alterations from tuberculosis as the lung.

The tuberculous virus may reach and spread throughout the lung along three distinct routes: the circulating blood, by inhalation through the bronchi, and by way of the lymph-vessels. In the first case we speak of a hematogenous or embolic tuberculosis, or of an acute miliary tuberculosis, because in this case the tuberculous eruptions at the time of death generally reach the size of millet seeds. This form of tuberculosis most frequently develops as the result of a tuberculous focus in some part of the body-e. g., a tuberculous lymphatic gland rupturing into a vein, the infectious material being carried by the blood to the right heart and thence into the lungs. A somewhat similar event occurs after the rupture of a tuberculous focus into a larger lymphatic vessel, followed by a transport of tuberculous material into the circulating blood. Circumscribed miliary tuberculosis of parts of the lung tissue may result from the breaking into an arterial branch of a preexisting tuberculous focus in the lung itself.

In all these cases there circulate in the blood tubercle bacilli that, if arrested in the capillaries, produce multiple, miliary, embolic, tuberculous foci, the beginning of which takes place in the capillary walls and their immediate surroundings.

As elsewhere, tubercle bacilli in the lungs cause first

along the bronchial tree or the lymphatic vessels, while presenting the same histologic changes in their inception, differ markedly in their further course.

By far the most frequent mode of tuberculous infection of the lung and of the body as a whole is by way of the inspiration. Through the respiratory passages the bacilli reach the small bronchial branches, where they become arrested and produce in the walls the earliest changes, or they reach the infundibula or alveoli, where the specific changes then develop. In the first case processes develop similar to those seen in the evolution of bronchopneumonia. Bronchitis, peribronchitis, and bronchopneumonia develop successively, the inflammation extending through the bronchial wall into the surrounding tissue ; histologically, these changes are modified only in so far as the specific effects on the tissues of the tubercle bacillus come into play. There is formation of nodules and then the caseous necrosis, which, as a rule, befalls tuberculous tissue at a certain stage.

It may be assumed that the bacilli are arrested in a plug of mucus in a small bronchus, and next come in contact with the epithelial cells of the walls; the toxic action of the bacilli at once induces a proliferation of the cells and leukocytic emigration, and a bronchial tubercle is formed. The nodules enlarge; the smaller the bronchus, the sooner the nodules coalesce; caseation occurs, and the caseous centers soon run together and form a partial or complete caseous ring around the bronchial lumen. At this point the neighborhood of the bronchus is extensively involved; the nodules spread to the external layers of the bronchial wall, which are destroyed and included in the caseous ring. Caseous material either partially or wholly fills the lumen, and, in consequence, the corresponding alveolar area sinks together in atelectasis. Furthermore, the peribronchial connective tissue and the alveoli adjacent thereto present consecutive changes: the alveolar walls are