It was very evident that the smaller bronchi and bronchioles were much more readily involved in a severe inflammatory reaction than the larger tubes. A purulent inflammation was not uncommonly found in the bronchioles of the lung when a pneumonic state with leucocytic infiltration was present. Even where such purulent infiltration of the walls of the bronchioles was readily demonstrable the trachea and main bronchi were devoid of this intense reaction. These purulent inflammations were not uniformly distributed in the bronchioles of the lung, but only occurred in those regions where the parenchymatous tissues were in themselves involved in a purulent reaction. It was difficult to find the evidence whether the purulent bronchitis preceded or followed the presence of a purulent pneumonia. The intimacy of the lung tissues with those of the small bronchioles makes it impossible for one or other of these structures to escape when one of them is implicated in a purulent reaction. It is equally important to appreciate that to a considerable extent the lung tissue surrounding the small bronchioles becomes involved by a direct radial extension through the walls of the thin respiratory tubes. Such extension laterally is assisted by the free lymphatic communication lying about the bronchioles and stretching into the lung parenchyma. Purulent processes of the small air tubes always showed a similar reaction in the interstitial tissues of the neighboring air sacs. Our material did not permit of following the bronchial reactions to their conclusion. In some instances we have found that where abscesses developed within the lung the contiguous bronchi and bronchioles either became eroded or suffered intense suppurative inflammatory lesions on their inner surface. The manner in which repair of the more common inflammatory processes of the bronchi is accomplished could not be demonstrated in the cases dying during the acute stage. In one case an organizing bronchitis was associated with an organizing lobular pneumonia. In this instance the connective tissues were proliferating freely from the inner wall of the bronchi, there being no evidence of a basement membrane at the point where the connective tissue was growing. The development of the connective tissue appeared to be spontaneous and was not taking place within an unresolved fibrinous exudate. In as much as the fibrosing process was largely scattered through all of the lobes, the numerical involvement of the respiratory tubes was quite great. In this instance the amount of obstruction which was imposed upon the respiratory tissues by the fibrosing pneumonia and bronchitis was sufficient to cause considerable distress and dyspnœa during the last few days of the patient’s life. The amount of dyspnœa was out of proportion to the clinical manifestations of pulmonary involvement, and from a clinical point of view it was difficult to arrive at a conclusion of the nature of the lung lesion.