remains in this pink ribbon and then the involvement seems to be primarily in the vessels of the wall. Not all the vessels are involved, and next to a hyaline thrombus in one, there may be fresh blood, usually red blood, in its neighbor. The alveolar epithelium is usually denuded and thus accentuates the intensity of the change. The acute death which involves the tracheal, bronchial, and bronchiolar epithelium and which may extend beyond the epithelium into the walls of these structures and kill en masse the walls of the alveoli, is a lesion which does not occur in other types of acute pulmonary infection. However, in influenza, as after exposure to pulmonary irritating gases, it is the lesion of characterization (158,159). The effects of this change, of course, where it involves the alveolar wall, will vary with the extent of the process; but given an absolutely necrotic wall, as yet unstrengthened by inflammatory reaction, an expected result would be its rupture with respiratory movement. The point of rupture is important, but where so many alveoli are involved, disturbance of continuity will occur, occasionally in such position that the result will be the escape of air into the interstitial tissues.[7] There is ample evidence that this happens. Indeed, among the clinical manifestations of the disease, interstitial emphysema of the lung spreading through the fascial planes to the subcutaneous tissues of neck and thorax is well known; the phenomenon is more frequent and extensive in influenza than in any other disease (8, 17, 52, 143). Interstitial emphysema is very striking at the post-mortem table. The escaped air appears as beads along the interlobular septa, but on account of their size they are always most conspicuous between the lobes and along the vessels toward the hilum (162) (Fig. XVIII). Histologically, a small bubble of escaped air confined to the interlobular septum compresses the surrounding tissue with almost complete atelectasis of many neighboring alveoli (Fig. XIX). _Summary._ The diffuse involvement of all the lung tissue, chiefly with a serous exudate in the subpleural, interstitial, perivascular, and peribronchial tissues, as well as in the alveoli, is associated with other elements which occur in aplastic reactions; red blood cells, fibrin, and bacteria. Added to the aplastic exudate is an acute necrosis of bronchial and alveolar epithelium involving at times the walls of these structures; consequently, the histology of this disease is almost as specific as that of any biological reaction. (2) LOCALIZATION AND NECROTIZATION OF THE PNEUMONIC PROCESS