The absence of cellular elements in the alveolar exudate is frequently observed in influenzal pneumonia (Figs. XXI, XXII, XXIII). This picture has been reproduced experimentally in animals which have been rendered aplastic with benzol, especially with reference to their myeloid elements (160). Pneumonia produced by intratracheal insufflation is more rapidly fatal in aplastic animals, and it is conceivable that the absence of cellular reaction is an explanation for the lack of resistance demonstrated by the high mortality of influenzal pneumonia. Frequently the fibrinoserous mass scattered diffusely throughout the lung is rich in bacteria. In the absence of cells of the polymorphonuclear series, the bacterial development seems to be unrestricted. The aplastic exudate is associated clinically with an absence of a myeloid reaction in the peripheral circulation. The leucocytic count may be definitely decreased, even though the tissues have been invaded by pyogenic organisms to which the usual response is a definite leucocytosis. The only explanation is that the myeloid structures have been injured, probably by the unknown virus of the disease. D. THE HYALINE NECROSIS OF THE PULMONARY TISSUE The hyalinization of the epithelium lining the ducti alveolares (47, 48) also merits special attention (Figs. V, XV, XVI). This process may extend through the wall of the duct and is often seen in the alveolar walls throughout the involved lung. The entire alveolar wall may be homogeneous in appearance, but, occasionally, the thrombus alone, which has formed in its vessels (41), presents this change (Fig. XVII). The alveolar as well as the bronchiolar wall is thickened by a homogeneous material in which cell-body and exudate cannot be differentiated. This acute necrosis, as has been mentioned, is encountered in gas poisoning but is unusual in other known types of respiratory infection. Doubtless, it is a precursor to the more destructive lesions commonly found in later stages of the disease—abscesses which extend through the bronchiolar walls (Fig. XXXI), necrotizing areas of pneumonia in which huge clumps of bacteria are found (Fig. XXXII), and true gangrene (Figs. XXXIII, XXXIV, XXXV). The destruction of the alveolar wall in the early stages of the disease plays a causal rôle in the production of subcutaneous emphysema (Figs. XVIII and XIX). This important phase of the histological change in influenzal pneumonia has received but little attention and, with one or two exceptions, is not mentioned in the literature (8, 162).