Gradually this phantom architecture, spotted only here and there with disintegrating polymorphonuclear leucocytes, ends in a ragged compressed border of a shaggy pink material which has no identifying qualities (Fig. XXXV). In the inner zone of pink an occasional vessel or, at times, a bronchiole more resistant to the process remains; frequently it is accentuated by the presence of partially destroyed polymorphonuclear leucocytes at its periphery. Probably these cells invade the necrotic areas along the sheath of the bronchus or vessel and not across the dead area. The thrombotic process described in the previous stage (Fig. LII) associated with an acute arteriolitis, may be associated with these gangrenous areas as well as with infarcts (82), but more likely gangrene is preceded by the acute diffuse necrosis of the alveolar wall which occurs in the fulminating cases. Furthermore, this is suggested where a typical grey hepatization is associated with marked thinning, but not actual disappearance, of the alveolar wall. Before concluding the description of this stage of the disease, mention should be made of the granular nodules of fibrin superimposed upon the swollen pleural cells and also of the older pleural exudate, either typically fibrinopurulent or more homogeneous with broken nuclear fragments (Fig. XXXVIII). _Summary._ In this stage of the disease the respiratory change is characterized by a localization of the inflammatory process with cellular invasion of the exudate. Pneumonia results, varying in extent from peribronchial to lobar, a pneumonia in which one of the most frequent complications is necrosis of the lung. Consequently, abscesses, even gangrene, are found. (3) ORGANIZATION OF BRONCHIOLAR AND PNEUMONIC PROCESSES. The processes described for the preceding group which involve not only the alveoli, but also the bronchi and the bronchioles, were predicted from the extensive hyalinization of these structures—a characteristic change in the more fulminating and acute phases of the disease. Likewise, it can be predicted that where death does not terminate the process such lesions will be followed by organization, which, by converting the exudate into scar, will produce deformities and offer serious mechanical interference with the ingress and egress of alveolar air and similar interference with the flow of blood through the pulmonary circulation (82). [Illustration: FIG. XXIV. AUTOPSY NO. 92. AN ALMOST PURE HEMORRHAGIC ALVEOLAR EXUDATE. COMPARE FIGURES VI, XXV, AND XXVI. ] [Illustration: