Pneumonia in Aves aside from that due to moulds is apparently much less common than among the Mammalia, one order only, the Passeres, showing an incidence comparable to the important orders of the latter class. The other orders, and this applies particularly to those of which we have an adequate number, are quite insusceptible to simple pneumonia, none of them showing over two per cent. There are listed for Aves three instances of lobar fibrinous pneumonia. These cases can be described together since in all the findings were about the same. A whole lung or goodly portion thereof was uniformly involved in a red or gray consolidation of rather fine granular character which on section study seemed to be made up of the same lesion all over, with fibrin a prominent part of the exudate. The coagula were largely within the secondary alveoli but the primaries also contained it. The microscopic section may not have represented the process at all places, and since the arrangement of fibrin is similar in definitely catarrhal lesions, these may of course have been instances of pseudolobar pneumonia. Our data are too few to draw any conclusions as to the behavior of the various orders but one note may be permitted. The passerine birds have a great tendency to dense cellular infiltrates while parrots show more coagulative or fluid exudates. PRODUCTION OF INSULAR PNEUMONIA IN BIRDS. Insular consolidations in which catarrhal and infiltrative processes are prominent, the bronchopneumonias, seem to arise in two ways. One course of events apparently follows infection _via_ the bronchial mucosa, the other _via_ the blood stream and a study of the resulting lesions may help toward an understanding of the development of pneumonia in man. When infection unquestionably has been superficial, that is _via_ the bronchus, the first thing to happen is a swelling of the septal prolongations dividing the primary alveoli and an extension of their ends farther into the secondary alveoli with the result that the inlet to the primary air sacs is narrowed and the space in the secondaries is reduced. Upon the surfaces there then develops the usual catarrhal exudate while in the deeper parts marked congestion makes its appearance. Fibrin may develop and be mixed with the cells both in the larger and smaller alveoli but it is more evident in the former. (Figs. 8, 9, 10.) [Illustration: FIG. 10.—LATER BRONCHOPNEUMONIA OF SUPERFICIAL ORIGIN. NOTE GREATER EXUDATE, GREATER SWELLING OF SEPTA. PRIMARY ALVEOLI PRACTICALLY ALL CLOSED. MUCH OF LUNG HAS BECOME CONSOLIDATED. ] [Illustration: FIG. 11.—INSULAR PNEUMONIA, BEGINNING AS CELLULAR INFILTRATION OF DEEPER PARTS OF SEPTA AND OF INTERSTITIAL TISSUE. FOUR AREAS OF DENSE AIRLESS CONSOLIDATION. ALL SECONDARY AND MANY PRIMARY ALVEOLI WIDELY OPEN. ]