There is no doubt that the character of the pneumonic process in the epidemic influenza was not the same in all localities. There have been not a few who have reported a large proportion of their pulmonary lesions as a definite broncho-pneumonia with an interstitial purulent involvement. The prominent reaction was a small circumscribed yellow focus about the bronchioles from which a bead of pus could be expressed. These pea-sized foci were scattered through several or all lobes. It is this type of reaction which appears to develop by a direct extension through the bronchial walls and to remain quite localized in the alveoli about these tubes. This reaction seems to be purulent from its very beginning and does not pass through the stages as we have described them above. There is more or less fibrin present in the exudate, but usually not in the quantity observed in lobar pneumonia. These lesions closely resemble those observed in the post-measles pneumonia, and it is claimed are the result of the same agent; the hemolytic streptococcus. In only one case did we observe a lesion of this kind. The small areas of broncho-pneumonia were confined to the left lower lobe and in the lower portion of the upper lobe. Each area was about the size of a split pea, was quite yellow and in fairly sharp contrast to the background of an acute sero-hemorrhagic pneumonia. The subsequent history of these interstitial purulent broncho-pneumonias is like that in measles, where the tendency toward an organizing pneumonia has been shown. The importance of the hemolytic streptococcus in inducing purulent interstitial lesions of the lung (and also of other organs) cannot be over-impressed. It is not so much the type of the reaction during its acute stage which attracts our attention, but the manner of the healing process. It is more than probable that the organizing pneumonias of influenza, not only of this distinct bronchial type, but also the lobular, confluent and lobar variety have had an associated streptococcus infection. The more intimate discussion of this type of pneumonia has been given by MacCallum. Our autopsy experience has led us to believe that the definite clinical signs of pneumonia are associated with the development of this gray consolidation of the lung. The lung tissue develops characters which permit the physical signs to be recognized. The tissue is more solid and more readily transmits the bronchial sounds. This is not true of the earlier stages where the inflammatory process is contained within a lung tissue which still is partially crepitant and when the so-called consolidation is due to an inflammatory œdema and not to the more solid fibrinous and cellular exudate. With the protean distribution of the gray lesion one does not wonder at the clinical difficulties in mapping out or even finding the consolidated tissues.