Study of the pathology of pneumonia experimentally produced in monkeys by the intratracheal injection of pneumococcus has shown that it is identical with the pathology of lobar pneumonia in man. It has been found that the pneumococcus primarily invades the pulmonary tissue at some point or points in the portion of the lobe proximal to the hilum, that it spreads rapidly throughout the lobe by way of the perivascular, peribronchial, and septal interstitial tissue and lymphatics, quickly reaching the pleura, and that it invades the alveolar structure primarily by way of the alveolar walls, subsequently passing into the alveolar spaces simultaneously with the outpouring of exudate into the alveoli. It has been shown that the initial mode of invasion may be by direct penetration at one or more points into the walls of the larger bronchi near the hilum. The possibility that primary invasion may occur in terminal bronchioles, alveolar ducts, or alveoli of the parenchyma near the hilum has not been certainly excluded, though the evidence is against this supposition. In harmony with the mode of distribution of pneurnococci it has been found that the initial lesions of lobar pneumonia are of the interstitial framework of the lung, with respect both to the grosser framework and to the alveolar framework. Hepatization begins centrally and spreads toward the periphery and is a constantly progressive process. With the development of hepatization the conspicuous interstitial lesions of the earliest stages gradually diminish and are often largely masked when complete lobar consolidation has developed. Resolution is frequently accompanied by a varying degree of organization of the grosser framework of the lung. A variable amount of organization of the alveolar exudate also may occur.

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