Inflammation of the pleura was a complication which varied in its extent and appearance. It appeared to us that a definite interval lapsed between the development of the lesions in the lung and the appearance of an inflammatory reaction upon the pleural surfaces. Although we have recorded evidence of a pleural reaction in 27 cases, this does not indicate that we have met with that number of pleurisies of clinical severity. In this group we include all gradations of pleural reaction from the merest evidence of irritation and slight dulling of the surface to the cases in which definite and marked inflammatory exudate accumulated within the cavity. In many cases we observed a slight increase in the amount of the fluid present in one or other pleural cavity, while there was little or no macroscopic evidence of a cellular or fibrinous exudate. An examination of the fluid showed the presence of lymphocytes and endothelial cells in small numbers, and sections of the pleural surface at points where a slight dulling of the serous membrane was seen at autopsy showed the presence of a very thin layer of a hyaline fibrin. By taking these reactions as indicative of pleurisy we have recorded 6 cases of acute fibrinous pleurisy, 20 of acute serofibrinous pleurisy, and 1 of acute fibrino-purulent pleurisy. An increase in the quantity of fluid in the pleural sacs was the most common indication of pleural irritation. The quantity varied from 50 to 500 c.c. of a clear or slightly turbid fluid. Not uncommonly this fluid was blood stained and evidence of superficial extravasation of blood could be recognized directly beneath the pleural membrane. These serous reactions accompanied the early acute stage, while hemorrhage was the accompaniment of the early period of the influenzal pneumonia when similar hemorrhages were found in the lung substance. The pleural reactions were almost entirely confined to the visceral pleura, and only in the very severe responses did we obtain a marked inflammatory reaction with hemorrhage upon the chest wall. Goodpasture and Burnett state that “there is commonly a moderate serous effusion in one or both pleural cavities amounting to 50 or 250 cubic centimeters. The fluid is clear and has the color of blood-stained serum. The pleural surfaces are smooth, shiny and wet, though occasionally a thin, granular fibrinous exudate may be seen by reflected light over limited areas. Often numerous small, red, discrete, or confluent pleural hemorrhages are present over consolidated portions, especially posteriorly on the surface of the lower lobes.” Where organisms other than the influenza bacillus had invaded the pleural sac and had been present for a sufficient time to obtain a reaction, the serous type of exudate observed in the early lesions changed to the turbid type of fluid accompanied by more or less fibrin deposit. There was one case where the intense reaction with fibrin and leucocytes gave rise to a new character