In gas poisoning it has been demonstrated that the initial damage to the epithelium of the larger air passages is followed by an invasion of the pulmonary parenchyma by the bacteria of the mouth. Repeated cultures from the mouth before the exposure of the animal to gas have been followed by the recovery of the same organisms, including the pneumococci, the streptococci, the staphylococci, and a gram-negative, hemoglobinophilic, small bacillus from the pneumonic lung. They find their way into the lung after the destruction or incapacitation of the protective mechanism (70) of the upper respiratory tract,—into a lung which has been so damaged by the irritative gas that bacteria innocuous in the normal pharynx now find a favorable medium for their development. The inflammatory reaction which develops into pneumonia, perhaps necrotizing, perhaps later organizing, can only be explained by the combined action of the corrosive gas and the organisms saprophytic in the normal mouth, but now pathogenic in varying degrees in the lung whose vital reactions have either been inhibited or impaired by the gas. [Illustration: FIG. XL. AUTOPSY NO. 140. LEFT LUNG. THE HISTOLOGY OF THE PULMONARY CHANGES IN THIS CASE IS ILLUSTRATED IN FIGURES XI, XLI, AND XLIV. THESE PROCESSES, ILLUSTRATED IN FIGURE XXXIX, ARE ACCENTUATED AND THERE IS ALSO AN ORGANIZATION OF THE EXTENSIVE PURULENT PLEURISY TO BE MADE OUT IN THE ABOVE FIGURE. ] There is no reason why this analogy should not be drawn, no reason why we should not consider that the unknown etiological agent in influenza produces a similar injury to, or even destruction of, the protective mechanism of the respiratory tract. Similarly, gas and influenza damage the pulmonary parenchyma itself, so that the bacteria of the air and of the mouth which find their way into the damaged lung[16] initiate processes and produce complications which may not be distinguished. V. PECULIARITIES OF THE HISTOLOGY OF INFLUENZAL PNEUMONIA A. THE EXTENT OF THE INITIAL PULMONARY LESION