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The pathology of influenza

Chapter 33: D. THE IMPORTANCE OF THE TRACHEA AND ITS RAMIFICATIONS AS A PROTECTIVE MECHANISM AGAINST INFECTION OF THE PULMONARY PARENCHYMA
By M. C. Winternitz
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The authors present a systematic pathological study of cases from the 1918 influenza epidemic, based on eighty-two autopsies, detailing gross and microscopic findings. They describe necrotizing hemorrhagic lesions of the trachea and bronchi and several pulmonary patterns including acute diffuse fulminant hemorrhagic pneumonia, localized necrotizing pneumonias, and organizing bronchiolar/alveolar exudates. The work documents extrarespiratory effects on lymphoid tissues, spleen, bone marrow, blood vessels, the alimentary and urinary tracts, central nervous system structures, and changes observed in pregnancy. A comparative analysis contrasts these lesions with those produced by inhaled poisonous gases and emphasizes peculiar histologic features such as hemorrhagic and hyaline necrosis and patterns of organization. Bacteriological findings and their relation to pleural involvement and pneumonic types conclude the study.

D. THE IMPORTANCE OF THE TRACHEA AND ITS RAMIFICATIONS AS A PROTECTIVE MECHANISM AGAINST INFECTION OF THE PULMONARY PARENCHYMA

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.

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.