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The pathology of influenza

Chapter 37: C. THE APLASTIC EXUDATE
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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.

C. THE APLASTIC EXUDATE

The absence of cellular elements in the alveolar exudate is frequently observed in influenzal pneumonia (Figs. XXI, XXII, XXIII). This picture has been reproduced experimentally in animals which have been rendered aplastic with benzol, especially with reference to their myeloid elements (160). Pneumonia produced by intratracheal insufflation is more rapidly fatal in aplastic animals, and it is conceivable that the absence of cellular reaction is an explanation for the lack of resistance demonstrated by the high mortality of influenzal pneumonia. Frequently the fibrinoserous mass scattered diffusely throughout the lung is rich in bacteria. In the absence of cells of the polymorphonuclear series, the bacterial development seems to be unrestricted. The aplastic exudate is associated clinically with an absence of a myeloid reaction in the peripheral circulation. The leucocytic count may be definitely decreased, even though the tissues have been invaded by pyogenic organisms to which the usual response is a definite leucocytosis. The only explanation is that the myeloid structures have been injured, probably by the unknown virus of the disease.