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Diffuse pulmonary edema, capable of arising in the absence of hemodynamic disorders is rare in infectious disease. They take on two different clinical appearances: a) acute edema of the lung with the syndrome of asphysia, b) a subacute dyspneic pneumonia with hypoxemia and hypo or normocapnia. These initial disorders can be followed by progressive respiratory failure secondary to the development of diffuse interstitial lesions with fibrosis and intra-alveolar hyaline deposits. The bronchiolo-alveolar lesions which induce a fibrin rich exudate are directly caused by the patogenic agent: myxovirus, essentially influenzae, and more rarely adeno or herpes virus. The role of bacteria and of certain parasites is more debateable.

Among the various infectious and parasitic disease liable to produce granulopenia, the authors selected certain diseases which represented their personal experience. Classically, leukopenia may occur during typhoid fever, but was not present in all of the series of 114 adults they observed with this disease. It only occurs after antibiotic treatment (Thiamphenicol in the majority of cases). During acute brucellosis (188 cases studied) granulopenia was constant. It occurs early and is lasting. It reappears during septicemic relapse. Leukopenia is corrected during treatment by tetracycline antibiotics. Neutropenia during disease is frequent but usually labile. This characteristic explains why there was no granulopenia in 90 cases of mumps and 64 cases of chickenpox. Finally, during Kala Azar, 8 cases confirmed certain already well known data: the considerable reduction in granulocytes but also anemia and thrombocytopenia.