title: Lung lesions in human leptospirosis: microscopic, immunohistochemical, and ultrastructural features related to thrombocytopenia.
abstract: Lung fragments from 12 patients were collected immediately after death and studied by light and electron microscopy and by immunohistochemistry to describe the main morphologic and ultrastructural aspects of the lung and platelets in leptospirosis (Weil's syndrome), to search for the possibility of disseminated intravascular coagulation (DIC), and to assess the relationship between endothelial lesions and local platelet aggregation and the leptospiral antigen distribution, as well as its relationship with the intensity of the lesions. The immunohistochemical results for fibrin aggregates were positive in the lumen and/or on the vascular endothelium in nine cases and on the alveolar surface in seven cases, leading to the diagnosis of the adult respiratory distress syndrome in these seven cases. Test results for leptospiral antigen by immunohistochemistry were positive in eight cases with no direct relationship between antigen deposits in the pulmonary vascular endothelium and intensity of the lesions. The ultrastructural findings were uniform and constant. Capillary lesions were characterized by swelling of endothelial cells, an increase in pinocytotic vesicles, and giant dense bodies in the cytoplasm of these cells. No necrosis, rupture, nor exposed subendothelial collagen was observed outside the hemorrhagic areas, and the intercellular junctions were preserved. The lung involvement in severe human leptospirosis presents as hemorrhagic pneumopathy with septal capillary lesions that are the usual cause of death. The thrombocytopenia that was verified in 11 of 12 patients in our study seems to bear no relationship to DIC and seems to be determined by activation, adhesion, and aggregation of platelets to the stimulated vascular endothelium, with an amorphous electron-dense substance between the endothelial cells and the adherent platelets in places where the subendothelial collagen was not exposed.
authors.affiliation: Department of Infectious Diseases, University of Sao Paulo Medical School, Brazil.
authors.forename: A C
authors.initials: AC
authors.lastname: Nicodemo
authors.forename: M I
authors.initials: MI
authors.lastname: Duarte
authors.forename: V A
authors.initials: VA
authors.lastname: Alves
authors.forename: C F
authors.initials: CF
authors.lastname: Takakura
authors.forename: R T
authors.initials: RT
authors.lastname: Santos
authors.forename: E L
authors.initials: EL
authors.lastname: Nicodemo
mesh_terms: D000328:Adult; D000942:Antigens, Bacterial / Q000032:analysis; D001792:Blood Platelets / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D002196:Capillaries / Q000469:parasitology / Q000648:ultrastructure; D002448:Cell Adhesion; D004730:Endothelium, Vascular / Q000378:metabolism / Q000469:parasitology / Q000648:ultrastructure; D005260:Female; D005337:Fibrin / Q000032:analysis / Q000276:immunology; D006470:Hemorrhage / Q000209:etiology; D006801:Humans; D007150:Immunohistochemistry; D007921:Leptospira interrogans / Q000276:immunology / Q000302:isolation & purification; D008168:Lung / Q000098:blood supply / Q000473:pathology* / Q000648:ultrastructure; D008171:Lung Diseases / Q000209:etiology; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D010974:Platelet Aggregation; D013921:Thrombocytopenia / Q000209:etiology* / Q000473:pathology; D014895:Weil Disease / Q000150:complications / Q000473:pathology*
chemical_list: D000942:Antigens, Bacterial; D005337:Fibrin