Lung lesions in human leptospirosis: microscopic, immunohistochemical, and ultrastructural features related to thrombocytopenia.

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.

Aspectos clinico-laboratoriais da nefrite intersticial da leishmaniose visceral. / Clinico-laboratorial aspects of interstitial nephritis of visceral leishmaniasis

O acometimento intersticial renal na leishmaniose visceral (LV) ja foi caracterizado com um componente proprio da doenca Fizemos um estudo retrospectivo de 104 casos de LV para verificar as repercussoes clinico-laboratoriais da nefrite intersticial da LV. Apesar da doenca de longa duracao, os pacientes sao admitos ao Hospital sem apresentarem dados clinicos ou laboratoriais que surgiram acometimento da funcao renal. Em alguns casos (6,38%) havia proteinuria discreta (variando de 1,0 a 2,0g/litro). Quatorze pacientes foram a obito, apresentando intercorrencias clinicas associadas a LV, infecciosas ou hemodinamicas. Em 6 casos constatou-se oliguria e uremia nos dias que precederam o obito. No exame histopatologico dos rins, encontrou-se nefrite intersticial de grau moderado ou intenso. O desenvolvimento de insuficiencia renal aguda nesses casos parece estar condicionado a intensidade da nefrite intersticial propria da LV quando os rins sao submetidos a fatores isquemiantes severos

Interstitial nephritis in human kala-azar.

Little is known about renal alterations in kala-azar. The renal histopathology of 21 patients admitted to hospital in São Paulo, Brazil, during the period 1960 through 1981 who either died or had a renal biopsy (two cases) is presented. All the specimens showed oedema and diffuse interstitial inflammatory infiltrate of lymphocytes and plasma cells with more compact foci of cells in some areas. In general, glomeruli did not show any important alterations. These aspects were interpreted as acute interstitial nephritis aetiologically related to later phase kala-azar. This interstitial alteration does not usually seem to determine any clinical manifestations. However, it seems that moderate and severe cortical intersitial damage contribute to the onset of renal insufficiency when severe clinical complications occur. The precise mechanisms of this lesion need further investigation since the aetiological agents have not been seen causing the damage locally.