In this paper the treatment of schistosomiasis is examined under the following headings: cercarial dermatitis, Katayama fever, schistosomiasis in the immunosuppressed host and treatment of therapeutic failures.

A esquistossomose apresenta-se clinicamente em três formas distintas: dermatite cercariana, esquistossomose aguda ou febre de Katayama e esquistossomose crônica. Há na literatura relatos de complicações da fase aguda. A ausencia de um marcador sorológico simples e confiável tem dificultado o diagnóstico precoce e, como consequência, o tratamento adequado de pacientes na fase aguda da doença. Recentemente, o teste de ELISA, realizado com o antígeno KLM (hemocianina do caramujo Megathura crenulata), tem se mostrado util na identificação dos pacientes com febre de Katayama. Evidências clínicas e experimentais apontam no sentido de uma ação sinérgica entre os corticosteróides e os esquistossomicidas no tratamento da esquistossomose toxêmica. Neste artigo, alguns aspectos clínicos, diagnósticos e terapêuticos da esquistossomose aguda são atualizados.

Three distinct syndromes caused by schistosomiasis have been described: cercarial dermatitis or swimmer's itch, acute schistosomiasis or Katayama fever, and chronic schistosomiasis. Complications of acute schistosomiasis have also been reported. The absence of a serological marker for the acute stage has hindered early diagnosis and treatment. Recently, an ELISA test using KLH (keyhole limpet haemocyanin) as antigen, has proved useful in differentiating acute from chronic schistosomiasis mansoni. Clinical and experimental evidence indicate that steroids act synergistically with schistosomicides in the treatment of Katayama syndrome. In this paper, clinical, diagnostic and therapeutic features of acute schistosomiasis are updated.

The post-treatment pulmonary alterations were evaluated in patients (Study 1) and in mice (Study 2) infected with Schistosoma mansoni. Study 1: the patients were examined pre and post-treatment (with ora oxamniquine) and the following exams were performed: sputum for eosinophils and chest x-ray. Study 2: four groups of mice (total = 64) were studied; Group I (infected and treated with oxamniquine); II (infected and not treated); III (not infected and treated) and IV (not infected and not treated). All were x-rayed to check for pulmonary abnormalities pre and post-treatment and lung specimens were studied by optical microscopy and immunofluorescence. We have found abnormalities in the parameters checked in both studies and the results suggest an immunological reaction, probably due to deposition of immune complexes in the lungs, with subsequent activation of the complement system. The experimental study showed that the alterations are not dependent of the presence of eggs and/or worms of S. mansoni in the lungs, thus corroborating the hypothesis of deposition of circulating material.