Pulmonary involvement in Schistosomiasis mansoni

Abstract

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.

IL‐10 Plays a Role in the Modulation of Human Granulomatous Hypersensitivity Against Schistosoma mansoni Eggs Induced by Immune Complexes

“…The possible interference of IC with cellular defence mechanisms against S. mansoni has been suggested by others [14,15]. In this work, our results show that IC isolated from sera of chronic intestinal schistosomiasis patients were able to suppress granulomatous hypersensitivity to S. mansoni egg antigens conjugated to polyacrylamide beads.…”

“…Although most of the studies on IC in schistosomiasis investigate their participation in pathologic mechanisms [14][15][16], a few have dealt with the participation of IC in suppressive mechanisms [17,18]. Using an in vitro model of granuloma formation [19] we have demonstrated that IC isolated from sera of schistosomiasis patients regulate granulomatous hypersensitivity to polyacrylamide beads conjugated to S. mansoni egg antigens (PB-SEA).…”

Acute Schistosomiasis: Report on Five Singular Cases

“…Patient 3 in our viewpoint presented a Löeffler-like syndrome due to lung deposition of embolic worms or/and immune complexes produced by dead worms after chemotherapy with oxamniquine (Lambertucci et al 1982, Greco et al 1987, Doenhoff et al 1988). As we know, praziquantel kills the worms a few hours after treatment but oxamniquine takes 7 to 10 days to have the same effect (unpublished observations).…”

Clinical, Laboratory and Ultrasonographic Evaluation of Patients with Acute Schistosomiasis Mansoni

“…The clinical features of the acute phase of schistosomiasis mansoni present a wide spectrum [42,43] and the relative contribution of host and parasite factors in the pathogenesis of the disease is not completely elucidated [20,[43][44][45]. According to Neves [46], the clinical forms of the disease will depend on the interaction of at least three sequential events: (a) the evolution phase of the worms, whether before or after oviposition and the deposition of eggs in the tissues; (b) the organ predominantly involved by young or mature worms and by their eggs; and (c) the type and the qualitative/quantitative deviation of the total and local host response to antigenic products derived from the disintegration of schistosomula, adult worms and their eggs.…”