The effects of a single dose (100 mg/kg-body weight of mouse) of oxamniquine on the worm's tegument and paranchyma in relation to the process of immunological granulomatous reaction of the host's liver are described under light and electron microscopy (EM). The lesions caused by the drug are sequentially and simultaneously described in form of swelling, surface bulble and disruption with erosions. Ulceration in the tubercules with loss of spines is often more extensive and severe in male worms and concentration of host's mononuclear cells is observed. The possible role of host's immune response is discussed.

Com o objetivo de observar as lesões renais iniciais na esquistossomose mansoni, foram selecionados 21 casos da forma hepato-esplênica, com idade média de 12 anos e que não apresentavam sinais clínicos ou laboratoriais de alterações renais. As biópsias foram realizadas durante esplenectomia e em seguida examinadas à microscopia ótica e à microscopia de fluorescência, sendo empregados conjugados anti IgG, IgM, IgA e C3, isoladamente. No exame microscópico, os 21 casos foram classificados em: 6 casos normais; 6 casos com lesões glomerulares consideradas mínimas e 9 casos com lesões mesangiais discretas ou moderadas. À imunofluorescência constatou-se presença de depósitos de IgM e de C3 predominantemente de localização mesangial, tanto nos casos de lesões mínimas, como nos casos de proliferação mesangial mais acentuada (Tabelas II e III). Constatou-se aind a depósitos de IgG em todos os casos, mesmo naqueles considerados normais, sendo entretanto localizados na parede capilar. Os autores acreditam que na esquistossomose mansoni as lesões glomerulares são provavelmente provocadas pela deposição inicial de imunoglobulinas M, formando imunocomplexos ligados a C3. A presença de IgG no mesangio, já descrita nos estágios mais avançados da glomerulopatia esquistossomótica, seria resultante de uma seqüência evolutiva.

Twenty one cases of hepatoesplenic schistosomiasis patients without clinical and laboratory evidence of renal disease, were studied by surgical biopsies using light microscopy and immunofluorescence. The cases were classified histologically as: normal pattern (6 cases); minimal changes (6 cases); and mesangial proliferative glomerulonephritis (9 cases). By the immunofluorescence microscopy using anti IgM, IgG, IgA and C3, the predominant finding in all biopsies, except the normal cases, was granular deposits of IgM in the mesangium along with C3. On the other hand, IgG was present in all cases including normal biopsies along the capillary walls. However IgG was also present in the mesangium only in cases with glomerular lesions. This finding may well be similar to that recently described as IgM mesangial nephropathy. According to our cases a mesangial proliferative glomerulonephritis, characterized by segmental cell proliferation and deposition of IgM in the mesangium, is probably the entity found in the early stages of mansonic schistosomiasis.