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The immunoglobulin E (IgE) response, a hallmark of helminthic infection, is generally considered a major host defense against schistosomiasis mansoni. In support, it was reported that mice with a null mutation of the Ce gene, which are thus incapable of making IgE, developed Schistosoma mansoni worm burdens 2-fold greater than wild-type mice. However, in another study, reduction of the IgE response in mice to a primary S. mansoni infection by anti-IgE treatment resulted in decreased worm burden and fecundity, suggesting that IgE plays a detrimental, rather than beneficial, role for the host in schistosomiasis. In a third study, S. mansoni worm burden and egg production in normal and in IL-4-deficient mice that produce negligible IgE levels did not differ significantly, and it appeared that IgE did not affect parasite survival or fecundity. In an attempt to resolve these controversies, we examined hepatic worm load and egg production in the liver and small intestine of IgE-deficient (SJA/9) and control IgE-producing (SJL/J) mice, 8 wk after S. mansoni infection. No differences were observed in worm burden, total egg production, and number of eggs produced per female worm in the 2 mouse strains, confirming the data that imply that IgE does not play an essential role in primary S. mansoni infection.

Five confirmed human cases of gnathostomiasis nipponica exhibiting creeping eruption and itching were found sporadically from the autumn of 1991 to the winter of 1992 in the northern region of the mainland of Japan. In all cases, a causative gnathostome with 3 transverse rows of hooklets on the head bulb was detected in biopsied skin. The morphological characteristics agreed with the advanced third-stage larvae of Gnathostoma nipponicum. Within a few weeks before development of symptoms, all patients had histories of eating raw freshwater fishes, kokanee (Salmo nerka nerka), carp (Cyprinus carpio), crucian carp (Carassius gibelio langsdorfi), or common ice-fish (Salangichthys microdon). However, they had never eaten raw loach, which is known as a source of human infections with G. nipponicum.

We previously demonstrated that neutrophils biosynthesize the Iinoleate epoxide, 9,10epoxy-12-octadecenoate, from Iinoleate and hydroxyl radical. This epoxide is highly cytotoxic, and has been termed leukotoxin. Wedetected leukotoxin in plasma from two patients with infectious endocarditis and circulatory shock. Maximal leukotoxin levels were 580 nmol/ml and 880 nmol/ml, respectively. The leukotoxin levels were affected by hemodialysis or hemofiltration. Disseminated intravascular coagulation was confirmed by blood coagulation studies in these two patients. Leukocytosis was also observed in these patients. In contrast, leukotoxin was not detected in plasma of normal volunteers. Accordingly, leukotoxin synthesized by recruited neutrophils might be a contributory factor in circulatory shock.

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