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ABSTRACT. Our previous reports indicated that C57BL/6 mice infected with a lethal variant of Plasmodium yoelii 17X (P. yoelii 17XL) produced high levels of interleukin 10 (IL-10) and interferon-γ (IFN-γ) while mice infected with the nonlethal variant of the parasite did not produce detectable levels of IL-10. In the present study, the involvement of IL-10 and IFN-γ in exacerbation or regulation of bloodstage malaria was investigated by using the lethal variant of P. yoelii 17XL and monoclonal antibodies (mAb) against the cytokines. C57BL/6 mice were injected intraperitoneally with a neutralizing anti-IL-10 mAb or anti-IFN-γ mAb after inoculation with P. yoelii 17XL. Treatment of mice with anti-IL-10 mAb resulted in substantial prolongation of survival and 60% of treated mice survived while 100% of control mice died by day 11. On the contrary, treatment of mice with anti-IFN-γ mAb exacerbated infection and all mice died after an earlier period than those treated with normal rat Ig. No differences in parasitemias were found between treated and untreated mice. To elucidate the involvement of nitric oxide in the host protection or exacerbation, mice were treated with aminoguanidine, an inhibitor of nitric oxide synthetase, after inoculation of P. yoelii 17XL. Neither mortality nor parasitemia was influenced by the treatment. These results indicate that an IFN-γ response is associated with protective immunity in mice infected with P. yoelii 17XL, while an IL-10

We investigated the induction of T-helper cell subsets during the course of lethal or nonlethal bloodstage Plasmodium yoelii 17X infection in C57BL/6 mice, which are relatively susceptible to these intraerythrocytic parasites. C57BL/6 mice infected with the nonlethal variant (PyNL) showed a moderate level of parasitemia and resolution of primary acute infection by week 4. Mice infected with the lethal variant (PyL) developed fulminating parasitemia and ultimately died. T-helper subset function was assessed during infection by determining the kinetics of in vitro production of the Th1-derived cytokine interferon-gamma (IFN-gamma) and the Th2-derived cytokine interleukin 10 (IL-10) by means of bioassay and enzyme-linked immunosorbent assay (ELISA), respectively. Spleen cells obtained from mice infected with PyL within the 1st week of infection produced high levels of IL-10 and IFN-gamma in response to malaria antigen. IL-10 also appeared in sera from PyL-infected mice at the same time at which the in vitro IL-10 response peaked. In contrast, spleen cells from mice infected with PyNL failed to produce IL-10 during the course of infection. CD4+ T-lymphocytes from mice infected with the lethal variant were a major source of IL-10, although non T-cells were also involved in the production of IL-10 during this malaria infection. In addition, the initial burst of IL-10 in response to malaria antigens was seen concomitantly with the production of IFN-gamma within the 1st week of infection. These results indicate that both Th1 and Th2 subsets of T-helper lymphocytes are activated during infection with the lethal variant of P. yoelii and support the contention of other investigators that a strong Th2 response early in infection is associated with the lethal outcome of malaria.

We report the clinical and radiologic features of 12 patients with acute intestinal anisakiasis. Diagnosis of anisakiasis was made immunologically by positive antibody to Anisakis larvae and a recent history of raw fish intake. Severe abdominal pain was a major symptom in these patients-half experienced fluid levels indicating ileus on plain x-ray films of the abdomen. Radiologic findings included irregular thickening of the jejunum, ileum, or colon, with mucosal edema and luminal narrowing with dilatation of the proximal intestine. In two cases a thread-like filling defect suggesting a worm was visualized on the x-ray film. These findings were interpreted as anisakiasis. Although ileus developed in some patients, all were treated and cured completely without surgery.

SUMMARY Two brothers with visceral larva migrans caused by Trichuris vulpis were diagnosed after they had been investigated for an eosinophilia. Both patients were almost asymptomatic. The diagnosis of visceral larva migrans was based on the results of immunoelectrophoretic studies and no liver biopsy was performed. After administration of thiabendazole, the number of eosinophils and serum total IgE levels gradually decreased, and the patients have remained well.The term visceral larva migrans (VLM) was first introduced by Beaver et al.1 to describe a syndrome in young children characterised by chronic extreme eosinophilia, hepatomegaly, and pulmonary symptoms. Causative parasites most often encountered are Toxocara canis and Toxocara cati.2-3 A hog ascaris, Ascaris suam, may also be an aetiological agent.5 Until now there have been no reports of VLM due to Tricharis vulpis infestation, and two such cases are now reported. Immunological methodsSerum antibodies against helminth antigens were detected by Ouchterlony's method and immunoelectrophoresis, using extracts of various helminths as antigens. The extracts were obtained by repeated freezing and thawing of the parasites, after grinding down in 0-1 % sodium chloride solution. After centrifugation, the supematants were dialysed and lyophilised. These antigens were dissolved in veronal-buffer before use.Details of immunoelectrophoresis have been described.6 Briefly, antigen was first developed by immunoelectrophoresis in agar gel. At the end of the separation, the serum was placed in a trough cut parallel to the path of electrophoretic migration. After incubation at 4°C, the slide was washed with saline containing veronal-buffer for 3 days and stained with amido black 10B. The arcs of precipitate were examined. Case 1. A 5-year-old boy was referred to Hiroshima University Hospital for further evaluation of a pronounced eosinophilia. His family had obtained a 10-month-old dog 4 months before he was admitted to hospital. He had been the product of a normal pregnancy and delivery. He started to have occasional asthmatic attacks at 21 years, but these had stopped by the age of 4. His father is currently in good health but he, too, had suffered from bronchial asthma in childhood.