Chagas' disease is caused by the protozoan Trypanosoma cruzi which infects 10-15 million people in endemic areas throughout Latin America and is naturally transmitted by insect vectors of the family Reduviidae. Infection can also occur by congenital passage, oral ingestion, laboratory accident, and in organ transplants and blood transfusions. There are 3 life-cycle forms of T. cruzi. Epimastigotes multiply in the midgut of the insect vector, differentiate in the hind-gut into infectious trypomastigotes, and are excreted with the feces or urine after a blood meal. They enter the body by mucous membranes or abraded skin, enter mammalian host cells, escape the phagolysosomal vacuole, and differentiate into amastigotes. Intracellular amastigotes multiply in host cells, redifferentiate to trypomastigotes, and are released upon cell rupture.
Acute Chagas' disease can be asymptomatic, or a mild to severe illness. Morbidity can be localized and/or systemic and is usually accompanied by general immunosuppression with blood and tissue parasitemia. It can be fatal. Usually, symptoms and parasitemia decrease within months, followed by a life-long, chronic infection with little morbidity and few apparent parasites. Serologically-positive, chronic asymptomatic patients are termed indeterminate (I). Morbidity develops in 20-30% of chronic patients after 10-30 years and often involves myocardiopathy (Cardiac disease; C), ranging from minor electrocardiographic changes to sudden death by heart failure. Severe “digestive” megasyndromes can also develop. Chagasic myocardial inflammatory infiltrates are associated with cardiac muscle and neuron destruction, followed by progressive fibrotic replacement. Asymptomatic Ipatients who die of unrelated causes have identical (but less intense) lesions.
Responses against T. cruzi antigens, their immunoregulation, and responses against related idiotypes (Ids) correlate with the presence of the different clinical forms of the infection. Although there are numerous findings of autoimmune lymphocyte and antibody reactivities in chagasic patients, a causal relationship is always difficult to prove. Chagasic patients' peripheral blood mononuclear cells (PBMC) respond to T. cruzi epimastigote antigens (EPI) with varying vigor. Almost all low responders are Cpatients, and their responses are usually augmented by removal of adherent macrophage suppressor cells or the addition of indomethacin. Chronic I-patients are medium or high responders, and exhibit little adherent cell-mediated immunoregulation. Western blotting studies indicate patients' Ab and cell-mediated responses to EPI show differences between C-and I-patients. PBMC from I-patients responded more often to high molecular weight components (100-150 kD), while both I-and C-patients responded well to moieties between 28-32 and 48-57 kD. All chagasic patients' sera had Abs and PBMC responses to T. cruzi GP57/51 antigen.
Chronic Chagas' patients have peripheral blood anti-Id T cells that respond to anti-EPI Abs purified from patients' sera. Some patients' PBMC anti-Id responses to anti-EPI Ids from C-patients (Id-C) are inhibited by chloroquine (Group 1), but some are not inhibited by chloroquine, anti-HLA Class II antigens, or sodium azide (Group 2). Most patients in Group 1 are asymptomatic, but all Group 2 patients have severe disease. Direct (non-processed; non-MHC-presented) stimulation of anti-Id T cells from C-patients by Ids expressed on anti-EPI Abs from C-patients could be immunopathogenic. Anti-Id specific rabbit sera detect Id differences in the anti-EPI Abs from pooled or individual C vs. I-cases. Competitive ELISA assays and Western blot analyses of Abs show that Ids on I-patients' anti-EPI Abs are primary structure expressions, while Ids on C-patients' anti-EPI Abs are defined by intact Ab molecules.

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Onchocerciasis is a widespread filarial disease in Nigeria that produces grave socio-economic effects. The great majority of the communities are mesoendemic for onchocerciasis while only few are hyperendemic especially in the savanna zone. Sexrelated infection depends on the degree of endemicity while age-infection increases gradually with advancing age. Visible and palpable nodules are more abundant around the pelvic region. The nodules are countered more in the rainforest zone even when microfilarial density (MFD) is moderate, while the nodules are less numerous in the savanna form with high MFD. The microfilariae in concert with host's immune response precipitate various skin lesions. The resulting pruritus, scratching and itching are generalized in the rainforest and localized in the savanna. In the eye, various ocular lesions are associated with the death of microfilariae. There is high incidence of eye lesion in the savanna zone than in the rainforest zone, especially the anterior lesions. The epidemiological picture presented by onchocerciasis in Nigeria is the summation of a complex array of contributing factors, both intrinsic to the microfilariae and resulting from the host-immune response, bioclimatic factors and vector species complex.

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The etiology of peripheral blood eosinophilia and hyperglobulinemia E, which are commonly found among residents in tropical area, were studied with two groups of Brazilian children from different primary schools. These two groups of children had different infection rates with soil-transmitted helminthiases, but similar positive rates of antibody against a common allergic antigen. The prevalence rate of children with eosinophilia or hyperglobulinemia E was significantly higher in a group with higher infection rate with soil-transmitted helminthiases than in another group with lower infection rate. It was suggested that eosinophilia and hyperglobulinemia E in this area were mainly caused by soil-transmitted helminthiases.

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The present study was designed to evaluate skin test preparations prepared from Leishmania panamensis promastigotes in 30 active cutaneous leishmaniasis patients. The crude antigen preparation (CA) used was 10, 000×g supernatant of the parasiteshomogenate. The soluble extract was further resolved into 4 preparations (FA-1 to-4) with the aid of a Sephacryl S-200 gel filtration. There was no significant difference in the positive ratio and the average induration size between CA (10 μg protein/test) and Montenegro's antigen (MA;5×10⁶ parasites/test). The reactivity of the delayed-type hypersensitivity to 10 μg dose of CA was shown with much the same intensity in the 25 μg dose of CA. In FAs (10 μg protein dose, except for 7.5 μg. in FA-4), the positive ratio was as follows : 90.0% in FA-1, 77.8% in FA-2, 75.0% in FA-3 and 37.5% in FA-4. The positive ratio and the intensity of skin test response in FA-4 were remarkably low in comparison with those in CA or MA. Significant difference was found in the intensity of response between FA-3 and CA or MA. Based on these results, therefore, we concluded that 10 pg protein dose of CA of L. panamensis and same dose of the fractionated preparations, FA-1 and-2, were very suitable for the diagnosis of cutaneous leishmaniasis in endemic areas of the New World. Furthermore, it was estimated that at least some or all of the 5 proteins, approximately 66, 55, 45, 28, and 26 kD, were related to a specific delayed-type hypersensitivity in cutaneous leishmaniasis of the New World.

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