Abstract. Trypanosoma cruzi infection in the Ecuadorian Amazon region has recently been reported. A seroepidemiologic survey conducted in four provinces in this region indicates a seroprevalence rate of 2.4% among the 6,866 samples collected in 162 communities. Among children Յ 10 years of age, 1.2% were seropositive. Risk factors for T. cruzi seropositivity were having been born and remaining in the Ecuadorian Amazon provinces, age, living in a house with a thatch roof and open or mixed wall construction, recognizing the vector insects, and reporting being bitten by a triatomine bug. These data suggest active transmission of Chagas' disease in the Ecuadorian Amazon region is associated with poor housing conditions, and highlight the need for further studies aimed at understanding the biology of the insect vectors, reservoir species, and the clinical impact of T. cruzi infection as the basis for future educational and control programs in this region.

Immunosuppression has been reported to occur in several protozoan parasitic infections. The significance of this suppression on host resistance or on parasite avoidance of immune destruction has not, however, been determined. In the present study two strains of mice that differ with respect to resistance to Trypanosoma cruzi were examined during the course of infection for differences in expression of suppression of blastogenic responses to phytohemagglutinin and an antigen preparation of these parasites. It was found that in vitro blastogenic responses were suppressed in both strains of mice: on day 12 for C57BL/6 mice (resistant strain) and on day 17 for C3H(He) mice (susceptible strain). Neither C3H(He) nor C57BL/6 lymph node cells (LNC) responded to a crude sonically treated antigen of these parasites, although C57BL/6 LNC were inhibited by this antigen later in infection. There was no abrogation of suppression of LNC responses late in infection, when decreases in spleen weight or total spleen cell numbers occurred, in the resistant C57BL/6 mice. LNC from normal uninfected mice were found to be completely suppressed in responsiveness to phytohemagglutinin when cultured at a 2:1 ratio with LNC from C57BL/6 mice with 18-day infections. Attempts to characterize the cell type responsible for this suppression showed it to be a non-thy 1.2-bearing, nylon wool-adherent cell.

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Isotypic analysis of anti-parasite humoral responses of C57B1/6 and C3H (He) mice surviving acute Trypanosoma cruzi infection showed that both mouse strains demonstrate IgG1, IgG2a, IgG2b, and IgM enzyme-linked immunosorbent assay titers from days 21 to 300 of infection. Using the western blot technique to determine the antigen specificity of the isotypic responses, 100-day infected C3H mice showed strong IgG1, IgG2a, and IgG2b responses to many antigens, whereas C57B1/6 mice showed weak responses to fewer antigens. Isotype western blots showed that reactivity to the T. cruzi antigen of 75-77 kDa is present in the humoral response of day 21-infected mice that will survive and missing in those that will not survive. In general, surviving immunized C3H mice respond with IgG1, IgG2a, and IgG2b reactions to the 75-77-kDa and other antigens, whereas resistant B6 mice concentrate their anti-T. cruzi response in the IgG2b isotype to the 75-77-kDa antigen. Perhaps induction of ineffective antibody responses to nonprotective antigens is beneficial to the parasite and detrimental to the host.

C57BL/6 mice exhibit low parasitemias and often survive Trypanosoma cruzi infections, whereas C3H(He) mice die during the acute phase with relatively high parasitemias. The present study showed that both strains of mice develop nonspecific immunosuppression to challenge with sheep erythrocytes during the course of infection. Several major differences in immunosuppression-related phenomena between the two strains of mice were determined, yet there is no apparent relationship between immunosuppression and resistance to T. cruzi. Both the number of direct plaque-forming cells and the titer of2-mercaptoethanol-sensitive agglutinating antibody were significantly lower on day 11 for C57BL/6 mice and day 9 for C3H(He) mice. The number of indirect plaque-forming cells and the titer of mercaptoethanol-resistant agglutinating antibody were reduced by day 36 of infection in C57BL/6 mice and 13 days postinfection in C3H(He) mice. In both strains the degree of humoral response suppression of mice increased concomitant with the period of infection, but was not correlated with the changes in spleen cell numbers. Preliminary experiments designed to explore the mechanism underlying the induction and maintenance of immunosuppression in this hostparasite model disclosed the presence of suppressor substance in the serum of T. cruzi-infected mice. The passive transfer ofserum from infected mice to syngeneic recipients elicited a state of immunosuppression to sheep erythrocytes, but did not diminish anti-erythrocyte activity in allogeneic recipients. The induction of immunosuppression in normal mice was further found to be dependent on the interval between serum transfer and challenge with antigen. No quantitative differences existed between the magnitude of suppressed humoral responses in mice infected for varying lengths of time and recipients of serum collected from similarly infected mice.