There are many potential mechanisms underlying the pathogenesis of chagasic heart disease. The frequent absence of parasites from the inflamed heart tissue of chronically infected individuals suggests that the disease may be, in part, autoimmune in nature. Mechanisms to explain the induction of T. cruzi induced autoimmunity include (i) polyclonal lymphocyte activation, induced by the parasite, (ii) bystander activation induced by tissue damage and stimulation of normally tolerant, self-reactive

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... lymphocytes, (iii) altered antigen processing leading to the generation and presentation of "cryptic self epitopes," and (iv) molecular mimicry, immunity to a parasite epitope that cross-reacts with a self epitope that "mimics" it. The genetics of host and parasite also determine susceptibility to T. cruzi induced autoimmunity. To date, there is little evidence that the T. cruzi induced autoimmunity directly causes pathology in human Chagas disease or even in mouse models of the disease. Therefore, public health interventions should focus on control of the insects that transmit the parasite, development of parasiticidal drugs and vaccines, and testing of blood products since they are important sources of potential new infections.