Immunopathology of Chagas disease

The main clinical forms of Chagas disease (acute, indeterminate and chronic cardiac) present strong evidences for the participation of the immune syst em on pathogenesis. Although parasite multiplication is evident during acut e infection, the intense acute myocarditis of this phase exhibits clear ult rastructural al signs of cell-mediated immune damage, inflicted to parasiti zed and non-parasitized myocardiocytes and to the endothelium of myocardial capillaries (microangiopathy). Inflammation subsides almost completely whe n immunity decreases parasite load and suppressor factors modulate host rea ction, but inflammation does not disappear when the disease enters the inde terminate phase. inflammation becomes mild and focal and undergoes cyclic c hanges leading to complete resolution. However; the process is maintained b ecause the disappearance of old focal lesions is balanced by the upsurge of new ones. This equilibrium allows for prolonged host survival in the absen ce of symptoms or signs of disease. The chronic cardiac form is represented by a delayed-type, cell-mediated diffuse myocarditis, that probably ensues when the suppressive mechanisms, operative during the indeterminate phase, become defaulted. The mechanism responsible for the transition from the in determinate to the cardiac form, is poorly understood.