Pathogenesis of chagasic myocarditis: an experimental study

With the propose to study the pathogenesis of chagasic myocarditis, white mice were inoculated with the Y strain of Trypanosoma cruzi. After confirmation of parasitemia, the animals were sacrificed: a) in the acute stage (first 30 days), 5 mice/day: b) in the subacute stage (days 30-90), 5 mice/week: c) in the chronic stage the remaining survivors, 365 days after inoculation. Parasitemia appeared on the sixth day and increased gradually until the maximum was reached in the third or fourth week, then decreasing until the thirtieth day, disappearing from the circulation after the 87th day. Parasitism occurred with parasitemia however, without a quantitative relationship. Starting from the sixth post-inoculation day the muscle fibers demonstrated parasites, with the presence of compact or loose amastigote nests. The nests, bursted during the evolution so that their contents (cytokine or interleukin?) could extravasate. While the nest was integral, there was no acute inflammatory reaction. During the chronic stage empty spaces remained and were occupied by the chronic inflammatory process: proliferation of fibroblasts. granulomas and residual fibrosis. The inflammatory edema replaced the interstitium. After rupture of the amastigote nests they were initially invaded by the acute inflammatory process and then by the chronic one with deposition of a fibrin network, proliferation of collagen, mastocytosis and terminating with fibrosis. It was not uncommon to find amastigote nests in various stages during the chronic phase in the myocardial fibers, characterizing the cyclical process of the parasitosis. The blood vessels were also, invaded by parasites. Causing thrombosis and necrotizing arteritis. The autonomous nervous system also was involved, with the presence of amastigote nests, ganglionitis, plexulitis with inflammation in scattered areas.