Chagas' Disease: a Clinical, Parasitological, Immunological, and Pathological Study in Rabbits

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  • Faculdade de Ciências da Saúde da Universidade de Brasília, 70.910, Brasília-DF, Brazil

Thirty-four rabbits were experimentally infected with trypomastigotes of either the Ernestina or the Albuquerque strains of Trypanosoma cruzi. These animals showed patent parasitemias, as demonstrated by xenodiagnosis, in the acute phases of the infections. Typical chagoma signs developed in two rabbits 1 week after parasite inoculation in the skin, although the acute phase of Chagas' disease in the rabbit model was usually asymptomatic. In the 6th month of infection the parasitemias became negative and the infections remained subpatent, as indicated by the persistence of positive serologic tests and of delayed-type skin reactions elicited in Chagas' rabbits against a microsomal T. cruzi antigen. This latent infection continued asymptomatically, in the absence of electrocardiographic (ECG) alterations. However, ECG changes consistent with enlargement and overload of cardiac chambers, alterations of ventricular repolarization, S-T changes and bundle-branch blocks were frequently recorded later in the chronic phase of Chagas' disease. The pathological manifestations of these ECG alterations were confirmed at the autopsy of each experimental rabbit. Congestive heart failure and pulmonary thromboemboli related to chronic myocarditis of Chagas' disease were frequent causes of death. Megacolon was seen in two rabbits inoculated with the Ernestina strain of the parasite. The relatively limited duration of detectable parasitemia even when xenodiagnosis is used, the lack of correlation between parasitemia and severity of pathological manifestations, and the fact that all infected animals showed histopathological evidence of myocarditis, destructive inflammatory lesions characterized by mononuclear infiltrates in skeletal muscles, as well as cutaneous delayed hypersensitivity to T. cruzi antigens, are notable observations in this animal model of the human disease.

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