It is still unclear whether the progression of acute to chronic
Chagas cardiomyopathy is predominantly associated with the limited efficacy of aetiological
chemotherapy, or with the pharmacological resistance profiles and pathogenicity of specific Trypanosoma cruzi strains. Thus, we tested the hypothesis that parasitic load could be a limited target of aetiological
chemotherapy to prevent chronic
cardiomyopathy in dogs infected by different T. cruzi strains. Animals were infected with
benznidazole-susceptible (Berenice-78) and -resistant (VL-10 and AAS) strains of T. cruzi. A quantitative real-time PCR strategy was developed to comparatively quantify the parasite load of the three different strains using a single standard curve. For dogs infected with the VL-10 strain,
benznidazole treatment reduced cardiac parasitism during the acute phase of
infection. However, similar parasite load and
collagen deposition were detected in the myocardium of treated and untreated animals in the chronic phase of the
infection. In animals infected with the AAS strain,
benznidazole reduced parasite load,
myocarditis and
type III collagen deposition in the acute phase. However, increased
type III collagen deposition was verified in the chronic phase. Dogs infected with the Berenice-78 strain showed a parasitological cure and no evidence of myocardial
fibrosis. Parasitic load and cardiac
fibrosis presented no correlation in acute or chronic phases of T. cruzi
infection. Our findings in a canine model of
Chagas disease suggest that parasite burden is a limited predictor for
disease progression after treatment and show that
benznidazole, although not inducing parasitological cure, is able to prevent total
fibrosis in the early stages of
infection, as well as complete prevention of cardiac damage when it eliminates parasites at the onset of
infection.