RESUMO
Trypanosoma cruzi causes a pan-infection, Chagas disease, in American mammals through fecal transmission by triatomine insects, resulting in an acute phase parasitemia with intracellularity mainly in the myocells and cells of the central nervous system (CNS).The parasites, due to the immune response, then decrease in number, characteristic of the life-long chronicity of the disease. We infected a mouse model with isolates obtained from reservoirs and vectors from rural and urban endemic areas in Venezuela. Intracellular proliferation and differentiation of the parasite in astrocytes, microglia, neurons, endothelial cells of the piarachnoid, cells of the Purkinje layer, and spinal ganglion cells, as well as extracellularly in the neuropil, were evaluated during the acute phase. Damages were identified as meningoencephalitis, astrocytosis, reactive microglia, acute neuronal degeneration by central chromatolysis, endothelial cell hyperplasia, edema of the neuropil, and satellitosis. This is the first time that satellitosis has been reported from a mammal infected with T. cruzi. Intracellular T. cruzi and inflammatory infiltrates were found in cardiac and skeletal myocytes and liver cells. No parasitism or alterations to the CNS were observed in the chronic mice, although they did show myocarditis and myocitis with extensive infiltrates. Our results are discussed in relation to hypotheses that deny the importance of the presence of tissue parasites versus the direct relationship between these and the damages produced during the chronic phase of Chagas disease. We also review the mechanisms proposed as responsible for the nervous phase of this parasitosis.
