Twenty young male Cebus apella monkeys were infected with CA1
Trypanosoma cruzi strain and reinfected with CA1 or Tulahuen
T.cruzi strains, with different doses and parasite source.
Subpatent parasitemia was usually demonstrated in acute and
chronic phases. Patent parasitemia was evident in one monkey
in the acute phase and in four of them in the chronic phase
after re-inoculations with high doses of CA1 strain.
Serological conversion was observed in all monkeys; titers
were low, regardless of the methods used to investigate
anti-T. cruzi specific antibodies. Higher titers were induced
only when re-inoculations were performed with the virulent
Tulahun strain or high doses of CA1 strain. Clinical,
electrocardiographic and ajmaline test evaluations did not
reveal changes between infected and control monkeys.
Histopathologically, cardiac lesions were always
characterized by focal or multifocal mononuclear infiltrates
and/or isolated fibrosis, as seen during the acute and
chronic phases; neither amastigote nests nor active
inflammation and fibrogenic processes characteristic of human
acute and chronic myocarditis respectively, were observed.
These morphological aspects more closely resemble those
found in the "indeterminate phase" and contrast with the more
diffuse and progressive pattern of the human chagasic chronic
myocarditis. All monkeys survived and no mortality was