Cardiomyopathy in Cebus apella monkeys experimentally infected with Trypanosoma cruzi.

Twenty four Cebus apella monkeys were studied as a biological model for the cardiac chronic form of Chagas' disease. Twelve were inoculated with Trypanosoma cruzi trypomastigotes, seven with the Brazilian Y strain and five with the Argentinian RA strain. Twelve monkeys were uninfected controls. The following parameters were studied: body weight, body temperature, direct parasitemia, xenodiagnosis, specific antibodies by IFA, clinical chemistry, hematology, ECG and chest X-ray. Three monkeys infected with Y strain were sacrificed at 4 months and 4 monkeys at 12 months after inoculation. Monkeys inoculated with RA strain were sacrificed at 48 months. Direct parasitemia was positive within a week after inoculation in all monkeys. Xenodiagnosis was positive until 49.0 +/- 3.0 and 79.0 +/- 6.0 weeks p.i. for Y and RA strains, respectively. In all inoculated monkeys an increase in antibody titers was detected within 3 weeks after inoculation. In all monkeys inoculated with the Y strain and 3/5 with the RA strain abnormal ECGs were observed within 1 or 2 weeks p.i., becoming more severe in the chronic phase. Y strain inoculated monkeys sacrificed at 4 months presented only a slight concentric hypertrophy of the heart left ventricle. Those sacrificed at 12 months had concentric left ventricle hypertrophy and 3/4 had an aneurism of the apex. Four out of 5 RA strain inoculated monkeys had an enlarged, flaccid heart; 3/5 aneurism of the apex and 2/5 concentric hypertrophy of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Chagas' disease in non-human primates. 1. Chronology of clinical events, clinical chemistry, ECG, radiology, parasitemia, and immunological parameters in the Cebus apella monkey.

Forty Cebus apella monkeys free from Chagas' disease were subcutaneously infected with 3 x 10(5) trypomastigotes of the Ypsilon strain of T. cruzi and followed-up for 6 months. Seventeen monkeys were controls. Body weight, temperature, direct parasitemia (DP), IgM and IgG were determined weekly. Hematology was performed weekly up to day 40 p.i. and monthly thereafter. Clinical chemistry was performed every two weeks up to day 33 p.i. and monthly thereafter. ECG was performed weekly up to day 47 p.i. and at 2,3, and 6 months p.i. Chest X-ray was done at 45 days, 4 and 6 months p.i. Xenodiagnosis was only performed after two negative DP. All infected monkeys developed fever, beginning 6.0 +/- 0.6 day p.i. and lasting 21.9 +/- 6.7 days, and lost 14% of their body weight the first month, 11% the third month and 7% the 6th month. DP was already detected 4.4 +/- 0.29 days after infection and it was detectable in all monkeys up to 96.0 +/- 6.9 days p.i. Cyclical peaks of parasitemia were observed throughout the study. IgM and IgG titers which permitted a diagnosis of T. cruzi infection occurred at 33.0 +/- 2.9 days p.i., respectively. Fifty-seven percent of infected monkeys presented ECG alterations one week after inoculation reaching a maximum of 86% at the third week. A normocytic, normochromic anemia was observed in all monkeys being significantly (p less than 0.02) more severe in the infected animals. No effects of T. cruzi on the clinical chemistry were observed.(ABSTRACT TRUNCATED AT 250 WORDS)