Infectivity and virulence of Trypanosoma evansi and Trypanosoma equiperdum Venezuelan strains from three different host species.

The infectivity and virulence of seven Trypanosoma evansi and Trypanosoma equiperdum Venezuelan strains isolated from horses, donkeys and capybaras were compared in a mouse model up to 41 days, for parasitemia, animal weight, survival rates, packed cell volume, haemoglobin and erythrocyte count. Two T. equiperdum strains and three of the T. evansi strains resulted in 100% mice mortality, while the two T. evansi donkey strains exhibited lower infectivity and mortality. T. equiperdum strains had shorter pre-patent periods (4 days) than the T. evansi strains (4-12 days). In terms of pathogenicity, only the T. evansi horse strain and the two capybara strains produced a significant decrease of the packed cell volume, in haemoglobin concentration and in red blood cell count. In contrast, the T. evansi donkey strains did not show any changes in the hematological parameters. From the seven variables studied, only pre-patent period, day of maximum parasitemia, day of first parasitemia peak and number of parasitemia peaks were statistically significant. Weight decrease was only observed in mice infected with the T. evansi horse strain. T. equiperdum strains showed the highest mice lethality (7% survival by day 8 post-infection) with no change in the hematological parameters. The three T. evansi horse and capybara strains showed 80%, 87% and 97% survival rates, respectively by day 12 post-infection. However, by day 20 post-inoculation all the mice infected with the T. evansi horse strain died, while 53% and 27% capybara strains infected survived. Whereas by day 40 post-infection, 53 and 73% of the mice infected with the T. evansi donkey strains had survived. These results demonstrate striking infectivity and virulence differences between Venezuelan T. evansi and T. equiperdum strains in NMRI mice and open new possibilities to characterize inter and intra-species variations that may contribute to the pathogenicity of these two species.

Evidence of reversible bradycardia and arrhythmias caused by immunogenic proteins secreted by T. cruzi in isolated rat hearts.

RATIONALE: Chagas cardiomyopathy, caused by the protozoan Trypanosoma cruzi, is characterized by alterations in intracellular ion, heart failure and arrhythmias. Arrhythmias have been related to sudden death, even in asymptomatic patients, and their molecular mechanisms have not been fully elucidated. OBJECTIVE: The aim of this study is to demonstrate the effect of proteins secreted by T. cruzi on healthy, isolated beating rat heart model under a non-damage-inducing protocol. METHODS AND RESULTS: We established a non-damage-inducing recirculation-reoxygenation model where ultrafiltrate fractions of conditioned medium control or conditioned infected medium were perfused at a standard flow rate and under partial oxygenation. Western blotting with chagasic patient serum was performed to determine the antigenicity of the conditioned infected medium fractions. We observed bradycardia, ventricular fibrillation and complete atrioventricular block in hearts during perfusion with >50 kDa conditioned infected culture medium. The preincubation of conditioned infected medium with chagasic serum abolished the bradycardia and arrhythmias. The proteins present in the conditioned infected culture medium of >50 kDa fractions were recognized by the chagasic patient sera associated with arrhythmias. CONCLUSIONS: These results suggest that proteins secreted by T. cruzi are involved in Chagas disease arrhythmias and may be a potential biomarker in chagasic patients.