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Clinical Science (2003) 104, (415–420) (Printed in Great Britain)

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Indeterminate Chagas' disease: Trypanosoma cruzi strain and re-infection are factors involved in the progression of cardiopathy

Juan M. BUSTAMANTE*, Héctor W. RIVAROLA*, Alicia R. FERNÁNDEZ*†, Julio E. ENDERS*, Ricardo FRETES‡, José A. PALMA* and Patricia A. PAGLINI-OLIVA*

*Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Santa Rosa 1085, 5000 Córdoba, Argentina, †Established Investigator, Consejo Nacional de Investigaciones Científicas y Técnicas, Argentina, and ‡Cátedra de Histología, Embriología y Genética II, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, 5016 Córdoba, Argentina

Key words: cardiac damage, indeterminate Chagas' disease, re-infection, strain, Trypanosoma cruzi.

Abbreviations: d.p.i., days post-infection.

Correspondence: Dr Patricia Paglini-Oliva, D. Rapela 3258, Residencial V. Sársfield, 5016 Córdoba, Argentina (e-mail ppaglini@mater.fcm.unc.edu.ar).

Chagas' disease is caused by Trypanosoma cruzi, which is transmitted by reduviid bugs. The World Health Organization has estimated that about 16–18 million people in the Americas are infected, and that more than 100 million are at risk. In the present study we have used a murine model to analyse if particular T. cruzi strains (Tulahuen strain and SGO-Z12 isolate from a chronic patient) and/or re-infection may determine, during the indeterminate phase of experimental Chagas' disease, changes that could explain the different evolution of cardiac lesions. Re-infected mice reached higher parasitaemias than those infected for the first time. The survival in the indeterminate phase of mice infected with Tulahuen strain was 50.0%, while the SGO-Z12-infected group presented a significantly higher survival rate (77.1%; P<0.01). The SGO-Z12-re-infected group showed a survival rate (70.9%) significantly higher than that of the Tulahuen-re-infected group (37.0%; P<0.01). Electrocardiographic abnormalities were found in 66% of Tulahuen-infected mice, while in SGO-Z12-infected group such abnormalities were found in only 36% of animals (P<0.01). The two groups exhibited similar percentages of electrocardiographic dysfunction on re-infection, although intraventricular blocks were more frequent in Tulahuen-re-infected mice (P<0.01). Hearts from infected or re-infected mice with either parasite showed mononuclear infiltrates. The SGO-Z12-re-infected and Tulahuen-re-infected groups exhibited a significantly diminished affinity (P<0.05) and a significantly increased density (P<0.05) of cardiac b-adrenergic receptors compared with the infected and non-infected groups. The indeterminate phase of Chagas' disease is defined as a prolonged period that is clinically silent, but the present findings show that different T. cruzi strains and re-infection are able to alter the host–parasite equilibrium, and these factors may be responsible for inducing progressive cardiopathy.

Received 18 September 2002/17 December 2002; accepted 31 January 2003

The Biochemical Society and the Medical Research Society © 2003