title: Indeterminate Chagas' disease: Trypanosoma cruzi strain and re-infection are factors involved in the progression of cardiopathy.
abstract: 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 beta-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.
authors.affiliation: Cátedra de Fi;sica Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Santa Rosa 1085, 5000 Córdoba, Argentina.
authors.forename: Juan M
authors.initials: JM
authors.lastname: Bustamante
authors.forename: Héctor W
authors.initials: HW
authors.lastname: Rivarola
authors.forename: Alicia R
authors.initials: AR
authors.lastname: Fernández
authors.forename: Julio E
authors.initials: JE
authors.lastname: Enders
authors.forename: Ricardo
authors.initials: R
authors.lastname: Fretes
authors.forename: José A
authors.initials: JA
authors.lastname: Palma
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Paglini-Oliva
mesh_terms: D000818:Animals; D002598:Chagas Cardiomyopathy / Q000401:mortality / Q000469:parasitology*; D018450:Disease Progression; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000469:parasitology*; D006790:Host-Parasite Interactions; D051379:Mice; D008815:Mice, Inbred Strains; D023421:Models, Animal; D018512:Parasitemia; D011485:Protein Binding; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D012008:Recurrence; D015996:Survival Rate; D014349:Trypanosoma cruzi / Q000502:physiology*
chemical_list: D011943:Receptors, Adrenergic, beta