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A. MUÑOZ et al. disease. In S Wendel, Z Brener, ME Camargo, A Rassi (ed.), Chagas disease (American trypanosomiasis): its impact on transfusion and clinical medicine, ISBT Brazil, São Paulo 237-247. 30. RASSI A JR, RASSI A, MARIN-NETO JA. 2010. Chagas disease.Lancet 375: 1388-1402. 31. STOPPANI AO. 1999. Quimioterapia de la enfermedad de Chagas. Medicina (B Aires) 59: 147-165. 32. TOLEDO M, PEREIRA MES, Y BRENER Z. 1990. Efects of immunosupression on the especific treatment of mice experimentally infected with Trypanosoma cruzi. Mem. Inst Oswaldo Cruz 85: 100. 33. TOLEDO MJO, BAHIA MT, CARNEIRO CM, et al. 2003. Chemotherapy with benznidazole and itraconazole for mice infected with different Trypanosoma 22 cruzi clonal genotypes. Antimicrob Agents Chemother 47: 223-230. 34. URBINA JA, DOCAMPO R. 1999. Specific chemotherapy of Chagas disease: controversies and advances. Trends Parasitol 19: 495-501. 35. VILLARREAL D, BARNABÉ C, SERENO D, TIBA- YRENC M. 2004. Lack of correlation between in vitro susceptibility to benznidazole and phylogenetic diversity of Trypanosoma cruzi, the agent of Chagas disease. Exp Parasitol 108: 24-31. 36. YUN O, LIMA MA, ELLMAN T, et al. 2009. Feasibility, drug safety, and effectiveness of etiological treatment programs for Chagas disease in Honduras, Guatemala, and Bolivia: 10-year experience of Médecins sans Frontières. PLoS Negl Trop Dis 3:e488. Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 14-22
Artículo Original Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 23-33 Edad del hospedero en la evolución de la infección experimental con Trypanosoma cruzi en un modelo murino ZÚÑIGA C. 1 , BINDER N. 1 , PALáU M.T. 4 , LARENAS J. 2 y VERGARA U. 1,3 1 Departamento de Medicina Preventiva, Facultad de Ciencias Veterinarias, Universidad de Chile. Avenida Santa Rosa 11735. La Pintana, Santiago - Chile. 2 Departamento de Patología Animal, Facultad de Ciencias Veterinarias, Universidad de Chile. Avenida Santa Rosa 11735. La Pintana, Santiago- Chile. 3 Escuela de Postgrado, Facultad de Medicina, Universidad de Chile. Independencia 1027, Santiago - Chile. 4 Escuela de Nutrición, Universidad Autónoma de Chile. ABSTRACT AGE EFFECT IN EVOLUTION OF EXPERIMENTAL TRYPANOSOMA CRUzI INFECTION IN A MURINE MODEL Two and eight months old Balb/c mice, were infected with 2000 Dm28c trypomastigotes of Trypanosoma. cruzi. Two weeks after initial infection the young males showed parasitemia of 5.1 x 10 5 parasites/mL and 50% of accumulated mortality, which reached 100% at 40 days after infection. Aged males reached 3.2 x 10 5 parasites/mL and 40% survival longer than four months. Histopathology showed differential distribution and severity of tissue lesions between the mouse groups. Increased damage and pseudocysts were found in heart of aged mice, which showed a long term tissue repair while lesions seemed to increase in the striated muscle of young mice, despite of the absence of detectable tissue or blood parasites. The differences in parasite burden, tissue damage and accumulated mortality observed in our infected mice, suggest that age may affect the effectiveness of the immune response in controlling parasite-dependent and/or immune-mediated damage in specific organs. Although there is no evidence for the pathogenic role of parasite persistence and/or autoimmunity in the evolution of the disease, the 100% of accumulated mortality observed in the young mice may be explained by neurological disturbances as those associated to malignant arrhythmias and sudden death observed in humans. These disturbances may not be triggered in the eight months old mice as a consequence of the decreased effectiveness of the immune system which comes with age. Key words: Trypanosoma cruzi, aged mice, parasitemia, histopathology. Recibido: 5 de Marzo de 2012. Aprobado: 28 de de Mayo de 2012. Correspondencia: U. Vergara Email: uvergara@uchile.cl C. Zuñiga Email: clzuniga@uchile.cl 23
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