Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/handle/123456789/10982
Title: Parasitaemia and parasitic load are limited targets of the aetiological treatment to control the progression of cardiac fibrosis and chronic cardiomyopathy in Trypanosoma cruzi-infected dogs.
Authors: Caldas, Ivo Santana
Menezes, Ana Paula de Jesus
Diniz, Lívia de Figueiredo
Nascimento, Alvaro Fernando da Silva do
Novaes, Rômulo Dias
Caldas, Sérgio
Bahia, Maria Terezinha
Keywords: Cardiovascular pathology
Experimental chemotherapy
Chagas disease
Issue Date: 2019
Citation: CALDAS, I. S. et al. Parasitaemia and parasitic load are limited targets of the aetiological treatment to control the progression of cardiac fibrosis and chronic cardiomyopathy in Trypanosoma cruzi-infected dogs. Acta Tropica, v. 189, p. 30-38, jan. 2019. Disponível em: <https://www.sciencedirect.com/science/article/pii/S0001706X18304637?via%3Dihub>. Acesso em: 25 fev. 2019.
Abstract: It is still unclear whether the progression of acute to chronic Chagas cardiomyopathy is predominantly associated with the limited efficacy of aetiological chemotherapy, or with the pharmacological resistance profiles and pathogenicity of specific Trypanosoma cruzi strains. Thus, we tested the hypothesis that parasitic load could be a limited target of aetiological chemotherapy to prevent chronic cardiomyopathy in dogs infected by different T. cruzi strains. Animals were infected with benznidazole-susceptible (Berenice-78) and -resistant (VL-10 and AAS) strains of T. cruzi. A quantitative real-time PCR strategy was developed to comparatively quantify the parasite load of the three different strains using a single standard curve. For dogs infected with the VL-10 strain, benznidazole treatment reduced cardiac parasitism during the acute phase of infection. However, similar parasite load and collagen deposition were detected in the myocardium of treated and untreated animals in the chronic phase of the infection. In animals infected with the AAS strain, benznidazole reduced parasite load, myocarditis and type III collagen deposition in the acute phase. However, increased type III collagen deposition was verified in the chronic phase. Dogs infected with the Berenice-78 strain showed a parasitological cure and no evidence of myocardial fibrosis. Parasitic load and cardiac fibrosis presented no correlation in acute or chronic phases of T. cruzi infection. Our findings in a canine model of Chagas disease suggest that parasite burden is a limited predictor for disease progression after treatment and show that benznidazole, although not inducing parasitological cure, is able to prevent total fibrosis in the early stages of infection, as well as complete prevention of cardiac damage when it eliminates parasites at the onset of infection.
URI: http://www.repositorio.ufop.br/handle/123456789/10982
metadata.dc.identifier.uri2: https://www.sciencedirect.com/science/article/pii/S0001706X18304637
ISSN: 0001706X
Appears in Collections:DECBI - Artigos publicados em periódicos

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