Persistence of Trypanosoma cruzi in Experimental Chagasic Cardiomyopathy

Estudio histopatológico de tejido cardiaco de roedores infectados con Trypanosoma cruzi capturados en barrios suburbanos de Mérida, México

“…Otro aspecto que pudo influir en el porcentaje de detección de nidos con formas de amastigotes en los roedores positivos por PCR, se refiere al hecho de que en el presente estudio no se empleó músculo esquelético, tejido que puede verse ampliamente afectado y ocupado por T. cruzi, sobre todo en infecciones crónicas, lo que restringió su distribución a otro órganos o tejidos (36,41). Asimismo, en modelos de ratón se ha observado que es posible que T. cruzi no persista en el tejido cardiaco previamente afectado (34,42), lo cual reduce la probabilidad de detectarlo en la observación histopatológica.…”

Trypanothione reductase inhibitors: Overview of the action of thioridazine in different stages of Chagas disease

“…Additionally, the suggestion that autoimmune processes could underlie the pathogenesis of chagasic myocardiopathy may have had a negative impact on the efforts to develop a vaccine against T. cruzi infection and to discover more effective and less toxic drugs for its chemotherapy (Zhang and Tarleton, 1999). The persistence of the parasite in the host tissues, on the other hand, has been demonstrated as a determining factor in inducing chronic Chagas disease (Zhang and Tarleton, 1999;Braga et al, 2000;Apt et al, 2005;Garcia et al, 2005;Bazán et al, 2012). This idea has been supported by the finding of T. cruzi DNA in hearts of patients with chagasic cardiomyopathy (Jones et al, 1992).…”

“…Several hypotheses have been raised to explain how cardiac pathology develops. Primary damage of the neuronal system, cell toxicity due to T. cruzi and/or T. cruzi-derived products, parasite-induced microvascular alterations, polyclonal B-cell activation, triggering of T-cell-mediated responses induced by persistent T. cruzi antigens and autoimmunity induced by T. cruzi-specific antigens or by the host antigens, are among the mechanisms that have been proposed to drive the pathogenesis of symptomatic chronic Chagas disease (Wood et al, 1982;Cossio et al, 1984;Morris et al, 1990;Kalil and Cunha-Neto, 1996;Tarleton and Zhang, 1999;Minoprio, 2001;Petkova et al, 2001;Bazán et al, 2012). A multiple background for the pathogenesis of chagasic cardiomyopathy can therefore not be ignored (Lescure et al, 2010;Haberland et al, 2013;Viotti et al, 2014).…”