Trypanosoma cruzi reinfections in mice determine the severity of cardiac damage

Influence of Pregnancy on Trypanosoma cruzi Parasitemia in Chronically Infected Women in a Rural Bolivian Community

“…27 Peak parasitemias after reinfection challenges in dogs and mice have been observed. 28,29 Therefore, controlling the level of exposure to vectors and of reinfection (i.e., the place of residence) appeared to be necessary in this study. Retrospectively, because women living in houses infested with T. infestans presented higher rates of T. cruzi parasitemia than those living without vectors, confirms the need to match for the risk of exposure.…”

Chagas heart disease: pathophysiologic mechanisms, prognostic factors and risk stratification

“…In contrast, whether one or more of the autoimmune events described in experimental models and human cases of Chagas disease can contribute to, or aggravate, this pathology, has been more controversial and difficult to validate (Tarleton 2003a, b). The evidence supporting this viewpoint can be summarised as follows: (i) in recent years, more powerful and sensitive methods of parasite detection, such as immunohistochemistry and polymerase chain reaction (PCR), have demonstrated a higher frequency of T. cruzi antigens and parasite DNA in chronic lesions; also, a significant correlation between parasite persistence and tissue inflammation has been clearly documented; therefore, the supposed absence of parasites at or near sites of disease (the mainstay of the autoimmune theory), probably reflects the use of insensitive histological techniques in past decades (Tarleton & Zhang 1999); (ii) interventions that lessen the parasite burden, such as aetiologic treatment with benznidazole or nifurtimox, reduce clinical disease in humans (Viotti et al 2006, Fabbro et al 2007) and experimental animals (Andrade et al 1991, Garcia et al 2005, in contrast to immunosuppressive treatments/situations that clearly increase T. cruzi parasitemia (Rassi et al 1997) and usually aggravate the inflammatory response (Sartori et al 2007); (iii) reinfection or continued exposure (due to continued residence in areas of active transmission) seems to increase the parasite load and disease severity in experimental models and in human cases (Bustamante et al 2002, Storino et al 2002; (iv) although anti-self responses are encountered in T. cruzi infection, the nature of anti-self antibodies in experimental and human chronic Chagas disease is heterophilic, with a poor correlation with the heart lesions (i.e., there is no direct and definitive evidence that the immune reactions against the mimicked auto-antigens are actually pathogenic) (Tarleton 2003a, b); and (v) data supporting the direct involvement of either molecular mimicry or polyclonal activation in the pathogenesis of myocardial lesions ascribed to T. cruzi infection are sparse and inconclusive.…”

Autonomic Dysfunction and Risk Factors Associated with Trypanosoma cruzi Infection among Children in Arequipa, Peru

“…The lower infection prevalence in Arequipa suggests a lower force of infection compared with study sites in Brazil, Argentina, or Bolivia, [33][34][35][36] whereas the relatively flat age prevalence curve supports the hypothesis that the parasite was only introduced into the periurban communities of Arequipa in the early 1990s. 26 Investigators have shown that repeated infection increases cardiac pathology in animal models 37,38 and have suggested that vector control, by decreasing reinfection rates, may be responsible for the milder disease now seen in formerly endemic communities. 39 Similarly, the children in our study may have had few repeated infections after their initial exposure.…”