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Trypanosoma rangeli is a non-pathogenic protozoan parasite that infects mammals, including humans, in Chagas disease-endemic areas of South and Central America. The parasite is transmitted to a mammalian host when an infected triatomine injects metacyclic trypomastigotes into the host′s skin during a bloodmeal. Infected mammals behave as parasite reservoirs for several months and despite intensive research, some major aspects of T. rangeli-vertebrate interactions are still poorly understood. In particular, many questions still remain unanswered, e.g. parasite survival and development inside vertebrates, as no parasite multiplication sites have yet been identified. The present study used an insect bite transmission strategy to investigate whether the vector inoculation spot in the skin behave as a parasite-replication site. Histological data from the skin identified extracellular parasites in the dermis and hypodermis of infected mice in the first 24 hours post-infection, as well as the presence of inflammatory infiltrates in a period of up to 7 days. However, qPCR analyses demonstrated that T. rangeli is eliminated from the skin after 7 days of infection despite being still consistently found on circulating blood and secondary lymphoid tissues for up to 30 days post-infection. Interestingly, significant numbers of parasites were found in the spleen and mesenteric lymph nodes of infected mice during different periods of infection and steady basal numbers of flagellates are maintained in the host′s bloodstream, which might behave as a transmission source to insect vectors. The presence of parasites in the spleen was confirmed by fluorescent photomicrography of free and cell-associated T. rangeli forms. Altogether our results suggest that this organ could possibly behave as a T. rangeli maintenance hotspot in vertebrates. Author summary: Trypanosoma rangeli development inside vertebrates is a highly controversial field of study, since there is no evidence of parasite multiplication in host tissues. One of the difficulties that turns it even more complex, it's the challenge to maintain T. rangeli infectivity, since its maintenance in culture decreases parasite's ability to infect its hosts. Our group developed a methodology in which parasites are kept in frequent passages through triatomines and mice, assuring its infectivity and allowing the development of studies more similar to natural transmission. In this study we used qPCR, flow cytometry and histological techniques to evaluate parasite persistence in different tissues and organs of mice infected by the bite of infected bugs, mimicking a natural infection. We found that after one week of infection, parasites as well as inflammatory infiltrates disappear from the inoculation site at the host´s skin. Evaluation of infected mice for a period of 30 days demonstrated that a stable basal amount of parasites was detected in circulating blood, although an increased amount of T. rangeli DNA was found in mesenteric lymph nodes and spleen. In spleen, through marking the parasite with a monoclonal antibody we confirmed the presence of live parasites which were seen in apparent close association with cells and also inside them as apparently amastigote forms, indicating that the parasite is preserved and possibly replicates in these tissues. Our study provides new insights into the interaction of T. rangeli with its vertebrate hosts. [ABSTRACT FROM AUTHOR]

Trypanosoma rangeli is a hemoflagelate parasite that infects domestic and sylvatic animals, as well as man, in Central and South America. T. rangeli has an overlapping distribution with T. cruzi, the etiological agent of Chagas disease, sharing several animal reservoirs and triatomine vectors. We have isolated T. rangeli strains in the State of Santa Catarina, in southern Brazil, which dramatically increased the distribution area of this parasite. This brief review summarizes several studies comparing T. rangeli strains isolated in Santa Catarina with others isolated in Colombia, Honduras and Venezuela. The different methods used include indirect immunofluorescence and western blot assays, lectin agglutination, isoenzyme electrophoresis and random amplified polymorphic DNA analysis, triatomine susceptibility, in vitro cell infection assays, and mini-exon gene analysis.