Abstract
AbstractIn this book chapter, we discuss the interactions between triatomines, two heteroxenous trypanosomatids—Trypanosoma cruzi, the etiologic agent of Chagas disease, and Trypanosoma rangeli, a sister species that is harmless to humans—and the diverse intestinal microbiota of triatomines, which include mutualistic symbionts. In order to colonize and proliferate, both species of trypanosomatids and their symbionts must survive the varying conditions in the different regions of the triatomine intestine. Trypanosoma cruzi multiplies mainly within the posterior midgut and in the rectum, where the infectious metacyclic trypomastigotes develop. In contrast, T. rangeli colonizes the whole intestinal tract, but predominantly the midgut, and subsequently invades and multiplies within the hemocoel, and then the salivary glands where metacyclogenesis occurs. The effect of triatomines on trypanosomes is evident in the differing susceptibility and refractoriness of different species/strains of triatomine to trypanosome infection. The diverse conditions in different regions of the triatomine intestine induce the development of specific forms of the trypanosomatids, which are also affected by the nutritional status of their triatomine vector, that is, by feeding and starvation. Reciprocally, the effect of the trypanosomatids on their triatomine vectors is strong in some T. rangeli-Rhodnius combinations, but is dependent on stressful conditions in T. cruzi infections of triatomines. Ingestion of blood-stage trypomastigotes induces intestinal humoral immunity, which in turn modifies the populations of bacteria present in the triatomine intestinal tract.KeywordsTriatomines Trypanosoma cruzi Trypanosoma rangeli Microbiota
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