An Update on the Knowledge of Parasite-Vector Interactions of Chagas Disease.

This review focusses on the interactions between the etiologic agent of Chagas disease, , and its triatomine vector. The flagellate mainly colonizes the intestinal tract of the insect. The effect of triatomines on trypanosomes is indicated by susceptibility and refractoriness phenomena that vary according to the combination of the strains. Other effects are apparent in the different regions of the gut. In the stomach, the majority of ingested blood trypomastigotes are killed while the remaining transform to round stages. In the small intestine, these develop into epimastigotes, the main replicative stage. In the rectum, the population density is the highest and is where the infectious stage develops, the metacyclic trypomastigote. In all regions of the gut, starvation and feeding of the triatomine affect . In the small intestine and rectum, starvation reduces the population density and more spheromastigotes develop. In the rectum, feeding after short-term starvation induces metacyclogenesis and after long-term starvation the development of specific cells, containing several nuclei, kinetoplasts and flagella. When considering the effects of on triatomines, the flagellate seems to be of low pathogenicity. However, during stressful periods, which are normal in natural populations, effects occur often on the behaviour, eg, in readiness to approach the host, the period of time before defecation, dispersal and aggregation. In nymphs, the duration of the different instars and the mortality rates increase, but this seems to be induced by repeated infections or blood quality by the feeding on infected hosts. Starvation resistance is often reduced by infection. Longevity and reproduction of adults is reduced, but only after infection with some strains of . Only components of the surface coat of blood trypomastigotes induce an immune reaction. However, this seems to act against gut bacteria and favours the development of