Trypanosoma rangeli is a protozoan that infects triatomines and mammals in Central and South America. Although it does not cause disease to humans, this parasite produces different levels of pathogenicity to its invertebrate host, mainly in species of the genus Rhodnius. In this study, we followed T. rangeli-infected and uninfected pairs throughout their adult lives and measured the amount of blood ingested, number of eggs laid, number of eggs hatched and proportion of infertile eggs, as well as female life expectancy. We found that all reproductive parameters were drastically decreased during infection, mainly due to the reduced amount of blood the infected insects ingested throughout their lives. Reproductive parameters were also affected by the reduction of the life expectancy of infected females, as survival was positively correlated with the number of eggs laid. The strategies used by the parasite to be transmitted are discussed in view of the pathological effects it causes in the insect.

Trypanosoma rangeli is a protozoan that infects triatomines and mammals in Latin America, sharing hosts with Trypanosoma cruzi, the etiological agent of Chagas disease. Trypanosoma rangeli does not cause disease to humans but is strongly pathogenic to its invertebrate hosts, increasing mortality rates and affecting bug development and reproductive success. We have previously shown that this parasite is also capable of inducing a general increase in the locomotory activity of its vector Rhodnius prolixus in the absence of host cues. In this work, we have evaluated whether infection impacts the insect–vertebrate host interaction. For this, T. rangeli-infected and uninfected R. prolixus nymphs were released in glass arenas offering single shelters. After a 3-day acclimatization, a caged mouse was introduced in each arena and shelter use and predation rates were evaluated. Trypanosoma rangeli infection affected all parameters analysed. A larger number of infected bugs was found outside shelters, both in the absence and presence of a host. Infected bugs also endured greater predation rates, probably because of an increased number of individuals that attempted to feed. Interestingly, mice that predated on infected bugs did not develop T. rangeli infection, suggesting that the oral route is not effective for these parasites, at least in our system. Finally, a smaller number of infected bugs succeeded in feeding in this context. We suggest that, although T. rangeli is not transmitted orally, an increase in the proportion of foraging individuals would promote greater parasite transmission rates through an increased frequency of very effective infected-bug bites.

The escape kinetics from the anterior midgut (AM) of Trypanosoma cruzi during the initial steps of infection was assessed in Triatoma infestans, as well as its ability to survive migration in the digestive tract of the vector. All the four strains evaluated survived and reached variable parasite densities. After 49–50 days, YuYu [discrete typing units (DTU) I] strain reached the highest parasite numbers in the rectum followed by Bug (DTU V), CL-Brener (DTU VI) and Dm28c (DTU I). All strains accomplished metacyclogenesis. Bug strain reached the highest numbers of metacyclic trypomastigotes followed by YuYu and CL-Brener/Dm28c. A remarkable parasite reduction in the AM for Bug strain, but not Dm28c was noticed at 72 h of infection. In the posterior midgut + rectum high densities of parasites from both strains were detected at this period indicating the parasites crossed the AM. For Dm28c strain, in infections initiated with trypomastigotes, parasites left AM faster than those starting with epimastigotes. In conclusion, T. cruzi strains from different DTUs were able to infect T. infestans reaching variable parasite densities. The kinetics of migration in the digestive tract may be affected by strain and/or the evolutive form used for infection.

Evidence is presented that Babesia microti may promote its transmission amongst rodents by enhancing the feeding success and survival of its tick vector, Ixodes trianguliceps. Both the mean engorged weight of larval ticks and the percentage moult of larvae to nymphs increased as larvae fed on naive hosts later in the parasitaemic cycle up to a point a few days beyond the loss of a patent infection. This increased feeding success and survival was not dependent on the level of infection by B. microti. Two possible, host-mediated mechanisms for the observed parasite–vector interactions are suggested, the anti-haemostatic effects induced by babesiosis and the interaction of the immunosuppressive effects of Babesia and the development of immunity to ixodid ticks by their vertebrate hosts.