Triatoma infestans susceptibility to different Trypanosoma cruzi strains: parasite development and early escape from anterior midgut.

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.

Extracellular vesicles isolated from Trypanosoma cruzi affect early parasite migration in the gut of Rhodnius prolixus but not in Triatoma infestans.

The protozoan Trypanosoma cruzi has the ability to spontaneously secrete extracellular vesicles (EVs). In this paper, T. cruzi EVs derived from epimastigote forms were evaluated during interaction with triatomine bugs Rhodnius prolixus and Triatoma infestans. T. cruzi EVs were purified and artificially offered to the insects prior to infection with epimastigote forms. No effect of EVs was detected in the parasite counts in the guts of both vectors after 49-50 days. On the other hand, pre-feeding with EVs delayed parasite migration to rectum only in the gut in R. prolixus after 21-22 days. Those data suggest a possible role of T. cruzi EVs during the earlier events of infection in the invertebrate host.

Salivary Gland Extract Modulates the Infection of Two Leishmania enriettii Strains by Interfering With Macrophage Differentiation in the Model of Cavia porcellus.

The subgenus Mundinia includes several Leishmania species that have human and veterinary importance. One of those members, Leishmania Mundinia enriettii was isolated from the guinea pig Cavia porcellus in the 1940s. Several histopathological studies have already been performed in this species in the absence of salivary gland extract (SGE), which are determinant and the early and future events of the infection. Our main hypothesis is that SGE could differentially modulate the course of the lesion and macrophage differentiation caused by avirulent and virulent L. enriettii strains. Here, the C. porcellus nasal region was infected using needles with two strains of L. enriettii (L88 and Cobaia) in the presence/absence of SGE and followed for 12 weeks. Those strains vary in terms of virulence, and their histopathological development was characterized. Some L88-infected animals could develop ulcerated/nodular lesions, whereas Cobaia strain developed non-ulcerated nodular lesions. Animals experimentally inoculated developed a protuberance and/or lesion after the 4th and 5th weeks of infection. Macroscopically, the size of lesion in L88-infected animals was smaller in the presence of SGE. Remarkable differences were detected microscopically in the presence of SGE for both strains. After the 6th and 7th weeks, L88-infected animals were heavily parasitized with an intense inflammatory profile bearing amastigotes and pro-inflammatory cells compared to those infected by Cobaia strain. Morphometry analysis revealed that L1+ macrophages were abundant in the L88 infection, but not in the Cobaia infection. In the presence of SGE, an increased CD163+ macrophage infiltrate by both strains was detected. Interestingly, this effect was more pronounced in Cobaia-infected animals. This study showed the role of SGE during the course of L. enriettii (strains L88 and Cobaia) infection and its role in modulating macrophage attraction to the lesion site. SGE decreased L1+ macrophages and this may favor an escaping mechanism for L88 parasites. On the other hand, in the presence of SGE, an increase in CD163+ cells during Cobaia infection may be important for its control. Although both strains healed at the end of the infection, the role of SGE was determinant for the kinetics of the immunopathological events in this dermotropic species.

An overview on Leishmania (Mundinia) enriettii: biology, immunopathology, LRV and extracellular vesicles during the host-parasite interaction.

One of the Leishmania species known to be non-infective to humans is Leishmania (Mundinia) enriettii whose vertebrate host is the guinea pig Cavia porcellus. It is a good model for cutaneous leishmaniasis, chemotherapeutic and molecular studies. In the last years, an increased interest has emerged concerning the L. (Mundinia) subgenus after the finding of Leishmania (M.) macropodum in Australia and with the description of other new/putative species such as L. (M.) martiniquensis and 'L. (M.) siamensis'. This review focused on histopathology, glycoconjugates and innate immunity. The presence of Leishmania RNA virus and shedding of extracellular vesicles by the parasite were also evaluated.