Abstract
Triatomine vectors transmit Trypanosoma cruzi, the etiological agent of Chagas disease in humans. Transmission to humans typically occurs when contaminated triatomine feces come in contact with the bite site or mucosal membranes. In the Southern Cone of South America, where the highest burden of disease exists, Triatoma infestans is the principal vector for T. cruzi. Recent studies of other vector-borne illnesses have shown that arthropod microbiota influences the ability of infectious agents to colonize the insect vector and transmit to the human host. This has garnered attention as a potential control strategy against T. cruzi, as vector control is the main tool of Chagas disease prevention. Here we characterized the microbiota in T. infestans feces of both wild-caught and laboratory-reared insects and examined the relationship between microbial composition and T. cruzi infection using highly sensitive high-throughput sequencing technology to sequence the V3-V4 region of the 16S ribosomal RNA gene on the MiSeq Illumina platform. We collected 59 wild (9 with T. cruzi infection) and 10 lab-reared T. infestans (4 with T. cruzi infection) from the endemic area of Arequipa, Perú. Wild T. infestans had greater hindgut bacterial diversity than laboratory-reared bugs. Microbiota of lab insects comprised a subset of those identified in their wild counterparts, with 96 of the total 124 genera also observed in laboratory-reared insects. Among wild insects, variation in bacterial composition was observed, but time and location of collection and development stage did not explain this variation. T. cruzi infection in lab insects did not affect α- or β-diversity; however, we did find that the β-diversity of wild insects differed if they were infected with T. cruzi and identified 10 specific taxa that had significantly different relative abundances in infected vs. uninfected wild T. infestans (Bosea, Mesorhizobium, Dietzia, and Cupriavidus were underrepresented in infected bugs; Sporosarcina, an unclassified genus of Porphyromonadaceae, Nestenrenkonia, Alkalibacterium, Peptoniphilus, Marinilactibacillus were overrepresented in infected bugs). Our findings suggest that T. cruzi infection is associated with the microbiota of T. infestans and that inferring the microbiota of wild T. infestans may not be possible through sampling of T. infestans reared in the insectary.
Highlights
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, infects an estimated six million people residing in 21 endemic countries in the Americas, with 30,000 new infections yearly [1]
Chagas disease in humans is caused by the parasite Trypanosoma cruzi and it is endemic to the Americas
Microbiota-mediated methods to control this vector-borne disease are being explored to determine whether microbes typically found in the vectors’ gut have a detrimental effect on T. cruzi and how they may be used to modify the vector and curb the ability for T. cruzi to be transmitted to humans
Summary
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, infects an estimated six million people residing in 21 endemic countries in the Americas, with 30,000 new infections yearly [1]. Beard et al leveraged the coprophagic habits of Rhodnius prolixus, another important triatomine vector of T. cruzi, to replace actinobacterial Rhodococcus rhodnii symbionts found ubiquitously in adult bugs with paratransgenic R. rhodnii carrying trypanocidal genes [16]. Another group utilized genetically modified R. rhodnii and Escherichia coli to induce RNA interference to affect redox state in the gut and reduce vector fitness [22]. Development of these and other novel vector control strategies is dependent upon a better understanding of the gut microbiome of triatomines and their relationship to T. cruzi infection and vector competence
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