2020 ESA Annual Meeting (August 3 - 6)

COS 169 Abstract - The gut microbial diversity of a Chagas disease vector varies across coinfection status and habitat type throughout central Panama

Kaylee Arnold1,2, Christina Pilar Varian2,3, Troy Kieran2,4, Azael Saldana5, Jose Calzada5, Franklin Samudio5, Travis C. Glenn4 and Nicole L. Gottdenker2,3, (1)Odum School of Ecology, University of Georgia, Athens, GA, (2)Center for the Ecology of Infectious Diseases, University of Georgia, Athens, GA, (3)College of Veterinary Medicine: Pathology, University of Georgia, Athens, GA, (4)Environmental Health Sciences, University of Georgia, Athens, GA, (5)Parasitology, Gorgas Memorial Institute for Health Studies, Panama City, Panama
Background/Question/Methods

Extensive research on how animal microbiomes differ across many host factors, such as infection status, geographic origin, and diet has been conducted. However, few systems have been systematically investigated in response to anthropogenic disturbances, such as deforestation. Understanding impacts of anthropogenic stressors on microbiomes is critical, especially in the context of disease ecology. The gut microbiome is also a crucial aspect of animal innate immune systems. Immunological resilience to disturbance can have significant implications for pathogen establishment within and transmission between vectors.

Chagas disease is caused by the parasite Trypanosoma cruzi that is carried in the guts of hematophagous triatomine vectors. Triatomines are often coinfected with the parasite T. rangeli, which is non-pathogenic to mammals but can reduce fitness of their triatomine hosts. This study examines the gut microbial diversity of coinfected and uninfected triatomines (n = 288) across a deforestation gradient throughout central Panama. We hypothesized that triatomine individuals found in more forested habitats would have greater gut microbial diversity in response to increased host and habitat diversity. Additionally, we expected that coinfected individuals would have greater gut microbial diversity than uninfected individuals due to pathogen-microbe interactions within the gut, which can facilitate the proliferation of different bacterial taxa.

Results/Conclusions

Coinfections were found in 30% of sampled individuals and they displayed significantly greater alpha and beta microbial diversity measurements (Kruskal-Wallis H Test, p = 0.001; (PERMANOVA p = 0.001 using Bray-Curtis dissimilarity). Beta diversity changed significantly across the gradient in forest cover (PERMANOVA p = 0.001 using Bray-Curtis dissimilarity). These results highlight patterns of microbial diversity which may be impacted by vector infection status and will be important to consider when developing vector control strategies.