Princeton University Library Catalog
- Elliott, Ryan J. [Browse]
- Senior thesis
- Graham, Andrea L. [Browse]
- Princeton University. Department of Ecology and Evolutionary Biology [Browse]
- Class year:
- 99 pages
- Summary note:
- The interactions between parasites and their vectors are important for understanding the ecology of disease transmission. One complex parasite-vector system is the Chagas disease system. Chagas disease is a neglected tropical disease leading to heart failure and digestive mega-syndromes that affects an estimated ten million people worldwide, mainly marginalized rural populations throughout Latin America. It is caused by the parasite Trypanosoma cruzi which is vector-borne by the triatomine “kissing bugs.” A second parasite in the system is Trypanosoma rangeli, which is apathogenic for mammals but considered pathogenic for triatomines. For this thesis, I examined the fitness consequences of mono-infection and co-infection with three strains of T. cruzi and one strain of T. rangeli in Rhodnius prolixus, the most epidemiologically-important Chagas disease vector in Colombia. I also estimated triatomine parasite loads using quantitative Polymerase Chain Reaction (qPCR) and explored associations between parasite loads and survival, fecundity, and fertility in R. prolixus.
I found that triatomines mono-infected with the T. cruzi “Gal 61” strain had the lowest survival and fecundity during their first egg-laying cycle. Triatomines co-infected with both T. rangeli and “Gal 61” T. cruzi had higher fecundity during both egg-laying cycles than triatomines mono-infected with either T. rangeli or “Gal 61” T. cruzi. These findings emphasize the variability of fitness outcomes with different trypanosome strains and species and the emergent nature of trypanosome co-infection in R. prolixus. In addition, triatomines with higher parasite loads generally had higher survival, fecundity, and fertility than those with lower parasite loads. Co-evolution of certain strains with R. prolixus towards a more tolerant immune response is posited as a potential explanation. Finally, parasite loads of triatomines co-infected with “Gal 61” T. cruzi and T. rangeli were not different from parasite loads in triatomines mono-infected with only “Gal 61” T. cruzi or T. rangeli. Further study of the interactions between triatomines and trypanosomes is vital to better understand the natural transmission of Chagas disease.