|Department:||Ecology and Evolutionary Biology|
|Keywords:||Chagas disease; co-infection; parasite strains; Rhodnius prolixus; Trypanosoma cruzi; Trypanosoma rangeli; Ecology; Parasitology; Entomology|
|Full text PDF:||http://arks.princeton.edu/ark:/88435/dsp01k930c028d|
Every interaction between species occurs in a heterogeneous environment that presents countless contexts that shape the interaction over time and space. The consequences of these interactions can regulate populations, as they trickle down to influence the genes that an individual passes on to its offspring, and then, in turn, scale back up to influence the genetic and phenotypic composition of future populations. In this work, I sought to uncover how these principles play out in the interactions between an invertebrate vector of human disease and the disease agent it carries. Disease vectors are often considered in a context that is faithful to the word as it is used in physics, where the vector is viewed as public transportation that moves the pathogen between hosts, experiencing no consequences of parasite infection. However, vectors face the challenge of how to maximize individual fitness in a stochastic environment with limited resources just as all other species do, so why would they be exempt from the effects of being parasitized? As such, I investigated the triatomine bug species Rhodnius prolixus when infected with the parasite Trypanosoma cruzi (etiological agent of Chagas disease), and co-infected with T. cruzi and its sister species, T. rangeli. I asked, does T. cruzi affect R. prolixus fitness, and under what contexts does this effect vary? I found a large range of variation in R. prolixus fitness when infected with T. cruzi, with the outcome being influenced by parasite strain, co-infection with T. rangeli, parasite dose, and the timing and order of infection. These factors did not act alone, but seemed to be dependent on one another: it was better to have a co-infection at lower T. rangeli doses, but at high T. rangeli doses, it was better to be infected with T. cruzi first, suggesting an interaction between dose, order and timing. These results illustrate the interactions across scales of both biological and spatio-temporal complexity that can be revealed when studying infectious disease through an ecological lens. Moreover, this work emphasizes the importance of taking into account the ecology of vector-borne neglected tropical diseases such as Chagas disease.