COS 61-10 - Identity and density of parasite exposures alters the outcome of co-infections in amphibians

Wednesday, August 14, 2019: 4:40 PM
L011/012, Kentucky International Convention Center
Chloe T. Ramsay1,2 and Jason R. Rohr1,2, (1)Integrative Biology, University of South Florida, Tampa, FL, (2)Biological Sciences, University of Notre Dame, Notre Dame, IN
Background/Question/Methods

Although much research has focused on density-dependent responses of hosts to single-parasite infections, hosts are exposed to numerous parasites simultaneously under natural conditions, and these co-infections can threaten host populations and ecosystem stability. Moreover, the spatiotemporal variation in abundance of co-occurring parasites might influence host responses to them and thus infection intensities. We investigated how the parasite density and identity alters within host co-infection dynamics by simultaneously exposing adult Cuban treefrogs (Osteopilus septentrionalis) to pairwise combinations of the chytrid fungus (Batrachochytrium dendrobatidis, Bd), the nematode Aplectana hamatospicula, and Ranavirus. For each parasite pair, the host was always exposed to the focal parasite at an intermediate density and to the non-focal parasite at a range of five densities. We quantified total parasite load and host survival and growth over four weeks. We hypothesized that the competitive advantage of a co-infecting parasite would be positively associated with its exposure dose, and we anticipated that this advantage would be amplified when the co-infecting parasites activate similar immune responses.

Results/Conclusions

Bd load was not influenced by exposure dose of the other two parasites, but Ranaviral load decreased with increasing exposure dose of Bd and A. hamatospicula. A. hamatospicula load was not affected by Ranaviral density but decreased with increasing Bd density. Host survival and growth were reduced by Bd infections relative to frogs that were not exposed to parasites, and these effects were independent of co-infection. Neither dose, A. hamatospicula, nor Ranavirus significantly affected host growth or survival.

As hypothesized, higher doses of the non-focal parasite caused a competitive disadvantage for the focal parasite which decreased the loads in some but not all cases. However, there was less evidence to support that these patterns would be amplified when parasites activate similar immune responses. Parasites that likely mount intercellular immune responses (i.e. Bd and Ranavirus) did not appear to indirectly compete more strongly with an extracellular parasite, A. hamatospicula. In my talk I will discuss some of the potential mechanisms for the patterns we found, such as the potential for immune-mediated interactions and for direct competition between the parasites for space or resources.