Predation is a fundamental ecological process with the potential to shape community structure. Because predator-prey interactions are embedded within complex systems, the direct effects of predators on their prey can produce cascading effects on other processes, such as host-pathogen interactions. While the impact of predators on disease dynamics has received considerable attention, research has focused on selective predation on infected prey. There is, however, substantial evidence that some predators avoid infected prey, preferentially attacking uninfected individuals. Such different strategies of prey selectivity by predators modulate host-parasite interactions changing the fitness payoffs both for hosts and their parasites. Do predators’ feeding preferences affect the co-evolutionary dynamics of their prey and prey’s parasites?
Here we take a first step towards answering this question by investigating the effects of selective predation on the evolution of host susceptibility. In particular, we use a host (Daphnia dentifera) - parasite (Metschnikowia bicuspidata) system to artificially manipulate predation to represent selective removal of infected or uninfected prey over multiple generations. We collected data on population patterns of D. dentifera, to examine differences in population densities and infection rates. Subsequently, we calculated population susceptibility to determine if predation treatment affects host susceptibility.
Results/Conclusions
After ten weeks of selective predation pressure on the D. dentifera populations, preliminary data suggest no differences in overall population densities across predation treatments. In contrast, there were trends suggesting differences in infection rates based on predation strategy. Populations in which uninfected individuals were removed to simulate selective predation had higher infection rates compared to populations where either infected or randomly selected individuals were removed. Despite strong predation pressure, there were no obvious changes in host susceptibly in response to selection over multiple generations. These preliminary patterns suggest that the benefits of low susceptibility in these predation treatments may be outweighed by associated tradeoffs (e.g., reduced fecundity). Alternatively, it may be that limited heritability precludes an evolutionary response in host susceptibility. Overall, these results suggest that while selective predation can alter infection rates, these effects do not always cascade across multiple generations through changes in genotype frequencies.