Impacts of Selective Predation on Infection Prevalence and Host Susceptibility

Abstract

Predation can alter diverse ecological processes, including host-parasite interactions. Selective predation, whereby predators preferentially feed on certain prey types, can affect prey density and selective pressures. Studies on selective predation in infected populations have primarily focused on predators preferentially feeding on infected prey. However, there is substantial evidence that some predators preferentially consume uninfected individuals. Such different strategies of prey selectivity likely modulate host-parasite interactions, changing the fitness payoffs both for hosts and their parasites. Here we investigated the effects of different types of selective predation on infection dynamics and host evolution. We used a host-parasite system in the laboratory (Daphnia dentifera infected with the horizontally transmitted fungus, Metschnikowia bicuspidata) to artificially manipulate selective predation by removing infected, uninfected, or randomly selected prey over approximately 8-9 overlapping generations. We collected weekly data on population demographics and host infection and measured susceptibility from a subset of the remaining hosts in each population at the end of the experiment. After 6 weeks of selective predation pressure, we found no differences in host abundance or infection prevalence across predation treatments. Counterintuitively, populations with selective predation on infected individuals had a higher abundance of infected individuals than populations where either uninfected or randomly selected individuals were removed. Additionally, populations with selective predation for uninfected individuals had a higher proportion of individuals infected after a standardized exposure to the parasite than individuals from the two other predation treatments. These results suggest that selective predation can alter the abundance of infected hosts and host evolution.

Keywords: Daphnia; Metschnikowia; evolution; parasite; pathogen; selection.

FIGURE 1

Population abundance across predation treatments in the microcosms. Selective predation was applied by removing infected or uninfected individuals, while the random predation removed both classes and acted as a control treatment. (A) Integrated abundance from the weekly subsamples did not statistically differ across treatments. Boxplots show median and interquartile range with lines showing the range without outliers and individual points showing each replicate (n = 10 for each treatment). (B) The time series of average population abundance in the subsample across treatments (±SE) is shown for weeks 4–10 when the predation treatments were applied.

FIGURE 2

The abundance of infected individuals across predation treatments in the microcosms. Selective predation was applied by removing infected or uninfected individuals, while the random predation removed both classes and acted as a control treatment. (A) Integrated infected abundance from the weekly subsamples was higher in the treatment where infected individuals were removed compared to the two other treatments. Boxplots show median and interquartile range with lines showing the range and individual points showing each replicate (n = 10 for each treatment). Treatments that share letters are not statistically different from one another. (B) The time series of average infected abundance in the subsample across treatments (±SE) is shown for weeks 4–10 when the predation treatments were applied.

FIGURE 3

The proportion of infected individuals across predation treatments in the microcosms. Selective predation was applied by removing infected or uninfected individuals, while the random predation removed both classes and acted as a control treatment. (A) Integrated proportion infected from the weekly subsamples did not statistically differ across treatments. Boxplots show median and interquartile range with lines showing the range and individual points showing each replicate (n = 10 for each treatment). (B) The time series of average infection prevalence in the subsample across treatments (±SE) is shown for weeks 4–10 when the predation treatments were applied.

FIGURE 4

Infection results from the population susceptibility experiment. Boxplots show median and interquartile range with lines showing the range and individual points showing the infection prevalence for each replicate (n = 10 for each treatment). Treatments that share the same letter do not statistically differ. Post‐microcosm infection prevalence was highest in the treatment with uninfected individuals removed compared to the two other predation treatments.