Virulent Disease Epidemics Can Increase Host Density by Depressing Foraging of Hosts.

AbstractAll else equal, parasites that harm host fitness should depress densities of their hosts. However, parasites that alter host traits may increase host density via indirect ecological interactions. Here, we show how depression of foraging rate of infected hosts can produce such a hydra effect. Using a foraging assay, we quantified reduced foraging rates of a zooplankton host infected with a virulent fungal parasite. We then parameterized a dynamical model of hosts, parasites, and resources with this foraging function, showing how foraging depression can create a hydra effect. Mathematically, the hydra arose when increased resource productivity exceeded any increase in resource consumption per host. Therefore, the foraging-mediated hydra effect more likely emerged (1) for hosts that strongly control logistic-like resources and (2) during larger epidemics of moderately virulent parasites. We then analyzed epidemics from 13 fungal epidemics in nature. We found evidence for a foraging-mediated hydra effect: large outbreaks depressed foraging rate and correlated with increased densities of both algal resources and Daphnia hosts. Therefore, depression of the foraging rate of infected hosts can produce higher host densities even during epidemics of parasites that increase host mortality. Such hydras might prevent the collapse of host populations but also could produce higher densities of infected hosts.

Ecological context influences epidemic size and parasite-driven evolution.

The occurrence and magnitude of disease outbreaks can strongly influence host evolution. In particular, when hosts face a resistance-fecundity trade-off, they might evolve increased resistance to infection during larger epidemics but increased susceptibility during smaller ones. We tested this theoretical prediction by using a zooplankton-yeast host-parasite system in which ecological factors determine epidemic size. Lakes with high productivity and low predation pressure had large yeast epidemics; during these outbreaks, hosts became more resistant to infection. However, with low productivity and high predation, epidemics remained small and hosts evolved increased susceptibility. Thus, by modulating disease outbreaks, ecological context (productivity and predation) shaped host evolution during epidemics. Consequently, anthropogenic alteration of productivity and predation might strongly influence both ecological and evolutionary outcomes of disease.