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Penczykowski, R. M.

Publications and source records attributed to Penczykowski, R. M..

2 recordsLinked to original sources

Virulent disease epidemics can increase host density by depressing foraging of hosts

All 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 infected host foraging rate 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 which 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 algae and hosts. Therefore, depression of foraging rate of infected hosts can produce higher host densities even during epidemics of parasites that increase host mortality. Such hydras might prevent collapse of host populations but also could produce higher densities of infected hosts.Competing Interest StatementThe authors have declared no competing interest.View Full Text

ecology

Facilitative priority effects drive parasite assembly under coinfection

Host individuals are often coinfected with diverse parasite assemblages, resulting in complex interactions among parasites within hosts. Within hosts, priority effects occur when the infection sequence alters the outcome of interactions among parasites. Yet, the role of host immunity in this process remains poorly understood. We hypothesized that the host response to first infection could generate priority effects among parasites, altering the assembly of later arriving strains during epidemics. We tested this by infecting sentinel host genotypes of Plantago lanceolata with strains of the fungal parasite, Podosphaera plantaginis, and measuring susceptibility to subsequent infection during experimental and natural epidemics. In these experiments, prior infection by one strain often increased susceptibility to other strains, and these facilitative priority effects altered the structure of parasite assemblages, but this effect depended on host genotype, host population, and parasite genotype. Thus, host genotype, spatial structure, and priority effects among strains all independently altered parasite assembly. Then, using a fine-scale survey and sampling of infections on wild hosts in several populations, we identified a signal of facilitative priority effects, which altered parasite assembly during natural epidemics. Together, these results provide evidence that within host priority effects by early arriving strains can drive parasite assembly, with implications for how strain diversity is spatially and temporally distributed during epidemics.

ecology