Submission Type
Poster
Abstract
Outbreaks of disease epidemics continue to erupt in host populations. Within these populations, parasites drive top-down effects. For example, when parasites kill their hosts, they can indirectly increase the hosts’ resource density, causing trophic cascades. This phenomena arises in a diversity of parasite-host-resource systems; however, the mechanisms of parasite-driven trophic cascades remain less clear. A straightforward density-mediated mechanism occurs when parasites increase host mortality, depressing host density. Alternatively, host traits such as body size could be affected, depressing host resource regulation. To disentangle connections between parasites and trophic cascades, we must measure mechanisms operating at both the population (density) and individual (trait) level. First, we created population-level experimental epidemics using a planktonic host-fungal parasite system. We used three clonal hosts that cover a wide span of trait space. Specifically, clones differ in their susceptibility and in their responses to infection. In experimental epidemics, we demonstrate strong resource release and reduction in host body size. Importantly, the clone with the most-reduced body size during epidemics had the greatest resource release. Then, to confirm mechanistically that fungal spores reduce host body size, we reared individuals along an algal resource and spore gradient. We found results consistent with the experimental epidemics: spores reduced host size and the magnitude of this effect varied across the three hosts. Together, these results illustrate a trait-mediated trophic cascade via reduced host size. We show that the size of trophic cascades is more strongly driven by parasite virulence on host size rather than by depressing host density.
Host size reduction in response to parasitic infection fuels trophic cascades
Outbreaks of disease epidemics continue to erupt in host populations. Within these populations, parasites drive top-down effects. For example, when parasites kill their hosts, they can indirectly increase the hosts’ resource density, causing trophic cascades. This phenomena arises in a diversity of parasite-host-resource systems; however, the mechanisms of parasite-driven trophic cascades remain less clear. A straightforward density-mediated mechanism occurs when parasites increase host mortality, depressing host density. Alternatively, host traits such as body size could be affected, depressing host resource regulation. To disentangle connections between parasites and trophic cascades, we must measure mechanisms operating at both the population (density) and individual (trait) level. First, we created population-level experimental epidemics using a planktonic host-fungal parasite system. We used three clonal hosts that cover a wide span of trait space. Specifically, clones differ in their susceptibility and in their responses to infection. In experimental epidemics, we demonstrate strong resource release and reduction in host body size. Importantly, the clone with the most-reduced body size during epidemics had the greatest resource release. Then, to confirm mechanistically that fungal spores reduce host body size, we reared individuals along an algal resource and spore gradient. We found results consistent with the experimental epidemics: spores reduced host size and the magnitude of this effect varied across the three hosts. Together, these results illustrate a trait-mediated trophic cascade via reduced host size. We show that the size of trophic cascades is more strongly driven by parasite virulence on host size rather than by depressing host density.
Comments
Turner DeBlieux, Indiana University
Spencer Hall, Indiana University