2020 ESA Annual Meeting (August 3 - 6)

COS 204 Abstract - From cascades to hydras during disease epidemics: An illustration using a predictive, trait-centered model-experiment iteration

Spencer Hall1, Jason C. Walsman1, Alex Strauss2, Carla Caceres3 and Meghan A. Duffy4, (1)Department of Biology, Indiana University, Bloomington, IN, (2)Ecology, Evolution, and Behavior, University of Minnesota, Saint Paul, MN, (3)University of Illinois, (4)Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI
Background/Question/Methods

Disease epidemics can potentially harm host populations by inflicting higher levels of mortality. The subsequent drop in host density can indirectly increase food resources of hosts, creating a disease-mediated trophic cascade. Additionally, many hosts depress feeding rate when exposed to infectious propagules of parasites in their environment. This mortality-feeding combination might seem to cause even larger cascades during epidemics. Given this verbal hypothesis, we first study a model of host-parasite-resource interactions. We test the model’s prediction that cascades should become larger during bigger epidemics suffered by hosts having higher susceptibility to virulent infection. Then, we test it using a waterflea host – algal resource – fungal parasite system. We stocked mesocosms with clonal genotypes of the Daphnia host chosen to spread a gradient of trait space. We then monitored epidemic size and density of hosts and their resources.

Results/Conclusions

In the experiment, we found that hosts having higher susceptibility to infection created larger trophic cascades (as predicted). However, density of the least susceptible hosts increased during epidemics to levels exceeding density in parasite-free controls. Clearly, some key assumption was missing from the initial model. In a second iteration, we first demonstrate varying sensitivity of the clones to parasite spores with experimental data. We then update the mathematical model with the re-parameterized foraging functions. This updated model shows that hosts having highly sensitive foraging response to spores but low susceptibility to infection can produce a hydra effect in the model. It arises because epidemics simultaneously increase primary production (by increasing resource density) but can lower per-host consumption of resources. At equilibrial conditions, this combination can trigger a hydra effect (more hosts and resources). Therefore, via this model-data iteration, we show how disease epidemics can cause host-resource systems to predictably respond along a range from cascades to hydras, depending on host traits.