Parasite-mediated depression of foraging rates: implications for consumer-resource-disease interactions
Consumer-resource interactions and disease can interact more intimately than our current theories anticipate. This intimacy arises perhaps most potently for hosts which become infected by eating their parasites. To illustrate these connections and their implications, we focus on depression of foraging rate by hosts when exposed to parasite propagules, using a planktonic (Daphnia) host-grazer, fungal parasite, and algal resource case study. In this system, foraging rates of host-grazers drop with higher exposure to fungal spores. High exposure can arise from (at least) four drivers: high spore density; large body size of hosts; faster (size-corrected feeding) of a given genotype; and low or intermediate resource density, depending on whether the host-grazer exhibits a type II or type III functional response, respectively. To test this prediction (high exposure depresses foraging), we fit data to a common model structure from experiments manipulating each of the four drivers. Then, armed with the parameterized foraging model, we evaluate implications of this parasite-mediated foraging depression for host-parasite-resource dynamics, partitioning of biomass among trophic levels, and epidemic size.
The first set of results establish the premise: each of the four drivers of exposure depress foraging rate. Indeed, the model predicts and the data show how: (1) high spore dose depresses foraging rate; (2) larger hosts (e.g., adults) experience higher foraging suppression relative to smaller ones (e.g., juveniles); (3) faster-feeding genotypes experience higher depression of foraging than do slower ones; and (4) given that hosts have a type III functional response, their foraging rate is most strongly depressed at intermediate resource density. Then, the second suite of results project why exposure-mediate depression may or may not matter for host-parasite-disease dynamics. For instance, foraging depression greatly stabilizes the propensity of consumer-resource systems to oscillate and exhibit other exotic, non-linear phenomena (especially if hosts have a type II functional response or even if they have a type III functional response). Additionally, foraging-depression elevates (mean) resource density, but can also increase host density during epidemics. However, this mechanism has nuanced implications for epidemic size, depending on interplay between exposure, parasite production, spore loss rates, and host density. Nonetheless, by embracing intimacy between consumer-resource interactions and disease, our model-data combination can reveal new insights into both consumer-resource and disease ecology.