Collaborative Research: How do predators spread disease? Tests of five ecological and eco-evolutionary mechanisms with disease in the plankton

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A practical goal of disease ecologists is to find ways to stop or slow the spread of infection from host to host. A popular idea is that predators control disease outbreaks by killing infected prey which are weaker and thereby easier to capture. However, this proposal warns that predators may sometimes spread disease in host populations. The researchers will use organisms living in lakes to test five ways in which predators could spread disease. These ideas are that predators: (1) while eating prey, physically spread parasites into prey habitat; (2) can increase food supply for prey, and more food can cause higher parasite production within infected hosts; (3) can shift the composition of prey populations towards certain ages and sizes that get infected more easily; (4) can kill other species that control disease; and (5) can cause genetic changes to prey populations, making them more susceptible to disease organisms. The project will focus on water fleas (the hosts), a deadly fungal parasite, and an insect predator to test these possibilities. The research uses these organisms as a model system: outbreaks of this fungus can be sampled in lakes, created in experiments within lakes and in the lab, and can be understood using mathematical models. These new ideas, once tested thoroughly in the lab and verified in nature, will help managers make prudent decisions on how to control disease outbreaks in wild and domestic animal populations. The project will train many students, and focus on engaging those in underrepresented groups. This project integrates three approaches. First, it will invest in a survey of fungal epidemics in water flea hosts in 40 lakes. The data from this large survey will be used to generate complex statistical models that test the first four mechanisms (ideas) given above. Second, it uses controlled experiments. One experiment will test mechanisms (2)-(4) with factorial manipulation of predatory insects and "competitor-diluters" (other water flea species which eat parasite propagules). A second experiment will investigate details of mechanisms (1)-(3). A third experiment investigates a tradeoff among clonal genotypes of the host; genotypes which better escape predation are more vulnerable to parasites. The hypothesis is that predators will shift host populations, via rapid evolution, towards bigger epidemics via this tradeoff. Third, this project develops a new suite of parameterized, mathematical (dynamical) models, designed to evaluate each of the mechanisms separately and together.