Ecological Context Influences Epidemic Size and Parasite-Driven Evolution

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Science  30 Mar 2012:
Vol. 335, Issue 6076, pp. 1636-1638
DOI: 10.1126/science.1215429

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Cost-Benefit Analysis

Mounting resistance to infection is costly, requires energetic input, and may thus compromise fecundity. Duffy et al. (p. 1636; see the cover) tested the relationships between productivity, predation, and mortality in a combination of observations of a natural lake and an experimental replica of a clonal zooplankton-parasitic yeast population. In the wild, epidemics of the yeast could exceed 60% and cause significant host mortality. In this situation, the clonal zooplankton host faces the physiological dilemma of either increasing resistance to deal with infection or of safeguarding fecundity. Zooplankton that feed quickly can reproduce quickly, but also end up ingesting more yeast spores. However, because fish tend to cull infected hosts, fish predation counters infection. Ultimately, both wild and model systems showed that lakes with high productivity (more nitrogen) and/or few fish supported greater epidemics of yeast and more resistant hosts, whereas less productive lakes, or those with more fish, had smaller epidemics and hosts with higher susceptibility to the yeast.


The occurrence and magnitude of disease outbreaks can strongly influence host evolution. In particular, when hosts face a resistance-fecundity trade-off, they might evolve increased resistance to infection during larger epidemics but increased susceptibility during smaller ones. We tested this theoretical prediction by using a zooplankton-yeast host-parasite system in which ecological factors determine epidemic size. Lakes with high productivity and low predation pressure had large yeast epidemics; during these outbreaks, hosts became more resistant to infection. However, with low productivity and high predation, epidemics remained small and hosts evolved increased susceptibility. Thus, by modulating disease outbreaks, ecological context (productivity and predation) shaped host evolution during epidemics. Consequently, anthropogenic alteration of productivity and predation might strongly influence both ecological and evolutionary outcomes of disease.

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