Thursday, August 9, 2007 - 10:30 AM

COS 113-8: Eating yourself sicker: Resource ecology of virulence in planktonic and plant systems

Spencer R. Hall1, Claes Becker1, Joseph Simonis2, C. Adam Brown1, Roger N. Nisbet3, Alan J. Tessier4, and Carla A. Caceres5. (1) Indiana University, (2) Florida State University, (3) University of California, Santa Barbara, (4) National Science Foundation, (5) University of Illinois

We all know that parasites can inflict virulent effects on survivorship and/or fecundity of their hosts.  Typically, explanations for variation in virulence invoke genetic match-mismatch mechanisms (e.g., allele matching, gene-for-gene models).  Here, we highlight another, potentially important source of variation of virulence: resource ecology of the host.  The idea is actually fairly simple: parasites that steal energy and/or materials (nutrients) from their hosts to build more parasites should depress growth, survivorship, and/or reproduction of their hosts.  It is more surprising that resource consumption by hosts can invoke variation in these virulent effects.  For instance, in both an experimental planktonic Daphnia-fungal parasite system and in various studies of plants and their parasites (especially in agricultural systems), we observed enhanced virulence as resource supply to hosts increases.  We captured these phenomena in both systems using simple models (dynamic energy and mass budgets for the plankton system; variable-stores based models for plants).  Despite some differences in their structure, these models emphasize that increased resource supply to hosts can fuel growth of parasites.  Layered on top of these links between resource quantity and virulence, we also see that food quality (digestibility and stoichiometric nutrient:carbon content) influences virulence in the Daphnia-fungus system in the lab.  Again, we can qualitatively capture these results using simple models that assume parasites act as consumers of resources within hosts.  Combined, these results highlight resource ecology as a potentially important driver of variation of virulence in disease systems.