COS 131-8 - Resources of hosts elevate disease in a planktonic host-parasite system

Thursday, August 9, 2012: 10:30 AM
D139, Oregon Convention Center

ABSTRACT WITHDRAWN

Spencer R. Hall, Indiana University; Claes Becker, Sweco Environment; Rachel M. Penczykowski, Georgia Institute of Technology; Meghan A. Duffy, University of Michigan; Carla E. Cáceres, University of Illinois at Urbana-Champaign

Background/Question/Methods

Species interactions can strongly influence the start and subsequent dynamics of disease epidemics.  We illustrate this point with focus on a interactions of hosts, their parasites, and their resources in a case study of environmentally-dispersed disease in lake plankton.  A priori, we suspected that resource quality and quantity could boost disease and explain variation in epidemic size – generally and in this particular system – for three reasons.  First, key traits (epidemiological and life history) vary plastically with resources.  In particular, parasite production and birth rate can both increase with resource-dependent condition of hosts.  Second, given this plasticity, a mathematical model predicts that increasing resource quality and quantity can boost disease.  Third, algal resources vary greatly among lakes.  Thus, we anticipate strong correlations between resources and variation in disease in this system.

Results/Conclusions

Experiments, a model, and observations revealed these predicted resource-epidemic links.  Laboratory-based experiments connected resources with host condition (indexed by growth rate) and yield of infectious stages (spores) of a virulent fungus (Metschnikowia bicuspitata) from infected hosts (Daphnia dentifera).  Whether we manipulated digestion resistance, fatty acid content, or phosphorus content of algae, better resources boosted spore yield.  Similarly, higher quality resources stimulated birth rate of hosts.  However, less digestible resources depressed transmission rate (infectivity) due to an exposure-based mechanism.  Since these traits influence disease spread (R0) differently, we used a mathematical model to predict R0 for an example contrasting the more easily digested alga Scenedemus with the more resistant Oocystis.  The model predicted larger epidemics with the better quality resource (because spore yield and birth rate effects overwhelmed transmission rate effects).  A follow-up mesocosm experiment confirmed this prediction.  In the field, positive links between epidemics and mean algal carbon (resource density, C) and carbon:phosphorus ratios (a quality index, C:P) emerged.  Both C and C:P correlated with spore yield and birth rate of hosts and then epidemic size.  Thus, these facets signal the same message: resources drive variation in epidemics.  Arguably, then, resources should play a more prominent role in growing theory for disease ecology.