Parasites can certainly harm host fitness.  Given such virulence, hosts should evolve strategies to resist, tolerate, and/or control infection.  But what governs those strategies – and the costs that they incur?  Furthermore, resistance, tolerance, and control can vary depending on environmental variation and G x E interactions.  How can we explain and predict these complex outcomes?  This study illustrates how a fecundity-resistance (transmission rate) tradeoff among genotypes of a zooplankton (Daphnia dentifera) infected by a virulent fungal microparasite (Metschnikowia) arises due to variation in resource acquisition (feeding rate) when hosts consume high quality resources.  Then, we show how and why this relationship reverses when hosts consume resources of poorer quality due to a power-efficiency tradeoff among host genotypes.   

Results/Conclusions

To make these connections and explain the shifting resistance-fecundity relationships, we used lab experiments and theoretical models that link feeding with transmission, energetics, resource quality, and fecundity.  Furthermore, a fecundity-survivorship tradeoff arose from similar feeding-based mechanisms.  Meanwhile, a variant on the parasite control-fecundity tradeoff, involving spore yield and fecundity when infected, arose from genetic variation in juvenile growth rate (another synthetic index of resource use) when food resources were good.  Yet, again, this relationship was reversed by the resource-based power-efficiency tradeoff.  Thus, mechanisms predicting key epidemiological tradeoffs and G x E interactions stem from genetic variation in resource ecology and tradeoffs associated with acquiring and using them.  These relationships between resource traits and infections genetics should undoubtedly shape ecological and rapid evolutionary dynamics of hosts during epidemics.  Furthermore, these synthetic links can also catalyze creation of new theory that integrates resource- and genetic-based responses of hosts to disease.