COS 108-9 - Ecological feedbacks reveal disease can accelerate host evolution of lower resistance

Wednesday, August 9, 2017: 4:20 PM
D137, Oregon Convention Center
Jason M. Walsman, Alexander T. Strauss and Spencer R. Hall, Department of Biology, Indiana University, Bloomington, IN

Understanding the forces shaping disease epidemics in natural populations requires working in the eco-evolutionary intersection of disease ecology, consumer-resource dynamics, and susceptibility evolution. A tradeoff between host fecundity and susceptibility to infection creates tension for the evolution of hosts during epidemics. The feedback between disease ecology and susceptibility evolution determines the resolution of this tension. In the absence of disease, hosts should evolve high susceptibility due to the accompanying high fecundity. In the presence of disease, especially large epidemics, hosts are typically expected to evolve lower susceptibility. However, in some scenarios (i.e. smaller epidemics) they may still evolve higher susceptibility, if increased fecundity is more valuable than reduced infection risk. Thus, conventional wisdom predicts that epidemics should reverse the evolution of high susceptibility or at least mitigate and slow it. But how does the inclusion of consumer-resource dynamics shape the effect of epidemics on evolution of susceptibility to infection? Here, we test this hypothesis with non-equilibrium modeling and a mesocosm experiment featuring an algal resource and multiple genotypes of Daphnia dentifera hosts evolving in the presence or absence of parasites (Metschnikowia bicuspidata). In both model and experiment, hosts face a tradeoff between per-resource fecundity and susceptibility to infection.


Inclusion of simple consumer-resource dynamics fundamentally alters the trajectory of host evolution during epidemics. Both the model and the mesocosms reveal the possibility of disease epidemics not only failing to mitigate susceptibility evolution, but instead accelerating evolution of high susceptibility. This can occur as disease epidemics increase host death rate and release resources in a parasite-driven trophic cascade. Host fecundity is resource-dependent so even a minor advantage in per-resource fecundity possessed by highly susceptible hosts is magnified by increased resources. This ecological feedback increases the strength and speed of selection for high susceptibility coupled with high per-resource fecundity. Thus, ecological feedbacks can drive faster evolution of high susceptibility during epidemics than in the absence of disease. Rapid host evolution is typically expected to moderate epidemics but these results caution that the exact opposite can occur and in a disease-accelerated fashion.