COS 57-4
Variation in host resistance and tolerance towards parasites with different exploitation strategies

Wednesday, August 7, 2013: 9:00 AM
L100E, Minneapolis Convention Center
Dylan C. Grippi, Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI
Stuart K. J. R. Auld, University of Stirling, Stirling, Scotland
Meghan A. Duffy, Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI

Host defense to infectious disease can be partitioned into both resistance and tolerance mechanisms. Both aim to limit the negative effects of parasitism, yet exert different selective pressures on parasite populations. Resistance limits or prevents infection and therefore reduces parasite fitness; in contrast, tolerance reduces the fitness impact of infections, and therefore does not reduce parasite fitness. Previous research has shown that investment in these strategies can vary with both host genotype and the density of parasites at time of initial infection. Here, we consider whether the way in which parasites exploit host resources may also drive variation in which defense a host uses. We consider two host exploitation strategies: rapid killers and castrators. In a fully factorial life-table experiment, we used 4 isofemale lines of Daphnia dentifera with two parasites: Metschnikowia bicuspidata, a rapid killer, and Pasteuria ramosa, a castrator, to explore variation in host defense between parasites, host genotype, and four parasite doses per parasite. We separated resistance and tolerance into specific mechanisms: infectivity, growth, total host fecundity, and early life fecundity compensation.


Infectivity resistance had a significant three-way interaction across host genotype, parasite dose, and parasite type (p < 0.005). Looking within each parasite, host genotypes responded differently to increasing dose for M. bicuspidata (p < 0.005) but not for P. ramosa (p = 0.68), indicating fundamentally different dose-response relationships to these two parasites. Variation in growth resistance differed with host genotype (p < 0.005), dose (p < 0.001), and parasite (p < 0.001), but this variation was consistent across main effects as there were no interactions. Interestingly, these data had a negative trend: the higher the initial dose, the lower the parasite’s yield. Host genotype and parasite identity significantly impacted total host fecundity (p < 0.005); hosts infected with the castrator had fewer offspring than those infected with the rapid killer. However, we found evidence of fecundity compensation in castrator-infected hosts. The difference between infected and uninfected animals’ first clutch size significantly varied across hosts (p < 0.01) and between parasites (p < 0.005); for some genotypes, P. ramosa-infected hosts had higher reproduction than control animals. These results indicate that D. dentifera employ different resistance and tolerance strategies against different microparasites, illustrating the importance of studying multiple parasites.