Disease epidemics can greatly reduce density of plant and wildlife hosts. Species interactions via the dilution effect could help contain epidemics in focal hosts, thereby alleviating some harm to their densities. However, these more resistant ‘diluter’ hosts often compete with focal hosts (in so-called ‘friendly competition’). In such dilution-competition scenarios, it becomes possible that disease plus competition inflict very large harm on hosts, from both virulence of parasites and from competition, possibly even their interaction. We illustrate this ecological doom inherent in joint dilution and competition using a plankton system. In this system, Daphnia focal hosts become infected with a virulent fungus (Metschnikowia) while competing with the disease diluter (Ceriodaphnia). We created disease epidemics in mesocosms with one clonal genotype. We then characterized harm from disease, competition, and both via interaction strengths calculated from fits of multivariate auto-regressive (MAR) models to time series data. We also compared this purely ecological outcome to two evolutionary scenarios. In the first, we stocked mesocosms with clonal genotypes of hosts having moderate mean competitive ability and infection risk (two key traits) but lower trait variation. In the other, we introduced clones having higher trait variation. This high standing trait variation, it turns out, enabled evolutionary rescue of hosts from friendly competition.
Results/Conclusions
The ecological doom of friendly competition arose in the experiment with one focal host. Here, both disease and competitors exerted strong, negative per capita interaction strengths on focal hosts. When together, the signal of competition was particularly large, diminishing host densities greatly. In the evolutionary experiment, the treatment with low trait diversity showed similar ecological harm. However, the treatments enabling rapid host evolution (due to larger standing trait variation) showed a much lower drop in host density. In this case, the evolutionary rescue arose from a weakening of these large, negative interaction strengths. The negative harm from both disease and dilution did not dissipate completely, but it did diminish considerably. Weakening of interaction strengths arose due to rapid evolution of competitive ability, not disease resistance, in all treatments – especially those with disease. Thus, the evolutionary rescue arose through a cryptic dynamic – interaction strengths weakened in this treatment with high clonal turnover and increase in competitive ability. These results highlight the importance of rapid host evolution in friendly competition. It may enable disease dilution without such large, negative harm to host populations observed in more purely ecological scenarios.