Canonical host-parasite theory suggests predation should reduce disease in wild populations by increasing host mortality, thereby decreasing density-dependent transmission of parasites. Intuitively, disease is further suppressed if predators preferentially feed on infected hosts, thereby also reducing total parasite density. Before turning to predator manipulations as means of controlling disease, we should assess if and when predators might also spread disease. Here, we evaluate the hypothesis that predators increase disease when they preferentially feed on less susceptible stages of hosts. Potential disease spread or control hinge on a life history trait (host body size) that protects hosts from predation but confers greater disease risk. Specifically, we investigate how gape-limited midge predators, Chaoborus punctipennis, spread epidemics of a virulent fungus, Metschnikowia bicuspidata in a dominant zooplankton grazer Daphnia dentifera. We employ individual and population experiments in order to evaluate predator feeding preferences and the consequences for host density, stage/size structure and disease risk. Then we look for signatures of predator-mediated disease spread in field populations which naturally vary in predation intensity by looking for predator-mediated shifts in host stage/size structure so that we may connect the variation in host size to variation in epidemic size.
Results/Conclusions
Individual experiments (infection assays; feeding trials), population experiments (mesocosms tracking host densities, sizes and infection prevalence under three levels of predation), and field data (30 lakes spanning the gradient of predation intensity) confirm predators increase disease despite lowering total host density. This counterintuitive finding is driven by a life history trade-off between predation risk (decreases with host body size) and disease risk (increases with body size). For disease, individual experiments indicate larger hosts are exposed at higher rates and produce more parasite propagules. For predators, individual trials indicate selectivity on smaller, juvenile hosts. In mesocosms, populations experiencing higher predation intensity undergo a shift towards larger, more easily infected individuals. Thus, net effect of predation increases disease even though populations with predators maintain lower total host density. Field data echo these findings: wild host populations are biased towards larger individuals when predators are present — a pattern that scales with intensity of predation. Further, populations where hosts are larger experience larger epidemics. Generally, if predators increase disease spread in hosts by shifting stage/size structure towards more easily infected and also more infectious animals, attempting to manage wild disease through predator manipulations could lead not only to fewer but fewer and sicker hosts.