Print PageParasites can be extremely potent natural enemies, capable of regulating host populations and even inducing catastrophic declines. However, disease is not severe everywhere: epidemics vary in size and severity in space and time. Environmental factors can cause this variation by modulating important host and parasite traits that govern disease spread. We illustrate the link between environmental factors, individual traits, and epidemic size using a case study of fungal disease in a freshwater zooplankton. Over two years we surveyed epidemics in populations of Daphnia dentifera. Epidemics varied extensively among 20 lakes (peak prevalence: 0-60%). Larger epidemics occurred in lakes with higher concentrations of potassium. Low potassium levels could limit epidemics by reducing host fecundity or susceptibility and parasite reproduction within hosts. Each of these traits enhances disease spread, i.e., R0 in epidemiological models. Thus, to connect potassium to traits that influence R0, we estimated relationships between potassium and susceptibility, fecundity, and spore yield with transmission and life table experiments using water from a single, low-potassium lake. Then, we used those data to parameterize a model built for this system’s epidemiology. Finally, we tested predictions of this model by adding potassium to large mesocosms installed in the same low-K lake.
Results/Conclusions
Potassium addition enhanced both uninfected host birth rate and parasite reproduction in infected hosts. However, K addition did not alter host susceptibility. The epidemiological model, once parameterized with these data, predicted that potassium addition could stimulate the index of disease spread (R0) roughly 10-fold in this lake. Finally, as qualitatively predicted by the model, potassium addition significantly increased the size of the experimentally-created epidemics. Thus, our results can explain the field pattern: potassium stimulates fungal epidemics. These results have two main implications. First, they indicate that other nutrients besides nitrogen and phosphorus can crucially influence host performance and production of parasites in hosts. Secondly, they show more generally how nutritional status of hosts can influence spread of disease. These connections between nutrition and disease can mechanistically explain why epidemics occur heterogeneously across the landscape. Ultimately, this research can provide insight into the influence of nutrients on disease and reveal new strategies for disease management in natural populations.
