Species interactions may profoundly influence disease outbreaks. However, disease ecology has only begun to integrate interactions between hosts and their food resources (foraging ecology) despite that hosts often encounter their parasites while feeding. A zooplankton-fungal system illustrated this central connection between foraging and transmission. Using experiments that varied food density for Daphnia hosts, density of fungal spores and body size of Daphnia, we produced mechanistic yet general models for disease transmission rate based on broadly applicable components of feeding biology. Best performing models could explain why prevalence of infection declined at high food density and rose sharply as host size increased (a pattern echoed in nature). In comparison, the classic mass-action model for transmission performed quite poorly. These foraging-based models should broadly apply to systems in which hosts encounter parasites while eating, and they will catalyse future integration of the roles of Daphnia as grazer and host.

Seasonal change in the intensity of fish predation affects succession in lake zooplankton communities. Predation affects not only the zooplankton prey, but also their parasites. Because the ability of a parasite to spread depends in part on the death rate of the hosts, seasonal reductions in the intensity of predation on zooplankton could lead to parasite epidemics. We examined seasonal population dynamics, mortality rate, and incidence of parasitism in lake populations of Daphnia to determine whether parasitism displayed seasonality and synchrony among lake populations and whether any such patterns are consistent with seasonal changes in predation rates. Infections of a bacterial parasite (Spirobacillus cienkowskii) in Daphnia dentifera populations were seasonal with epidemics in many lakes occurring synchronously in autumn. In situ foraging behavior of the dominant fish planktivores, bluegill sunfish, is highly selective on infected Daphnia. Mortality rates on the Daphnia drop just prior to the initiation of epidemics. An epidemiological model shows that this magnitude of decrease in mortality rate, if driven largely by a reduction in predation, can account for the seasonal occurrence of epidemics in our Daphnia populations. Together, these results suggest that parasitism in Daphnia populations may be seasonally restricted by fish predation.Historically, ecologists studying food webs regarded parasites as add-ons (Marcogliese and Cone 1997), while ecologists studying parasitism focused on the isolated interactions of hosts and parasites. Yet the ability of a parasite to spread and persist in a host population depends critically on the other members of the community (e.g., competitors and predators;Packer et al. 2003).

Epidemiologists increasingly realize that species interactions (e.g. selective predation) can determine when epidemics start and end. We hypothesize here that resource quality can also strongly influence disease dynamics: epidemics can be inhibited when resource quality for hosts is too poor and too good. In three lakes, resource quality for the zooplankton host (Daphnia dentifera) was poor when fungal epidemics (Metschnikowia bicuspidata) commenced and increased as epidemics waned. Experiments using variation in algal food showed that resource quality had conflicting effects on underlying epidemiology: high-quality food induced large production of infective propagules (spores) and high birth rate but also reduced transmission. A model then illustrated how these underlying correlations can inhibit the start of epidemics (when spore production/birth rate are too low) but also catalyse their end (when transmission becomes too low). This resource quality mechanism is likely to interface with other ones controlling disease dynamics and warrants closer evaluation.

It remains challenging to predict variation in the magnitude of disease outbreaks. The dilution effect seeks to explain this variation by linking multiple host species to disease transmission. It predicts that disease risk increases for a focal host when host species diversity declines. However, when an increase in species diversity does not reduce disease, we are often unable to diagnose why. Here, we increase mechanistic and predictive clarity of the dilution effect with a general trait-based model of disease transmission in multi-host communities. Then, we parameterise and empirically test our model with a multi-generational case study of planktonic disease. The model-experiment combination shows that hosts that vary in competitive ability (R*) and potential to spread disease (R0 ) can produce three qualitatively disparate outcomes of dilution on disease: the dilution effect can succeed, fail, or be ambiguous/irrelevant.

Models of the evolution of virulence have typically focused on increased mortality, one of two negative effects that parasites can inflict on their host. Those that consider the other effect, fecundity reduction, can predict that parasites should completely sterilize their hosts. Although this prediction seems extreme, sterilization features prominently in a fascinating strategy, parasitic castration. Such castration can be accompanied by gigantism (unusually large growth of infected hosts), long infectious periods, and fecundity compensation (where, before heavy parasite burdens ensue, newly infected hosts reproduce earlier/more than they would if not infected). Using a model of dynamic energy budgets (DEB), we show how these results readily emerge, assuming that parasites consume energy reserves of the host. The simple, but mechanistic, DEB model follows energy flow though hosts and parasites, starting with ingestion, and continuing with storage of assimilated energy, and use of those reserves for growth and reproduction, as allocated by the host according to the "κ-rule". Using this model, we compare and contrast two strategies for parasites. "Consumers" only steal energy from their hosts, thereby indirectly altering allocation of energy to growth and reproduction, reducing fecundity, and enhancing mortality. "Castrators" steal energy but also directly modify the scheme by which hosts allocate reserve energy, shunting resources from reproduction to growth. Not surprisingly, the model predicts that this strategy should promote gigantism, but it also forecasts longer infectious periods and fecundity compensation. Thus, commonly observed characteristics of parasitic castration readily emerge from a mechanistic model of energy flow using a minimal number of assumptions. Finally, the DEB model for both "consumers" and "castrators" highlight that variation in resources supplied to hosts promotes variation in virulence in a given host-parasite system, holding all else equal. Such predictions highlight the potential importance of resource ecology for virulence in disease systems.