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.

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.

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.

We investigated the effects of various mineral and biochemical limitations on Daphnia magna. These daphniids have much lower saturation thresholds for growth for the polyunsaturated fatty acids (PUFA) eicosapentaenoic acid (EPA), and arachidonic acid (ARA) than has been previously described for other Daphnia species. Daphniids take up large amount of fatty acids from food, and different fatty acids are handled differently by D. magna. The saturated fatty acid (20:0; EPA) was not retained, and metabolized, the PUFAs were preferably stored. There were also differences among the PUFAs: EPA was found in higher concentrations in the eggs than ARA. In contrast, although there were some variations in D. magna phosphorus levels with varying levels of phosphorus in the food, these differences were small compared with the changes in D. magna fatty-acid concentrations. Independent of these small changes, the P content of eggs was constant at 14 mg P (g dry wt)Ϫ1 . Storage of EPA, but not P, fully compensated D. magna growth during periods of bad food quality. Egg production was a major drain of fatty acids from female D. magna.

Parasites can certainly harm host fitness. Given such virulence, hosts should evolve strategies to resist or tolerate infection. But what governs those strategies and the costs that they incur? This study illustrates how a fecundity‐susceptibility trade‐off among clonally reared genotypes of a zooplankton (Daphnia dentifera) infected by a fungal parasite (Metschnikowia) arises due to variation in resource acquisition and use by hosts. To make these connections, we used lab experiments and theoretical models that link feeding with susceptibility, energetics, and fecundity of hosts. These feeding‐based mechanisms also produced a fecundity‐survivorship trade‐off. Meanwhile, a parasite spore yield–fecundity trade‐off arose from variation in juvenile growth rate among host clones (another index of resource use), a result that was readily anticipated and explained by the models. Thus, several key epidemiological trade‐offs stem from variation in resource acquisition and use among clones. This connection should catalyze the creation of new theory that integrates resource‐ and gene‐based responses of hosts to disease.

The differences in the impact of two major groups of herbivorous zooplankton (Cladocera and Copepoda) on summer phytoplankton in a mesotrophic lake were studied. Field experiments were performed in which phytoplankton were exposed to different densities of two major types of herbivorous zooplankton, cladocerans and copepods. Contrary to expectation, neither of the two zooplankton groups signi®cantly reduced phytoplankton biomass. However, there were strong and contrasting impacts on phytoplankton size structure and on individual taxa. Cladocerans suppressed small phytoplankton, while copepods suppressed large phytoplankton. The unaffected size classes compensated for the loss of those affected by enhanced growth. After contamination of the copepod mesocosms with the cladoceran Daphnia, the combined impact of both zooplankton groups caused a decline in total phytoplankton biomass.

We investigated the changes in life histories imposed on the water flea, Daphnia magna, due to biochemical and mineral limitations. Phosphorus-deficient Scenedesmus obliquus were incubated with or without a single essential fatty acid, eicosapentaenoic acid (EPA). Additionally, the algae were spiked with dissolved phosphorus to create a range of C : P ratios from 600 to 200. This procedure created the possibility to study the importance of different essential resources. We found that somatic growth is retarded until a C : P ratio (molar) ϳ350 is reached. Adding more phosphorus did not further increase growth. At the same time, at high C : P ratios the addition of EPA did not make a difference in growth, whereas below the nutrient threshold (C : P ϭ 350), the fatty acid had a strong positive impact on growth. In a second experiment we studied how the food conditions (with regard to EPA) affected the growth and investment in reproduction and whether this effect was passed on to the next generation. We found that animals fed EPA made an earlier and larger investment in reproduction. Also, the EPA-enriched animals had a higher mortality. The juveniles from mothers fed EPA-enriched algae had a higher growth rate than neonates from control mothers.In recent years, numerous studies on the effect of food quality differences on herbivorous zooplankton have appeared (e.g

The "dilution effect" concept in disease ecology offers the intriguing possibility that clever manipulation of less competent hosts could reduce disease prevalence in populations of more competent hosts. The basic concept is straightforward: host species vary in suitability (competence) for parasites, and disease transmission decreases when there are more incompetent hosts interacting with vectors or removing free-living stages of a parasite. However, host species also often interact with each other in other ecological ways, e.g., as competitors for resources. The net result of these simultaneous, multiple interactions (disease dilution and resource competition) is challenging to predict. Nonetheless, we see the signature of both roles operating concurrently in a planktonic host-parasite system. We document pronounced spatiotemporal variation in the size of epidemics of a virulent fungus (Metschnikowia bicuspidata) in Midwestern U.S. lake populations of a dominant crustacean grazer (Daphnia dentifera). We show that some of this variation is captured by changes in structure of Daphnia assemblages. Lake-years with smaller epidemics were characterized by assemblages dominated by less suitable hosts ("diluters," D. pulicaria and D. retrocurva, whose suitabilties were determined in lab experiments and field surveys) at the start of epidemics. Furthermore, within a season, less suitable hosts increased as epidemics declined. These observations are consistent with a dilution effect. However, more detailed time series analysis (using multivariate autoregressive models) of three intensively sampled epidemics show the signature of a likely interaction between dilution and resource competition between these Daphnia species. The net outcome of this interaction likely promoted termination of these fungal outbreaks. Should this outcome always arise in "friendly competition" systems where diluting hosts compete with more competent hosts? The answers to this question lie at a frontier of disease ecology.