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.
The relationship between energy reserves (biomass and triacylglycerol) and starvation time is investigated for two planktonic Cladocera, Daphnia. galeata mendotae and Daphnia magna. Triacylglycerol storage is correlated to total individual biomass independently of body size. Adult biomass increases twofold to threefold during the intermolt, with triacylglycerol accounting for 16% of the total increase. The amount of triacylglycerol transferred into each egg depends on the adult’s feeding success. Starvation time is correlated to body mass; however, triacylglycerol storage and reproductive allocation modify the relationship. Although adult biomass and percentage of lipid both increase during intermolt, animals in late intermolt starve sooner than those in early‐middle intermolt because of the transfer of energy reserves to the ovaries for reproduction. Daphnia magna neonates with high maternal lipid survived twice as long as neonates with low maternal lipid but similar body mass.
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.
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