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Community ecology can link habitat to disease via interactions among
habitat, focal hosts, other hosts, their parasites, and predators.
However, complicated food web interactions (i.e., trophic interactions
among predators, and their impacts on host density and diversity) often
obscure the important pathways regulating disease. Here, we disentangle
community drivers in a case study of planktonic disease, using a two-step
approach. In step one, we tested univariate field patterns linking
community interactions to two disease metrics. Density of focal hosts
(Daphnia dentifera) was related to density but not prevalence of fungal
(Metschnikowia bicuspidata) infections. Both disease metrics appeared to
be driven by selective predators that cull infected hosts (fish, e.g.
Lepomis macrochirus), sloppy predators that spread parasites while feeding
(midges, Chaoborus punctipennis), and spore predators that reduce contact
between focal hosts and parasites (other zooplankton, especially
small-bodied Ceriodaphnia sp.). Host diversity also negatively correlated
with disease, suggesting a dilution effect. However, several of these
univariate patterns are initially misleading, due to confounding
ecological links among habitat, predators, host density, and host
diversity. In step two, path models uncovered and explained these
misleading patterns, and grounded them in habitat structure (refuge size).
First, rather than directly reducing infection prevalence, fish predation
drove disease indirectly through changes in density of midges and
frequency of small spore predators (which became more frequent in lakes
with small refuges). Second, small spore predators drove the two disease
metrics through fundamentally different pathways: They directly reduced
infection prevalence, but indirectly reduced density of infected hosts by
lowering density of focal hosts (likely via competition). Third, the
univariate diversity-disease pattern (signaling a dilution effect) merely
reflected the confounding direct effects of these small spore predators.
Diversity per se had no effect on disease, after accounting for the links
between small spore predators, diversity, and infection prevalence. In
turn, these small spore predators were regulated by both size-selective
fish predation and refuge size. Thus, path models not only explain each of
these surprising results, but also trace their origins back to habitat
structure.
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