As disease outbreaks increase in natural populations, epidemiologists and ecologists continue to search for mechanistic drivers of disease. Parasites harm hosts, virulently depressing their survival and/or fecundity. These effects on individuals can reduce host densities, shape ecological communities, and catalyze evolutionary change through parasite-mediated selection. Within a given host population, disease prevalence can vary substantially through time. Despite recent progress, it remains challenging to understand this variance in epidemic size in space and time. In the last few decades, zooplankton (especially Daphnia) have emerged as a model system for examining the ecological and evolutionary roles of parasites in populations, communities and ecosystems. Our research group integrates epidemiology, rapid evolution and community ecology to understand the distribution and abundance of infectious diseases. In particular, some aspects of habitat seem to enhance the spread of disease whereas others inhibit it. We have identified mechanisms that connect habitat to epidemiology using a case study of disease in plankton. We see a pronounced relationship between the basin shapes of lakes and fungal (Metschnikowia bicuspidata) disease in the zooplankton grazer Daphnia dentifera. Several mechanisms could explain why Daphnia in some lakes are sicker. We can eliminate some hypotheses and find support for others involving food-web players. Furthermore, we identify physical mechanisms (gravity currents, turbulence) that could lead to greater transport of fungal spores to habitat occupied by Daphnia hosts in some lakes in some years. Our results highlight how habitat structure, through its effects on food-web structure and physical processes, can shape wildlife disease.