OOS 22-4 - Plant disease ecology meets urban ecology: Effects of microclimate and urbanization on plant disease

Urbanization involves dramatic changes to the environment which can alter the frequency and outcomes of ecological interactions including parasitism. These include changes in habitat connectivity and genetic diversity, increases in temperature (i.e., the "urban heat island" effect), and modification of other physical, chemical, and biological aspects of the environment. Indeed, a meta-analysis of >100 published studies revealed wildlife face significantly greater risk of parasite infection in urban areas. However, the mechanisms by which urban environmental changes alter prevalence of disease remain poorly characterized, particularly for plant disease systems. Moreover, assessment of land cover and climate changes at the landscape or population scale does not capture fine-scale heterogeneity in habitat structure and microclimate that can impact an individual host's susceptibility to infection. Understanding the role of this fine-scale environmental heterogeneity in host-parasite interactions is especially critical for predicting whether disease can persist in pockets of suitable microclimate under scenarios of continued warming.

Our goals were to document patterns of disease in wild host populations across a gradient of urbanization, and to test how certain environmental changes associated with urbanization -- including climatic variation at landscape and microhabitat scales -- influence infection prevalence. To achieve these goals, we performed observational and experimental studies using a tractable system of weedy host plants (Plantago spp.) and their host-specific foliar fungal pathogens (powdery mildews). In each of four years, we performed field surveys of urban, suburban, and rural Plantago populations in the Greater St. Louis region (Missouri, USA). Epidemics of powdery mildew were generally larger in more urban populations in all four years. Results of complementary field and laboratory experiments which control for host genotype suggest that this field pattern is not due to rural hosts being more resistant to the focal pathogens. Additionally, we observed greater prevalence of disease in shaded than full-sun microhabitats across levels of urbanization. A field experiment manipulating shade suggests that this relationship is causal, where microclimate conditions associated with shade promote pathogen growth and transmission. Together, our findings highlight the importance of taking fine-scale habitat heterogeneity into account when establishing links between climate or land cover context and prevalence of disease. Overall, our results provide novel insights into the ecological processes that drive variation in plant-pathogen interactions across levels of urbanization.