Emily Bruns

Evidence that climate change will impact the ecology and evolution of individual plant species is growing. However, little, as yet, is known about how climate change will affect interactions between plants and their pathogens. Climate drivers could affect the physiology, and thus demography, and ultimately evolutionary processes affecting both plant hosts and their pathogens. Because the impacts of climate drivers may operate in different directions at different scales of infection, and, furthermore, may be nonlinear, abstracting across these processes may mis-specify outcomes. Here, we use mechanistic models of plant–pathogen interactions to illustrate how counterintuitive outcomes are possible, and we introduce how such framing may contribute to understanding climate effects on plant–pathogen systems. We discuss the evidence-base derived from wild and agricultural plant–pathogen systems that could inform such models, specifically in the direction of estimates of physiological, demographic and evolutionary responses to climate change. We conclude by providing an overview of knowledge gaps and directions for future research in this important area. This article is part of the theme issue ‘Infectious disease ecology and evolution in a changing world’.

Pathogen transmission mode is a key determinant of epidemiological outcomes. Theory shows that host density can influence the spread of pathogens differentially depending on their mode of transmission. Host density could therefore play an important role in determining the pathogen transmission mode. We tested theoretical expectations using floral arrays of the alpine carnation Dianthus pavonius in field experiments of spore dispersal of the anther‐smut fungus, Microbotryum , by vector (pollinator)‐based floral transmission and passive aerial transmission at a range of host densities. Pollinators deposited fewer spores per plant at high host density than at lower density (ranging from a 0.2–2 m spacing between plants), and vector‐based spore deposition at higher densities declined more steeply with distance from diseased plant sources. In contrast, while aerial spore deposition declined with distance from the diseased source, the steepness of this decline was independent of host density. Our study indicates that the amount and distance of vector‐based transmission are likely to be a nonmonotonic function of host density as a result of vector behavior, which is not readily encapsulated by fixed dispersal functions. We conclude that the spatial spread of pathogens by vectors is likely to be greater at lower and intermediate densities, whereas the spatial spread of aerially transmitted pathogens would be greater at high densities. These contrasting patterns could lead to differential importance of each transmission mode in terms of its contribution to subsequent infections across host densities.