Abstract
Pathogen transport by biotic or abiotic processes (e.g. mechanical vectors, wind, rain) can increase disease transmission by creating more opportunities for host exposure. But transport without replication has an inherent trade‐off, that creating new venues for exposure decreases the average pathogen abundance at each venue. The host dose‐response relationship is therefore required to correctly assess infection risk. We model and analyse two examples—biotic mechanical vectors in plant–pollinator networks, and abiotic‐facilitated long‐distance pathogen dispersal—to illustrate how oversimplifying the dose‐response relationship can lead to incorrect epidemiological predictions. When the minimum infective dose is high, mechanical vectors amplify disease transmission less than suggested by simple compartment models, and may even dilute transmission. When long‐distance dispersal leads to infrequent large exposures, models that assume a linear force of infection can substantially under‐predict the speed of epidemic spread. Our work highlights an important general interplay between dose‐response relationships and pathogen transport.