Gregory F. Albery

Pathogen traits can vary greatly and heavily impact the ability of a pathogen to persist in a population. Although this variation is fundamental to disease ecology, little is known about the evolutionary pressures that drive these differences, particularly where they interact with host behaviour. We hypothesized that host behaviours relevant to different transmission routes give rise to differences in contact network structure, constraining the space over which pathogen traits can evolve to maximize fitness. Our analysis of 232 contact networks across mammals, birds, reptiles, amphibians, arthropods, fish and molluscs found that contact network topology varies by contact type, most notably in networks that are representative of fluid-exchange transmission. Using infectious disease model simulations, we showed that these differences in network structure suggest pathogens transmitted through fluid-exchange contact types will need traits associated with high transmissibility to successfully proliferate, compared to pathogens that transmit through other types of contact. These findings were supported through a review of known traits of pathogens that transmit in humans. Our work demonstrates that contact network structure may drive the evolution of compensatory pathogen traits according to transmission strategy, providing essential context for understanding pathogen evolution and ecology.

Exposure and susceptibility underlie every organism's infection status, and an untold diversity of factors can drive variation in both. Often, both exposure and susceptibility change in response to a given factor, and they can interact, such that their relative contributions to observed disease dynamics are obscured. These independent and interlinked changes often complicate empirical inference in disease ecology and ecoimmunology. Although many disease ecology studies address this problem, it is often implicit rather than explicit and requires a specific set of tools to tackle. Moreover, as yet, there is no established conceptual framework for disentangling susceptibility and exposure processes. Here, we consolidate previous theory and empirical understanding regarding the entwined effects of susceptibility and exposure, which we refer to as ‘the Twin Pillar Problem’. We provide a framework for conceptualising exposure–susceptibility interactions, where they obscure, confound, induce or counteract one another, providing some well‐known examples for each complicating mechanism. We synthesise guidelines for anticipating and controlling for covariance between exposure and susceptibility, and we detail statistical and operational methodology that researchers have employed to deal with them. Finally, we discuss novel emerging frontiers in their study in ecology, and their potential for further integration in the fields of wildlife and human health. Read the free Plain Language Summary for this article on the Journal blog.