Summary: 1. Ecological immunology and disease ecology are two relatively young disciplines that apply ecological approaches and principles to traditionally non‐ecological fields. In both cases, an ecological perspective has allowed new insights to emerge by focusing attention on variation over space and time, and by emphasizing the role of the environment in shaping individual responses and the outcome of host‐pathogen interactions. Here we review the growing conceptual interface between these two rapidly evolving fields.2. Areas of synergy between ecological immunology and disease ecology aim to translate variation in within‐host processes (e.g. immunity) into between‐host dynamics (e.g. parasite transmission). Emerging areas of synergy include potential immune mechanisms that underlie host heterogeneity in disease susceptibility, teasing apart the effects of environmental factors such as seasonality and climate on host susceptibility and pathogen dynamics, and predicting the outcome of co‐infection by functionally distinct groups of parasites that elicit different immune responses.3. In some cases, practical limitations have constrained the merging of ideas in ecological immunology and disease ecology. We discuss several logistical challenges, including dissecting the relative roles of host exposure and susceptibility, establishing links between measures of immunity and pathogen resistance in wild populations, and incorporating relevant immune variation into prevailing disease ecology modeling frameworks.4. Future work at the interface of these two fields should advance understanding of life‐history theory, host‐pathogen dynamics, and physiological ecology, and will also contribute to targeted approaches for wildlife health and zoonotic disease prevention.

Nature's “responsible” response to disease: With the emergence of the COVID-19 pandemic, there have been global calls for the implementation of “social distancing” to control transmission. Throughout the world, some have resisted this requirement with the unfounded argument that it is unnecessary or ineffective. Social distancing, however, is a natural consequence of disease across animals, both human and nonhuman. Stockmaier et al. reviewed responses to disease across animal taxa and reveal how these responses naturally limit disease transmission. Understanding such natural responses and their impacts on pathogenic transmission provides epidemiological insight into our own responses to pandemic challenges. Science , this issue p. eabc8881

Animal behaviour and the ecology and evolution of parasites are inextricably linked. For this reason, animal behaviourists and disease ecologists have been interested in the intersection of their respective fields for decades. Despite this interest, most research at the behaviour–disease interface focuses either on how host behaviour affects parasites or how parasites affect behaviour, with little overlap between the two. Yet, the majority of interactions between hosts and parasites are probably reciprocal, such that host behaviour feeds back on parasites and vice versa. Explicitly considering these feedbacks is essential for understanding the complex connections between animal behaviour and parasite ecology and evolution. To illustrate this point, we discuss how host behaviour–parasite feedbacks might operate and explore the consequences of feedback for studies of animal behaviour and parasites. For example, ignoring the feedback of host social structure on parasite dynamics can limit the accuracy of predictions about parasite spread. Likewise, considering feedback in studies of parasites and animal personalities may provide unique insight about the maintenance of variation in personality types. Finally, applying the feedback concept to links between host behaviour and beneficial, rather than pathogenic, microbes may shed new light on transitions between mutualism and parasitism. More generally, accounting for host behaviour–parasite feedbacks can help identify critical gaps in our understanding of how key host behaviours and parasite traits evolve and are maintained.

Individual heterogeneity can influence the dynamics of infectious diseases in wildlife and humans alike. Thus, recent work has sought to identify behavioural characteristics that contribute disproportionately to individual variation in pathogen acquisition (super-receiving) or transmission (super-spreading). However, it remains unknown whether the same behaviours enhance both acquisition and transmission, a scenario likely to result in explosive epidemics. Here, we examined this possibility in an ecologically relevant host–pathogen system: house finches and their bacterial pathogen, Mycoplasma gallisepticum , which causes severe conjunctivitis. We examined behaviours likely to influence disease acquisition (feeder use, aggression, social network affiliations) in an observational field study, finding that the time an individual spends on bird feeders best predicted the risk of conjunctivitis. To test whether this behaviour also influences the likelihood of transmitting M. gallisepticum , we experimentally inoculated individuals based on feeding behaviour and tracked epidemics within captive flocks. As predicted, transmission was fastest when birds that spent the most time on feeders initiated the epidemic. Our results suggest that the same behaviour underlies both pathogen acquisition and transmission in this system and potentially others. Identifying individuals that exhibit such behaviours is critical for disease management.

Ever since Mycoplasma gallisepticum emerged among house finches in North America, it has been suggested that bird aggregations at feeders are an important cause of the epidemic of mycoplasmal conjunctivitis because diseased birds could deposit droplets of pathogen onto the feeders and thereby promote indirect transmission by fomites. In this paper we bring the first experimental evidence that such transmission (bird-to-feeder-to-bird) does actually take place. House finches infected via this route, however, developed only mild disease and recovered much more rapidly than birds infected from the same source birds but directly into the conjunctiva. While it is certainly probable that house finch aggregations at artificial feeders enhance pathogen transmission, to some degree transmission of M. gallisepticum by fomites may serve to immunize birds against developing more severe infections. Some such birds develop M. gallisepticum antibodies, providing indication of an immune response, although no direct evidence of protection.

Host individuals and populations often vary in their responses to infection, with direct consequences for pathogen spread and evolution. While considerable work has focused on the mechanisms underlying differences in resistance-the ability to kill pathogens-we know little about the mechanisms underlying tolerance-the ability to minimize fitness losses per unit pathogen. Here, we examine patterns and mechanisms of tolerance between two populations of house finches (Haemorhous [formerly Carpodacus] mexicanus) with different histories with the bacterial pathogen Mycoplasma gallisepticum (MG). After infection in a common environment, we assessed two metrics of pathology, mass loss and eye lesion severity, as proxies for fitness. We calculated tolerance using two methods, one based on pathology and pathogen load at the peak of infection (point tolerance) and the other based on the integrals of these metrics over time (range tolerance). Alabama birds, which have a significantly longer history of exposure to MG, showed more pronounced point tolerance than Arizona birds, while range tolerance did not differ between populations. Alabama birds also displayed lower inflammatory cytokine signaling and lower fever early in infection. These results suggest that differences in inflammatory processes, which can significantly damage host tissues, may contribute to variation in tolerance among house finch individuals and populations. Such variation can affect pathogen spread and evolution in ways not predictable by resistance alone and sheds light on the costs and benefits of inflammation in wild animals.