We know much about pathogen evolution and the emergence of new disease strains, but less about host resistance and how it is signaled to other individuals and subsequently maintained. The cline in frequency of black-coated wolves ( Canis lupus ) across North America is hypothesized to result from a relationship with canine distemper virus (CDV) outbreaks. We tested this hypothesis using cross-sectional data from wolf populations across North America that vary in the prevalence of CDV and the allele that makes coats black, longitudinal data from Yellowstone National Park, and modeling. We found that the frequency of CDV outbreaks generates fluctuating selection that results in heterozygote advantage that in turn affects the frequency of the black allele, optimal mating behavior, and black wolf cline across the continent.

Sex‐based differences in physiology, behaviour and demography commonly result in differences in disease prevalence. However, sex differences in prevalence may reflect exposure rather than transmission, which could affect disease control programmes. One potential example is chronic wasting disease (CWD), which has been observed at greater prevalence among male than female deer. We used an age‐ and sex‐structured simulation model to explore harvest‐based management of CWD under three different transmission scenarios that all generate higher male prevalence: (1) increased male susceptibility, (2) high male‐to‐male transmission or (3) high female‐to‐male transmission. Both female and male harvests were required to limit CWD epidemics across all transmission scenarios (approximated by R₀), though invasion was more likely under high female‐to‐male transmission. In simulations, heavily male‐biased harvests controlled CWD epidemics and maintained large host populations under high male‐to‐male transmission and increased male susceptibility scenarios. However, male‐biased harvests were ineffective under high female‐to‐male transmission. Instead, female‐biased harvests were able to limit disease transmission under high female‐to‐male transmission but incurred a trade‐off with smaller population sizes. Synthesis and applications. Higher disease prevalence in a sex or age group may be due to higher exposure or susceptibility but does not necessarily indicate if that group is responsible for more disease transmission. We showed that multiple processes can result in the pattern of higher male prevalence, but that population‐level management interventions must focus on the sex responsible for disease transmission, not just those that are most exposed.

Predators may create healthier prey populations by selectively removing diseased individuals. Predators typically prefer some ages of prey over others, which may, or may not, align with those prey ages that are most likely to be diseased. The interaction of age‐specific infection and predation has not been previously explored and likely has sizable effects on disease dynamics. We hypothesize that predator cleansing effects will be greater when the disease and predation occur in the same prey age groups. We examine the predator cleansing effect using a model where both vulnerability to predators and pathogen prevalence vary with age. We tailor this model to chronic wasting disease (CWD) in mule deer and elk populations in the Greater Yellowstone Ecosystem, with empirical data from Yellowstone grey wolves and cougars. Model results suggest that under moderate, yet realistic, predation pressure from cougars and wolves independently, predators may decrease CWD outbreak size substantially and delay the accumulation of symptomatic deer and elk. The magnitude of this effect is driven by the ability of predators to selectively remove late‐stage CWD infections that are likely the most responsible for transmission, but this may not be the age class they typically select. Thus, predators that select for infected young adults over uninfected juveniles have a stronger cleansing effect, and these effects are strengthened when transmission rates increase with increasing prey morbidity. There are also trade‐offs from a management perspective—that is, increasing predator kill rates can result in opposing forces on prey abundance and CWD prevalence. Our modelling exploration shows that predators have the potential to reduce prevalence in prey populations when prey age and disease severity are considered, yet the strength of this effect is influenced by predators' selection for demography or body condition. Current CWD management focuses on increasing cervid hunting as the primary management tool, and our results suggest predators may also be a useful tool under certain conditions, but not necessarily without additional impacts on host abundance and demography. Protected areas with predator populations will play a large role in informing the debate over predator impacts on disease.

Significance: How do social and infectious disease dynamics interact in group-living mammals? A significant cost to group living is increased transmission of pathogens. When a pathogen invades a group, members will be more vulnerable to mortality, Allee effects, and, ultimately, group extinction. The presence of a pathogen reduces the size of the population by reducing the number of social groups, allowing uninfected groups to grow larger from a reduction in intergroup aggression. Concomitantly, Allee effects are exacerbated in infected groups; this reduces the probability of pathogen persistence as infected groups die out more rapidly. Social structuring changes prevalence across scales and influences pathogen invasion and persistence. The models described here provide a framework for understanding the dynamics of these interactions.

Population genetic theory posits that molecular variation buffers against disease risk. Although this “monoculture effect” is well supported in agricultural settings, its applicability to wildlife populations remains in question. In the present study, we examined the genomics underlying individual‐level disease severity and population‐level consequences of sarcoptic mange infection in a wild population of canids. Using gray wolves (Canis lupus) reintroduced to Yellowstone National Park (YNP) as our focal system, we leveraged 25 years of observational data and biobanked blood and tissue to genotype 76,859 loci in over 400 wolves. At the individual level, we reported an inverse relationship between host genomic variation and infection severity. We additionally identified 410 loci significantly associated with mange severity, with annotations related to inflammation, immunity, and skin barrier integrity and disorders. We contextualized results within environmental, demographic, and behavioral variables, and confirmed that genetic variation was predictive of infection severity. At the population level, we reported decreased genome‐wide variation since the initial gray wolf reintroduction event and identified evidence of selection acting against alleles associated with mange infection severity. We concluded that genomic variation plays an important role in disease severity in YNP wolves. This role scales from individual to population levels, and includes patterns of genome‐wide variation in support of the monoculture effect and specific loci associated with the complex mange phenotype. Results yielded system‐specific insights, while also highlighting the relevance of genomic analyses to wildlife disease ecology, evolution, and conservation.