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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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Micro‐ and macroparasites are a leading cause of mortality for humans, animals, and plants, and there is great need to understand their origins, transmission dynamics, and impacts. Disease ecology formed as an interdisciplinary field in the 1970s to fill this need and has recently rapidly grown in size and influence. Because interdisciplinary fields integrate diverse scientific expertise and training experiences, understanding their composition and research priorities is often difficult. Here, for the first time, we quantify the composition and educational experiences of a subset of disease ecology practitioners and identify topical trends in published research. We combined a large survey of self‐declared disease ecologists with a literature synthesis involving machine‐learning topic detection of over 18,500 disease ecology research articles. The number of graduate degrees earned by disease ecology practitioners has grown dramatically since the early 2000s. Similar to other science fields, we show that practitioners in disease ecology have diversified in the last decade in terms of gender identity and institution, with weaker diversification in race and ethnicity. Topic detection analysis revealed how the frequency of publications on certain topics has declined (e.g., HIV, serology), increased (e.g., the dilution effect, infectious disease in bats), remained relatively common (e.g., malaria ecology, influenza, vaccine research and development), or have consistently remained relatively infrequent (e.g., theoretical models, field experiments). Other topics, such as climate change, superspreading, emerging infectious diseases, and network analyses, have recently come to prominence. This study helps identify the major themes of disease ecology and demonstrates how publication frequency corresponds to emergent health and environmental threats. More broadly, our approach provides a framework to examine the composition and publication trends of other major research fields that cross traditional disciplinary boundaries. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The spatial organization of a population can influence the spread of information, behaviour and pathogens. Group territory size and territory overlap and components of spatial organization, provide key information as these metrics may be indicators of habitat quality, resource dispersion, contact rates and environmental risk (e.g. indirectly transmitted pathogens). Furthermore, sociality and behaviour can also shape space use, and subsequently, how space use and habitat quality together impact demography.Our study aims to identify factors shaping the spatial organization of wildlife populations and assess the impact of epizootics on space use. We further aim to explore the mechanisms by which disease perturbations could cause changes in spatial organization.Here we assessed the seasonal spatial organization of Serengeti lions and Yellowstone wolves at the group level. We use network analysis to describe spatial organization and connectivity of social groups. We then examine the factors predicting mean territory size and mean territory overlap for each population using generalized additive models.We demonstrate that lions and wolves were similar in that group‐level factors, such as number of groups and shaped spatial organization more than population‐level factors, such as population density. Factors shaping territory size were slightly different than factors shaping territory overlap; for example, wolf pack size was an important predictor of territory overlap, but not territory size. Lion spatial networks were more highly connected, while wolf spatial networks varied seasonally. We found that resource dispersion may be more important for driving territory size and overlap for wolves than for lions. Additionally, canine distemper epizootics may have altered lion spatial organization, highlighting the importance of including infectious disease epizootics in studies of behavioural and movement ecology.We provide insight about when we might expect to observe the impacts of resource dispersion, disease perturbations, and other ecological factors on spatial organization. Our work highlights the importance of monitoring and managing social carnivore populations at the group level. Future research should elucidate the complex relationships between demographics, social and spatial structure, abiotic and biotic conditions and pathogen infections. [ABSTRACT FROM AUTHOR]

Abstract: Many parasites infect multiple hosts, but estimating the transmission across host species remains a key challenge in disease ecology. We investigated the within and across host species dynamics of canine distemper virus (CDV) in grizzly bears (Ursus arctos) and wolves (Canis lupus) of the Greater Yellowstone Ecosystem (GYE). We hypothesized that grizzly bears may be more likely to be exposed to CDV during outbreaks in the wolf population because grizzly bears often displace wolves while scavenging carcasses. We used serological data collected from 1984 to 2014 in conjunction with Bayesian state‐space models to infer the temporal dynamics of CDV. These models accounted for the unknown timing of pathogen exposure, and we assessed how different testing thresholds and the potential for testing errors affected our conclusions. We identified three main CDV outbreaks (1999, 2005, and 2008) in wolves, which were more obvious when we used higher diagnostic thresholds to qualify as seropositive. There was some evidence for increased exposure rates in grizzly bears in 2005, but the magnitude of the wolf effect on bear exposures was poorly estimated and depended upon our prior distributions. Grizzly bears were exposed to CDV prior to wolf reintroduction and during time periods outside of known wolf outbreaks, thus wolves are only one of several potential routes for grizzly bear exposures. Our modeling approach accounts for several of the shortcomings of serological data and is applicable to many wildlife disease systems, but is most informative when testing intervals are short. CDV circulates in a wide range of carnivore species, but it remains unclear whether the disease persists locally within the GYE carnivore community or is periodically reintroduced from distant regions with larger host populations. [ABSTRACT FROM AUTHOR]