Predator-prey interactions present heightened opportunities for pathogen spillover, as predators are at risk of exposure to infectious agents harbored by prey. Epizootics with high morbidity and mortality have been recorded following prey-to-predator spillover events, which have had significant conservation implications for sensitive species. Using felids as a detailed case study, we have documented both virulent and clinically silent infections in apex predators following transfer of microbes from prey. We draw on these examples and others to examine the mechanisms that determine frequency and outcome of predator exposure to prey-based pathogens. We propose that predator-prey dynamics should be more thoroughly considered in empirical research and disease dynamic modeling approaches in order to reveal answers to outstanding questions relating to pathogen bioaccumulation.

Infectious diseases play an important role in wildlife population dynamics by altering individual fitness, but detecting disease-driven natural selection in free-ranging populations is difficult due to complex disease–host relationships. Chronic wasting disease (CWD) is a fatal infectious prion disease in cervids for which mutations in a single gene have been mechanistically linked to disease outcomes, providing a rare opportunity to study disease-driven selection in wildlife. In Wyoming, USA, CWD has gradually spread across mule deer ( Odocoileus hemionus ) populations, producing natural variation in disease history to evaluate selection pressure. We used spatial variation and a novel temporal comparison to investigate the relationship between CWD and a mutation at codon 225 of the mule deer prion protein gene that slows disease progression. We found that individuals with the ‘slow’ 225F allele were less likely to test positive for CWD, and the 225F allele was more common in herds exposed to CWD longer. We also found that in the past 2 decades, the 225F allele frequency increased more in herds with higher CWD prevalence. This study expanded on previous research by analysing spatio-temporal patterns of individual and herd-based disease data to present multiple lines of evidence for disease-driven selection in free-ranging wildlife.

Though far less obvious than direct effects (clinical disease or mortality), the indirect influences of pathogens are difficult to estimate but may hold fitness consequences. Here, we disentangle the directional relationships between infection and energetic reserves, evaluating the hypotheses that energetic reserves influence infection status of the host and that infection elicits costs to energetic reserves. Using repeated measures of fat reserves and infection status in individual bighorn sheep ( Ovis canadensis ) in the Greater Yellowstone Ecosystem, we documented that fat influenced ability to clear pathogens ( Mycoplasma ovipneumoniae ) and infection with respiratory pathogens was costly to fat reserves. Costs of infection approached, and in some instances exceeded, costs of rearing offspring to independence in terms of reductions to fat reserves. Fat influenced probability of clearing pathogens, pregnancy and over-winter survival; from an energetic perspective, an animal could survive for up to 23 days on the amount of fat that was lost to high levels of infection. Cost of pathogens may amplify trade-offs between reproduction and survival. In the absence of an active outbreak, the influence of resident pathogens often is overlooked. Nevertheless, the energetic burden of pathogens likely has consequences for fitness and population dynamics, especially when food resources are insufficient.

Efficient learning about disease dynamics in free‐ranging wildlife systems can benefit from active surveillance that is standardized across different ecological contexts. For example, active surveillance that targets specific individuals and populations with standardized sampling across ecological contexts (landscape‐scale targeted surveillance) is important for developing a mechanistic understanding of disease emergence, which is the foundation for improving risk assessment of zoonotic or wildlife‐livestock disease outbreaks and predicting hotspots of disease emergence. However, landscape‐scale targeted surveillance systems are rare and challenging to implement. Increasing experience and infrastructure for landscape‐scale targeted surveillance will improve readiness for rapid deployment of this type of surveillance in response to new disease emergence events. Here, we describe our experience developing and rapidly deploying a landscape‐scale targeted surveillance system for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) in two free‐ranging deer species across their ranges in the United States. Our surveillance system was designed to collect data across individual, population, and landscape scales for future analyses aimed at understanding mechanisms and risk factors of SARS‐CoV‐2 transmission, evolution, and persistence. Our approach leveraged partnerships between state and federal public service sectors and academic researchers in a landscape‐scale targeted surveillance research network. Methods describe our approach to developing the surveillance network and sampling design. Results report challenges with implementing our intended sampling design, specifically how the design was adapted as different challenges arose and summarize the sampling design that has been implemented thus far. In the discussion, we describe strategies that were important for the successful deployment of landscape‐scale targeted surveillance, development and operation of the research network, construction of similar networks in the future, and analytical approaches for the data based on the sampling design.

Feline foamy virus (FFV) is a retrovirus that has been detected in multiple feline species, including domestic cats (Felis catus) and pumas (Puma concolor). FFV results in persistent infection but is generally thought to be apathogenic. Sero-prevalence in domestic cat populations has been documented in several countries, but the extent of viral infections in nondomestic felids has not been reported. In this study, we screened sera from 348 individual pumas from Colorado, Southern California and Florida for FFV exposure by assessing sero-reactivity using an FFV anti-Gag ELISA. We documented a sero-prevalence of 78.6% across all sampled subpopulations, representing 69.1% in Southern California, 77.3% in Colorado, and 83.5% in Florida. Age was a significant risk factor for FFV infection when analyzing the combined populations. This high prevalence in geographically distinct populations reveals widespread exposure of puma to FFV and suggests efficient shedding and transmission in wild populations.

Bighorn sheep (Ovis canadensis) across North America commonly experience population-limiting epizootics of respiratory disease. Although many cases of bighorn sheep pneumonia are polymicrobial, Mycoplasma ovipneumoniae is most frequently associated with all-age mortality events followed by years of low recruitment. Chronic carriage of M. ovipneumoniae by adult females serves as a source of exposure of naïve juveniles; relatively few ewes may be responsible for maintenance of infection within a herd. Test-and-remove strategies focused on removal of adult females with evidence of persistent or intermittent shedding (hereafter chronic carriers) may reduce prevalence and mitigate mortality. Postmortem confirmation of pneumonia in chronic carriers has been inadequately reported and the pathology has not been thoroughly characterized, limiting our understanding of important processes shaping the epidemiology of pneumonia in bighorn sheep. Here we document postmortem findings and characterize the lesions of seven ewes removed from a declining bighorn sheep population in Wyoming, USA, following at least two antemortem detections of M. ovipneumoniae within a 14-mo period. We confirmed that 6/7 (85.7%) had variable degrees of chronic pneumonia. Mycoplasma ovipneumoniae was detected in the lung of 4/7 (57.1%) animals postmortem. Four (57.1%) had paranasal sinus masses, all of which were classified as inflammatory, hyperplastic lesions. Pasteurella multocida was detected in all seven (100%) animals, while Trueperella pyogenes was detected in 5/7 (71.4%). Our findings indicate that not all chronic carriers have pneumonia, nor do all have detectable M. ovipneumoniae in the lung. Further, paranasal sinus masses are a common but inconsistent finding, and whether sinus lesions predispose to persistence or result from chronic carriage remains unclear. Our findings indicate that disease is variable in chronic M. ovipneumoniae carriers, underscoring the need for further efforts to characterize pathologic processes and underlying mechanisms in this system to inform management.