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Quantifying spatiotemporally explicit interactions within animal populations facilitates the understanding of social structure and its relationship with ecological processes. Data from animal tracking technologies (Global Positioning Systems ["GPS"]) can circumvent longstanding challenges in the estimation of spatiotemporally explicit interactions, but the discrete nature and coarse temporal resolution of data mean that ephemeral interactions that occur between consecutive GPS locations go undetected. Here, we developed a method to quantify individual and spatial patterns of interaction using continuous‐time movement models (CTMMs) fit to GPS tracking data. We first applied CTMMs to infer the full movement trajectories at an arbitrarily fine temporal scale before estimating interactions, thus allowing inference of interactions occurring between observed GPS locations. Our framework then infers indirect interactions—individuals occurring at the same location, but at different times—while allowing the identification of indirect interactions to vary with ecological context based on CTMM outputs. We assessed the performance of our new method using simulations and illustrated its implementation by deriving disease‐relevant interaction networks for two behaviorally differentiated species, wild pigs (Sus scrofa) that can host African Swine Fever and mule deer (Odocoileus hemionus) that can host chronic wasting disease. Simulations showed that interactions derived from observed GPS data can be substantially underestimated when temporal resolution of movement data exceeds 30‐min intervals. Empirical application suggested that underestimation occurred in both interaction rates and their spatial distributions. CTMM‐Interaction method, which can introduce uncertainties, recovered majority of true interactions. Our method leverages advances in movement ecology to quantify fine‐scale spatiotemporal interactions between individuals from lower temporal resolution GPS data. It can be leveraged to infer dynamic social networks, transmission potential in disease systems, consumer–resource interactions, information sharing, and beyond. The method also sets the stage for future predictive models linking observed spatiotemporal interaction patterns to environmental drivers. [ABSTRACT FROM AUTHOR]

Ecological context—the biotic and abiotic environment, along with its influence on population mixing dynamics and individual susceptibility—is thought to have major bearing on epidemic outcomes. However, direct comparisons of wildlife disease events in contrasting ecological contexts are often confounded by concurrent differences in host genetics, exposure histories, or pathogen strains. Here, we compare disease dynamics of a Mycoplasma ovipneumoniae spillover event that affected bighorn sheep populations in two contrasting ecological contexts. One event occurred on the herd's home range near the Rio Grande Gorge in New Mexico, while the other occurred in a captive facility at Hardware Ranch in Utah. While data collection regimens varied, general patterns of antibody signal strength and symptom emergence were conserved between the two sites. Symptoms appeared in the captive setting an average of 12.9 days postexposure, average time to seroconversion was 24.9 days, and clinical signs peaked at approximately 36 days postinfection. These patterns were consistent with serological testing and subsequent declines in symptom intensity in the free‐ranging herd. At the captive site, older animals exhibited more severe declines in body condition and loin thickness, higher symptom burdens, and slower antibody response to the pathogen than younger animals. Younger animals were more likely than older animals to clear infection by the time of sampling at both sites. The patterns presented here suggest that environment may not be a major determinant of epidemiological outcomes in the bighorn sheep—M. ovipneumoniae system, elevating the possibility that host‐ or pathogen‐factors may be responsible for observed variation. [ABSTRACT FROM AUTHOR]

A respiratory disease epizootic at the National Bison Range (NBR) in Montana in 2016–2017 caused an 85% decline in the bighorn sheep population, documented by observations of its unmarked but individually identifiable members, the subjects of an ongoing long‐term study. The index case was likely one of a small group of young bighorn sheep on a short‐term exploratory foray in early summer of 2016. Disease subsequently spread through the population, with peak mortality in September and October and continuing signs of respiratory disease and sporadic mortality of all age classes through early July 2017. Body condition scores and clinical signs suggested that the disease affected ewe groups before rams, although by the end of the epizootic, ram mortality (90% of 71) exceeded ewe mortality (79% of 84). Microbiological sampling 10 years to 3 months prior to the epizootic had documented no evidence of infection or exposure to Mycoplasma ovipneumoniae at NBR, but during the epizootic, a single genetic strain of M. ovipneumoniae was detected in affected animals. Retrospective screening of domestic sheep flocks near the NBR identified the same genetic strain in one flock, presumptively the source of the epizootic infection. Evidence of fatal lamb pneumonia was observed during the first two lambing seasons following the epizootic but was absent during the third season following the death of the last identified M. ovipneumoniae carrier ewe. Monitoring of life‐history traits prior to the epizootic provided no evidence that environmentally and/or demographically induced nutritional or other stress contributed to the epizootic. Furthermore, the epizootic occurred despite proactive management actions undertaken to reduce risk of disease and increase resilience in this population. This closely observed bighorn sheep epizootic uniquely illustrates the natural history of the disease including the (presumptive) source of spillover, course, severity, and eventual pathogen clearance. [ABSTRACT FROM AUTHOR]