Chronic wasting disease (CWD) is a fatal disease of deer, elk, and moose transmitted through direct, animal-to-animal contact, and indirectly, via environmental contamination. Considerable attention has been paid to modeling direct transmission, but despite the fact that CWD prions can remain infectious in the environment for years, relatively little information exists about the potential effects of indirect transmission on CWD dynamics. In the present study, we use simulation models to demonstrate how indirect transmission and the duration of environmental prion persistence may affect epidemics of CWD and populations of North American deer. Existing data from Colorado, Wyoming, and Wisconsin's CWD epidemics were used to define plausible short-term outcomes and associated parameter spaces. Resulting long-term outcomes range from relatively low disease prevalence and limited host-population decline to host-population collapse and extinction. Our models suggest that disease prevalence and the severity of population decline is driven by the duration that prions remain infectious in the environment. Despite relatively low epidemic growth rates, the basic reproductive number, R 0, may be much larger than expected under the direct-transmission paradigm because the infectious period can vastly exceed the host's life span. High prion persistence is expected to lead to an increasing environmental pool of prions during the early phases (i.e. approximately during the first 50 years) of the epidemic. As a consequence, over this period of time, disease dynamics will become more heavily influenced by indirect transmission, which may explain some of the observed regional differences in age and sex-specific disease patterns. This suggests management interventions, such as culling or vaccination, will become increasingly less effective as CWD epidemics progress.

Infectious disease contributed to historical declines and extirpations of bighorn sheep (Ovis canadensis) in North America and continues to impede population restoration and management. Reports of pneumonia outbreaks in freeranging bighorn sheep following contact with domestic sheep have been validated by the results of 13 captive commingling experiments. However, ecological and etiological complexities still hinder our understanding and control of respiratory disease in wild sheep. In this paper, we review the literature and summarize recent data to present an overview of the biology and management of pneumonia in bighorn sheep. Many factors contribute to this population-limiting disease, but a bacterium (Mycoplasma ovipneumoniae) host-specific to Caprinae and commonly carried by healthy domestic sheep and goats, appears to be a primary agent necessary for initiating epizootics. All-age epizootics are usually associated with significant population declines, but mortality rates vary widely and factors influencing disease severity are not well understood. Once introduced, M. ovipneumoniae can persist in bighorn sheep populations for decades. Carrier females may transmit the pathogen to their susceptible lambs, triggering fatal pneumonia outbreaks in nursery groups, which limit recruitment and slow or prevent population recovery. The demographic costs of disease persistence can be equal to or greater than the impacts of the initial epizootic. Strain typing suggests that spillover of M. ovipneumoniae into bighorn sheep populations from domestic small ruminants is ongoing and that consequences of spillover are amplified by movements of infected bighorn sheep across populations. Therefore, current disease management strategies focus on reducing risk of spillover from reservoir populations of domestic sheep and goats and on limiting transmission among bighorn sheep.

1. Surveying wildlife communities provides data for informing conservation and management decisions that affect multiple species. Autonomous recording units (ARUs) can efficiently gather community data for a variety of taxa, but generally require software algorithms to classify each recorded call to a species. Species classification Surveying wildlife communities provides data for informing conservation and management decisions that affect multiple species. Autonomous recording units (ARUs) efficiently gather community data by passively recording animal vocalizations (Gibb, Browning, Glover-Kapfer, & Jones, 2019), generally for multiple time periods ('visits') at each surveyed location ('site'). These data, including counts of call recordings and corresponding species classifications, can be used to investigate various ecological questions and are applicable for surveying multiple taxa (e.g. anurans, bats, birds). However, due to the large volumes of data typically collected, most studies using acoustic surveys require classification software to identify the species of each call recording (Gibb et al., 2019). This automated process includes species classification errors that lead to both false-negative and false-positive detections. For instance, when a species is present, false-negative detections can result from successfully recording its calls but misclassifying them as alternative species. These errors are in addition to false negatives from failing to record any of its calls. False-positive detections at sites where a species is absent are often due to misclassifying recorded calls from another species. Estimating the ecological parameters of interest, while addressing these errors is an important consideration when analysing ARU data. Occupancy models (MacKenzie et al., 2002) are a natural framework for analysing ARU data when visits are summarized to detection/non-detection observations for each species (e.g. Banner et al., 2018; Rodhouse et al., 2019). Originally developed to account for false negatives, standard occupancy models assume that all false positives are removed (MacKenzie et al., 2002). Completely eliminating false positives from ARU data is generally cost prohibitive because it requires manually confirming at least one recording for every visit. False positives are an important source of errors in many

BackgroundGray wolves (Canis lupus) were reintroduced into Yellowstone National Park (YNP) after a >70 year absence, and as part of recovery efforts, the population has been closely monitored. In 1999 and 2005, pup survival was significantly reduced, suggestive of disease outbreaks.Methodology/Principal FindingsWe analyzed sympatric wolf, coyote (Canis latrans), and red fox (Vulpes vulpes) serologic data from YNP, spanning 1991–2007, to identify long-term patterns of pathogen exposure, identify associated risk factors, and examine evidence for disease-induced mortality among wolves for which there were survival data. We found high, constant exposure to canine parvovirus (wolf seroprevalence: 100%; coyote: 94%), canine adenovirus-1 (wolf pups [0.5–0.9 yr]: 91%, adults [≥1 yr]: 96%; coyote juveniles [0.5–1.5 yrs]: 18%, adults [≥1.6 yrs]: 83%), and canine herpesvirus (wolf: 87%; coyote juveniles: 23%, young adults [1.6–4.9 yrs]: 51%, old adults [≥5 yrs]: 87%) suggesting that these pathogens were enzootic within YNP wolves and coyotes. An average of 50% of wolves exhibited exposure to the protozoan parasite, Neospora caninum, although individuals’ odds of exposure tended to increase with age and was temporally variable. Wolf, coyote, and fox exposure to canine distemper virus (CDV) was temporally variable, with evidence for distinct multi-host outbreaks in 1999 and 2005, and perhaps a smaller, isolated outbreak among wolves in the interior of YNP in 2002. The years of high wolf-pup mortality in 1999 and 2005 in the northern region of the park were correlated with peaks in CDV seroprevalence, suggesting that CDV contributed to the observed mortality.Conclusions/SignificanceOf the pathogens we examined, none appear to jeopardize the long-term population of canids in YNP. However, CDV appears capable of causing short-term population declines. Additional information on how and where CDV is maintained and the frequency with which future epizootics might be expected might be useful for future management of the Northern Rocky Mountain wolf population.