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In the current era of global change, the emergence of infectious diseases at the wildlife–livestock interface poses risks to biodiversity, agricultural economies, and public health. Driven by anthropogenic influence, increased sharing of resources between wildlife and livestock can promote cross‐species transmission, the consequences of which are challenging to predict. Mycoplasma bovis , an economically important bacterial pathogen in cattle, has recently emerged as a threat to other ungulate species. This study reports on a case of M. bovis in an intensively monitored free‐ranging mule deer (Odocoileus hemionus ) in Colorado, USA, which presented an opportunity to describe the disease in a novel host and infer transmission and infection dynamics from GPS collar data. Following a mortality signal from a GPS‐collared adult female mule deer, field investigation revealed predation while postmortem examination further revealed severe, acute, fibrinosuppurative and necrotizing pleuropneumonia. Histopathological analysis, immunohistochemistry, and real‐time PCR confirmed M. bovis as the etiology. GPS collar data demonstrated spatial overlap with dairy cattle in the 50 days prior to death, implicating potential spillover from cattle as the transmission pathway. Reduced movement was identified 19 days prior to death, indicative of sickness behavior due to acute pneumonia. This case underscores the potential for M. bovis to cause severe disease in wild ungulates and highlights the value of thorough postmortem investigations as a routine component of studies involving wildlife tracking. The retrospective use of GPS collar data provides valuable insights into the movement ecology of wildlife exposed to novel pathogens, aiding in the understanding of cross‐species transmission and informing management strategies to reduce the potential for spillover. Mycoplasma bovis is bacterial pathogen of cattle that is rarely detected in wildlife. Our intensive monitoring of free‐ranging mule deer led to the discovery of Mycoplasma bovis as the cause of death in an animal that had recently selected for use of a dairy premise. Our findings highlight the potential for spillover inference from intensively monitored wildlife, while also contributing foundational knowledge about a specific emerging infectious disease at the wildlife‐livestock interface.

Mycoplasma bovis is 1 of several bacterial pathogens associated with pneumonia in cattle. Its role in pneumonia of free-ranging ungulates has not been established. Over a 3-month period in early 2019, »60 free-ranging pronghorn with signs of respiratory disease died in northeast Wyoming, USA. A consistent finding in submitted carcasses was severe fibrinosuppurative pleuropneumonia and detection of M. bovis by PCR and immunohistochemical analysis. Multilocus sequence typing of isolates from 4 animals revealed that all have a deletion in 1 of the target genes, adh-1. A retrospective survey by PCR and immunohistochemical analysis of paraffin-embedded lung from 20 pronghorn that died with and without pneumonia during 2007-2018 yielded negative results. These findings indicate that a distinct strain of M. bovis was associated with fatal pneumonia in this group of pronghorn.

Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.

Wildlife translocations are a commonly used strategy in endangered species recovery programmes. Although translocations require detailed assessment of risk, their impact on parasite distribution has not been thoroughly assessed. This is despite the observation that actions that alter host–parasite distributions can drive evolution or introduce new parasites to previously sequestered populations. Here, we use a contemporary approach to amplify viral sequences from archived biological samples to characterize a previously undocumented impact of the successful genetic rescue of the Florida panther ( Puma concolor coryi ). Our efforts reveal transmission of feline immunodeficiency virus (FIV) during translocation of pumas from Texas to Florida, resulting in extirpation of a historic Florida panther FIV subtype and expansion of a genetically stable subtype that is highly conserved in Texas and Florida. We used coalescent theory to estimate viral demography across time and show an exponential increase in the effective population size of FIV coincident with expansion of the panther population. Additionally, we show that FIV isolates from Texas are basal to isolates from Florida. Interestingly, FIV genomes recovered from Florida and Texas demonstrate exceptionally low interhost divergence. Low host genomic diversity and lack of additional introgressions may underlie the surprising lack of FIV evolution over 2 decades. We conclude that modern FIV in the Florida panther disseminated following genetic rescue and rapid population expansion, and that infectious disease risks should be carefully considered during conservation efforts involving translocations. Further, viral evolutionary dynamics may be significantly altered by ecological niche, host diversity and connectivity between host populations.

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. Pathogen transmission in wildlife populations depends on ecological factors that feed back across the scales of individuals, populations, and landscapes. We developed and deployed a disease surveillance design for aligning data collection across these multiple biological scales (landscape‐scale targeted surveillance) to enable future analyses to identify ecological drivers of disease transmission and predict hotspots of disease emergence in wildlife. We describe our experience with the deployment of landscape‐scale targeted surveillance of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) in two free‐ranging deer species across their ranges in the United States. We identify strategies that are important for successful deployment of landscape‐scale targeted surveillance in wildlife using a research‐based surveillance network.

Integrating host movement and pathogen data is a central issue in wildlife disease ecology that will allow for a better understanding of disease transmission. We examined how adult female mule deer (Odocoileus hemionus) responded behaviorally to infection with chronic wasting disease (CWD). We compared movement and habitat use of CWD‐infected deer (n = 18) to those that succumbed to starvation (and were CWD‐negative by ELISA and IHC; n = 8) and others in which CWD was not detected (n = 111, including animals that survived the duration of the study) using GPS collar data from two distinct populations collared in central Wyoming, USA during 2018–2022. CWD and predation were the leading causes of mortality during our study (32/91 deaths attributed to CWD and 27/91 deaths attributed to predation). Deer infected with CWD moved slower and used lower elevation areas closer to rivers in the months preceding death compared with uninfected deer that did not succumb to starvation. Although CWD‐infected deer and those that died of starvation moved at similar speeds during the final months of life, CWD‐infected deer used areas closer to streams with less herbaceous biomass than starved deer. These behavioral differences may allow for the development of predictive models of disease status from movement data, which will be useful to supplement field and laboratory diagnostics or when mortalities cannot be quickly retrieved to assess cause‐specific mortality. Furthermore, identifying individuals who are sick before predation events could help to assess the extent to which disease mortality is compensatory with predation. Finally, infected animals began to slow down around 4 months prior to death from CWD. Our approach for detecting the timing of infection‐induced shifts in movement behavior may be useful in application to other disease systems to better understand the response of wildlife to infectious disease. Our manuscript characterizes how infection with chronic wasting disease (CWD) alters the movement and habitat use of free‐ranging mule deer. We demonstrate that movement data (i.e., locations from GPS collars) are predictive of disease status as early as 4–6 months prior to death from CWD. We further demonstrate that behavioral changes (e.g., decreased movement speed, increased use of riparian habitat) in CWD‐infected deer can be distinguished from similar behavioral shifts in other pathologic states such as malnutrition and starvation.

Feline immunodeficiency virus (FIV) is a naturally occurring T-cell tropic lentiviral disease of felids with many similarities to HIV/AIDS in humans. Similar to primate lentiviral-host interactions, feline APOBEC3 (A3) has been shown to inhibit FIV infection in a host-specific manner and feline A3 degradation is mediated by FIV Vif. Further, infection of felids with non-native FIV strains results in restricted viral replication in both experimental and naturally occurring infections. However, the link between molecular A3-Vif interactions and A3 biological activity during FIV infection has not been well characterized. We thus examined expression of the feline A3 genes A3Z2, A3Z3 and A3Z2-Z3 during experimental infection of domestic cats with host-adapted domestic cat FIV (referred to as FIV) and non-adapted Puma concolor FIV (referred to as puma lentivirus, PLV). We determined A3 expression in different tissues and blood cells from uninfected, FIV-infected, PLV-infected and FIV/PLV co-infected cats; and in purified blood cell subpopulations from FIV-infected and uninfected cats. Additionally, we evaluated regulation of A3 expression by cytokines, mitogens, and FIV infection in cultured cells. In all feline cells and tissues studied, there was a striking difference in expression between the A3 genes which encode FIV inhibitors, with A3Z3 mRNA abundance exceeding that of A3Z2-Z3 by 300-fold or more. Interferon-alpha treatment of cat T cells resulted in upregulation of A3 expression, while treatment with interferon-gamma enhanced expression in cat cell lines. In cats, secondary lymphoid organs and peripheral blood mononuclear cells (PBMC) had the highest basal A3 expression levels and A3 genes were differentially expressed among blood T cells, B cells, and monocytes. Acute FIV and PLV infection of cats, and FIV infection of primary PBMC resulted in no detectable change in A3 expression with the exception of significantly elevated A3 expression in the thymus, the site of highest FIV replication. We conclude that cat A3 expression is regulated by cytokine treatment but, by and large, lentiviral infection did not appear to alter expression. Differences in A3 expression in different blood cell subsets did not appear to impact FIV viral replication kinetics within these cells. Furthermore, the relative abundance of A3Z3 mRNA compared to A3Z2-Z3 suggests that A3Z3 may be the major active anti-lentiviral APOBEC3 gene product in domestic cats.

Identifying drivers of transmission—especially of emerging pathogens—is a formidable challenge for proactive disease management efforts. While close social interactions can be associated with microbial sharing between individuals, and thereby imply dynamics important for transmission, such associations can be obscured by the influences of factors such as shared diets or environments. Directly-transmitted viral agents, specifically those that are rapidly evolving such as many RNA viruses, can allow for high-resolution inference of transmission, and therefore hold promise for elucidating not only which individuals transmit to each other, but also drivers of those transmission events. Here, we tested a novel approach in the Florida panther, which is affected by several directly-transmitted feline retroviruses. We first inferred the transmission network for an apathogenic, directly-transmitted retrovirus, feline immunodeficiency virus (FIV), and then used exponential random graph models to determine drivers structuring this network. We then evaluated the utility of these drivers in predicting transmission of the analogously transmitted, pathogenic agent, feline leukemia virus (FeLV), and compared FIV-based predictions of outbreak dynamics against empirical FeLV outbreak data. FIV transmission was primarily driven by panther age class and distances between panther home range centroids. FIV-based modeling predicted FeLV dynamics similarly to common modeling approaches, but with evidence that FIV-based predictions captured the spatial structuring of the observed FeLV outbreak. While FIV-based predictions of FeLV transmission performed only marginally better than standard approaches, our results highlight the value of proactively identifying drivers of transmission—even based on analogously-transmitted, apathogenic agents—in order to predict transmission of emerging infectious agents. The identification of underlying drivers of transmission, such as through our workflow here, therefore holds promise for improving predictions of pathogen transmission in novel host populations, and could provide new strategies for proactive pathogen management in human and animal systems.

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.

Bovine tuberculosis (bTB) is endemic in freeranging white-tailed deer (Odocoileus virginianus) in MI, USA. Currently, the rates of farm visitation by deer and couse of forage resources by cattle and deer are poorly understood. To evaluate the extent deer and livestock may share forage resources, we investigated farm, yard, and cattle-use area visitation by white-tailed deer and compared visitation with common livestock management practices. We fitted 25 female white-tailed deer near the bTB-infected zone in Michigan’s Lower Peninsula with global positioning system collars. Livestock management practices associated with farm visitation included presence of confined feeding pastures, number of cattle water sources, and the number of cattle pastures. Fewer farm visits occurred at night than during the day. A higher proportion of nighttime visits occurred between midnight and sunrise. Visitation to yards and cattle-use areas were similar: a higher proportion of visits occurred at night, and a higher proportion of nighttime visits occurred between midnight and sunrise. Multiple visits during the same day were common. Visitation increased through spring and peaked during the fawning season. Results suggest that mitigation and control efforts to guard against potential transmission of bTB should include the season and time of day during which deer visitation occurs. Furthermore, specific livestock management practices may contribute to farm visitation by deer. Deer visiting multiple farms may contribute to local area spread of bTB. Focusing risk mitigation efforts on individual deer that aremost likely to visit farms may reduce potential bTB transmission.