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Plague is a flea‐vectored disease introduced to North America c. 1900. It is lethal to many American mammal species, causes major die‐offs (epizootics) in some populations, and may be ecologically disruptive even at lower interepizootic (enzootic) levels of transmission. We sought to determine the effects of enzootic plague on survival of Mexican woodrats (Neotoma mexicana) and to test the hypothesis that the causative bacterium Yersinia pestis can be maintained by a highly plague‐susceptible species like these woodrats. We compared apparent survival for woodrats in groups with and without plague management. Woodrat groups were (1) treated for vector control with an insecticide (deltamethrin), (2) vaccinated against plague, (3) treated with both vaccine and vector control, and (4) without plague management treatments. Flea prevalence on woodrats was reduced >90% in response to deltamethrin. Apparent survival during May–September, 2010, was 31.1% for non‐vaccinated adult woodrats living in deltamethrin‐treated nests, compared to 9.6% for woodrats in non‐treated nests. During May–September of 2010 and 2011, vaccinated juvenile woodrat survival was 16.8%, compared to 8.4% for non‐vaccinated juveniles. Peak numbers of woodrats captured were 139 for the first trapping session of 2010 and 76 for the first session of 2011, suggesting a population decline consistent with the relatively low estimated survival rates. Survival results suggest that this highly plague‐susceptible species can locally maintain enzootic plague while encountering substantial rates of mortality. [ABSTRACT FROM AUTHOR]

Plague, a disease caused by Yersinia pestis introduced into North America about 100 years ago, is devastating to prairie dogs and the highly endangered black-footed ferret. Current attempts to control plague in these species have historically relied on insecticidal dusting of prairie dog burrows to kill the fleas that spread the disease. Although successful in curtailing outbreaks in most instances, this method of plague control has significant limitations. Alternative approaches to plague management are being tested, including vaccination. Currently, all black-footed ferret kits released for reintroduction are vaccinated against plague with an injectable protein vaccine, and even wild-born kits are captured and vaccinated at some locations. In addition, a novel, virally vectored, oral vaccine to prevent plague in wild prairie dogs has been developed and will soon be tested as an alternative, preemptive management tool. If demonstrated to be successful, oral vaccination of selected prairie dog populations could decrease the occurrence of plague epizootics in key locations, thereby reducing the source of bacteria while avoiding the indiscriminate environmental effects of dusting. Just as rabies in wild carnivores has largely been controlled through an active surveillance and oral vaccination program, we believe an integrated plague management strategy would be similarly enhanced with the addition of a cost-effective, bait-delivered, sylvatic plague vaccine for prairie dogs. Control of plague in prairie dogs, and potentially other rodents, would significantly advance prairie dog conservation and black-footed ferret recovery. [ABSTRACT FROM AUTHOR]

• Simulating realistic social networks is important for modeling diseases transmitted by direct contact between individuals • Uncertainties in the mechanisms of plague transmission in fleas contributes substantially to variation in model outcomes • In our simulations, initiation of plague infections in fleas versus hosts resulted in different disease dynamics • Our results elucidate the complexity of the flea-plague-prairie dog system and reiterate the importance of research on Yersinia pestis transmission mechanisms to provide a full understanding of this disease. The development of models to elucidate the transmission pathways and dynamics of wildlife diseases remains challenging. Sylvatic plague, caused by the bacterium Yersinia pestis (Yp), is an infectious zoonotic disease that primarily affects wild rodents, including prairie dogs (Cynomys spp.) in North America. Proposed transmission pathways for Yp include flea bites, direct contacts between hosts, and environmental reservoirs (e.g. soil, carcasses). We developed a spatially explicit, agent-based model of Yp transmission to explore the effects of alternative transmission pathways, different disease initiation mechanisms (host or fleas), parameter uncertainty, and spatial structure of hosts. A particularly novel aspect of our model was the integration of ecological models with traditional disease models. Specifically, we used estimates from spatial capture-recapture models to generate data-driven spatial distributions, densities, and contact rates to capture the spatial structure of prairie dogs. We simulated ~9 million scenarios across a wide range of parameter values and conducted sensitivity analyses to determine the most influential parameters on the number of flea-days (sum of the mean number of fleas on hosts each day of the simulation), number of newly infected hosts per day, the time to depopulation (<20 prairie dogs remaining), and the proportion of the prairie dog population remaining at the end of the simulation (after 150 days). When including spatial structure, we found the probability of transmission via environmental sources of Yp (i.e. carcasses) had the greatest influence on model results when Yp infection was initiated in prairie dog hosts, rather than in fleas. Conversely, the mechanism of transmission by fleas to prairie dogs had the greatest influence on model results when Yp infection was initiated in fleas (i.e. via introduction by carnivores, a migrant prairie dog, or other mammalian host). Uncertainty in parameter estimates, particularly those related to the transmission pathways of Yp, continue to hamper efforts to realistically model plague dynamics in wild rodents. Our results elucidate the complexity of the flea-plague-prairie dog system and reiterate the importance of research on Yp transmission mechanisms to provide a full understanding of this disease. Our results also emphasize the importance of realistic estimates of spatial structure for exploring transmission dynamics of wildlife diseases and provide a framework for generating a data-driven description of spatial structure. [ABSTRACT FROM AUTHOR]