Search

Utah prairie dogs (Cynomys parvidens) are federally threatened due to eradication campaigns, habitat destruction, and outbreaks of plague. Today, Utah prairie dogs exist in small, isolated populations, making them less demographically stable and more susceptible to erosion of genetic variation by genetic drift. We characterized patterns of genetic structure at neutral and putatively adaptive loci in order to evaluate the relative effects of genetic drift and local adaptation on population divergence. We sampled individuals across the Utah prairie dog species range and generated 2955 single nucleotide polymorphisms using double digest restriction site‐associated DNA sequencing. Genetic diversity was lower in low‐elevation sites compared to high‐elevation sites. Population divergence was high among sites and followed an isolation‐by‐distance model. Our results indicate that genetic drift plays a substantial role in the population divergence of the Utah prairie dog, and colonies would likely benefit from translocation of individuals between recovery units, which are characterized by distinct elevations, despite the detection of environmental associations with outlier loci. By understanding the processes that shape genetic structure, better informed decisions can be made with respect to the management of threatened species to ensure that adaptation is not stymied. [ABSTRACT FROM AUTHOR]

Plague is a lethal zoonotic disease associated with rodents worldwide. In the western United States, plague outbreaks can decimate prairie dog (Cynomys spp.) colonies. However, it is unclear where the causative agent, Yersinia pestis, of this flea-borne disease is maintained between outbreaks, and what triggers plague-induced prairie dog die-offs. Less susceptible rodent hosts, such as mice, could serve to maintain the bacterium, transport infectious fleas across a colony, or introduce the pathogen to other colonies, possibly facilitating an outbreak. Here, we assess the potential role of two short-lived rodent species, North American deer mice (Peromyscus maniculatus) and Northern grasshopper mice (Onychomys leucogaster) in plague dynamics on prairie dog colonies. We live-trapped short-lived rodents and collected their fleas on black-tailed (Cynomys ludovicianus, Montana and South Dakota), white-tailed (Cynomys leucurus, Utah and Wyoming), and Utah prairie dog colonies (Cynomys parvidens, Utah) annually, from 2013 to 2016. Plague outbreaks occurred on colonies of all three species. In all study areas, deer mouse abundance was high the year before plague-induced prairie dog die-offs, but mouse abundance per colony was not predictive of plague die-offs in prairie dogs. We did not detect Y. pestis DNA in mouse fleas during prairie dog die-offs, but in three cases we found it beforehand. On one white-tailed prairie dog colony, we detected Y. pestis positive fleas on one grasshopper mouse and several prairie dogs live-trapped 10 days later, months before visible declines and plague-confirmed mortality of prairie dogs. On one black-tailed prairie dog colony, we detected Y. pestis positive fleas on two deer mice 3 months before evidence of plague was detected in prairie dogs or their fleas and also well before a plague-induced die-off. These observations of plague positive fleas on mice could represent early spillover events of Y. pestis from prairie dogs or an unknown reservoir, or possible movement of infectious fleas by mice. [ABSTRACT FROM AUTHOR]