Molecular epidemiology of a fatal sarcoptic mange epidemic in endangered San Joaquin kit foxes (Vulpes macrotis mutica)

Jaime L Rudd,Joshua M Hull,Deana L Clifford,Janet E Foley,Brian L Cypher,A Jane Riner

doi:10.1186/s13071-020-04328-3

Abstract

BackgroundIn 2013, sarcoptic mange, caused by Sarcoptes scabiei mites, precipitated a catastrophic decline of the formerly stable urban population of endangered San Joaquin kit foxes (Vulpes macrotis mutica) in Bakersfield, California, USA. In 2019, a smaller sarcoptic mange outbreak affected kit foxes 58 km southwest of Bakersfield in the town of Taft, California. To determine whether the Taft outbreak could have occurred as spillover from the Bakersfield outbreak and whether epidemic control efforts must involve not only kit foxes but also sympatric dogs (Canis lupus familiaris), coyotes (Canis latrans), and red foxes (Vulpes vulpes), we evaluated genotypes and gene flow among mites collected from each host species.MethodsWe used 10 Sarcoptes microsatellite markers (SARM) to perform molecular typing of 445 S. scabiei mites collected from skin scrapings from twenty-two infested kit foxes, two dogs, five coyotes, and five red foxes from Bakersfield, Taft, and other nearby cities.ResultsWe identified 60 alleles across all SARM loci; kit fox- and red fox-derived mites were relatively monomorphic, while genetic variability was greatest in Bakersfield coyote- and dog-derived mites. AMOVA analysis documented distinct mite populations unique to hosts, with an overall FST of 0.467. The lowest FST (i.e. closest genetic relationship, FST = 0.038) was between Bakersfield and Taft kit fox-derived mites while the largest genetic difference was between Ventura coyote- and Taft kit fox-derived mites (FST = 0.843).ConclusionsThese results confirm the close relationship between the Taft and Bakersfield outbreaks. Although a spillover event likely initiated the kit fox mange outbreak, mite transmission is now primarily kit fox-to-kit fox. Therefore, any large-scale population level intervention should focus on treating kit foxes within the city.

Highlights

In 2013, sarcoptic mange, caused by Sarcoptes scabiei mites, precipitated a catastrophic decline of the formerly stable urban population of endangered San Joaquin kit foxes (Vulpes macrotis mutica) in Bakersfield, California, USA
Collection of Sarcoptes scabiei mites Sampling was opportunistic, consisting of male and female animals aged 4 months and older, and that were found dead, euthanized for humane reasons, or euthanized because of threats to public safety or domestic animals. These included foxes found dead or euthanized due to mange provided by the Endangered Species Recovery Program (ESRP) and the California Department of Fish and Wildlife (CDFW), ill stray dogs from Kern County Animal Services and Bakersfield Animal Care Center, and coyotes found dead due to vehicular strike, euthanized due to severe mange (Ventura), hit by vehicles, or euthanized for depredation by the United States Department of Agriculture Wildlife Services (USDA, Fig. 1)
Bakersfield mites from kit and red foxes, and mites from Taft kit foxes, had relatively few alleles and low heterozygosity compared to dogs and coyotes, comprising an obvious cluster differentiated from other host species regardless of geographical area

Summary

Introduction

In 2013, sarcoptic mange, caused by Sarcoptes scabiei mites, precipitated a catastrophic decline of the formerly stable urban population of endangered San Joaquin kit foxes (Vulpes macrotis mutica) in Bakersfield, California, USA. In 2019, a smaller sarcoptic mange outbreak affected kit foxes 58 km southwest of Bakersfield in the town of Taft, California. To determine whether the Taft outbreak could have occurred as spillover from the Bakersfield outbreak and whether epidemic control efforts must involve kit foxes and sympatric dogs (Canis lupus familiaris), coyotes (Canis latrans), and red foxes (Vulpes vulpes), we evaluated genotypes and gene flow among mites collected from each host species. Sarcoptes scabiei appears to be a single but highly variable mite species with many host-restricted genetic variants [7,8,9,10,11,12,13]. Documentation of the host specificity of each variant can help determine the host that served as the original source of the epidemic, how many species are involved, and how best to intercede

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Conclusion