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Reevaluation of the Role of Blocked Oropsylla hirsuta Prairie Dog Fleas (Siphonaptera: Ceratophyllidae) in Yersinia pestis (Enterobacterales: Enterobacteriaceae) Transmission.

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Miarinjara A(1)(2), Eads DA(3), Bland DM(1), Matchett MR(4), Biggins DE(3), Hinnebusch BJ(1). Author information: (1)Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, NIH, Hamilton, MT, USA. (2)Department of Environmental Sciences, Emory University, Atlanta, GA, USA. (3)U.S. Geological Survey, Fort Collins Science Center, Fort Collins, CO, USA. (4)U.S. Fish and Wildlife Service, Lewistown, MT, USA. Prairie dogs in the western United States experience periodic epizootics of plague, caused by the flea-borne bacterial pathogen Yersinia pestis. An early study indicated that Oropsylla hirsuta (Baker), often the most abundant prairie dog flea vector of plague, seldom transmits Y. pestis by the classic blocked flea mechanism. More recently, an alternative early-phase mode of transmission has been proposed as the driving force behind prairie dog epizootics. In this study, using the same flea infection protocol used previously to evaluate early-phase transmission, we assessed the vector competence of O. hirsuta for both modes of transmission. Proventricular blockage was evident during the first two weeks after infection and transmission during this time was at least as efficient as early-phase transmission 2 d after infection. Thus, both modes of transmission likely contribute to plague epizootics in prairie dogs. Published by Oxford University Press on behalf of Entomological Society of America 2022. DOI: 10.1093/jme/tjac021 PMID: 35380675

Evaluation of a liquid carbaryl formulation to control burrow fleas following a die-off of black-tailed prairie dogs ( Cynomys ludovicianus) caused by plague ( Yersinia pestis) in Converse County, Wyoming

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Russell E Enscore  1 , Ying Bai  2 , Lynn M Osikowicz  2 , Christopher Sexton  2 , Daniel R O’Leary  3   4
Affiliations

Free article

No abstract available

References

    1. Bai, Y., V. Motin, R.E. Enscore, L. Osikowicz, M.R. Rizzo, A. Hojgaard, M. Kosoy, and R.J. Eisen. 2020. Pentaplex real-time PCR for differential detection of <italic>Yersinia pestis</italic> and Y. pseudotuberculosis and application for testing fleas collected during plague epizootics. MicrobiologyOpen, 11 pp., doi: 10.1002/mbo3.1105.
    1. Barnes, A.M., L.J. Ogden, and E.G. Campos. 1972. Control of the plague vector, <italic>Opisocrostis</italic> hirsutus, by treatment of prairie dog (<italic>Cynomys ludovicianus</italic>) burrows with 2% carbaryl dust. J. Med. Entomol. 9: 330–333.
    1. Barnes, A.M. 1982. Surveillance and control of bubonic plague in the United States. Symp. Zool. Soc. Lond. 50: 237–270.
    1. Biggins, D.E., J.L. Godbey, K.L. Gage, L.G. Carter, and J.A. Montenieri. 2010. Vector control improves survival of three species of prairie dogs (<italic>Cynomys</italic>) in areas considered enzootic for plague. Vector-Borne Zoonotic Dis. 10: 17–26.
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A novel mechanism of streptomycin resistance in Yersinia pestis: Mutation in the rpsL gene

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Abstract

Streptomycin is considered to be one of the effective antibiotics for the treatment of plague. In order to investigate the streptomycin resistance of Y. pestis in China, we evaluated strep- tomycin susceptibility of 536 Y. pestis strains in China in vitro using the minimal inhibitory concentration (MIC) and screened streptomycin resistance-associated genes (strA and strB) by PCR method. A clinical Y. pestis isolate (S19960127) exhibited high-level resis- tance to streptomycin (the MIC was 4,096 mg/L). The strain (biovar antiqua) was isolated from a pneumonic plague outbreak in 1996 in Tibet Autonomous Region, China, belonging to the Marmota himalayana Qinghai–Tibet Plateau plague focus. In contrast to previously reported streptomycin resistance mediated by conjugative plasmids, the genome sequenc- ing and allelic replacement experiments demonstrated that an rpsL gene (ribosomal protein S12) mutation with substitution of amino-acid 43 (K43R) was responsible for the high-level resistance to streptomycin in strain S19960127, which is consistent with the mutation reported in some streptomycin-resistant Mycobacterium tuberculosis strains. Streptomycin is used as the first-line treatment against plague in many countries. The emergence of strep- tomycin resistance in Y. pestis represents a critical public health problem. So streptomycin susceptibility monitoring of Y. pestis isolates should not only include plasmid-mediated resistance but also include the ribosomal protein S12 gene (rpsL) mutation, especially when treatment failure is suspected due to antibiotic resistance.

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