Prevalence of fluoroquinolone resistance and mutations in the gyrA, parC and parE genes of Riemerella anatipestifer isolated from ducks in China

Author:

Zhu Dekang,Zheng Mingyu,Xu Jinge,Wang Mingshu,Jia Renyong,Chen Shun,Liu Mafeng,Zhao Xinxin,Yang Qiao,Wu Ying,Zhang Shaqiu,Huang Juan,Liu Yunya,Zhang Ling,Yu Yanling,Pan Leichang,Chen Xiaoyue,Cheng AnchunORCID

Abstract

Abstract Background Riemerella anatipestifer is one of the most serious infectious disease-causing pathogens in the duck industry. Drug administration is an important method for prevention and treatment of infection in duck production, leading to widespread drug resistance in R. anatipestifer. Methods For a total of 162 isolates of R. anatipestifer, the MICs were determined for a quinolone antimicrobial agent, namely, nalidixic acid, and three fluoroquinolones, namely, ciprofloxacin, enrofloxacin and ofloxacin. The gyrA, parC, and parE gene fragments were amplified by PCR to identify the mutation sites in these strains. Site-directed mutants with mutations that were detected at a high frequency in vivo were constructed (hereafter referred to as site-directed in vivo mutants), and the MICs of these four drugs for these strains were determined. Results In total, 100, 97.8, 99.3 and 97.8% of the 137 R. anatipestifer strains isolated between 2013 and 2018 showed resistance to nalidixic acid, ciprofloxacin, enrofloxacin, and ofloxacin, respectively. The high-frequency mutation sites were detected in a total of 162 R. anatipestifer strains, such as Ser83Ile and Ser83Arg, which are two types of substitution mutations of amino acid 83 in GyrA; Val799Ala and Ile811Val in ParC; and Val357Ile, His358Tyr, and Arg541Lys in ParE. MIC analysis results for the site-directed in vivo mutants showed that the strains with only the Ser83Ile mutation in GyrA exhibited an 8–16-fold increase in MIC values, and all mutants showed resistance to ampicillin and ceftiofur. Conclusions The resistance of R. anatipestifer to quinolone agents is a serious problem. Amino acid 83 in GyrA is the major target mutation site for the fluoroquinolone resistance mechanism of R. anatipestifer.

Funder

National Key Research and Development Program of China

China Agricultural Research System

Sichuan Veterinary Medicine and Drug Innovation Group of China Agricultural Research System

International S&T Cooperation Program of Sichuan Province

Science and Technology Innovation Program of Guizhou Academy of Agricultural Science

Publisher

Springer Science and Business Media LLC

Subject

Microbiology (medical),Microbiology

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