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Resistance and Virulence Mechanisms of Escherichia coli Selected by Enrofloxacin in Chicken

文献类型： 外文期刊

作者： Li, Jun 1 ; Hao, Haihong 1 ; Dai, Menghong 3 ; Zhang, Heying 1 ; Ning, Jianan 1 ; Cheng, Guyue 3 ; Shabbir, Muhammad A 1 ;

作者机构： 1.Natl Reference Lab Vet Drug Residues HZAU, Wuhan, Hubei, Peoples R China

2.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing, Jiangsu, Peoples R China

3.Minist Agr, Lab Qual & Safety Risk Assessment Livestock & Pou, Wuhan, Hubei, Peoples R China

4.Huazhong Agr Univ, Hubei Collaborat Innovat Ctr Anim Nutr & Feed Saf, Wuhan, Hubei, Peoples R China

5.Abdul Wali Khan Univ Mardan, Coll Vet Sci & Anim Husb, Mardan, KP, Pakistan

关键词： Escherichia coli; fluoroquinolones; multidrug resistance; resistance mechanisms

期刊名称：ANTIMICROBIAL AGENTS AND CHEMOTHERAPY （ 影响因子：5.191； 五年影响因子：5.346 ）

ISSN： 0066-4804

年卷期： 2019 年 63 卷 5 期

页码：

收录情况： SCI

摘要： This study aimed to investigate the genetic characteristics, antibiotic resistance patterns, and novel mechanisms involved in fluoroquinolone (FQ) resistance in commensal Escherichia coli isolates. The E. coli isolates were recovered from a previous clinical study and subjected to antimicrobial susceptibility testing and molecular typing. Known mechanisms of FQ resistance (target site mutations, plasmid-mediated quinolone resistance [PMQR] genes, relative expression levels of efflux pumps and porins) were detected using DNA sequencing of PCR products and real-time quantitative PCR. Whole-genome shotgun sequencing was performed on 11 representative strains to screen for single nucleotide polymorphisms (SNPs). The function of a key SNP (A1541G) was investigated by site-directed mutagenesis and allelic exchange. The results showed that long-term enrofloxacin treatment selected multidrug-resistant (MDR) E. coli isolates in the chicken gut and that these E. coli isolates had diverse genetic backgrounds. Multiple genetic alterations, including double mutations on GyrA (S83L and D87N), a single mutation on ParC (S80I) and ParE (S458E), activation of efflux pumps, and the presence of the QnrS1 protein, contributed to the high-level FQ resistance (enrofloxacin MIC [MICENR] >= 128 mu g/ml), while the relatively low-level FQ resistance (MICENR = 8 or 16 mu g/ml) was commonly mediated by decreased expression of the porin OmpF, besides enhancement of the efflux pumps. No significant relationship was observed between resistance mechanisms and virulence genes. Introduction of the A1541G mutation on aegA was able to increase FQ susceptibility by 2-fold. This study contributes to a better understanding of the development of MDR and the differences underlying the mechanisms of high-level and low-level FQ resistance in E. coli.

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