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首页> 外文期刊>Microbial drug resistance: MDR : Mechanisms, epidemiology, and disease >Prevalence and molecular characterization of fluoroquinolone resistance in escherichia coli isolates from dairy cattle with endometritis in China
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Prevalence and molecular characterization of fluoroquinolone resistance in escherichia coli isolates from dairy cattle with endometritis in China

机译:中国患有子宫内膜炎的奶牛大肠杆菌分离株对氟喹诺酮耐药的流行及其分子特征

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Fluoroquinolones are frequently used to treat infectious disease that is caused by Escherichia coli in dairy cattle. However, fluoroquinolone resistance occurs and is due either to chromosomal mutations in the bacterial topoisomerase genes and/or to plasmid-mediated resistance genes. The purpose of this study was to determine the prevalence and molecular characteristics of fluoroquinolone resistance determinants in E. coli strains (n=148) isolated from dairy cattle with bovine endometritis in Inner Mongolia (China). Analysis of the mutations in the quinolone resistance-determining regions of resistant E. coli isolates confirmed previously reported substitutions in the GyrA and ParE. However, we identified additional substitutions in the ParC and GyrB that have not been reported earlier. No plasmid-mediated quinolone resistance genes in any of the isolates were found. The number of point mutations found per isolate correlated with an increase in the minimum inhibitory concentration of ciprofloxacin. Overall, 45.5% of the isolates were positive for the class I integrase gene along with four gene cassettes that were responsible for resistance to trimethoprim (dfr1 and dfrA17) and aminoglycosides (aadA1 and aadA5), respectively. The prevalence of extended-spectrum β-lactamases (ESBLs) was 100%, and the blaTEM gene was predominant in all of the isolates. In conclusion, our results identify the mechanism of quinolone resistance for the first time and reveal the prevalence of integron and ESBLs in E. coli isolates from dairy cattle with bovine endometritis in China after 20 years of quinolone usage in cattle.
机译:氟喹诺酮类药物通常用于治疗奶牛大肠杆菌引起的传染病。但是,发生氟喹诺酮耐药性是由于细菌拓扑异构酶基因中的染色体突变和/或质粒介导的耐药基因引起的。这项研究的目的是确定从内蒙古(中国)奶牛子宫内膜炎分离的大肠杆菌(n = 148)菌株中氟喹诺酮耐药性决定因素的发生率和分子特征。对耐药大肠杆菌分离物的喹诺酮耐药性决定区域中的突变进行分析,证实了先前报道的GyrA和ParE中的取代。但是,我们在ParC和GyrB中发现了其他较早的替代报道。在任何分离物中均未发现质粒介导的喹诺酮抗性基因。每个分离株发现的点突变数量与环丙沙星的最低抑菌浓度增加相关。总体而言,有45.5%的分离物对I类整合酶基因呈阳性,另外还有四个基因盒分别对甲氧苄啶(dfr1和dfrA17)和氨基糖苷(aadA1和aadA5)产生抗性。广谱β-内酰胺酶(ESBLs)的患病率为100%,而blaTEM基因在所有分离株中均占主导。总之,我们的结果首次确定了喹诺酮耐药性的机制,并揭示了在牛中使用喹诺酮20年后,在患有牛子宫内膜炎的奶牛大肠杆菌分离物中,整合子和ESBLs的流行。

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