A study of plasmid-mediated aac(6′)-Ib gene determination and quinolone resistance

doi:10.3969/j.issn.1673-8640.2013.03.007

Abstract

Abstract: Objective　To investigate the quinolone resistance to Escherichia coli isolates，and to identify the relationship of existence of plasmid-mediated aac (6′)-Ib genes with the resistance of quinolones. Methods　Kirby-Bauer(k-B) method was performed for 121 Escherichia coli isolates from urine samples collected from March 2010 to March 2011 in Renji Hospital. The aac (6′)-Ib genes in Escherichia coli isolates were determined by polymerase chain reaction(PCR). The amplification fragment of positive isolates were selected to be sequenced，and the genotypes were determined. Results　Escherichia coli isolates′ resistance rates of nalidixic acid，ciprofloxacin，norfloxacin and levofloxacin were all higher than 75%. The determination rate of aac(6′)-Ib gene was 14.0% (17/121)，and the mutation rate was 82.4%(14/17). The aac (6′)-Ib gene positive isolates had higher resistance rates of ampicillin-sulbactam，piperacillin-tazobactam，cefazolin，cefaclor，cefuroxime，amikacin，ciprofloxacin，norfloxacin and levofloxacin than the negative isolates. There was statistical significance(P<0.05). Conclusions　Quinolone resistance to Escherichia coli isolates in Renji Hospital is serious. With the plasmid-mediated aac (6′)-Ib genes，the Escherichia coli isolates may have an increasing resistance rates to quinolones and decreasing susceptibility to beta-lactamase inhibitors and cephalosporins antibiotics.

Key words: Plasmid-mediation, aac(6′)-Ib gene, Mutation isolate, Quinolone antibiotic, Resistance mechanism

ZHAO Qian，WANG Yaping，YING Chunmei，ZHENG Bing，ZHANG Haomin，YANG Jun. A study of plasmid-mediated aac(6′)-Ib gene determination and quinolone resistance[J]. , 2013, 28(3): 199-202.

References

[1]叶任高.临床肾脏病学[M].第2版.北京:人民卫生出版社，2007:339.
[2]Chenia HY，Pillay B，Pillay D. Analysis of the mechanisms of fluoroquinolone resistance in urinary tract pathogens[J].J Antimicrob Chemother，2006，58(6):1274-1278. 
[3]Ruiz J. Mechanisms of resistance to quinolones: target alterations，decreased accumulation and DNA gyrase protection[J]. J Antimicrob Chemother，2003，51(5):1109-1117.
[4]Sáenz Y，Ruiz J，Zarazaga M，et al. Effect of the efflux pump inhibitor Phe-Arg-beta-naphthylamide on the MIC values of the quinolones，tetracycline and chloramphenicol，in Escherichia coli isolates of different origin[J].J Antimicrob Chemother，2004，53(3):544-545.
[5]Park CH，Robicsek A，Jacoby GA，et al.Prevalence in the United States of aac(6′)-Ib-cr encoding a ciprofloxacin-modifying enzyme[J]. Antimicrob Agents Chemother，2006，50(11):3953-3955.
[6]肖时超，吕火祥，沈蓓琼，等.2003年至2007年大肠埃希菌的临床分离及耐药趋势分析[J]. 中国微生态学杂志，2008，20(4):407-409.
[7]Robicsek A，Sahm DF，Strahilevitz J，et al. Broader distribution of plasmid-mediated quinolone resistance in the United States[J]. Antimicrob Agents Chemother，2005，49(7):3001-3003.
[8]Morgan-Linnell SK，Becnel Boyd L，Steffen D，et al.Mechanisms accounting for fluoroquinolone resistance in Escherichia coli clinical isolates[J]. Antimicrob Agents Chemother，2009，53(1):235-241.
[9]朱东安，孙景勇，范惠清.一株福氏志贺菌中同时检出CTX-M-3型超广谱β-内酰胺酶和质粒介导的喹诺酮基因qnrS[J].检验医学，2009，24（7）:489-492.
[10]汪雅萍，应春妹，张灏旻，等.氟喹诺酮耐药志贺菌中质粒介导qnr基因的检测[J].检验医学，2011，26（10）：645-647.
[11]Robicsek A，Strahilevitz J，Jacoby GA，et al. Fluoroquinolone-modifying enzyme: a new adaptation of a common aminoglycoside acetyltransferase [J]. Nat Med，2006，12(1):83-88.