喹诺酮耐药性大肠埃希菌临床分离株中parC基因突变的检测
Detection of mutations in parC in quinolone-resistant clinical isolates of Escherichia coli.
作者信息
Vila J, Ruiz J, Goñi P, De Anta M T
机构信息
Department of Microbiology, University of Barcelona, Spain.
出版信息
Antimicrob Agents Chemother. 1996 Feb;40(2):491-3. doi: 10.1128/AAC.40.2.491.
Abstract
The gene parC encodes the A subunit of topoisomerase IV of Escherichia coli. Mutations in the parC region analogous to those in the quinolone resistance-determining region of gyrA were investigated in 27 clinical isolates of E. coli for which ciprofloxacin MICs were 0.0007 to 128 micrograms/ml. Of 15 isolates for which ciprofloxacin MICs were > or = 1 microgram/ml, 8 showed a change in the serine residue at position 80 (Ser-80), 4 showed a change in Glu-84, and 3 showed changes in both amino acids. No mutations were detected in 12 clinical isolates for which ciprofloxacin MICs were < or = 0.25 micrograms/ml. These findings suggest that ParC from E. coli may be another target for quinolones and that mutations at residues Ser-80 and Glu-84 may contribute to decreased fluoroquinolone susceptibility.
摘要
基因parC编码大肠杆菌拓扑异构酶IV的A亚基。在环丙沙星MIC为0.0007至128微克/毫升的27株临床分离大肠杆菌中，研究了parC区域与gyrA喹诺酮耐药决定区域类似的突变。在环丙沙星MIC≥1微克/毫升的15株分离株中，8株在第80位丝氨酸残基（Ser-80）处有变化，4株在Glu-84处有变化，3株在这两个氨基酸处均有变化。在环丙沙星MIC≤0.25微克/毫升的12株临床分离株中未检测到突变。这些发现表明，大肠杆菌的ParC可能是喹诺酮类药物的另一个靶点，并且Ser-80和Glu-84残基处的突变可能导致氟喹诺酮敏感性降低。
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