Molecular characterization of cefoxitin-resistant Escherichia coli from Canadian hospitals
Molecular characterization of cefoxitin-resistant Escherichia coli from Canadian hospitals
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DOI：
10.1128/aac.49.1.358-365.2005
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发表时间：
2005-01-01
影响因子：
4.9
通讯作者：
Paton, S
中科院分区：
文献类型：
--
作者：
Mulvey, MR;Bryce, E;Paton, S
描述了一项旨在获得加拿大对头孢西丁耐药的大肠杆菌菌株的基线信息的研究。作为超广谱β-内酰胺酶监测计划的一部分，在12个参与的医院地点共筛选了29,323株大肠杆菌。在截至2000年9月30日的一年时间里，共有411株对NCCLS推荐的β-内酰胺类药物敏感性降低的临床显著、非重复分离株被提交到中心实验室。经鉴定，232株细菌对头孢西丁耐药。用脉冲场凝胶电泳法对所有头孢西丁耐药菌株进行分型，其中182株有独特的指纹图谱，1株无法分型。对AmpC基因启动子区域进行了PCR和序列分析，发现51个不同的启动子或衰减型变异体和14个野生型启动子。3个启动子区域被插入元件打断，2个含有IS10元件，1个含有IS911变异体。通过获得ACT-1/MIR-1、CMY-2或Fox序列分析检测获得性AmpC酶耐药性，发现25株菌株含有CMY-2，其中7株含有野生型启动子。菌株指纹和启动子区域的相当大的遗传变异性表明，AmpC耐药可能是通过敏感菌株的突变而不是通过菌株或质粒在医院的传播而自发出现的。
A study designed to gain baseline information on strains of Escherichia coli displaying resistance to cefoxitin in Canada is described. A total of 29,323 E. coli isolates were screened at 12 participating hospital sites as part of an extended-spectrum beta-lactamase surveillance initiative. A total of 411 clinically significant, nonrepeat isolates displaying reduced susceptibilities to the NCCLS-recommended beta-lactams were submitted to a central laboratory over a 1-year period ending on 30 September 2000. Two hundred thirty-two isolates were identified as resistant to cefoxitin. All cefoxitin-resistant strains were subtyped by pulsed-field gel electrophoresis, and of these, 182 strains revealed a unique fingerprint and 1 strain was untypeable. PCR and sequence analysis of the ampC promoter region revealed 51 different promoter or attenuator variants and 14 wild-type promoters. Three promoter regions were interrupted by insertion elements, two contained IS10 elements, and one contained an IS911 variant. PCR and sequence analysis for the detection of acquired AmpC resistance (by the acquisition of ACT-1/MIR-1, CMY-2, or FOX) revealed that 25 strains contained CMY-2, including 7 of the strains found to have wild-type promoters. The considerable genetic variability in both the strain fingerprint and the promoter region suggests that AmpC-type resistance may emerge spontaneously by mutation of sensitive strains rather than by the spread of strains or plasmids in the hospital setting.