Emergence of Serratia marcescens, Klebsiella pneumoniae, and Escherichia coli isolates possessing the plasmid-mediated carbapenem-hydrolyzing β-lactamase KPC-2 in intensive care units of a Chinese hospital
Emergence of Serratia marcescens, Klebsiella pneumoniae, and Escherichia coli isolates possessing the plasmid-mediated carbapenem-hydrolyzing β-lactamase KPC-2 in intensive care units of a Chinese hospital
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DOI：
10.1128/aac.01539-07
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发表时间：
2008-06-01
影响因子：
4.9
通讯作者：
Chen, Gong-Xiang
中科院分区：
文献类型：
--
作者：
Cai, Jia Chang;Zhou, Hong Wei;Chen, Gong-Xiang
从我院重症监护室（ICU）中回收了21株粘质沙雷菌、10株肺炎克雷伯菌和1株具有碳青霉烯耐药或碳青霉烯敏感性降低的大肠埃希菌分离株。肠杆菌重复基因间共有序列PCR和脉冲场凝胶电泳结果表明，所有的S。marcescens菌株为克隆菌株，10 K. pneumoniae分离株之间没有区别或彼此密切相关。亚胺培南、美罗培南和厄他培南对所有分离株的MIC均为2 ~ 8 μ g/ml，但对K. pneumoniae K10（MIC为128、256和>256 μ g/ml）。等电聚焦、PCR和DNA测序结果表明，所有S. marcescens分离株产生KPC-2和pI为6.5的β-内酰胺酶。所有K。肺炎分离株产生TEM-1、KPC-2、CTX-M-14和pI为7.3的β-内酰胺酶。急诊大肠杆菌E1分离株产生KPC-2、CTX-M-15和pI为7.3的β-内酰胺酶。用E.大肠杆菌（EC 600）中仅检测到bla（KPC-2）基因的转移。大肠杆菌接合子。质粒酶切分析显示所有E.大肠杆菌接合子。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳和外膜蛋白ompK 35/36基因序列分析表明，K. pneumoniae K10不能表达OmpK 36，这是由于插入序列ISEcp 1的插入失活。以上结果表明，产KPC-2的S. marcescens，K. pneumoniae和E.我院ICU出现大肠埃希菌分离株。KPC-2与孔蛋白缺陷联合导致克雷伯氏菌对碳青霉烯类抗生素产生高水平的耐药性。肺炎。同一个bla（KPC-2）编码质粒在三个不同的属中传播。
Twenty-one Serratia marcescens, ten Klebsiella pneumoniae, and one Escherichia coli isolate with carbapenem resistance or reduced carbapenem susceptibility were recovered from intensive care units (ICUs) in our hospital. Enterobacterial repetitive intergenic consensus-PCR and pulsed-field gel electrophoresis demonstrated that all the S. marcescens isolates belonged to a clonal strain and the 10 K. pneumoniae isolates were indistinguishable or closely related to each other. The MICs of imipenem, meropenem, and ertapenem for all isolates were 2 to 8 mu g/ml, except for K. pneumoniae K10 (MICs of 128, 256, and >256 mu g/ml). Isoelectric focusing, PCRs, and DNA sequencing indicated that all S. marcescens isolates produced KPC-2 and a beta-lactamase with a pI of 6.5. All K. pneumoniae isolates produced TEM-1, KPC-2, CTX-M-14, and a beta-lactamase with a pI of 7.3. The E. coli E1 isolate produced KPC-2, CTX-M-15, and a beta-lactamase with a pI of 7.3. Conjugation studies with E. coli (EC600) resulted in the transfer of reduced carbapenem susceptibility compared to that of the original isolates, and only the bla(KPC-2) gene was detected in E. coli transconjugants. Plasmid restriction analysis showed identical restriction patterns among all E. coli transconjugants. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and ompK35/36 gene sequence analysis of outer membrane proteins revealed that K. pneumoniae K10 failed to express OmpK36, because of insertional inactivation by an insertion sequence ISEcp1. All these results indicate that KPC-2-producing S. marcescens, K. pneumoniae, and E. coli isolates emerged in ICUs in our hospital. KPC-2 combined with porin deficiency results in high-level carbapenem resistance in K. pneumoniae. The same bla(KPC-2)-encoding plasmid was spread among the three different genera.