首页> 外文期刊>Microbial drug resistance: MDR : Mechanisms, epidemiology, and disease >Characterization of KPC-2-Producing Escherichia coli, Citrobacter freundii, Enterobacter cloacae, Enterobacter aerogenes, and Klebsiella oxytoca Isolates from a Chinese hospital
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Characterization of KPC-2-Producing Escherichia coli, Citrobacter freundii, Enterobacter cloacae, Enterobacter aerogenes, and Klebsiella oxytoca Isolates from a Chinese hospital

机译:一家中国医院生产KPC-2的大肠杆菌,弗氏柠檬酸杆菌,阴沟肠杆菌,产气肠杆菌和产氧克雷伯菌的鉴定

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Twelve nonduplicated KPC-2-producing enterobacterial isolates, including three Escherichia coli, two Citrobacter freundii, two Enterobacter cloacae, four Enterobacter aerogenes, and one Klebsiella oxytoca, were collected from various clinical samples within 18 months (March 2011 to September 2012). Two of the 12 patients died from infections caused by KPC-2-producing pathogens, while the rest of the patients with KPC-2-producing pathogens improved or were cured. The majority of the clinical isolates exhibited a high-level of resistance to oxyimino-cephalosporins and carbapenems, and possessed self-transferable blaKPC-2-carrying plasmids with sizes ranging from 20 to 120?kb. Most isolates carried blaCTX-M and plasmid-mediated quinolone resistance genes, while some isolates produced 16S rRNA methylases (ArmA or RmtB). The genetic environment of blaKPC-2 of most clinical strains was consistent with the genetic structure surrounding blaKPC-2 on the plasmid pKP048, which contains an integration structure of a Tn3-based transposon and partial Tn4401 segment. Inserted fragments (truncated bla TEM) were detected upstream of the blaKPC-2 gene for two E. aerogenes strains. In conclusion, the enterobacterial isolates exhibited sporadic emergence and did not arise by clonal spread at our hospital. The outcome of infections caused by KPC-producing enterobacterial isolates and their mortality were closely associated with the baseline condition of patients. The spread of blaKPC-2 gene between different enterobacterial species in China was mainly mediated by horizontal transfer of the Tn3-based transposons and not the blaKPC-2-carrying plasmids.
机译:在18个月内(2011年3月至2012年9月)从各种临床样本中收集了十二种无重复KPC-2产肠细菌,包括三株大肠杆菌,两株弗氏柠檬酸杆菌,两株阴沟肠杆菌,四株产气肠杆菌和一株产酸克雷伯菌。 12名患者中有2名死于由KPC-2产生病原体引起的感染,而其余的KPC-2产生病原体患者则有所改善或已治愈。大多数临床分离株表现出对氧亚氨基头孢菌素和碳青霉烯类的高水平抗性,并具有大小为20至120?kb的自转移性blaKPC-2携带质粒。大多数分离株带有blaCTX-M和质粒介导的喹诺酮抗性基因,而一些分离株则产生16S rRNA甲基化酶(ArmA或RmtB)。大多数临床菌株的blaKPC-2的遗传环境与质粒pKP048上blaKPC-2周围的遗传结构一致,该质粒包含基于Tn3的转座子和部分Tn4401区段的整合结构。在两个Kererogenes菌株的blaKPC-2基因上游检测到插入的片段(截短的bla TEM)。总之,肠杆菌分离株表现出零星的出现,而不是由于我们医院的克隆传播而出现的。由生产KPC的肠杆菌分离株引起的感染的结果及其死亡率与患者的基线状况密切相关。 blaKPC-2基因在中国不同肠道细菌之间的传播主要是通过基于Tn3的转座子的水平转移而不是携带blaKPC-2的质粒介导的。

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