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首页> 外文期刊>Journal of Clinical Microbiology >Outbreak Caused by an Ertapenem-Resistant, CTX-M-15-Producing Klebsiella pneumoniae Sequence Type 101 Clone Carrying an OmpK36 Porin Variant
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Outbreak Caused by an Ertapenem-Resistant, CTX-M-15-Producing Klebsiella pneumoniae Sequence Type 101 Clone Carrying an OmpK36 Porin Variant

机译:由抗Ertapenem,生产CTX-M-15的肺炎克雷伯氏菌序列类型101克隆携带OmpK36孔蛋白变体引起的暴发

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Although numerous studies have documented outbreaks of carbapenem-resistant Klebsiella pneumoniae (CRKP) possessing various carbapenemases, reports on outbreaks due to CRKP possessing extended-spectrum β-lactamases (ESBLs) and/or AmpCs with porin lesions have been limited. Here, we describe an outbreak caused by an ertapenem-resistant, CTX-M-15-producing clonal K. pneumoniae strain expressing an OmpK36 porin variant. From May 2012 to November 2012, 37 ertapenem-resistant K. pneumoniae isolates phenotypically negative for carbapenemase production were recovered from 19 patients hospitalized in the intensive care unit of a Greek hospital. The isolates were either susceptible or intermediate to other carbapenems and resistant to all remaining β-lactams but cefotetan. Phenotypic and molecular analysis revealed the presence in all isolates of the blaCTX-M-15 gene on a conjugative 100-kb plasmid, disruption in the expression of the ompK35 gene, and the production of an Ompk36 porin variant. The index case was a patient admitted from another hospital. Active surveillance upon admission and on a weekly basis was immediately initiated; environmental samples were also periodically tested. Molecular typing showed that all clinical isolates as well as two ertapenem-resistant environmental K. pneumoniae isolates belonged to the same clonal type and were assigned to multilocus sequence typing (MLST) sequence type 101 (ST101). As all colonized/infected patients were hospitalized during overlapping periods, cross-infection was considered the main route for the dissemination of the outbreak strain. Despite reinforcement of infection control measures and active surveillance, the outbreak lasted approximately 7 months. Identification of hidden carriers upon admission and by screening on a weekly basis was found valuable for early recognition and subsequent successful management of the outbreak.
机译:尽管许多研究已经证明具有多种碳青霉烯酶的耐碳青霉烯的肺炎克雷伯菌肺炎(CRKP)的暴发,但由于CRKP具有广谱β-内酰胺酶(ESBLs)和/或带有孔蛋白病变的AmpC引起的暴发的报道仍然有限。在这里,我们描述了由表达OmpK36孔蛋白变异体的抗埃他培南,产生CTX-M-15的克隆性肺炎克雷伯菌引起的暴发。从2012年5月至2012年11月,从希腊一家医院的重症监护病房住院的19名患者中回收了37种表型对碳青霉烯酶产生阴性的抗ertapenem肺炎克雷伯菌。分离株对其他碳青霉烯敏感或对其他碳青霉烯敏感,并且对除头孢替坦以外的所有其余β-内酰胺类耐药。表型和分子分析表明,在结合的100kb质粒上,所有 bla CTX-M-15 基因的分离株均存在,从而破坏了的表达。 ompK35 基因和Ompk36孔蛋白变异体的产生。索引病例是另一家医院收治的患者。入院时每周一次进行主动监测;还定期测试环境样品。分子分型显示,所有临床分离株以及两种耐厄他培南的环境肺炎克雷伯菌分离株均属于同一克隆类型,并被分配为多基因座序列分型(MLST)序列类型101(ST101)。由于所有定植/感染的患者都在重叠期间住院,因此交叉感染被认为是传播暴发菌株的主要途径。尽管加强了感染控制措施和积极监测,但疫情仍持续了大约7个月。发现隐藏的携带者在入院时和每周进行筛查的发现对于早期识别和随后成功控制暴发非常有价值。

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