Department of Microbiology, Serres General Hospital, Serres, Greece.
J Clin Microbiol. 2013 Oct;51(10):3176-82. doi: 10.1128/JCM.01244-13. Epub 2013 Jul 12.
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.
尽管有大量研究记录了碳青霉烯类耐药肺炎克雷伯菌 (CRKP) 爆发的情况,这些菌株携带各种碳青霉烯酶,但有关携带超广谱β-内酰胺酶 (ESBLs) 和/或 AmpC 且孔蛋白受损的 CRKP 爆发的报告却很有限。在此,我们描述了一起由产 CTX-M-15 的厄他培南耐药克隆肺炎克雷伯菌菌株引起的爆发,该菌株表达 OmpK36 孔蛋白变体。2012 年 5 月至 11 月,希腊一家医院重症监护病房的 19 名住院患者中分离出 37 株表型上不产碳青霉烯酶的厄他培南耐药肺炎克雷伯菌。这些分离株对其他碳青霉烯类药物敏感或中介,对所有其他β-内酰胺类药物耐药,但对头孢替坦敏感。表型和分子分析显示,所有分离株均携带blaCTX-M-15 基因,位于可接合的 100kb 质粒上,ompK35 基因表达受阻,同时产生 Ompk36 孔蛋白变体。首例患者为从另一家医院转入的患者。入院时和每周进行主动监测,并定期对环境样本进行检测。分子分型显示,所有临床分离株以及 2 株厄他培南耐药环境肺炎克雷伯菌分离株均属于同一克隆类型,被归为多位点序列分型 (MLST) 序列型 101(ST101)。由于所有定植/感染患者在重叠期间住院,因此认为交叉感染是爆发菌株传播的主要途径。尽管加强了感染控制措施和主动监测,但疫情仍持续了大约 7 个月。入院时和每周筛查时发现隐匿性携带者对于早期识别和随后成功管理疫情非常有价值。