Ergani-Ozcan Ayla, Naas Thierry, Baysan Betil Ozhak, Ogunc Dilara, Inan Dilara, Colak Dilek, Nordmann Patrice
Medical Microbiology Department, Akdeniz University School of Medicine, Antalya, Turkey.
J Antimicrob Chemother. 2008 May;61(5):1033-9. doi: 10.1093/jac/dkn066. Epub 2008 Mar 4.
Despite growing concern about vancomycin-resistant enterococci (VRE) as nosocomial pathogens, especially in the USA, they have been rarely isolated in Turkish hospitals. After initial description in 2001 of unrelated VRE isolates, we report now the molecular characterization of a nosocomial outbreak at the Akdeniz University Hospital, Antalya, Turkey.
VRE isolates were from either clinical or rectal swab specimens. Identification, susceptibility testing and molecular characterization were performed according to standard techniques. Virulence genes (encoding aggregation substance, gelatinase, cytolysin, enterococcal surface protein and hyaluronidase) were sought by PCR.
Thirty-six VRE were isolated from 10 patients between June and October 2005 in the Department of Paediatrics. Six patients were only carriers, two had urinary tract infections and two had bloodstream infections. All isolates were Enterococcus faecium, of vanA genotype and belonged either to a main pulsotype (A) or to three minor pulsotypes (B, C and D). The epidemic strain A, found in eight patients, expressed high-level glycopeptide resistance (MIC of vancomycin 256 mg/L and MIC of teicoplanin 64 mg/L) and was of multilocus sequence typing sequence type (ST) 31, whereas the minor strain D, found in two patients, expressed heterogeneous glycopeptide resistance (MIC of vancomycin 8 to 256 mg/L) and was ST18. Strains B and C were only found in single patients either with strain A or alone. The two epidemic strains A and D were esp gene-positive. Their vanA genes were located on transposons similar to Tn1546, except for deletion of the transposition genes and the presence of IS1542, inserted upstream of the vanA operon, and IS1216, inserted at the 3' end of the vanX gene. VRE outbreak was contained by early identification and implementation of measures for patient isolation and of stringent hand and environmental disinfection policies.
This work underlines the emergence in Turkey of epidemic VRE clones that belong to the clonal complex-17 (CC-17) and that are esp-positive.
尽管人们越来越关注耐万古霉素肠球菌（VRE）作为医院病原体的问题，尤其是在美国，但在土耳其医院中很少分离到这种病菌。在2001年首次描述了不相关的VRE分离株后，我们现在报告土耳其安塔利亚阿克德尼兹大学医院一次医院感染暴发的分子特征。
VRE分离株来自临床或直肠拭子标本。根据标准技术进行鉴定、药敏试验和分子特征分析。通过聚合酶链反应（PCR）寻找毒力基因（编码聚集物质、明胶酶、细胞溶素、肠球菌表面蛋白和透明质酸酶）。
2005年6月至10月期间，在儿科从10名患者中分离出36株VRE。6名患者只是携带者，2名患者有尿路感染，2名患者有血流感染。所有分离株均为粪肠球菌，属于vanA基因型，要么属于主要脉冲型（A），要么属于三种次要脉冲型（B、C和D）。在8名患者中发现的流行株A表现出高水平糖肽耐药性（万古霉素MIC为256mg/L，替考拉宁MIC为64mg/L），多位点序列分型序列类型（ST）为31，而在2名患者中发现的次要株D表现出异质性糖肽耐药性（万古霉素MIC为8至256mg/L），为ST18。株B和株C仅在与株A在一起或单独的单一患者中发现。两种流行株A和D的esp基因呈阳性。它们的vanA基因位于类似于Tn1546的转座子上，但转座基因缺失，并且在vanA操纵子上游插入了IS1542，在vanX基因的3'端插入了IS1216。通过早期识别并实施患者隔离措施以及严格的手部和环境消毒政策，控制了VRE暴发。
这项工作强调了土耳其出现了属于克隆复合体-17（CC-17）且esp呈阳性的流行VRE克隆。
