Tedim Ana P, Ruíz-Garbajosa Patricia, Rodríguez Maria Concepción, Rodríguez-Baños Mercedes, Lanza Val F, Derdoy Laura, Cárdenas Zurita Gonzalo, Loza Elena, Cantón Rafael, Baquero Fernando, Coque Teresa M
Microbiology Department, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain.
Unidad de Resistencia a Antibióticos y Virulencia Bacteriana asociada al Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain.
J Antimicrob Chemother. 2017 Jan;72(1):48-55. doi: 10.1093/jac/dkw366. Epub 2016 Sep 21.
To investigate the population structure of Enterococcus faecium causing bloodstream infections (BSIs) in a tertiary Spanish hospital with low glycopeptide resistance, and to enhance our knowledge of the dynamics of emergence and spread of high-risk clonal complexes.
All available E. faecium causing BSIs (n = 413) in our hospital (January 1995-May 2015) were analysed for antibiotic susceptibility (CLSI), putative virulence traits (PCR, esp, hyl) and clonal relationship (SmaI-PFGE, MLST evaluated by goeBURST and BAPS).
The increased incidence of BSIs caused by enterococci [2.3‰ of attended patients (inpatients and outpatients) in 1996 to 3.0‰ in 2014] significantly correlated with the increase in BSIs caused by E. faecium (0.33‰ of attended patients in 1996 to 1.3‰ in 2014). The BSIs Enterococcus faecalis:E. faecium ratio changed from 5:1 in 1996 to 1:1 in 2014. During the last decade an increase in E. faecium BSIs episodes in cancer patients (10.9% in 1995-2005 and 37.1% in 2006-15) was detected. Ampicillin-susceptible E. faecium (ASEfm; different STs/BAPS) and ampicillin-resistant E. faecium (AREfm; ST18/ST17-BAPS 3.3a) isolates were recovered throughout the study. Successive waves of BAPS 2.1a-AREfm (ST117, ST203 and ST80) partially replaced ASEfm and ST18-AREfm since 2006.
Different AREfm clones (belonging to BAPS 2.1a and BAPS 3.3a) consistently isolated during the last decade from BSIs might be explained by a continuous and dense colonization (favouring both invasion and cross-transmission) of hospitalized patients. High-density colonization by these clones is probably enhanced in elderly patients by heavy and prolonged antibiotic exposure, particularly in oncological patients.
在一家糖肽耐药率较低的西班牙三级医院中，调查引起血流感染（BSIs）的粪肠球菌的种群结构，并增进我们对高危克隆复合体出现和传播动态的了解。
对我院（1995年1月至2015年5月）所有引起BSIs的粪肠球菌（n = 413）进行抗生素敏感性分析（CLSI）、推定毒力特征分析（PCR、esp、hyl）和克隆关系分析（SmaI-PFGE、通过goeBURST和BAPS评估的多位点序列分型）。
肠球菌引起的BSIs发病率增加[1996年为就诊患者（住院患者和门诊患者）的2.3‰，2014年为3.0‰]与粪肠球菌引起的BSIs增加显著相关（1996年为就诊患者的0.33‰，2014年为1.3‰）。粪肠球菌血症中粪肠球菌与屎肠球菌的比例从1996年的5:1变为2014年的1:1。在过去十年中，检测到癌症患者中屎肠球菌BSIs发作增加（1995 - 2005年为10.9%，2006 - 15年为37.1%）。在整个研究过程中均分离出对氨苄西林敏感的粪肠球菌（ASEfm；不同的STs/BAPS）和对氨苄西林耐药的粪肠球菌（AREfm；ST18/ST17 - BAPS 3.3a）菌株。自2006年以来，连续几波BAPS 2.1a - AREfm（ST117、ST203和ST80）部分取代了ASEfm和ST18 - AREfm。
在过去十年中从BSIs中持续分离出的不同AREfm克隆（属于BAPS 2.1a和BAPS 3.3a）可能是由于住院患者的持续密集定植（有利于侵入和交叉传播）所致。老年患者中，尤其是肿瘤患者，因大量且长期使用抗生素，这些克隆的高密度定植可能会增强。
