屎肠球菌高耐庆大霉素转座子Tn5281的检测

目的　研究高耐庆大霉素 (HLGR)屎肠球菌耐药性与转座子的关系。方法　用聚合酶链反应 (PCR)检测 48株HLGR屎肠球菌Tn5 2 81转座子 ,扩增产物用斑点杂交和测序法验证。结果　 48株HLGR屎肠球菌中 ,13株含有完整的Tn5 2 81,2 6株含有缺少右侧插入序列IS2 5 6的Tn5 2 81缺失型 ,9株不含Tn5 2 81,总阳性率为 81. 3 %。结论　Tn5 2 81在屎肠球菌高耐庆大霉素中起着重要作用。     

氨基苷类高水平耐药肠球菌的耐药性及修饰酶基因分布

目的明确临床分离的氨基苷类高水平耐药肠球菌（HLAR）耐药性及修饰酶基因类型。方法用琼脂筛选法筛选出HLAR、庆大霉素高水平耐药肠球菌（HLGR）及链霉素高水平耐药肠球菌（HLSR）；采用K—B法测定粪肠球菌及屎肠球菌对12种抗菌药物的耐药性；PCR及序列分析法检测7种氨基苷类修饰酶基因。结果肠球菌中HLAR为73．6％。利奈唑胺、万古霉素和替考拉宁对HLAR的抗菌作用最好，未检出耐药株。屎肠球菌中B内酰胺类抗生素耐药株以及喹诺酮类药物耐药株明显高于粪肠球菌。所有的屎肠球菌氨基苷类高耐株对氨苄西林、氨苄西林-舒巴坦及环丙沙星均耐药。aac（6′）-Ie-aph（2″）-Ia基因是HLGR的主要耐药基因，占HLGR的92．6％；3株HLGR存在与aph（2″）-Id高同源性的基因。而6′-ant、3″-ant及str基因在HLSR中的检出率低。结论HLAR已成为医院感染的重要耐药菌。HLGR主要通过aac（6′）-Ie-aph（2″）-Ia基因编码的修饰酶造成对庆大霉素高度耐药。     

粪肠球菌和屎肠球菌的临床分布及耐药监测研究

目的 研究临床感染患者中粪肠球菌和屎肠球菌的临床分布、对抗菌药物的敏感性以及耐药情况。方法北京积水潭医院2014年1月至2015年12月临床送检的感染标本,分离粪肠球菌和屎肠球菌进行鉴定和药敏分析。结果 分离出粪肠球菌184株,屎肠球菌109株。粪肠球菌药物敏感性从高到低依次为万古霉素、替考拉宁、氨苄西林、呋喃妥因、利奈唑胺、高浓度庆大霉素。屎肠球菌药物敏感性从高到低依次为替考拉宁、利奈唑胺、万古霉素、四环素、高浓度庆大霉素。检测出耐高浓度庆大霉素(HLGR)粪肠球菌75株,分离率为40.76%,HLGR屎肠球菌48株,分离率为44.04%。检测出2株耐万古霉素的粪肠球菌,分离率为1.09%,9株耐万古霉素霉素的屎肠球菌,分离率为8.26%。结论 肠球菌属的总体耐药率较高,且综合评价屎肠球菌的耐药性高于粪肠球菌,但肠球菌属对于万古霉素、利奈唑胺、替考拉宁等仍然保持较高的敏感性,临床上应选用合适的方法对肠球菌属进行耐药性检测,根据药敏结果选择适当的抗菌药物治疗。     

儿科临床分离肠球菌的耐药性监测及大环内酯类耐药机制研究

目的 研究儿科临床分离肠球菌的流行情况及红霉素耐药株基因ermB、mefA、tetM与转座子整合酶基因int-Tn分布特点.方法 采用KB纸片法对北京、上海、广州和重庆5家儿科专科医院2000-2006年临床分离粪、屎肠球菌进行8种抗菌药敏感性试验,并用琼脂稀释法测定225株红霉素耐药粪、屎肠球菌对大环内酯类及四环素最小抑菌浓度.PCR检测红霉素耐药基因ermB和mefA,四环素耐药基因tetM,以及转座子Tn1545的整合酶基因int-Tn.结果 4地5家儿童医院分离所得肠球菌对红霉素耐药率最高,平均耐药率86.5%;对氨苄西林、高浓度链霉素、高浓度庆大霉素、环丙沙星及利福平的耐药率分别为48.0%、47.6%、60.5%、45.4%、63.6%;未发现对万古霉素耐药的肠球菌.225株红霉素耐药粪、屎肠球菌ermB基因阳性率为70.7%,仅发现1株对mefA阳性的菌株.tetM基因阳性率为75.1%.Tn1545基因阳性株组ermB和tetM的携带率分别为84.8%和83.7%,高于阴性组60.9%和70.0%,且差异均有统计学意义(P均＜0.05).结论 我国儿科临床分离粪、屎肠球菌对多种抗菌药均有较高耐药率,对糖肽类抗菌药均保持较好敏感性,分离株对红霉素和四环素耐药主要机制分别是ermB编码的靶位改变和tetM编码的核糖体保护作用;接合性转座子Tn1545与tetM和ermB存在关系密切,可能是肠球菌多重耐药的重要机制之一.     

肠球菌庆大霉素高水平耐药机理的研究进展

肠球菌已成为医院感染的重要病原。从70年代首次报道肠球菌高耐庆大霉素开始,肠球菌对庆大霉素等氨基糖苷类药物的高水平耐药不断增加,如希腊在1993～1994年粪肠球菌和屎肠球菌对庆大霉素高水平耐药(HLGR)发生率2 0 %左右,1996～1997年则分别达到4 3 7%和2 6 3% ;北京四家医院1997～2 0 0 1年临床分离肠球菌耐药性的分析结果显示粪肠球菌和屎肠球菌HLGR发生率高达4 7 4 %和6 4 9% [1] ,屎肠球菌的耐药率明显高于粪肠球菌[2 ] 。近年来,肠球菌对庆大霉素高水平耐药的机理已有了较深入的研究,对其全面了解将有助于指导临床合理用药、新…     

儿童肠球菌多重耐药与Ⅰ类整合子的检测

目的了解儿童临床分离肠球菌的耐药特征及其多重耐药与Ⅰ类整合子的相互关系。方法采用琼脂稀释法测定常用抗菌药物对152株肠球菌的最低抑菌浓度(MIC),用聚合酶链反应(PCR)检测肠球菌Ⅰ类整合子和Ⅰ类整合酶基因。结果屎肠球菌对氨苄西林、阿莫西林-克拉维酸、环丙沙星的耐药率分别为96.8%、95.2%和84.1%,粪肠球菌对上述3种抗菌药物的耐药率分别为23.6%、18.0%和49.4%,屎肠球菌的耐药率明显高于粪肠球菌(P<0.001);粪肠球菌中有2株对万古霉素的MIC为8μg/mL,粪肠球菌和屎肠球菌对替考拉宁均敏感。儿童多重耐药肠球菌发生率高达93.7%。屎肠球菌耐药模式以耐氨苄西林、红霉素、环丙沙星、利福平、四环素、高水平庆大霉素6种抗菌药物为主,占屎肠球菌的59%,粪肠球菌以耐四环素、红霉素、利福平、氯霉素、高水平庆大霉素5种抗菌药物为主,占粪肠球菌的26%。全部152株肠球菌未检测到Ⅰ类整合子,仅有5株检测到Ⅰ类整合酶基因。结论儿童肠球菌多重耐药十分严重,儿童肠球菌多重耐药与Ⅰ类整合子和Ⅰ类整合酶基因尚无明显关系。     

临床分离肠球菌的耐药性分析

目的了解2017年本院临床分离肠球菌耐药状况。方法采用法国梅里埃VITK2-compact全自动细菌鉴定和药敏系统进行鉴定和药敏实验,参照CLSI(美国临床实验室标准化协会)2017年版判读结果,数据分析应用WHONET5.6软件。结果 2017年收集非重复临床分离肠球菌共86株,其中粪肠球菌36株,屎肠球菌47株,鹑鸡肠球菌3株;大部分分离株来自尿液标本,且以泌尿外科分离率最高。粪肠球菌对高浓度庆大霉素和高浓度链霉素的耐药率分别为36.1%和22.2%;屎肠球菌对高浓度庆大霉素和高浓度链霉素的耐药率分别为68.1%和61.7%,屎肠球菌耐药率明显高于粪肠球菌,未检出万古霉素耐药株。结论我院临床分离肠球菌以粪肠球菌和屎肠球为主,且屎肠球菌耐药率高于粪肠球菌,临床应合理选择抗生素,以延缓耐药肠球菌的增多。     

耐万古霉素肠球菌耐药基因、转座子结构和多位点序列分析

目的分析耐万古霉素肠球菌(VRE)耐药基因和多位点序列分型(MLST)情况。方法收集三亚中心医院临床分离的耐万古霉素的80株屎肠球菌和12株粪肠球菌,采用VITEK MS微生物鉴定系统进行菌种鉴定。采用VITEK 2 Compact自动化鉴定药敏仪测定VRE对14种常用抗菌药物的敏感性。采用微量肉汤稀释法测定VRE对万古霉素和替考拉宁的最小抑菌浓度(MIC),并确定耐药表型;采用聚合酶链反应(PCR)筛选VRE的毒力基因(esp、hyl、gelE、asal、cy1A、efaA、ace)和转座子结构;对VRE进行MLST。结果质谱鉴定结果为80株屎肠球菌和12株粪肠球菌。体外药物敏感性试验结果表明,屎肠球菌和粪肠球菌对万方霉素的耐药率均为100%,对氨苄西林的耐药率分别为97.5%和50.0%,但对呋喃妥因的耐药率较低。92株VRE对万古霉素和替考拉宁的MIC分别为192～256和32～256μg/mL,均为VanA表型;92株VRE基因型均为vanA,以esp毒力基因所占比例最高(82.5%);屎肠球菌以esp-hyl基因组合最常见,粪肠球菌以多基因组合为主;通过Tn1546基因转座子结构分析可分为A～E 5个型别;92株VRE的MLST包括7个ST型别,分别为ST17(43.5%)、ST78(32.6%)、ST203(6.5%)、ST363(5.4%)、ST555(4.3%)、ST1392(4.3%)和ST1394(3.4%),其中ST17和ST78均属于CC17克隆复合体。结论 92株VRE均为多重耐药株、vanA基因型和CC17克隆复合体,耐药基因和毒力基因携带率均较高,临床应引起重视。     

肠球菌氨基糖苷类高水平耐药基因的检测

目的调查肠球菌对高水平氨基糖苷类的耐药情况，并检测其耐药基因。方法琼脂稀释法筛选对氨基糖苷类高水平耐药的肠球菌，PCR扩增5种高耐药基因：双功能酶AAC(6′)-APH(2″)的编码基因aac(6′)-Ie—aph(2″)-Ia，磷酸转移酶APH(2″)-Id、APH(2″)-Ib的编码基因aph(2″)-Id、aph(2″)-Ib，核苷酸转移酶ANT(6-′)、ANT(3″)(9)的编码基因ant(6′)-Ia和ant(3″)(9)，并通过PCR产物的基因测序及寡核苷酸探针斑点杂交试验验证结果的可靠性。结果粪肠球菌对氨基糖苷类高水平耐药率达63％，屎肠球菌达84％。95％以上庆大霉素高耐肠球菌(HLGR)检测到aac(6′)-Ie—aph(2″)-Ia、3株HLGR肠球菌检测到aph(2″)-Id，99％以上HLSR肠球菌检测到ant(6′)-Ia。结论肠球菌对氨基糖苷类高水平耐药十分普遍，双功能酶AAC(6′)-APH(2″)、核苷转移酶ANT(6′)分别介导了大多数肠球菌对庆大霉素、链霉素的耐药。     

福州市134株肠球菌的耐药性分析

目的了解肠球菌的耐药状况,指导临床合理用药。方法对临床分离的134株肠球菌,用法国生物梅里埃公司的全自动细菌鉴定仪VITEK-32进行鉴定分析。结果134株肠球菌中,粪肠球菌113株(占84.3%),屎肠球菌19株(占14.2%),鸡肠球菌与铅黄肠球菌各1株(占1.5%),耐万古霉素肠球菌(VRE)与庆大霉素高水平耐药(HLGR)肠球菌分别占肠球菌感染标本总数的4.5%和52.3%,未发现对万古霉素和高浓度庆大霉素双重耐药株。结论肠球菌对临床常用8种抗生素以万古霉素、呋喃妥因最敏感,对其他抗生素均有不同程度耐药。对肠球菌引起的感染应选择根据分离株的耐药特点和药敏显示敏感的抗生素来治疗。     

Plasmid heterogeneity and identification of a Tn5281-like element in clinical isolates of high-level gentamicin-resistant Enterococcus faecium isolated in the UK.

Ten clinical isolates of high-level gentamicin-resistant (HLGR) Enterococcus faecium, collected from six hospitals throughout the UK, were studied to determine whether HLGR was attributed to widespread dissemination of a single plasmid or whether different plasmid types were implicated in the dissemination of this phenotype. HLGR was attributed to the presence of the AAC6'-APH2" bifunctional aminoglycoside modifying enzyme. The aac6'-aph2" gene was present on a 70 kb plasmid in all ten isolates. Conjugation studies indicated that the HLGR marker could transfer with varying frequency, with or without the associated 70 kb plasmid. Detailed molecular genetic analysis suggested that four of the isolates harboured a transposon similar to Tn5281, originally identified in Enterococcus faecalis strain HH22 isolated in the USA. The UK transposon, however, lacked the two symmetrically located HaeIII sites found in Tn5281. The six remaining isolates appeared to have a Tn5281-truncated structure in which the aac6'-aph2" gene is flanked by an IS256 element at the 5' end. Further studies with nine restriction endonucleases showed that the aac6'-aph2" gene was associated with two different plasmid types in E. faecium. Pulsed-field gel electrophoresis (PFGE) analysis identified three different patterns. The four E. faecium isolates harbouring the Tn5281-like structure were indistinguishable from each other, while the remaining six isolates exhibited two distinct PFGE patterns. This is the first study to indicate that there is heterogeneity among the plasmids that confer the HLGR phenotype in E. faecium isolates in the UK and to report on the presence of a transposon, similar to Tn5281, in E. faecium harbouring the aac6'-aph2" gene.     

Diversity among high-level aminoglycoside-resistant enterococci

A total of 55 Enterococcus faecalis and 21 Enterococcus faecium non-replicate isolates were obtained from routine clinical specimens, during a 1 year period, in a tertiary care hospital in Athens, Greece. The most common isolation site was the urinary tract (44% of E. faecalis and 33% of E. faecium isolates). No vancomycin resistance was detected. Ampicillin-resistant isolates did not produce beta-lactamase. High-level gentamicin resistance was detected in 22% and 0% of E. faecalis and E. faecium isolates, respectively. The corresponding figures for high-level streptomycin resistance were 40% and 33%. The aminoglycoside-modifying enzyme gene aac(6')+aph(2") was detected by PCR in 10 of 12 high-level gentamicin-resistant E. faecalis isolates, and the ant(6)-I gene in all high-level streptomycin-resistant isolates of both species. DNA fingerprinting by PFGE grouped 31 of 55 E. faecalis isolates into 10 clusters, and 10 of 21 E. faecium isolates into two clusters, containing two to seven isolates each. Two E. faecalis PFGE types, comprising isolates expressing high-level aminoglycoside resistance, and not observed among non-high-level aminoglycoside-resistant strains, were disseminated in building A of the hospital. In contrast, high-level aminoglycoside resistance seemed to have been acquired nosocomially by a number of genotypically different E. faecium types. Molecular typing was therefore instrumental in understanding the differences in the mode of spread and acquisition of high-level aminoglycoside resistance among these two different enterococcal species.     

Genetic relatedness among Enterococcus faecalis with transposon-mediated high-level gentamicin resistance in Swedish intensive care units

We studied 45 isolates of Enterococcus faecalis with high-level gentamicin resistance (HLGR), all but one concomitantly resistant to ciprofloxacin, and 25 ciprofloxacin-resistant isolates without HLGR for genetic relatedness using pulsed-field gel electrophoresis (PFGE). E. faecalis were isolated from patients admitted to intensive care units at eight hospitals in southern Sweden from December 1996 through December 1998. Genomic analysis by PFGE resulted in three clusters of genetically related isolates (designated clusters I, II and III) and 23 unique clones. Cluster I was found predominantly in the eastern and central parts of southern Sweden and clusters II and III in south-western Sweden. Among the 45 isolates with HLGR, 69% belonged to cluster I, 20% to cluster II, and 11% had unique PFGE patterns, which suggests that the majority of isolates with HLGR are closely related. Among the 25 ciprofloxacin-resistant isolates without HLGR, 68% had unique PFGE patterns, 12% belonged to cluster I and 20% to cluster III, which suggests the ciprofloxacin-resistant isolates are not related. All isolates with HLGR contained the aac(6')Ie-aph(2")Ia gene, which was carried on a Tn5281-like transposon in all isolates except one. We conclude that HLGR in E. faecalis was mainly due to dissemination of genetically related clones during the time studied, and that HLGR in these isolates was due to the presence of the aac(6')Ie-aph(2")Ia gene.     

Comparison of high-level gentamicin-resistant Enterococcus faecium isolates from different continents.

Eight clinical isolates of Enterococcus faecium highly resistant to gentamicin (MIC, > 1,000 mg/liter) from patients in six hospitals on three continents were investigated for evidence of spread of either a clone of high-level gentamicin-resistant (HLGR) E. faecium or wide dissemination of a gentamicin resistance (Gmr) plasmid. A combination of ribotypes, plasmid profiles, and extended antimicrobial susceptibilities enabled us to distinguish all but two of the isolates and did not suggest clonal dissemination of a single strain. Two isolates from hospitals situated close together appeared identical by these methods. All of the isolates carried Gmr plasmids which appeared to be closely related following digestion with restriction endonucleases. Cross-hybridization studies confirmed extensive DNA homology between these plasmids. The fragments of these plasmids which hybridized with a probe specific for the aac6'aph2" resistance gene did not resemble those seen in the Gmr transposon Tn5281, which was characterized previously in E. faecalis HH22. This study suggests that there has been widespread dissemination of a single Gmr plasmid and its derivatives amongst isolates of HLGR E. faecium, although a Gmr plasmid from an HLGR E. faecium isolated in the United States showed little homology with the other Gmr plasmids studied.     

258株肠球菌耐药性分析及耐万古霉素基因检测

目的研究肠球菌的耐药率及耐万古霉素肠球菌(VRE)的耐药表型和基因型。方法按照美国临床和实验室标准化研究所(CLSI)2009年推荐的微量稀释法进行临床分离肠球菌对各类药物的最小抑菌浓度(MIC)检测,VRE进一步用E-test药敏试验确认;PCR法检测VRE的耐药基因。结果 2010年7月至2011年11月沈阳军区总医院共检出粪肠球菌95株,屎肠球菌163株。粪肠球菌对万古霉素、替考拉宁保持较高敏感度,对氨苄西林、青霉素、呋喃妥因三种抗菌药物敏感度也在65%以上,对其他抗菌药物敏感度低,统计期内未检出耐万古霉素粪肠球菌菌株。屎肠球菌对多数抗菌药物表现为耐药,对氯霉素敏感率为70%,对万古霉素、替考拉宁敏感度下降,为90.7%。期间检出15株VRE,其耐药表型为多重耐药,PCR扩增结果显示,15株万古霉素耐药屎肠球菌VanA基因扩增均为阳性,产物长度在700～1000bp之间,约783bp,符合预期;VanB、VanC引物扩增均阴性。15株万古霉素耐药屎肠球菌对多数抗菌药物耐药,仅对氯霉素、四环素相对敏感,对万古霉素MIC>256mg/L,对替考拉宁也表现为耐药。结论屎肠球菌耐药性高于粪肠球菌,VRE多为多重耐药,给临床治疗带来困难,医院应加强对其预防监测。     

Nature of transposon-mediated high-level gentamicin resistance in Enterococcus faecalis isolated in the United Kingdom

Forty-two high-level gentamicin-resistant (MIC > 1000 mg/L) strains of Enterococcus faecalis, isolated from diverse geographical locations throughout the UK between 1993 and 1995, were studied to identify the nature of the high-level gentamicin-resistant determinants and the possibility of these determinants being associated with a transposon. High-level gentamicin resistance was attributed to the synthesis of the bifunctional (AAC6'-APH2") aminoglycoside-modifying enzyme. The aac6'-aph2" gene, which was present on a 70 kb plasmid in all 42 isolates, could be transferred by conjugation in association with the 70 kb plasmid in 39 of the isolates studied. In three E. faecalis isolates, however, the high-level gentamicin resistance was transferable independent of the 70 kb plasmid, suggesting the presence of a conjugative transposon. Long-PCR studies showed that all 42 clinical isolates harboured a transposon similar to Tn5281, originally identified in E. faecalis strain HH22 isolated in the USA. Restriction endonuclease and Southern hybridization analysis of the UK transposon showed that it is closely related to the high-level gentamicin resistance-conferring transposon Tn5281. However, the UK transposon lacks the HaeIII site identified in Tn5281. Pulsed-field gel electrophoresis analysis identified seven different patterns. Further studies with nine restriction endonucleases showed that the aac6'-aph2" gene was associated with nine different plasmid types in E. faecalis.     

Glycopeptide susceptibility among Danish Enterococcus faecium and Enterococcus faecalis isolates of animal and human origin and PCR identification of genes within the VanA cluster.

The MICs of vancomycin and avoparcin were determined for isolates of Enterococcus faecium and isolates of Enterococcus faecalis recovered from the feces of humans and animals in Denmark. Two hundred twenty-one of 376 (59%) isolates of E. faecium and 2 of 133 (1.5%) isolates of E. faecalis were resistant to vancomycin (MICs, 128 to > or = 256 micrograms/ml), and all vancomycin-resistant isolates were resistant to avoparcin (MICs, 64 to > or = 256 micrograms/ml). All vancomycin-resistant isolates examined carried the vanA, vanX, and vanR genes, suggesting that a gene cluster similar to that of the transposon Tn1546 was responsible for the resistance.     

Aminoglycoside resistance genes aph(2")-Ib and aac(6')-Im detected together in strains of both Escherichia coli and Enterococcus faecium

Escherichia coli SCH92111602 expresses an aminoglycoside resistance profile similar to that conferred by the aac(6')-Ie-aph(2")-Ia gene found in gram-positive cocci and was found to contain the aminoglycoside resistance genes aph(2")-Ib and aac(6')-Im (only 44 nucleotides apart). aph(2")-Ib had been reported previously in Enterococcus faecium SF11770. aac(6')-Im had not been detected previously in enterococci and was found to be present also 44 nucleotides downstream from aph(2")-Ib in E. faecium SF11770. aph(2")-Ib and aac(6')-Im are separate open reading frames, each with its own putative ribosome binding site, whereas aac(6')-Ie-aph(2")-Ia appears to be a fusion of two genes with just one start and one stop codon. The deduced AAC(6')-Im protein exhibits 56% identity and 80% similarity to the AAC(6')-Ie domain of the bifunctional enzyme AAC(6')-APH(2"). Our results document the existence of a member of the aph(2") family of genes in gram-negative bacteria and provide evidence suggesting the horizontal transfer of aph(2")-Ib and aac(6')-Im as a unit between gram-positive and gram-negative bacteria.     

Molecular epidemiology of high-level aminoglycoside-resistant enterococci isolated from patients in a university hospital in southern Italy

OBJECTIVES: We evaluated the genetic and molecular basis of high-level resistance to gentamicin and amikacin in 91 clinical isolates of Enterococcus faecalis and Enterococcus faecium in a university hospital in southern Italy from 1987 to 2003. METHODS: Antibiotic susceptibility was evaluated by disc diffusion and microdilution methods. Genotyping was performed by PFGE and dendrogram analysis. Aminoglycoside resistance genes were analysed by multiplex PCR. Aminoglycoside resistance gene transfer was performed by filter mating. RESULTS: In our strain collection, 44% of E. faecalis and 52% of E. faecium were high-level-resistant to gentamicin. Fifty-two PFGE profiles were identified for E. faecalis and 15 for E. faecium. Although the majority of PFGE patterns were single isolates, four patterns (two for E. faecalis and two for E. faecium) were isolated each in 8 and 4, and 6 and 4 different patients, respectively. The aac(6')-Ie-aph(2')-Ia gene was responsible for high-level resistance to gentamicin and amikacin in E. faecalis and E. faecium; the aph(2')-Id gene responsible for resistance to gentamicin was also isolated in E. faecium; the aph(3')-IIIa and ant(4')-Ia genes responsible for resistance to amikacin were also isolated in E. faecalis and E. faecium. High-level resistance to gentamicin, along with the aac(6')-Ie-aph(2')-Ia gene, was transferred at a frequency of about 10(-5) to 10(-8) per recipient cell in 14 of 17 E. faecalis and 3 of 4 E. faecium different genotypes. CONCLUSIONS: The spread of the aac(6')-Ie-aph(2')-Ia gene was responsible for high-level resistance to gentamicin and amikacin among enterococci isolated from patients in our geographical area.     

肠球菌耐药现状调查及抗感染用药探讨

目的了解肠球菌尤其是对万古霉素耐药肠球菌（ＶＲＥ）和庆大霉素高水平耐药（ＨＬＧＲ）肠球菌的耐药状况,指导临床合理用药。方法对北京５家教学医院感染标本中分离出的１６１４株肠球菌,分别进行纸片扩散法药敏试验和β内酰胺酶测试,并以“ＷＨＯＮＥＴ４”软件对试验数据进行分析处理。结果ＶＲＥ和ＨＬＧＲ肠球菌分别占肠球菌感染标本总数的３．４％和５２．６％,产β内酰胺酶的肠球菌占５．８％;对常用抗生素的耐药率,屎肠球菌明显高于粪肠球菌,ＨＬＧＲ株明显高于低耐株;万古霉素和高浓度庆大霉素多重耐药株检出率为０．９％。结论肠球菌对临床常用的８种抗生素以万古霉素最敏感。对不同特征肠球菌感染应采取不同的治疗方案。