湖北地区肠球菌体外耐药监测与基因分型研究

目的：监测湖北地区肠球菌耐药性并对耐药株进行基因分型及流行病学研究。方法：对9所大型综合医院感染标本中分离的335株肠球菌进行鉴定和药敏试验，以“WHONET4“软件分析；并以随机扩增多态性DNA分型法（RAPD）进行基因分型。结果：对耐氨苄西林肠球菌（ARE）分离率17.0%，对耐氨基糖苷类肠球菌（HLAR）分离率38.2%，对耐万古霉素肠球菌（VRE）分离率为0%，HLAR合并ARE的分离率为5.4%，万古霉素中介肠球菌（VIE）分离率2.1%；21株ARE分为16型，43株HLAR分为26型，7株HLAR合并ARE分为5型。结论：湖北地区肠球菌耐药性呈上升趋势，其感染在本地区呈散在流行态势；临床微稗室应严密关注多重耐药肠球菌的产生及播散流行。     

重症监护病房肠球菌感染及体外药敏监测

目的 研究医院重症监护病房(ICU)内肠球菌的感染现状并对其耐药性进行体外药敏监测。方法 用法国-生物梅里埃公司生产的VITEK32全自动细菌鉴定系统鉴定肠球菌，用K-B法及E-test试条法监测肠球菌耐药率。结果 ICU内116株肠球菌中，以粪肠球菌分离率最高，为75．0％，屎肠球菌为10．3％，居第2位，116株肠球菌中检出耐氨苄西林肠球菌(ARE)16．4％，氨基糖苷类高水平耐药肠球菌(HLAR)38．8％，氨基糖苷类高水平耐药合并氨苄西林耐药株6．9％，未检出耐万古霉素肠球菌(VRE)，但检出万古霉素中介肠球菌(VIE)3．4％。结论 ICU内肠球菌耐药率呈上升趋势，须严密监测，预防耐药肠球菌的暴发流行。     

肠球菌耐药分析

目的：为了了解肠球菌特别是氨基糖苷类高水平耐药肠球菌（HLAR）及耐万古霉素肠球菌（VRE）的耐药状况，指导临床合理用药，方法：对两年中天津地区7所医院各类住院患者标本分离出的肠球菌，采用纸片扩散法进行耐药分析。结果：在215 株肠球菌中，以粪肠球菌和屎肠球菌的分离率最高，占总数的99．1％，分离出氨基糖苷类高水平耐药肠球菌（HLAR）56株，分离率为45．2％，分离出耐万古霉素肠球菌（VRE）9株，分离率为4．6％，结论：肠球菌耐药性呈上升趋势，提示临床在治疗此类菌感染时，应根据分离株的耐药特点和药敏试验结果合理选用抗生素，以减少耐药菌株的产生和耐药基因的传播。     

耐氨基苷类高水平肠球菌医院感染的危险因素及氨基糖苷类耐药相关基因研究

目的 了解耐氨基糖苷类高水平肠球菌(HLAR)的耐药性和医院感染的危险因素,研究HLAR氨基糖苷类耐药相关基因类型分布.方法 采用全自动微生物鉴定仪VITEK-AMS对857株肠球菌属进行鉴定及抗菌药物敏感性检测;PCR法检测HLAR氨基糖苷类耐药相关基因,并对PCR结果进行测序分析.结果 肠球菌属中HLAR占50.4％,利奈唑胺、万古霉素和替考拉宁对HLAR的抗菌作用最好,但有3株屎肠球菌对万古霉素和替考拉宁耐药,粪肠球菌对氯霉素和四环素的耐药率高于屎肠球菌,而屎肠球菌对其他常用抗菌药物的耐药率明显高于粪肠球菌,粪肠球菌和屎肠球菌的耐药谱明显不同,aac(6')-Ie-aph(2〃)-Ia基因为耐庆大霉素高水平肠球菌(HLGR)的主要耐药基因,占HLGR的88.0％,严重的基础疾病、侵入性操作和头孢三代抗菌药物和激素的应用是肠球菌属医院感染的常见危险因素.结论 HLAR已成为医院感染的重要耐药菌,HLGR产生的主要机制是aac(6')-Ie-aph(2〃)-Ia基因介导对庆大霉素高水平耐药,控制常见医院感染危险因素,合理使用抗菌药物,可减少HLAR医院感染的发生.     

临床分离肠球菌分布及其耐药性监测

目的 了解某院临床分离肠球菌的菌群分布及其耐药情况。方法 采用全自动微生物分析仪VITEK AMS 32对分离自各类临床标本的206株肠球菌进行鉴定及药敏试验，并对耐万古霉素的菌株用K—B法作进一步验证。结果 206株肠球菌中，以粪肠球菌(80．10％)和屎肠球菌(11．65％)为主。菌株来源以痰液(21．84％)、前列腺液(20．87％)、脓液(20．39％)、尿液(10．68％)为主。耐万古霉素肠球菌(VRE)中，粪肠球菌为1．82％，屎肠球菌为4．17％，鸟肠球菌为14．29％，鸡肠球菌为100％。粪肠球菌中高浓度庆大霉素耐药株(HLGR)占56．36％，高浓度链霉素耐药株(HLSR)占54．55％；屎肠球菌中HLGR为79．17％，HLSR为45．83％。结论 肠球菌所致感染以下呼吸道医院感染占首位。各菌种对抗菌药物的敏感率相差较大，微生物室必须做好菌种鉴定及药敏试验，以指导临床合理用药。     

肠球菌的分离及耐药性

目的：了解肠球菌的临床分离状况和对常用抗菌药物的耐药性及与感染性疾病的关系。方法：对1993年1月01998年12月6年间本院临床标本中分离的359株肠球菌，分别进行纸片扩散法药敏试验和β内酰胺酶测定，病例回顾性分析。结果：各年肠球菌的分离率为2．6％，3．1％，4．3％,5．1％，5．3％，5．2％；产β－内酰胺酶的肠球菌占5．0％；359株肠球菌对常用的抗菌药物的耐药率以万古霉素最低为1．7％，其次为氨苄西林／舒巴坦耐药率12．5％，氨苄西林为14．8％，亚胺培南为16．4％，哌拉西林为18．9％，对其他抗菌药物耐药率均超过50％；8屎肠球 对抗菌药物的耐药率明显高于粪肠球菌；肠球菌引起的不同系统的医院感染，呼吸系统感染为46．1％；其次为泌尿系统感染占39．1％，腹腔感染占8．2％，结论：肠球菌感染有逐年增高的趋势，对万古霉素敏感率最高，对其他常用的抗菌药物显示有很强的耐药性，可引起不同系统的医院感染，以呼吸系统感染最为常见。     

尿路感染病原菌分布及耐药性检测

目的 探讨尿路感染病原菌的分布及耐药性特征，为临床合理选用抗生素、控制医院感染提供依据。方法 收集我院尿路感染患者标本中分离的151株病原菌进行鉴定，同时对G^-杆菌进行ESBLs的检测，肠球菌属进行氨基糖昔类高水平耐药(HLAR)的筛选。结果 尿路感染病原菌分布占前几位的细菌为大肠埃希菌53．64％、肠球菌属9．27％、凝固酶阴性葡萄球菌7．95％、假单胞菌5．96％；产ESBLs大肠埃希菌的检出率为13．58％，产ESBLs肺炎克雷伯菌的检出率为16．67％，HLAR肠球菌属检出率为57．14％。结论 重视尿路感染病原菌耐药性检测，对控制医院感染、合理使用抗生素十分重要。     

引起肠球菌感染上升的原因及其耐药性分析

目的 探讨引起肠球菌感染上升的原因，并对其耐药性进行分析。方法 采用回顾性调查，对我院2000～2001年度1918例呼吸道感染患者，在做痰培养前1周内使用头孢菌素类和其他抗生素后，分离出肠球菌的情况和对2001年度肠球菌的耐药性进行分析。结果 2001年度的982例患者中使用头孢菌素类的616例，分离出肠球菌98例，分离率为15．9％，366例使用其他抗生素的患者分离出肠球菌16例，分离率为4．4％，二者差异有显著性(P＜0．01)，2000年度的936例患者中分离出肠球菌46例，其中使用头孢菌素(318例)的患者中分离出肠球菌36例，分离率为11．3％，在2001年度共分离出的114株肠球菌中耐万古霉素(VRE)的4株，分离率为3．5％。结论 由肠球菌所致的医院内呼吸道感染呈增高趋势，头孢菌素类抗生素的使用可能是原因之一，在治疗此类菌引起的感染时，应根据细菌培养结果合理选择抗生素，避免盲目使用对肠球菌无效的头孢菌素类。     

肝移植患者术后肠球菌属感染与体外药敏分析

目的 调查肝移植患者术后肠球菌属的感染状况,并对其耐药性进行体外药敏检测,为肠球菌属感染的治疗提供参考及指导.方法 采用法国生物梅里埃公司生产的VITEK32全自动细菌鉴定系统或常规生化法鉴定肠球菌属到种,用K-B纸片法监测其耐药率.结果 分离出的387株肠球菌属中以屎肠球菌的分离率最高,为73.9%,粪肠球菌分离率21.4%,居第2位,检出耐高浓度氨基糖苷类肠球菌(HLAR)346株,占89.4%,仅检出1株耐万古霉素肠球菌(VRE).结论 肝移植患者术后感染肠球菌属以屎肠球菌为主,其耐药性明显高于粪肠球菌,提示临床医师在治疗肝移植患者术后感染肠球菌时应根据分离株种类、耐药特点及药敏试验合理选用抗菌药物.     

临床分离273株肠球菌属分析

目的 探讨2008年1-12月医院临床分离肠球菌属的易感因素及耐药情况,为临床用药提供证据.方法 按操作进行细菌的培养、分离及鉴定;运用VITEK-2分析仪进行菌株的鉴定及药敏检测;调查病历了解患者资料.结果 共分离出273株肠球菌属,其中粪肠球菌158株,屎肠球菌109株,其他肠球菌6株;其中耐高浓度氨基糖苷类肠球菌(HLAR)屎肠球菌10株,HLAR粪肠球菌80株,两者间分离率差异有统计学意义(P<0.05);屎肠球菌对氨苄西林、氨苄西林/舒巴坦、亚胺培南、红霉素、环丙沙星、莫西沙星的耐药率明显高于粪肠球菌,糖肽类抗菌药物(万古霉素和替考拉宁)和利奈唑烷对肠球菌属保持高度敏感性.结论 医院HLAR粪肠球菌产生率高,肠球菌属的耐药性较为严重;医院应加强抗菌药物使用的管理,严格掌握糖肽类抗菌药物的使用指针,降低细菌耐药率.     

耐万古霉素肠球菌的目标性监测与分析

目的 了解临床耐万古霉素肠球菌的分离和耐药性,探索耐万古霉素肠球菌感染病例的监控措施.方法 对2010年医院临床分离的病原菌进行目标性监测,统计耐万古霉素肠球菌的株数以及耐药性,并对临床耐万古霉素肠球菌感染病例实施监控.结果 共分离出肠球菌属582株,其中耐万古霉素肠球菌占2.20％,对抗菌药物耐药率较高;全院未发生耐万古霉素肠球菌的暴发和流行.结论 耐万古霉素肠球菌分离株数较多,耐药率较高,应该加强临床合理使用抗菌药物的管理,对耐万古霉素肠球菌感染病例实施监控,预防和减少多药耐药菌的产生,控制医院感染.     

Vancomycin-resistente Enterokokken – Krankenhausküche als Vektor? Eine Erhebung aus der Praxis

Vancomycin-resistant enterococci (VRE) were first detected in the UK and France in 1986. The characteristic of glycopeptid-resistance was spread worldwide, especially in the US, so that nowadays enterococci have become an important cause of nosocomial infections. Within the frame work of a hospital's internal investigation the prevalence of VRE carriage in intensive care patients reached 21%. In order to scrutinize to what extent the hospital kitchen is involved in the spreading of VRE, 200 food samples and 552 environmental samples, RODAC (= Replicate Organism Direct Agar Contact) -plates and wet-dry double swabs, were tested over 10 inspections in the course of six months. The isolation of enterococci and VRE was determined by the BgVV-method. Enterococci were isolated from 37 of 200 (18,5%) food samples. Seven isolated strains of enterococci were classified as VRE due to the fact that they grow on CATC-agar with 8 mg vancomycin-supplement and are biochemically and morphologically specified as E. faecalis, E. casseliflavus and E. gallinarum-group. The microdilution-test (MHK) for examination of glycopeptide-resistance showed only one intermediate reacting strain. The other six VRE-suspicious strains were classified as vancomycin-sensitive. Concerning the environmental samples, enterococci were isolated from 74 of 302 (24,5%) RODAC-plates. Eight isolated strains of enterococci, specified as E. casseliflavus, grew on CATC-agar with vancomycin-supplement. However, the MHK-test distinguished them all as vancomycin-sensitive. With the wet-dry double swab technique no enterococci could be detected although this method included an enrichment step. The possibility, VRE-suspicious strains might be carrier of resistance genes without expressing vancomycin-resistance by MHK-test, has been ruled out by PCR. However, in all the 10 inspections there were multiple deficits concerning the hospital kitchen hygiene status and measures. Against this background it can be concluded that although VRE-detection was negative, in case of using VRE-contaminated raw material, the possibility of spreading VRE by re- and cross-contaminating processed foods, equipment and staff were to be taken into account.     

Eradication of vancomycin resistant Enterococcus faecium from a paediatric oncology unit and prevalence of colonization in hospitalized and community-based children

We previously reported an outbreak of vancomycin resistant enterococci (VRE) in a paediatric oncology unit in December 1995 which was associated with widespread environmental contamination of the unit with VRE. We undertook this study to evaluate the effectiveness of the infection control policy instituted subsequent to the outbreak and to investigate the underlying prevalence of VRE colonization in hospitalized, outpatient and community-based children. We sought to establish the molecular similarity of VRE isolates from the study. Stool specimens were obtained from outpatients at risk of VRE, hospital inpatients and from healthy community-based children. VRE colonization was eradicated from the inpatient unit within 11 months, but in outpatients, 16 months after the outbreak, 4 of 137 (2.9 %) attending oncology outpatients, 5 of 65 (7.7%) with cystic fibrosis and 1 of 12 (8.3 %) with liver disease were found to be colonized with VRE. The isolates were all Enterococcus faecium, Van A phenotype except one E. casseliflavus of the Van C phenotype. All were unique in SmaI DNA macrorestriction patterns with the exception of two isolates, which were similar to the original outbreak strain and three further isolates of a single strain but which differed from the outbreak strain. Of 315 hospital inpatients, 2.5 % were colonized with VRE of the Van C resistance phenotype but VRE was not detected in 116 healthy, community-based children. We conclude that effective strategies can successfully control spread of VRE but despite a low prevalence of VRE colonization in hospital patients and in community-based children, outbreaks can occur when infection control practices are not optimal. Continued vigilance to detect VRE and limit spread within hospitals is therefore necessary.     

Vancomycin resistant enterococci in the Netherlands

Enterococci (Enterococcus faecalis and Enterococcus faecium) are relatively avirulent enteric bacteria that usually only cause infections in immunocompromised patients. Antimicrobial treatment, however, is hampered as enterococci are intrinsically resistant to many antibiotics. For years, vancomycin was considered the last available antibiotic. Plasmid-mediated resistance against vancomycin among enterococci was first described in the nineteen-eighties and since then incidences of infection caused by vancomycin-resistant enterococci (VRE) have increased dramatically, especially in the United States. In 2000, three outbreaks of VRE occurred in hospitals in the Netherlands and a set of infection-control measures was proposed to limit further transmission. These measures were based on the simultaneous isolation of VRE from multiple patients. All three outbreaks were controlled by these measures and no new outbreaks in Dutch hospitals have been reported since then. Epidemiological studies have shown that hospital outbreaks on three continents were caused by a subpopulation of E. faecium, which is characterized by the presence of a potential virulence gene (variant esp) and resistance to amoxicillin. This 'hospital strain' of E. faecium has probably been prevalent within hospital settings for some time, but only became clinically relevant when it had acquired vancomycin-resistance. Current advice is to implement the set of infection control measures formulated in 2000, only in those patients colonized by amoxicillin-resistant VRE. The potential dangers of VRE were recently underlined by the proven transmission of the vancomycin-resistance gene from VRE to methicillin-resistant Staphylococcus aureus (MRSA) in two patients in the United States. It is in the interest of the patients that prevalence of VRE and MRSA in Dutch hospitals should be kept as low as possible.     

肠球菌的菌种分布和耐药性分析

目的 为了解深圳市人民医院临床分离的肠球菌的菌种分布和耐药性。方法 用Kirby-Bauer法对全院2001年7月至2003年7月临床分离的206株肠球菌进行药敏试验并对其菌种分布进行分析。结果 206株肠球菌中以粪肠球菌和屎肠球菌分离频率最高,分别占总体的65％和16％。粪肠球菌对替考拉宁、万古霉素、氨苄西林的耐药率低,分别为0、1．5％和4．8％;屎肠球菌对万古霉素和替考拉宁的耐药率均为0,其它肠球菌对万古霉素的耐药率为5．6％;粪肠球菌对氨苄西林的耐药率显著低于屎肠球菌。约30％的肠球菌高耐庆大霉素。结论万古霉素、替考拉宁对肠球菌有较强的抗菌作用,但VRE的出现应引起高度重视。氨苄西林对不同肠球菌的抗菌作用存在显著差异,29．7％的粪肠球菌、50％屎肠球菌和25．7％的其它肠球菌为高耐庆大霉素。     

妇幼专科医院病原体菌群分布及耐药分析

目的：对送检标本中分离的致病菌分布及耐药趋势进行分析,旨在做好防控措施和指导临床合理使用抗菌药物。方法进行常规培养分离鉴定,药敏试验应用K-B纸片扩散法,按CLSI/NCCLS规定的标准进行。结果3年共分离到1071株细菌,其中G＋菌414株,占38．65％,G-菌465株,占43．41％。 MRSA检出率明显上升,分别为：3％、9％、13％。纳入目标性监测的多重耐药菌（MDRO）包括：耐甲氧西林金黄色葡萄球菌（MRSA）20株、多重耐药的大肠埃希菌25株、多重耐药的肺炎克雷伯菌4株、耐万古霉素肠球菌（ VRE）1株、多重耐药的铜绿假单胞菌1株。2013年金黄色葡萄球菌开始出现万古霉素耐药株,耐药率为16％。结论妇幼专科医院病原菌群相比综合医院病种少,病原菌也相对较少,但是病原菌群也同样随着时间推移在不断变迁,耐药性逐年增长,加强监测防控,指导临床合理用药也很有意义。