36株多重耐药鲍曼不动杆菌对氨基糖苷类药物耐药基因的流行病学研究

目的了解多重耐药鲍曼不动杆菌中氨基糖苷类耐药基因的存在情况。方法收集2012年8—11月江苏大学附属医院和镇江市第一人民医院住院患者的临床标本中分离到的多重耐药鲍曼不动杆菌菌株36株。应用KB纸片扩散法检测多重耐药鲍曼不动杆菌对抗菌药物的敏感性、应用PCR检测细菌对氨基糖苷类药物的耐药基因。结果36株多重耐药鲍曼不动杆菌对头孢哌酮一舒巴坦有较高的敏感率（33．3％）,对其他抗菌药物的敏感率均较低（20．0％）。36株多重耐药鲍曼不动杆菌中氨基糖苷类耐药基因aac（3）-I、aac（6’）Ib、aph（3’）-I和16SrRNA甲基化酶基因armA的阳性率分别为72．2％（26株）、72．2％（26株）、80．6％（29株）和80．6％（29株）。结论本组多重耐药鲍曼不动杆菌多耐药情况比较严重,其对氨基糖苷类药物耐药与氨基糖苷类耐药基因的存在密切相关。     

鲍曼不动杆菌对氨基糖苷类药物的耐药机制研究

目的探讨鲍曼不动杆菌对氨基糖苷类药物耐药机制。方法K-B法检测19株鲍曼不动杆菌对4种氨基糖苷类药物的敏感性,聚合酶链反应(PCR)检测氨基糖苷类修饰酶基因。结果14株鲍曼不动杆菌携带aacA4基因,检出率为74%。结论aacA4型氨基糖苷类修饰酶是鲍曼不动杆菌对氨基糖苷类药物耐药的重要机制。     

多重耐药鲍曼不动杆菌氨基糖苷类耐药基因的研究

目的调查山东省潍坊市人民医院临床分离的多重耐药鲍曼不动杆菌氨基糖苷类耐药基因的流行情况,为院内感染控制提供依据。方法采用VITEK2全自动微生物仪对2013年11月26日至12月12日山东省潍坊市人民医院临床分离的9株多重耐药鲍曼不动杆菌进行细菌鉴定和药敏试验,部分抗菌药物的敏感度检测采用纸片扩散法。聚合酶链反应检测氨基糖苷类耐药基因,对部分阳性基因进行测序。结果 9株多重耐药鲍曼不动杆菌中,2株aac(3)-Ⅰ基因阳性,3株ant(3″)-Ⅰ基因阳性,3株aac(6′)-Ⅰ基因阳性,9株armA基因阳性。所有菌株对氨基糖苷类抗菌药物阿米卡星、庆大霉素和妥布霉素耐药。5株标本来源于重症监护病房,3株标本来源于神经外科病房。所有标本来源于痰液。结论该院这段时间分离的多重耐药鲍曼不动杆菌对阿米卡星、庆大霉素和妥布霉素同时耐药与携带armA氨基糖苷类耐药基因有关。院感部门应重点监测重症监护病房和神经外科病房多重耐药鲍曼不动杆菌引起的院内感染。     

鲍曼不动杆菌对氨基糖苷类药物耐药机制研究

目的研究对氨基糖苷类抗菌药物耐药的鲍曼不动杆菌分子流行病学特征和耐药机制。方法采用琼脂稀释法检测抗菌药物对鲍曼不动杆菌的最低抑菌浓度(MIC),采用肠杆菌科基因间重复一致性序列(ERIC)-聚合酶链反应(PCR)研究耐药菌株的分子流行病学特征,采用特异性PCR、序列分析和接合试验研究介导耐药的分子机制。结果临床分离菌株对包括氨基糖苷类抗菌药物在内的多种药物广泛耐药,同源性分析显示属于7个流行克隆型。所有分离菌株均扩增出介导氨基糖苷类抗菌药物耐药的修饰酶和药物"外排泵"基因,部分菌株扩增出甲基化酶基因。结论修饰酶和甲基化酶介导鲍曼不动杆菌临床分离株对氨基糖苷类药物耐药,药物"外排泵"参与介导耐药机制形成,垂直传播和通过耐药性质粒的水平传递可能是耐药菌株播散的主要方式。     

鲍曼不动杆菌多重耐药机制研究进展

鲍曼不动杆菌是医院感染重要条件致病菌。近年来,鲍曼不动杆菌感染日益增多,仅次于金黄色葡萄球菌和大肠埃希菌,并且呈现多重耐药现象,已引起临床医生和微生物工作者的高度关注。鲍曼不动杆菌耐药机制包括染色体基因突变,外膜孔蛋白改变,药物主动外排系统和产生灭活酶等。细菌耐药基因通过接合性质粒、转座子、整合型噬菌体、整合子的水平传递等发生传递。我们就鲍曼不动杆菌多重耐药机制,尤其是整合子与鲍曼不动杆菌多重耐药性的有关研究作一详细综述。     

广泛耐药鲍曼不动杆菌氨基糖苷类药物获得性耐药基因研究

目的了解重症监护病房（ICU）患者分离的广泛耐药（XDR）-鲍曼小动杆菌（AB）对氨基糖苷类药物获得性耐药基因情况。方法用phoenix-100全自动细菌鉴定药物敏感性分析仪对AB进行细菌鉴定和药物敏感性试验,gyrA和parC基因扩增测序确定AB。聚合酶链反应（PCR）测定20株XDR—AB的10种氨基糖苷类修饰酶基因、6种16SrRNA甲基化酶基因和外排泵adeB基因,并用DNA测序比对。结果20株XDR—AB中,氨基糖苷类修饰酶基因aac（3）-I、aac（6’）-Ib、ant（3”）-I、aph（3’）-I检出率分别为90．0％、30．0％、95．0％、95．0％,而aac（3）-lI、aac（6’）-Iad、aac（6’）-lI、ant（2”）-I、ant（4’）-I及aph（3’）-VIa基因均未检出。armA型16SrRNA甲基化酶基因和外排泵adeB基因检出率均为100％。结论20株XDR—AB均携带rarmA和adeB基因,同时aac（3）-I、ant（3”）-I和aph（3）-I检出率较高,提示ICU分离的XDR—AB对氨基糖苷类药物高水平耐药可能与携带的耐药基因有关。     

鲍曼不动杆菌整合子流行现状与多重耐药相关性研究

[目的]了解我院鲍曼不动杆菌整合子流行情况,并探讨整合子与鲍曼不动杆菌多重耐药的关系。[方法]收集我院2009年9月至2010年1月临床分离的鲍曼不动杆菌共56株,用纸片扩散法检测鲍曼不动杆菌对19种抗生素的敏感性,用整合酶PCR方法检测I类、Ⅱ类和Ⅲ类整合子基因。[结果]鲍曼不动杆菌耐药现象十分严重。56株菌株中有41株检出I类整合子,阳性率73．2％,其中8株为I类和Ⅱ类杂交整合子,2株为I类和Ⅲ类杂交整合子。I类整合子阳性株对多种药物的耐药率均高于阴性株,且I类整合子阳性株多重耐药率（90．2％）明显高于阴性株（30％）（P〈0．0L）。[结论]I类整合子在我院鲍曼不动杆菌中检出率很高并与其多重耐药性关系密切。     

导致氨基糖苷类药物双圈耐药型鲍曼不动杆菌的相关携带基因研究

目的 探讨在K-B法药物敏感试验中对氨基糖苷类抗菌药物双圈耐药的鲍曼不动杆菌耐药基因携带状况及药物诱导对耐药基因mRNA表达量的影响.方法 收集42株携带Ⅰ类整合子酶基因的鲍曼不动杆菌;PCR法扩增其整合子可变区;联合RFLP和DNA测序技术分析可变区耐药基因;用RT-PCR的方法分析药物诱导前后细菌耐药基因表达量.结...     

鲍曼不动杆菌对氨基糖苷类抗菌药物双圈耐药现象的初步探讨

目的 探讨鲍曼不动杆菌对氨基糖苷类抗菌药物的双圈耐药现象.方法 用琼脂稀释法检测庆大霉素、阿米卡星、妥布霉素、依替米星等4种氨基糖苷类药物对56株鲍曼不动杆菌的最低抑菌浓度(MIC).用阿米卡星诱导试验检测该药对该表型的基因是否存在诱导现象.用PCR法检测该类菌是否携带整合子.结果 庆大霉素、依替米星对56株鲍曼不动杆菌的MIC均＞1 024 mg/L;71.4%(40/56)的鲍曼不动杆菌妥布霉素的MIC≥1 024 mg/L;阿米卡星的MIC呈抑制后再生长现象,大多在512 mg/L出现抑制,而到4 096 mg/L又开始生长. 用K-B法进行诱导试验,传至15代双圈耐药现象转为完全耐药.56株菌中53株检测到Ⅰ类整合子.结论 MIC试验证实了K-B法中的双圈现象,介导这一现象的基因呈诱导型表达,这类菌大多携带Ⅰ类整合子.     

High tigecycline resistance in multidrug-resistant Acinetobacter baumannii

OBJECTIVES: Multidrug-resistant (MDR) Acinetobacter baumannii is increasing in our hospital and worldwide, raising the necessity of finding effective therapies. We aimed to evaluate the in vitro activity of tigecycline against MDR A. baumannii clones isolated before tigecycline was used in our institution. METHODS: Eighty-two unique patient clinical isolates of multidrug-resistant A. baumannii collected in 2003 were studied. Species identification and antibiotic susceptibilities were determined by Vitek-2. Tigecycline MIC was determined by Etest. Clonal relatedness was determined by PFGE. RESULTS: MDR A. baumannii possessed 19 different pulsotypes. Sixty-six percent of the isolates were resistant to tigecycline, 12% were intermediate and 22% were susceptible. The MIC(50) and MIC(90) of tigecycline were 16 and 32 mg/L, respectively, with a wide MIC range of 1-128 mg/L. Variability in MIC of tigecycline was evident between and within the same pulsotype. CONCLUSIONS: We report here high resistance rates to tigecycline, and higher than previously described MICs, in multiple clones of MDR A. baumannii. As tigecycline represents a new treatment choice for infections caused by A. baumannii, these findings are worrisome.     

Heteroresistance to colistin in multidrug-resistant Acinetobacter baumannii

Multidrug-resistant Acinetobacter baumannii has emerged as a significant clinical problem worldwide and colistin is being used increasingly as "salvage" therapy. MICs of colistin against A. baumannii indicate its significant activity. However, resistance to colistin in A. baumannii has been reported recently. Clonotypes of 16 clinical A. baumannii isolates and ATCC 19606 were determined by pulsed-field gel electrophoresis (PFGE), and colistin MICs were measured. The time-kill kinetics of colistin against A. baumannii ATCC 19606 and clinical isolate 6 were investigated, and population analysis profiles (PAPs) were conducted. Resistance development was investigated by serial passaging with or without exposure to colistin. Five different PFGE banding patterns were found in the clinical isolates. MICs of colistin against all isolates were within 0.25 to 2 microg/ml. Colistin showed early concentration-dependent killing, but bacterial regrowth was observed at 24 h. PAPs revealed that heteroresistance to colistin occurred in 15 of the 16 clinical isolates. Subpopulations (<0.1% from inocula of 10(8) to 10(9) CFU/ml) of ATCC 19606, and most clinical isolates grew in the presence of colistin 3 to 10 microg/ml. Four successive passages of ATCC 19606 in broth containing colistin (up to 200 microg/ml) substantially increased the proportion of the resistant subpopulations able to grow in the presence of colistin at 10 microg/ml from 0.000023 to 100%; even after 16 passages in colistin-free broth, the proportion only decreased to 2.1%. This represents the first demonstration of heterogeneous colistin-resistant A. baumannii in "colistin-susceptible" clinical isolates. Our findings give a strong warning that colistin-resistant A. baumannii may be observed more frequently due to potential suboptimal dosage regimens recommended in the product information of some products of colistin methanesulfonate.     

Acinetobacter baumannii: an emerging multidrug-resistant threat

Amid the recent attention focused on the growing impact of methicillin-resistant Staphylococcus aureus and multidrug-resistant Pseudomonas aeruginosa infections, the pathogen Acinetobacter baumannii has been stealthily gaining ground as an agent of serious nosocomial and community-acquired infection. Historically, Acinetobacter spp. have been associated with opportunistic infections that were rare and of modest severity; the last two decades have seen an increase in both the incidence and seriousness of A. baumannii infection, with the main targets being patients in intensive-care units. Although this organism appears to have a predilection for the most vulnerable patients, community-acquired A. baumannii infection is an increasing cause for concern. The increase in A. baumannii infections has paralleled the alarming development of resistance it has demonstrated. The persistence of this organism in healthcare facilities, its inherent hardiness and its resistance to antibiotics results in it being a formidable emerging pathogen. This review aims to put into perspective the threat posed by this organism in hospital and community settings, describes new information that is changing our view of Acinetobacter virulence and resistance, and calls for greater understanding of how this multifaceted organism came to be a major pathogen.     

Acinetobacter baumannii: an emerging multidrug-resistant threat

Amid the recent attention focused on the growing impact of methicillin-resistant Staphylococcus aureus and multidrug-resistant Pseudomonas aeruginosa infections, the pathogen Acinetobacter baumannii has been stealthily gaining ground as an agent of serious nosocomial and community-acquired infection. Historically, Acinetobacter spp. have been associated with opportunistic infections that were rare and of modest severity; the last two decades have seen an increase in both the incidence and seriousness of A. baumannii infection, with the main targets being patients in intensive-care units. Although this organism appears to have a predilection for the most vulnerable patients, community-acquired A. baumannii infection is an increasing cause for concern. The increase in A. baumannii infections has paralleled the alarming development of resistance it has demonstrated. The persistence of this organism in healthcare facilities, its inherent hardiness and its resistance to antibiotics results in it being a formidable emerging pathogen. This review aims to put into perspective the threat posed by this organism in hospital and community settings, describes new information that is changing our view of Acinetobacter virulence and resistance, and calls for greater understanding of how this multifaceted organism came to be a major pathogen.     

多重耐药鲍曼不动杆菌感染危险因素分析

目的：了解本地区多重耐药鲍曼不动杆菌感染的危险因素及耐药状况。方法回顾性分析80例多重耐药鲍曼不动杆菌患者与48例非多重耐药鲍曼不动杆菌感染患者的基本资料,以及菌株药敏试验检测结果;采用Logistic回归分析方法分析多重耐药菌株感染的独立危险因素。结果多重耐药鲍曼不动杆菌感染的独立危险因素包括入住重症监护病房（IC U ）、侵入性操作、两种及其以上抗菌药物序贯使用或联合使用。多重耐药鲍曼不动杆菌对左氧氟沙星、氨苄西林/舒巴坦、亚胺培南、替卡西林/克拉维酸的耐药率均大于60％,对除上述4种药物以外抗菌药物的耐药率均超过90％。结论多重耐药鲍曼不动杆菌感染的独立危险因素包括入住IC U、侵入性操作、两种及其以上抗菌药物序贯使用或联合使用。严格进行医院环境的消毒和医院感染的监测,合理使用抗菌药物,是控制多重耐药鲍曼不动杆菌感染的重要手段。     

多重耐药鲍曼不动杆菌携带碳青霉烯类水解酶基因情况的研究

目的 研究浙江省瑞安市人民医院多重耐药鲍曼不动杆菌中金属-内酰胺酶(IMP、VIM)、 KPC酶、 OXA-23型水解酶基因的携带情况,探讨各种碳青霉烯类水解酶在多重耐药鲍曼不动杆菌中的作用。 方法 采用Whonet 5.4 软件分析多重耐药鲍曼不动杆菌的标本类型和病区分布,以及药敏资料;设计特异性引物,用PCR方法扩增IMP、VIM、KPC和OXA-23特异基因,并用琼脂糖电泳分析其产物。 结果 70株多重耐药鲍曼不动杆菌均未检测到IMP、VIM及KPC基因,其中58株亚胺培南耐药菌株均携带OXA-23基因,阳性率为82.86%。 结论 OXA-23型水解酶是造成瑞安市人民医院鲍曼不动杆菌对临床常用碳青霉烯类抗生素耐药的主要原因。     

ICU多药耐药鲍曼不动杆菌耐药监测分析

目的 分析重症监护病房(ICU)多药耐药鲍曼不动杆菌(MDR-AB)耐药性及耐药基因.方法 对分离自ICU送检痰标本的5株鲍曼不动杆菌进行药敏试验,采用聚合酶链反应(PCR)及测序技术进行耐药基因分析.结果 5株鲍曼不动杆菌对对β-内酰胺类、喹诺酮类药物耐药,均检出C、D类β-内酰胺酶基因ADC和OXA-23,及外膜蛋白CarO突变.结论应采取有效措施控制鲍曼不动杆菌的传播,加强耐药性监测,防止鲍曼不动杆菌院内扩散及耐药性变迁.     

多重耐药性鲍曼不动杆菌耐药基因及菌株聚类分析

目的了解临床分离到的鲍曼不动杆菌耐药相关基因存在状况和菌株间的亲缘性。方法药敏试验用PhoenixTM100系统检测。用PCR扩增β-内酰胺酶基因、氨基糖甙类药物修饰酶基因、DNA拓扑异构酶基因等,并用DNA测序仪证实。结果247株鲍曼不动杆菌对亚胺培南和美洛培南耐药率最低,仅为3.2%、4.1%。20株多重耐药性鲍曼不动杆菌中,17株具TEM型β-内酰胺酶基因,氨基糖甙类药物修饰酶基因aac（3）-Ⅰ、aac（3）-Ⅱ、aac（3）-Ⅲ、aac（3）-Ⅳ、aac（6′）-Ⅰ、ant（2″）-Ⅰ、ant（3″）-Ⅰ基因检出率分别为80%、15%、30%、70%、15%、55%、80%。20株对环丙沙星耐药的鲍曼不动杆菌gyrA密码子均由TCA→TTA,氨基酸由Ser83→Leu,而85%菌株（17/20）的ParC氨基酸序列发生Ser80→Leu替代。聚类分析显示存在2株克隆株,其耐药表型基本一致。结论本院鲍曼不动杆菌携带多种β-内酰胺酶、氨基糖甙类修饰酶等耐药基因,喹诺酮耐药决定区基因突变是细菌耐受喹诺酮类药物重要原因。聚类分析表明,本院的鲍曼不动杆菌存在克隆传播。     

Novel bis-indole agents active against multidrug-resistant Acinetobacter baumannii

The in vitro activity of 5 novel Microbiotix bis-indole agents (MBXs) (Microbiotix, Worcester, MA) against 30 multidrug-resistant (MDR) Acinetobacter baumannii (including 18 resistant to carbapenems) was evaluated. Overall, MIC(90)'s ranged from 1 to 8 μg/mL, whereas those for imipenem were >64 μg/mL. MBX 1196 was the most potent (MIC(90), 1 μg/mL). MBXs are compounds that are highly effective against MDR A. baumannii.