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目的了解不同医院间肺炎克雷伯菌连续分离株质粒AmpC基因存在情况和耐药性。方法应用聚合酶链反应(PCR)法对耐药的肺炎克雷伯菌连续分离株进行AmpC酶DHA和ACT-1基因检测和分析。结果PCR结果显示A院44株肺炎克雷伯菌中DHA基因阳性4株(9.1%);B院25株肺炎克雷伯菌中DHA基因阳性8株(32.0%),ACT-1基因二家均为阴性,二家医院DHA基因检出率有明显差别(P〈0.05)。结论质粒型AmpC酶基因可通过转化、接合等方式转移给其他同种或不同种菌,易于传播。二家医院DHA基因检出率有明显差别,并均己有流行的迹象。 相似文献
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目的 通过Solexa高通量测序法研究肺炎克雷伯菌的质粒与耐药性的关系.方法 菌株为7年临床分离的206株肺炎克雷伯菌.提取所有菌的全部质粒DNA,Solexa高通量测序获得大规模的短序列.SOAP软件对质粒基因进行分析拼接,分析结果与相关数据库进行比对.MAQ软件分析质粒基因组包含的超广谱β-内酰胺酶(ESBL)多样性及单核苷酸多态性(SNP)情况.结果 肺炎克雷伯菌质粒基因组中已知的直接与耐药相关的基因就有13种.质粒基因组中存在多个ABC主动外排转运系统.发现4种编码β-内酰胺酶的ORF,其中SHV型ESBLs分布最广.系统分析了206株肺炎克雷伯菌质粒基因组中SHV型ESBLs的SNPs位点,发现存在着大量的非同义替换SNPs位点.结论 发现质粒中SHV型ESBLs基因可能受到选择压力,存在着大量的非同义替换SNPs位点.肺炎克雷伯菌质粒存在外排药物耐药方式,从而形成低水平的非特异多重耐药. 相似文献
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通过PCR基因测序分析两种酶的基因类型,用接合转移试验了解肺炎克雷伯菌耐药基因转移方式,并用纸片扩散试验和微量稀释法测定细菌对17种抗生素的敏感性,现报道如下。 相似文献
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目的 了解邢台地区产超广谱β-内酰胺酶(ESBLs)肺炎克雷伯菌的分子流行病学特点,为临床感染预防和治疗提供依据.方法 采用最小抑菌浓度(MIC)法检测产ESBLs肺炎克雷伯菌的耐药性,选取13种特异性引物采用聚合酶链反应(PCR)的方法检测产ESBLs肺炎克雷伯菌的基因类型.结果 2013年1月至2014年3月从邢台人民医院分离出的125株非重复的产ESBLs肺炎克雷伯菌菌株,耐药基因以blaCTX-M的阳性率最高,为92.0%,blaSHV和blaTEM次之,为82.9%和73.2%.所有菌株均携带1种或1种以上的耐药基因.结论 产ESBLs肺炎克雷伯菌多重耐药现象严重,耐药基因以blaCTX-M、blaSHV和blaTEM为主.医院应加强对ESBLs的监测,降低ESBLs的感染率以及耐药基因的突变,提高治疗感染的效率,防止医院感染的发生. 相似文献
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目的 研究儿童多重耐药肺炎克雷伯杆菌(MDR-KP)脓毒症感染的危险因素和有效治疗方法。方法 选取2016年1月~2019年1月在我院治疗的50例MDR-KP脓毒症感染患儿为研究对象,将其设为为观察组。选取同期在我院诊治的50例非MDR-KP脓毒症感染患儿设为对照组,比较两组患儿感染前使用抗生素情况、治疗效果、预后、住院时间、机械通气时间,采用多元Logistic回归分析MDR-KP脓毒症感染的危险因素。结果 观察组患儿感染前使用抗生素的种类、感染前使用三代头孢和碳青霉素类抗生素均高于对照组,机械通气时间、住院时间均长于对照组,差异有统计学意义(P<0.05);对照组患儿治疗总有效率为98.00%,高于观察组的82.00%,差异有统计学意义(P<0.05);Logistic回归分析显示,感染前使用抗生素的种类、感染前使用三代头孢和碳青霉素类抗生素是MDR-KP脓毒症感染的独立危险因素(P<0.05)。结论 临床依据实际病情合理选择抗生素治疗,可有效预防和降低MDR-KP感染发生。 相似文献
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产AmpC酶大肠埃希菌和肺炎克雷伯菌中整合子与多重耐药的研究 总被引:1,自引:0,他引:1
目的探讨整合子介导的耐药机制在产AmpC酶大肠埃希菌和肺炎克雷伯菌多重耐药中的作用.方法5株产AmpC酶大肠埃希菌和肺炎克雷伯菌分离自2002年1月-2004年5月间我院呼吸科住院的患者,采用E-test试验条进行药敏试验、电转化试验,筛选、分离耐药质粒.PCR扩增Ⅰ型整合子基因盒插入序列,分子克隆和序列分析.结果所有产酶菌株通过电转化试验可将头孢西丁耐药性传递给受体菌,5个产AmpC酶耐药质粒中,有4个检出整合酶序列,其中3个携带2种抗药性基因盒,包括氨基糖苷乙酰转移酶基因aacA4;氨基糖苷腺苷转移酶基因aadA5;二氢叶酸还原酶基因dfrA17;氯霉素外排蛋白编码基因cmL44.结论整合子介导的抗药性基因盒参与了产质粒AmpC酶大肠埃希菌和肺炎克雷伯菌多重耐药的形成,应引起高度重视. 相似文献
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目的 检测质粒介导的喹诺酮类外排基因qepA在临床分离的产超广谱β-内酰胺酶(ESBLs)的肺炎克雷伯菌中的分布情况,并对阳性菌株进行同源性分析.方法 41株细菌的鉴定和药敏采用Vitek-2 Compact系统;采用PCR法检测qepA并进行序列测定、比对.应用Rep-PCR法采用Diversilab系统对qepA阳性菌株进行同源性分析;同时了解阳性株上的rmtB分布情况.结果 5株肺炎克雷伯菌上检测到qepA基因,检出率为12.2%.Diversilab分析结果表明其中两株的qepA阳性菌同源性超过99%.包含qepA的肺炎克雷伯菌中2株(40%)检出rmtB.结论 在肺炎克雷伯菌临床菌株上检出质粒介导的喹诺酮类外排基因qepA.Abstract: Objective To investigate the prevalence of qepA, quinolone efflux protein, among 41 unique clinical strains of K. pneumoniae producing ESBLs and to study the qepA-bearing isolates using the Diversilab system. Methods Identification and antimicrobial susceptibility were performed by Vitek-2 Compact System. Screening of qepA was carried out by PCR amplification. The NCBI BLAST program was utilized for sequence comparisons. qnr-bearing strains was evaluated by the Repetitive-sequence-based PCR(Rep-PCR) employing the Diversilab system. And the existence of rmtB was detected among these qepA contained isolates. Results qepA were detected in 5 isolates( 12.2% ). The Rep-PCR profiles produced by the Diversilab system showed that 2/5 of isolates were indistinguishable. And 60% of qepA-positive isolates were detected to harbor rmtB gene. Conclusion The data suggest the emergence of qepA-borne K. pneumoniae. 相似文献
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肺炎克雷伯菌(Klebsiella pneumoniae)是临床常见的院内感染致病菌,常引起泌尿系统、呼吸系统以及血流感染等。近年来,肺炎克雷伯菌生物膜引起的慢性感染日益得到重视,对肺炎克雷伯菌生物膜的研究也越来越多。为了适应周围环境,肺炎克雷伯菌会形成生物膜(biofilm),这是一种相对于浮游细菌的生存方式,生物膜由细菌及其自身分泌的代谢产物(胞外多糖、蛋白质、胞外DNA、脂质等)组成。生物膜状态下的肺炎克雷伯菌耐药性极强,容易逃避机体的免疫攻击,难以彻底清除,使临床抗感染变得更加棘手。本文就生物膜形成过程、生物膜状态细菌的耐药机制、生物膜测定方法以及生物膜防治作简要综述。 相似文献
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WEI FENG SHI SU JIAN WANG JIAN PING QIN 《中华微生物学和免疫学杂志(英文版)》2007,5(2):158-162
Klebsiella pneumoniae ( K. pneumoniae) is one of the main gmn-negative bacilli in clinical practice. Nosocomial infections caused by K. pneumoniae producing extended-spectrum β-lactamases (ESBLs) are very difficult to treat. This paper investigated the resistant characteristics of K. pneumoniae producing ESBLs and their aminoglycoside-modifying enzyme gene expressions including Nacetyltransferases and O-adenyltransferases. Bacteria identification and ESBLs confirmatory tests were performed by Phoenix^TM-100 system. And minimum inhibitory concentrations (MICs) of gentamicin, amikacin, kanamycin, tobranycin, netilmicin and neomycin in 53 K. pneumoniae isolates were detected by agar dilution. In addition, six aminoglycoside-modifying enzyme genes were amplified by polymerase chain reaction (PCR) and verified by DNA sequencer. It was found that imipenem and meropenem against 120 K. pneumoniae isolates produced powerful antimicrobial activities. The resistant rates of gentamicin and amikacin were 55.0% and 46.7%, respectively. Except neomycin, MIC50 and MIC90 of gentamicin, amikacin, kanamycin, tobramycin and netilmicin in 53 K. pneumoniae were all 〉 128 μg/ml, and the resistant rates were 83.0%, 52.3%, 75.5%, 81.1% and 69.8%, respectively. However, neomycin was only 39.6%. In addition, five modifying enzyme genes, including aac(3)-Ⅰ, aac(3)-Ⅱ, aac(6')-Ⅰb, ant(3")-Ⅰ, ant(2")-Ⅰ genes, were found in 53 isoaltes except aac (6')-Ⅱ, and their positive rates were 11.3%, 67.9%, 47.2%, 1.9% and 39.6%, respectively. It was also confirmed by nucleotide sequence analysis that the above resistant genes shared nearly 100% identities with GenBank published genes. The results obtained in the present study indicated that K. pneumoniae producing ESBLs strains are rapidly spreading in our hospital, and their resistance to aminoglycosides may be associated with aminoglycoside-modifying enzyme gene expressions. 相似文献
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I. Galani E. Xirouchaki K. Kanellakopoulou G. Petrikkos H. Giamarellou 《Clinical microbiology and infection》2002,8(9):579-588
Objective To investigate the underlying resistance mechanisms in 10 Klebsiella pneumoniae isolates.
Methods Ten K. pneumoniae strains according to distinct bacteriocin typing and REP-PCR, were examined for their plasmid content, their ability to transfer their resistance to aminoglycosides and third-generation cephalosporins, and their production of aminoglycoside-modifying enzymes and β -lactamases.
Results Transfer of resistance to the above-mentioned antibiotics as well as to co-trimoxazole and tetracycline in Escherichia coli strain RC 85 at a frequency of 5–106 was achieved for all strains by conjugation. Similar strains harbor a self-transferable multiresistant plasmid (80 kb) with similar Eco RI and Hind III restriction patterns. This plasmid encodes an extended-spectrum β -lactamase which confers high-level resistance to third-generation cephalosporins and aztreonam. It produces SHV-5 β -lactamase, as demonstrated by isoelectric focusing and DNA sequencing. Aminoglycoside resistance was co-transferred, and AAC(6')-I, mediating resistance to gentamicin, tobramycin, netilmicin and amikacin, and AAC(3)-I, mediating resistance to gentamicin and sisomycin, were encoded in all isolates and their transconjugants, while APH(3')-I, mediating resistance to kanamycin and neomycin, was encoded in seven strains.
Conclusions It appears that a multiresistant transferable plasmid encoding the SHV-5 β -lactamase, causing unusually high resistance to ceftazidime and aztreonam, and the combination AAC(6')-I + AAC(3)-I of acetylating enzymes causing, also resistance to all clinically available aminoglycosides, is established in K. pneumoniae in Greece. 相似文献
Methods Ten K. pneumoniae strains according to distinct bacteriocin typing and REP-PCR, were examined for their plasmid content, their ability to transfer their resistance to aminoglycosides and third-generation cephalosporins, and their production of aminoglycoside-modifying enzymes and β -lactamases.
Results Transfer of resistance to the above-mentioned antibiotics as well as to co-trimoxazole and tetracycline in Escherichia coli strain RC 85 at a frequency of 5–10
Conclusions It appears that a multiresistant transferable plasmid encoding the SHV-5 β -lactamase, causing unusually high resistance to ceftazidime and aztreonam, and the combination AAC(6')-I + AAC(3)-I of acetylating enzymes causing, also resistance to all clinically available aminoglycosides, is established in K. pneumoniae in Greece. 相似文献
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目的 探讨氟喹诺酮体外诱导耐药肺炎克雷伯菌(KPn)膜孔蛋白表达变化.方法 取2008年9月至2009年6月本院临床分离对环丙沙星敏感的KPn 20株,分为对照组和实验组,每组10株.对照组直接涂布于含环丙沙星128 mg/L的平板,观察其对环丙沙星的敏感性.实验组应用不同浓度梯度环丙沙星逐级诱导成为高度耐药株,观察应用环丙沙星前后KPn敏感株和耐药株膜孔蛋白表达的差异.结果 对照组10株KPn直接涂布于含环丙沙星128 mg/L的平板培养后无一存活.3对KPn菌株R9、S9、R4、S4、R3、S3环丙沙星诱导前后膜孔蛋白相对表达量分别是3.86±0.11、6.44±0.26、5.46±0.18、9.58±0.34、1.75±0.06和9.78±0.36,诱导耐药的KPn较相应敏感株膜孔蛋白表达明显减少(均P<0.05).结论 氟喹诺酮体外诱导耐药KPn膜孔蛋白表达减少,可能通过细菌外膜通透性改变在KPn诱导耐药中起重要作用. 相似文献
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探讨环丙沙星诱导耐药肺炎克雷伯菌(KPn)对几类常见的抗生素的耐药性。方法 琼脂二倍稀释法测定环丙沙星对20株临床分离KPn敏感株的最低抑菌浓度(MIC),用环丙沙星对其进行体外多步诱导成耐药株。诱导前和诱导后K-B纸片扩散法进行药敏试验检测其对头孢他啶、头孢西丁、氨曲南、亚胺培南、莫西沙星、阿米卡星的敏感性。诱导后进行产超广谱β-内酰胺酶(ESBL)初筛和确证实验。结果 20株KPn有17株成功诱导成环丙沙星高度耐药株,ESBL筛选和确证实验显示17株诱导耐药株无一产ESBL。诱导耐药株对莫西沙星全部耐药,对头孢他啶、亚胺培南、氨曲南全部敏感,对阿米卡星的敏感率为88.2%(15/17),而对头孢西丁耐药率达88.2% (15/17)、中介率12.8%(2/17)。结论 KPn在长期低剂量接触环丙沙星后可产生耐药性,且对莫西沙星和头孢西丁有交叉耐药。环丙沙星诱导耐药的KPn对头孢西丁交叉耐药的机制可能相似。 相似文献
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目的 研究碳青霉烯类耐药肺炎克雷伯菌临床儿童分离株的耐药特点及分子流行病学特征.方法 收集温州医学院附属第二医院2010年7月-2011年6月从儿童标本中分离的耐碳青霉烯类肺炎克雷伯菌12株,所有菌株为非重复菌株,菌种鉴定采用全自动微生物分析仪.改良的Hodge试验筛选产碳青霉烯酶阳性菌株,采用PCR法检测KPC、IMP、bla(s)、VIM、SPM和整合酶基因,测序确定基因型.对菌株进行质粒结合试验、质粒消除试验检测质粒的转移性.脉冲场凝胶电泳(PFGE)分析耐药菌株的同源性.结果 12株耐碳青霉烯类肺炎克雷伯菌对庆大霉素、妥布霉素、阿米卡星、环丙沙星、左氧氟沙星、复方磺胺甲噁唑的敏感率分别为8.3%、41.7%、58.3%、8.3%、8.3%、33.3%;12株菌均携带有KPC-2基因,且同时携带有TEM-1和SHV型β-内酰胺酶基因,其中SHV-11-like和SHV-1 2-like各6株;11株携带CTX-M型基因,其中4株为CTX-M-14-like基因,6株CTX-M-15-like基因;2株携带有OXA-10型基因,1株携带有PER-1基因.未检出NDM-1、GIM、SPM、SIM、VIM型碳青霉烯酶基因.12株均为Ⅰ类整合酶基因(int1)阳性.2株通过接合试验把质粒传递给受体菌EC600.所有接合子blaTEM-1基因阳性、超广谱β-内酰胺酶(ESBL)基因阳性及对亚胺培南、庆大霉素、阿米卡星、妥布霉素和头孢噻肟耐药,接合子ESBL基因型与供菌一致.2株菌经质粒消除后对亚胺培南的MIC值均有较大程度降低,消除后KPC-2基因扩增为阴性.12株KPC-2基因阳性菌株经PFGE分成5个基因型,主要为B型和C型.结论 KPC-2型碳青霉烯酶基因已经在儿童肺炎克雷伯菌中播散,常伴随携带多种类型的ESBL基因和Ⅰ类整合酶基因,部分耐药基因可通过质粒播散. 相似文献
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S. Brisse T. van Himbergen K. Kusters J. Verhoef 《Clinical microbiology and infection》2004,10(10):942-945
A rapid method combining gyrA PCR-restriction fragment length polymorphism analysis, parC PCR and adonitol fermentation was developed to identify Klebsiella pneumoniae phylogenetic groups KpI, KpII and KpIII. Analysis of 420 clinical isolates from 26 hospitals showed that the three groups were widespread geographically. KpI comprised 80.3% of 305 isolates from blood and 82.2-97.2% of isolates from other clinical sources. KpIII was never found among isolates from urinary tract infections. KpI isolates from blood were generally less susceptible than KpIII isolates to the ten antimicrobial agents tested, with KpII being intermediate. The frequencies of ceftazidime resistance were 21.6% and 8.6% in KpI and KpIII isolates, respectively (p 0.01). 相似文献
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目的 调查我院产ESBL肺炎克雷伯菌临床分离株16S rRNA甲基化酶基因的分布以及与耐药谱的关系,并初步探讨其在分子流行病学分析中的作用.方法 收集我院临床2010年3月至9月分离出69株非重复产ESBL肺炎克雷伯菌,采用PCR法检测16S rRNA 甲基化酶基因,并对阳性菌株进行ESBL基因及整合子基因分析,通过DNA直接测序确定.质粒接合试验和质粒消除试验确定16S rRNA甲基化酶基因的传播途径,利用ERIC-PCR技术进行基因分型.结果 69株产ESBL肺炎克雷伯菌中有rmtB阳性菌株20株(28.9%),其中2株同时携带有rmtB和armA.在20株产16SrRNA甲基化酶菌株中,均携带有CTX-M基因,测序显示14株CTX-M-14基因,6株CTX-M-15基因;14株携带有TEM-1基因;8株携带有SHV基因,测序显示5株SHV-12基因,3株SHV-11基因;3株携带有OXA-10基因;3株携带有VBE-1基因.另有12株携带有int1阳性,含有5种不同的耐药基因盒,分别携带drfA25、drfA1、drfA12、aadA1、aadA2、sat和blaVEB-1基因.ERIC-PCR法显示20株16SrRNA甲基化酶基因阳性的肺炎克雷伯菌主要分为5型,A型为优势流行克隆株.质粒接合和消除试验发现A型克隆株KP5和KP16 rmtB均位于一质粒上并通过接合传播.结论 本院产ESBL肺炎克雷伯菌临床分离株中存在16S rRNA甲基化酶基因rmtB的普遍流行,导致对多种氨基糖苷类抗生素高水平耐药.rmtB可通过水平基因传播和克隆传播的两种方式进行播散,并且存在同时产ESBLs、16S rRNA甲基化酶和Ⅰ类整合子的肺炎克雷伯菌的传播. 相似文献
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目的:了解耐喹诺酮类肺炎克雷伯杆菌的体外抗菌活性及CCCP对喹诺酮类药物体外抗菌活性的影响。方法:从99株肺炎克雷伯杆菌临床分离株中选取对环丙沙星耐药(M IC≥4μg/m l)菌株14株。采用琼脂二倍稀释法测定抗菌药的最低抑菌浓度(M IC),同时测CCCP对喹诺酮类药物M IC的影响。结果:14株肺炎克雷伯杆菌对5种喹诺酮类药物无一株敏感,且表现出较高水平的耐药。对其它抗生素的耐药率由高到低依次是氨苄西林、哌拉西林、氯霉素、庆大霉素、氨曲南、阿米卡星、头孢噻肟和头孢吡肟。亚胺培南未发现有耐药株。喹诺酮类药物与CCCP合用后,在部分菌中的M IC中出现了明显的降低。结论:耐喹诺酮类肺炎克雷伯杆菌对喹诺酮类呈交叉耐药,且呈较高水平耐药;CCCP可以明显提高部分喹诺酮类药物对肺炎克雷伯杆菌的体外抗菌活性;亚胺培南、第三代头孢菌素、氨曲南和阿米卡星对耐喹诺酮肺炎克雷伯杆菌仍有一定作用。 相似文献