膝关节液中产气巴斯德菌的耐药性及耐药机制研究

目的 探讨产气巴斯德菌耐药性及耐药机制.方法 用美国BD公司PhoenixTMl00全自动细菌鉴定/药敏仪,对膝关节炎患者膝关节液分离的1株病原菌进行鉴定,并对21种抗菌药物的敏感性进行检测,应用头孢硝噻吩(Ncf)试验检测其β-内酰胺酶(BLs),多底物纸片法分类检测β-内酰胺酶.结果 PhoenixTMl00细菌鉴定仪鉴定该菌为产气巴斯德菌,可信度(ID)为94.0％;对氨曲南、头孢他啶耐药,对氨苄西林、氨苄西林/舒巴坦、阿莫西林/克拉维酸、哌拉西林、哌拉西林/他唑巴坦、头孢唑林、头孢西丁、头孢噻肟、头孢吡肟、碳青霉烯类、氨基糖苷类、四环素类、氯霉素、多黏菌素、氟喹诺酮类、磺胺甲噁唑/甲氧苄啶敏感;BLs的分类检测中,氨曲南为6 mm,耐药,与头孢他啶/克拉维酸、氨苄西林/舒巴坦均无协同及拮抗,头孢他啶为10 mm,耐药,头孢他啶/克拉维酸及头孢噻肟均为14 mm,头孢噻肟/克拉维酸为16 mm,头孢西丁为28 mm,均敏感.结论 该产气巴斯德菌临床分离株仅对部分β-内酰胺类药物耐药(耐药性较低),其机制为产BLs,耐药表型及克拉维酸协同试验阳性,推测为产某种产超广谱β-内酰胺酶(ESBLs).     

佳木斯地区大肠埃希菌和阴沟肠杆菌质粒介导头孢菌素酶、超广谱β-内酰胺酶基因型分布

目的 了解佳木斯地区临床分离的大肠埃希菌和阴沟肠杆菌中质粒介导头孢菌素酶(AmpC酶)和超广谱β-内酰胺酶(ESBLs)流行情况及主要的基因型别.方法 127株临床分离无重复大肠埃希菌81株与阴沟肠杆菌46株,采用酶提取物三维实验检测产AmpC酶和ESBLs菌株,聚合酶链反应(PCR)扩增质粒型AmpC酶与ESBLs基因及其序列测定以确定其基因亚型.结果 46株阴沟肠杆菌中,单产AmpC酶者、单产ESBLs者、高产AmpC酶并产ESBLs者分别占21.7％、28.3％、6.5％;81株大肠埃希菌中,单产AmpC酶者、单产ESBLs者、高产AmpC酶并产ESBLs者分别占19.8％、38.3％、9.9％.大肠埃希菌ESBLs基因型为TEM、SHV、CTX-M,质粒AmpC酶基因型为DHA.阴沟肠杆菌ESBLs基因型为TEM、SHV、CTX-M,质粒AmpC酶基因型为DHA.结论 CTX-M型和DHA-1型分别是本地区大肠埃希菌和阴沟肠杆菌ESBLs和质粒介导AmpC酶的主要流行基因型.     

阴沟肠杆菌产AmpC酶和ESBLs的检测及药物敏感性分析

目的 了解阴沟肠杆菌的耐药特性及其产AmpCβ-内酰胺酶(AmpC酶)和产超广谱β-内酰胺酶(ESBLs)的情况。方法 药敏实验和AmpC酶检测采用WalkAway-40全自动微生物分析仪,FSBLs俭测采用NCCLS纸片确证试验。结果 阴沟肠杆菌的标本来源主要为痰液、尿液、创口分泌物等,以烧伤科为多。ESBLs检出率为51．8％,AmpC酶检出率为53．2％。业胺培南敏感率为92．8％,其余抗生素敏感率均低于50％。结论 阴沟肠杆菌Ampc酶和ESBLs检出率较高,耐药性严苇,治疗应首选亚胺培南。     

连续4年临床分离阴沟肠杆菌耐药监测与对策

目的 探讨阴沟肠杆菌引起医院内感染的特点以及对抗菌药物耐药性的变化趋势.方法 应用Walkaway40型全自动细菌鉴定仪对2007～2010年分离的256株阴沟肠杆菌进行鉴定和药敏试验,并进行统计学分析.结果 256株阴沟肠杆菌来源主要为伤口分泌物、痰及咽拭子、尿液、血液等,分别占51.6%、18.8%、12.5%、7.4%.对亚胺培南敏感性最高,耐药率较低(0.8%),对头孢西丁耐药率高达98.0%.近年来阴沟肠杆菌多重耐药得到有效控制,临床常用药物的耐药呈下降趋势.结论 加强阴沟肠杆菌的耐药监测、了解其耐药性变迁可合理指导临床用药,有效控制阴沟肠杆菌耐药菌株的产生.     

医院感染阴沟肠杆菌产金属酶及耐药性分析

目的:了解临床分离的阴沟肠杆菌的耐药性及产金属β内酰胺酶的基因分布状况。方法:临床分离的40株阴沟肠杆菌用法国梅里埃公司的V ITEK-2全自动微生物分析系统鉴定,K-B法进行抗生素敏感试验,采用纸片协同法检测金属酶,PCR法扩增金属酶基因,并对PCR产物进行电泳后纯化,测序比对确定基因型。结果:阴沟肠杆菌对头孢他啶、头孢西丁、亚胺培南、美罗培南、阿米卡星、头孢吡肟、环丙沙星的耐药率分别为52.5%、92.5%、7.5%、5.5%、65.0%、12.5%、85.0%。其中40株阴沟肠杆菌中产金属酶的3株,3株菌中有2株扩增出金属酶IMP基因。结论:院内感染标本分离的阴沟肠杆菌对临床常用的多种抗生素耐药,由于金属酶菌株的存在,阴沟肠杆菌对亚胺培南等碳青霉烯类药物的耐药性增加。     

河南某医院569株阴沟肠杆菌临床分布及耐药分析

目的 调查阴沟肠杆菌的临床分布特点及耐药情况,为临床治疗阴沟肠杆菌感染提供实验室依据.方法 根据临床实验室操作规程对医院2010-2014年分离的569份阳性标本进行鉴定及药敏试验,统计其临床分布特点及药敏试验结果.结果 阴沟肠杆菌主要感染人群为外科病人和婴幼儿,临床分布以神经外科(15.60％)、新生儿科(14.10％)、泌尿外科(10.90％)为主,标本主要来自于尿液(38.70％)、痰液(29.00％)及血液(8.79％),药敏试验结果示对亚胺培南、美罗培南、头孢哌酮/舒巴坦较为敏感,敏感率分别是97.46％、96.78％和90.23％.结论 肠杆菌耐药现象严重,要尽快建立该菌在医院的耐药谱,加强耐药监测,根据药敏试验,合理规范使用抗菌药物.     

Emergence of colistin resistance in Enterobacter aerogenes from Croatia

A colistin-resistant Enterobacter aerogenes [study code 12264] was isolated from the tracheal aspirate of a 71-year-old male patient in the General Hospital [GH] in Pula, Croatia. The patient was previously treated in University Hospital Centre in Rijeka with colistin in order to eradicate Acinetobacter baumannii isolate, susceptible only to colistin and tigecycline. Genes encoding ESBLs [bla_TEM, bla_SHV, bla_CTX-M, bla_PER-1] were screened by PCR. The strain was shown to possess bla_CTX-M-15 and bla_TEM-1 genes. To asses genes possibly involved in resistance to colistin the chromosomal enconding mgrB gene and the plasmid-mediated mcr-1 and mcr-2 genes were screened as described previously. Mcr-1 and mcr-2 genes were not detected and mgrB gene presented a wild-type sequence. PCR-based Replicon typing method [PBRT] conducted on an E. aerogenes isolate, showed that the strain carried an IncN plasmid. Adaptive mechanisms such as changes of the bacterial cell outer membrane that cause porin decrease or presence of an efflux pump, due to selection pressure exerted by the therapeutic administration of colistin, could be responsible for the development of colistin resistance in our strain, as recently reported in E. aerogenes from France. Due to effective infection control measures, the colistin-resistant strain did not spread to other patients or hospital wards. This is the first report of an ESBL-producing, colistin-resistant E. aerogenes in clinically relevant samples such as endotracheal aspirate and blood culture, showing the presence of this rare resistance profile among Gram-negative bacteria.     

TEM-24 extended-spectrum β-lactamase-producing Enterobacter aerogenes: long-term clonal dissemination in French hospitals

Objective To investigate interstrain relatedness of TEM-24-producing Enterobacter aerogenes clinical strains isolated between 1993 and 1998 in 10 French hospitals from nine areas by pulsed-field gel electrophoresis (PFGE) and plasmid patterns.
Methods Fifteen TEM-24 - producing strains and a set of 16 control strains having various other antibiotic resistance phenotypes were genotyped by PFGE. Plasmid DNA from TEM-24 - producing strains and transconjugants was analyzed .
Results Analysis of Xba I macrorestriction patterns revealed only minor variations, and showed that all 15 TEM-24 - producing strains were closely related. Some isolates originating from distant areas had indistinguishable patterns . According to their clustering correlation coefficients, they were also genomically distant from the control strains . Two plasmid patterns were observed in TEM-24-producing strains, one of them in 13 of the strains. Large plasmids of 85 kb encoding TEM-24 β-lactamase were present in all isolates and, in all except one strain, could be transferred with high frequency by conjugation .
Conclusions These results confirm that the spread of the TEM-24 extended-spectrum β-lactamase in France was essentially due to the dissemination of a single clone .     

In vitro selective concentrations of cefepime and ceftazidime for AmpC β-lactamase hyperproducer Enterobacter cloacae variants

This study aimed to compare the selective concentrations of cefepime and ceftazidime on Enterobacter cloacae. A mixed culture of a wild-type ceftazidime/cefepime-susceptible (4±10⁷ CFU/mL) strain and an ampC derepressed Enterobacter cloacae (10⁵ CFU/mL) strain (relative proportions 99.75% and 0.25%) was challenged for 4 h with different antibiotic concentrations of ceftazidime and cefepime (0.03–4096 mg/L), and then transferred to drug-free medium. The proportion of wild-type versus derepressed population was evaluated after 24 h.
Ceftazidime and cefepime selected the derepressed variant at concentrations ranging from 1 to 4096 and from 0.12 to 16 mg/L respectively.
These results suggest that serum concentrations attainable with a 2 g/8 h cefepime dosage may be able to suppress the emergence of derepressed ampC mutants.