耐碳青霉烯类铜绿假单胞菌的耐药机制研究

目的探讨新疆地区临床分离的铜绿假单胞菌产金属β-内酰胺酶、外排泵Mex AB-oprM和外膜蛋白OprD2表达水平及其与碳青霉烯类抗菌药物耐药性之间的关系。方法聚合酶链反应(PCR)和测序法分别检测1~4组铜绿假单胞菌的金属β-内酰胺酶;RT-PCR检测1、2、4组铜绿假单胞菌外排泵Mex AB-oprM和孔蛋白OprD2的表达水平。结果含亚胺培南耐药和美罗培南耐药组均有≥42.9%检出亚胺培南(IMP)、VIM金属酶基因型;OprD2显著低于表达在亚胺培南与美罗培南同时耐药组(87.5%),高于亚胺培南与美罗培南同时敏感组(20.0%),差异有统计学意义;Mex AB-oprM在各组中分别有60.0%、57.1%、37.5%的高表达,差异无统计学意义。结论外膜的低通透性、金属β-内酰胺酶的水解和主动外排泵过度表达,三者相互协同作用是该地区耐碳青霉烯类铜绿假单胞菌的主要机制。     

铜绿假单胞菌对亚胺培南耐药机制的研究

目的 研究铜绿假单胞菌对亚胺培南耐药机制。方法 用PCR法对铜绿假单胞菌亚胺培南耐药相关的金属β-内酰胺酶IMP、VIM基因和外膜蛋白OprD2基因等3种主要耐药基因进行了检测与分析。结果 35株耐亚胺培南铜绿假单胞菌IMP和VIM型金属酶基因检测均阴性，35株耐亚胺培南铜绿假单胞菌OprD2基因检测均阴性，但35株铜绿假单胞菌23S rRNA基因扩增阳性。结论 研究表明湖北襄樊地区铜绿假单胞菌不产生金属酶，但从遗传学角度证实外膜蛋白OprD2基因缺失是襄樊铜绿假单胞菌对亚胺培南耐药的重要机制。     

5年间耐亚胺培南铜绿假单胞菌耐药性监测及耐药机制探讨

目的检测2004-2008年临床分离铜绿假单胞菌对亚胺培南的耐药性,并探讨其耐药机制。方法采用K-B法检测临床分离铜绿假单胞菌对抗菌药物的敏感性,采用PCR方法检测碳青酶烯酶基因和外膜通道蛋白基因。结果 2004-2008年共分离铜绿假单胞菌1947株,耐亚胺培南的菌株573株,耐药率29.4%;2006-2008年与2004-2005年相比耐亚胺培南的铜绿假单胞菌有上升趋势,从14.4%上升到31.8%;耐亚胺培南的铜绿假单胞菌中以阿米卡星最敏感,其次为头孢他啶和头孢哌酮/舒巴坦,哌拉西林/他唑巴坦的敏感率下降明显;23株耐亚胺培南的铜绿假单胞菌IMP基因阳性4株(17.4%),VIM基因阳性4株(17.4%),OprD2缺失18株(79.3%)。结论耐亚胺培南铜绿假单胞菌携带多种金属酶基因,但主要是由于外膜通道蛋白基因OprD2缺失引起,阿米卡星与头孢他啶或头孢哌酮/舒巴坦联合是有效的治疗手段。     

耐亚胺培南铜绿假单胞菌外膜孔蛋白与β-内酰胺酶研究

目的探讨铜绿假单胞菌外科监护室分离株对碳青酶烯类抗菌药物耐药机制。方法琼脂稀释法测定抗菌药物最低抑菌浓度(MIC);提取β-内酰胺酶进行三维水解试验及等电聚焦电泳;紫外分光光度计测定酶活性;用PCR扩增IMP、VIM金属酶基因;用Western印迹分析外膜孔蛋白OprD2表达水平。结果从外科监护室分离的49株铜绿假单胞菌,有41株对亚胺培南耐药;耐药组34株菌产AmpC酶,其中8株同时产ESBLs酶,2株仅产ESBLs,未筛选出产金属酶菌株;亚胺培南耐药组酶活性(74.32±53.42)μmmol/mg与亚胺培南敏感组酶活性(8.7±16.16)μmmol/mg比较差异有统计学意义(P<0.01);耐药组OprD2表达均有不同程度的降低或缺失,而敏感组均正常表达OprD2,耐药组OprD2相对表达量(0.20±0.27)与敏感组(3.10±2.20)比较差异有统计学意义(P<0.01);未扩增出IMP、VIM金属酶基因。结论外膜孔蛋白OprD2表达降低或缺失以及高活性AmpC酶,是外科监护室耐亚胺培南铜绿假单胞菌的主要原因,与IMP、VIM金属酶关系不大。     

医院耐亚胺培南铜绿假单胞菌的耐药机制研究

目的研究医院铜绿假单胞菌(PAE)耐药情况及对亚胺培南的耐药机制分布。方法对医院临床分离的150株非重复铜绿假单胞菌对亚胺培南(IMP)等14种常用抗菌药物的最低抑菌浓度(MIC)进行检测;进一步对耐亚胺培南铜绿假单胞菌(IRPA)64株作为受试株,进行耐药机制表型初筛试验及基因检测。结果 IRPA共64株,占42.6%,其中9株为产金属β-内酰胺酶(MBL)阳性,占试验菌株的14.06%,4株携带VIM基因和3株携带IMP基因,其他为阴性结果;17株主动外排表型筛选阳性,5株同时检测出oprM、mexB基因、有9株仅扩增出oprM基因而没有mexB基因、有3株未扩增出外排基因;oprD2基因缺失共11株,占17.19%。结论调查结果显示,铜绿假单胞菌对亚胺培南的耐药机制主要有金属酶的产生;主动外排的过度表达;孔道蛋白OprD2的缺失。     

耐亚胺培南铜绿假单胞菌耐药分析及产金属β-内酰胺酶检测

目的:研究临床分离的耐亚胺培南铜绿假单胞菌对12种抗菌药物的耐药性及产金属β-内酰胺酶菌株情况。方法:采用K-B法进行药物敏感性试验,2-巯基丙酸纸片协同试验筛选金属酶菌株。结果:60株耐亚胺培南铜绿假单胞菌呈多重耐药,对临床常用的多种抗菌药物耐药率分别为:IPM100%、CTX98.3%、TIM96.7%、TZP85.0%、LEV78.3%、ATM78.3%、FEP73.3%、AK73.3%。纸片协同试验产金属β-内酰胺酶4株,检出率为6.7%。结论:耐亚胺培南铜绿假单胞菌呈多重耐药。产金属β-内酰胺酶是铜绿假单胞菌耐亚胺培南的机制之一。密切监视产金属β-内酰胺酶菌株,合理使用抗生素,减少耐药菌株传播。     

耐亚胺培南铜绿假单胞菌的耐药性分析

目的探讨耐亚胺培南铜绿假单胞菌的耐药性,为临床合理用药提供参考。方法对医院2012年耐亚胺培南铜绿假单胞菌感染患者的临床分布、标本来源进行统计分析,比较耐亚胺培南和非耐亚胺培南铜绿假单胞菌对常用抗菌药物的耐药率,采用WHONE 5.6软件进行统计分析。结果 2012年共分离出铜绿假单胞菌837株,其中耐亚胺培南铜绿假单胞菌195株,分离率为23.30%;主要分布在ICU、神经内科,分别占25.64%、14.37%;标本主要来源于痰液、分泌物,分别占69.23%和12.31%;耐亚胺培南铜绿假单胞菌对常用抗菌药物的耐药率明显高于非耐亚胺培南铜绿假单胞菌(P<0.05)。结论耐亚胺培南铜绿假单胞菌的耐药现象极为严重,需加强对耐亚胺培南铜绿假单胞菌的耐药性监测,合理使用抗菌药物,对患者严格实施标准预防和接触隔离的措施,防止交叉感染。     

铜绿假单胞菌对亚胺培南的耐药水平调查及药敏分析

目的了解2009年3月-2010年7月岳阳市一人民医院住院患者送检标本分离的铜绿假单胞菌对亚胺培南的耐药水平,并分析亚胺培南耐药株对其他常用抗菌药物的耐药性。方法临床标本分离的铜绿假单胞菌用常规K-B法进行药物敏感试验,若结果判定为耐药和中介,则进一步采用琼脂倍比稀释法检测铜绿假单胞菌对亚胺培南及其他9种抗菌药物的MIC。结果铜绿假单胞菌对亚胺培南的耐药率为13.5%,20株耐亚胺培南的铜绿假单胞菌对9种常用抗菌药物的耐药率也普遍较高,有2株铜绿假单胞菌对受试的10种抗菌药物全部耐药。结论铜绿假单胞菌对亚胺培南的耐药率较高,并对多种抗菌药物耐药,应密切关注本地区细菌耐药性的变迁,适时调整治疗方案,合理应用抗菌药物。     

铜绿假单胞菌对碳青霉烯类抗生素耐药性

目的探讨铜绿假单胞菌对碳青霉烯类抗生素的耐药性和耐药机制。方法选取温州医学院附属第一医院162株铜绿假单胞菌临床分离株,采用琼脂稀释法检测抗生素亚胺培南和美罗培南对铜绿假单胞菌的最低抑菌浓度(M IC);PCR扩增分离株外膜蛋白基因OprD2和碳青霉烯酶基因VIM、IMP、SPM、KPC,对阳性产物测序确定基因亚型;羰基氰氯苯腙(CCCP)协同抑制试验检测膜外排机制。结果 162株分离菌株中,亚胺培南和美罗培南的耐药率分别为37.0%和30.9%;60株耐亚胺培南和/或美罗培南菌株(简称耐药株)中,50株对2种抗生素均耐药,另10株仅对亚胺培南耐药;耐药株中有18株OprD2基因缺失,102株不耐亚胺培南或美罗培南菌株(简称敏感株)中有20株OprD2基因缺失;耐药株中检出13株碳青霉烯酶阳性,其中5株产VIM型,8株产IMP型,敏感株中未检出VIM、IMP基因,所有菌株中未检出SPM-1、KPC基因;耐药株有48.3%外排泵表型试验阳性,以亚胺培南和美罗培南作为底物的分别有19株和24株,敏感株有10.8%外排试验阳性。结论铜绿假单胞菌对碳青霉烯类抗生素耐药严重,与外膜蛋白OprD2缺失、产碳青霉烯酶和主动外排共同作用有关。     

重症监护病房耐亚胺培南铜绿假单胞菌的耐药性及产金属酶分析

目的 了解医院重症监护病房(ICU)分离的铜绿假单胞菌耐亚胺培南药物及产金属酶情况.方法 对医院ICU 2007年1-12月临床分离的铜绿假单胞菌标本来源的药敏试验结果及金属酶检测结果进行回顾性分析,同时与历年的耐药率进行比较,药敏试验采用K-B法,金属酶检测采用CAZ-EDTA协同试验.结果 共检出60株铜绿假单胞菌,其中对亚胺培南敏感菌株40株(66.7%),耐亚胺培南菌株20株(33.3%);20株耐药株产金属酶7株;在耐亚胺培南菌株中,对美罗墙南、庆大霉素、妥布霉素以及环丙沙星、复方新诺明耐药率＞90.0%,对哌拉西林、哌拉西林/他唑巴坦耐药率＞80.0%;对头孢他啶、头孢吡肟的耐药率均为50.0%;对多黏菌素E的耐药率较低;20株菌全部为耐＞3类药物,显著高于亚胺培南敏感菌株的27.5%.结论 ICU耐亚胺培南铜绿假单胞菌的耐药率维持较高水平,其产金属酶是对亚胺培南抗菌药物耐药的重要机制之一,应加强对临床产酶株的检测,指导临床合理使用抗菌药,减少耐药株的产生.     

Carbamate resistance in Anopheles albimanus. Cross resistance spectrum and stability of resistance

Carbamate resistance induced in a field strain of A. albimanus from El Salvador by laboratory selection with propoxur remained fairly stable on relaxation of selection pressure for 12 generations. Studies on cross and multiple resistance showed that this strain was not resistant to the pyrethroids bioresmethrin, bioallethrin, and CRC 11451, although resistance to cismethrin was 2.3-fold. Resistance to 10 carbamates of various structural configurations covered a broad spectrum, being for example >100× to Bay 38799, Ciba 17474, and Ciba 18107, 74.8× to carbaryl, 20.57× to carbanolate, and 2.27× to Stauffer R 15396. The possible causes of the presence or absence of cross resistance and the implications of stability of resistance and cross resistance are discussed.     

HIV-1 drug resistance and resistance testing

The global scale-up of antiretroviral (ARV) therapy (ART) has led to dramatic reductions in HIV-1 mortality and incidence. However, HIV drug resistance (HIVDR) poses a potential threat to the long-term success of ART and is emerging as a threat to the elimination of AIDS as a public health problem by 2030. In this review we describe the genetic mechanisms, epidemiology, and management of HIVDR at both individual and population levels across diverse economic and geographic settings. To describe the genetic mechanisms of HIVDR, we review the genetic barriers to resistance for the most commonly used ARVs and describe the extent of cross-resistance between them. To describe the epidemiology of HIVDR, we summarize the prevalence and patterns of transmitted drug resistance (TDR) and acquired drug resistance (ADR) in both high-income and low- and middle-income countries (LMICs). We also review to two categories of HIVDR with important public health relevance: (i) pre-treatment drug resistance (PDR), a World Health Organization-recommended HIVDR surveillance metric and (ii) and pre-exposure prophylaxis (PrEP)-related drug resistance, a type of ADR that can impact clinical outcomes if present at the time of treatment initiation. To summarize the implications of HIVDR for patient management, we review the role of genotypic resistance testing and treatment practices in both high-income and LMIC settings. In high-income countries where drug resistance testing is part of routine care, such an understanding can help clinicians prevent virological failure and accumulation of further HIVDR on an individual level by selecting the most efficacious regimens for their patients. Although there is reduced access to diagnostic testing and to many ARVs in LMIC, understanding the scientific basis and clinical implications of HIVDR is useful in all regions in order to shape appropriate surveillance, inform treatment algorithms, and manage difficult cases.     

大肠埃希菌对氟喹诺酮类的耐药性及其机制研究

目的 探讨大肠埃希菌(ECO)对氟喹诺酮类药物的耐药率及耐药机制.方法 K-B法测定100株ECO对5种氟喹诺酮抗菌药物的耐药性,试管稀释法测定耐环丙沙星和左氧氟沙星的最低抑菌浓度(MIC);错配PCR技术检测耐环丙沙星ECO gyrA基因和parC基因的突变.结果 100株ECO中耐环丙沙星有65株;环丙沙星MIC50、MIC90分别是32、128 μg/ml,左氧氟沙星MIC50、MIC90是16、64 μg/ml;基因位点结果显示,耐环丙沙星的65株中,有60株发生gyrA、parC一个或多个基因位点的突变,有5株未发生突变.结论 gyrA、parC基因突变是该地区ECO,对氟喹诺酮类药物耐药的重要机制,且基因突变位点越多其耐药程度越高.     

铜绿假单胞菌的耐药性及耐药基因研究

目的分析临床分离铜绿假单胞菌的耐药性,检测耐药基因,探讨耐药基因与耐药性的关系。方法采用美国德灵Microscan WalkAway 40系统对病原菌进行鉴定及药敏试验;采用PCR扩增技术对临床分离铜绿假单胞菌耐药性相关基因TEM、CARB、OXA-10、VIM、VEB、IMP、DHA、aac(6′)-Ⅰb、aac(6′)-Ⅱ、ant(2′)-Ⅰ、qacE△1-sul1、oprD2进行检测。结果 67株铜绿假单胞菌耐药严重,对哌拉西林/他唑巴坦、哌拉西林、替卡西林/克拉维酸的耐药率达100.0%;检出TEM、CARB、OXA-10、aac(6′)-Ⅰb、aac(6′)-Ⅱ、ant(2′)-Ⅰ、qacE△1-sul1、VIM、VEB基因,检出阳性率分别为98.6%、82.1%、88.1%、92.6%、92.6%、71.7%、83.6%、13.4%、1.5%,未检出IMP、DHA基因。结论β-内酰胺酶耐药是多机制联合作用的结果,氨基糖苷类修饰酶基因的高检出率与铜绿假单胞菌对氨基糖苷类的耐药关系有待进一步探讨,医院分离铜绿假单胞菌对季铵类、双胍类消毒剂耐药。     

鲍氏不动杆菌耐药性及相关耐药基因检测分析

目的检测分析鲍氏不动杆菌耐药性及相关耐药基因。方法采用K-B法(CLSI 2008年标准)测定鲍氏不动杆菌临床分离株耐药性;PCR方法检测TEM、SHV、CTX-M、I MP、VI M、OXA-23、OXA-24耐药基因以及Ⅰ、Ⅱ类整合酶。结果 130株鲍氏不动杆菌,除阿米卡星和碳青霉烯类外,对其他抗菌药物耐药率非常高,TEM、SHV、CTX-M、Int1、Int2基因阳性率分别为68.5%、10.8%、17.7%、75.4%、0;51株耐碳青霉烯类鲍氏不动杆菌中I MP、VI M、OXA-23、OXA-24基因阳性率分别为25.5%、19.6%、72.5%、0。结论鲍氏不动杆菌耐药性较高,携带TEM型β-内酰胺酶、OXA-23、I MP和VI M型碳青霉烯酶基因和Ⅰ类整合酶;产生OXA-23型碳青霉烯酶和金属酶是医院鲍氏不动杆菌对碳青霉烯类耐药的主要机制。     

Conceptualizing resistance

The 1990s saw a proliferation of sociological work applying Foucault's ideas on governmentality to health promotion and public health. This work characterized public health discourses as regimes of power and knowledge employed in the regulation and surveillance of individuals and populations. This article is concerned with the question of how and to what extent those who are subject to such regimes are able to resist them. We seek to identify the various forms in which resistance to such regimes of power have been manifest in empirical studies of health and illness. Our aims are threefold. The first is to alert empirical researchers who wish to examine resistance in the context of health and health care to the subtle and nuanced ways in which such resistance can be manifested both within and outside encounters with health professionals. This is achieved through tracing both the evolution of Foucault's own concepts around resistance and the way in which these ideas have been mobilized in empirical studies. The second, and related, aim is to demonstrate the complex forms which such resistance takes, problematizing the simplistic assumptions that adherence to health promotion advice necessarily implies the collapse of agency, and that resistance necessarily involves the rejection of advice and interventions. The third is to highlight the potentially problematic normative qualities that may be assigned to resistance.