细菌耐药机制及抗生素合理应用的研究

目的 探讨如何合理使用抗生素来应对细菌的耐药性.方法 分析细菌的耐药机制和抗生素的作用机制.结果 细菌是通过产生钝化酶、改变靶位蛋白及细胞膜渗透性等耐药.结论 循环使用或联合使用抗生素可减轻细菌的耐药性对临床治疗的影响,减少新的耐药性的产生.     

细菌的耐药机制及对策

目的:了解细菌产生耐药性的机制及如何消除由此引发的治疗危机.方法:对细菌的耐药机制研究进展、如何处理细菌耐药性进行综述.结果:细菌的耐药机制总体分为两类,即遗传学机制和生化机制.结论:细菌产生耐药性的原因多种多样,如靶点的改变、结构的修饰、遗传、抗生素灭活酶的产生、抗生素的泵出等.正确合理的使用抗生素,遏制抗生素的滥用;研发新的抗耐药菌型抗生素;可以降低或彻底消除耐药性的产生.     

基因盒-整合子系统与细菌的耐药性

近年来,细菌对抗生素耐药性不断上升和耐药性快速传播已经成为临床感染性疾病治疗的难题。研究表明,细菌的耐药性大多在外环境诱导下经可动遗传因子,如质粒（plasmid）、转座子（transposon）、噬菌体（bacteriophage）、整合子（integron）／基因盒（genecas-sette）等的传递获得。目前,由具有捕获及表达外来耐药基因盒能力的整合子系统介导的细菌耐药机制越来越引起研究者们的关注,其对多重耐药性研究有着非常重要的意义。整合子1989年由StokesHW等首次提出。     

由细菌耐药机制探讨临床抗生素的合理应用

目的：通过对细菌耐药机制的分析,探讨临床上抗生素的合理使用,以应对细菌的耐药性。方法：结合已有文献报道和多年临床经验,分析细菌的耐药机制,探讨临床抗生素的合理应用原则和方法。结果：细菌的耐药机制分为遗传学机制和生化机制,其耐药性的产生与抗生素灭活酶的产生、膜通透性改变、新靶位的产生和改变等有关。结论：合理使用抗生素,防止其滥用,能有效较少细菌耐药性的产生。     

抗生素耐药机制研究进展

随着抗生素的广泛大量的使用，细菌的耐药性及耐药水平越来越高，病原菌对常用抗生素，如β-内酰胺类、氨基糖甙类和喹诺酮类药物的耐药性尤为突出，给疾病的治疗和临床用药造成了诸多困难。及时了解细菌的耐药机制和抗生素的发展及应用，对预防和治疗细菌性感染，研制新的抗菌药物及控制耐药性的蔓延非常重要。     

临床分离致病菌耐药机制及抗感染研究进展

随着抗生素在临床上的大量应用,细菌耐药现象日益严重,研究其耐药机制,防止细菌的耐药性的产生和蔓延,合理使用抗生素治疗感染性疾病,防止院内感染,减少患者痛苦及经济费用尤为重要,为此,针对临床分离常见菌的耐药性和抗感染治疗作如下综述。     

抗生素耐药性机理及对策

本文就细菌对抗生素的耐药机制研究进展、及如何处理细菌对抗生素的耐药性作出综述,旨在控制抗生素耐药性问题上提出一些策略和建议。     

Amp C酶及其耐药性

本文叙述了Amp C酶的定义、Amp C酶的基因结构与功能、Amp C酶的合成、Amp C酶的耐药性及其耐药机制，以及Amp C酶的检测方法。Amp C酶是由肠杆菌科细菌和铜绿假单胞菌等产生的一类头孢菌素酶，可水解头孢菌素类抗生素，导致细菌对这类抗生素产生耐药性。编码产生Amp C酶的基因包括结构基因-amp C和四种调控基因-ampR、ampD、ampE以及ampG,但其具体的转录、调控机制目前尚未完全明了。Amp C酶的合成具有明显的诱导性，其诱导有菌种依赖性、抗生素依赖性和生长条件依赖性。Amp C酶的耐药机制主要是作用于头胞菌素的β-内酰胺环上的羰基，形成酰化酶中间体，然后在水分子的作用下导致β-内酰胺环开环而失活。大部分Amp C酶都是由细菌染色体所介导，但近年来陆续在质粒上发现这些基因，并在肺炎克雷伯菌、大肠埃希菌、产气肠杆菌和沙门菌中持续高水平的表达，还可以通过质粒在细菌间相互传播，导致耐药菌的广泛传播。产Amp C酶菌株的检测以改良的酶提取物三维试验法较佳。     

临床耐药菌株的出现及其对策

细菌对抗生素耐药已成为全球化趋势， 且耐药情况日益严重。其直接的后果是由细菌感染导致的病死率增高， 医疗费用增加。遗憾的是细菌耐药的严重性并没有引起足够的重视， 为此， 本文就细菌耐药原因、 耐药机制及控制耐药对策等进行了概述。抗生素的滥用滥用抗生素是导致细菌耐药的主要原因。滥用抗生素的途径可能是多方面的， 如： 抗生素销售管理不严， 患者可以随意在药店购买到抗生素；商业抗生素广告盛行， 一定程度上纵容和扩大了抗生素的滥用；医师滥用抗生素， 包括理由不充分的经验性治疗过多、 疗程过长， 不必要或过长的预防性…     

多重耐药鲍曼不动杆菌耐药性及碳青霉烯酶相关耐药基因研究

目的研究鲍曼不动杆菌(acinetobacter baumannii,Ab)耐药性及对β-内酰胺酶基因的耐药存在情况。方法收集分离我院自2012年至2013年住院患者多重耐药鲍曼不动杆菌株53株,用Walkway96SI细菌鉴定系统检测其耐药性及敏感性,采用聚合酶联反应(PCR)检测碳青霉烯酶等相关基因:OXA-23,OXA24,OXA-58,IMP,VIM。结果对15种抗菌药物的抗菌活性中,亚胺培南为54.7%,头孢他啶,头孢噻肟,哌拉西林均达到了86.8%,其他抗菌药物的耐药率均在70%以上。对53株Ab菌进行基因检测结果为:43.4%的菌株OXA-23阳性(23/53),9.5%的菌株OXA-58阳性(5/53),3.8%的菌株IMP阳性(2/53),18.8%的菌株VIM阳性(10/53),OXA-24全部为阴性。结论 OXA-23阳性时对抗生素耐药及其对抗生素的MIC分布有重要关系,泛耐药同时携带多种耐药基因是导致其对所有常用药物均耐药的重要原因。     

大肠埃希菌和肺炎克雷伯菌外膜蛋白与耐药机制的研究进展

细菌的膜孔蛋白及其形成的孔道是细菌与外界交流的主要途径,也是抗生素透过细菌细胞膜的重要通道。细菌膜孔蛋白合成降低或膜孔蛋白缺失可阻碍抗生素进入细菌,从而引起细菌对抗生素耐药。在细菌的耐药机制研究方面,膜孔蛋白的作用日益受到关注,文章从大肠埃希菌和肺炎克雷伯菌入手,对其膜孔蛋白的特点、构成、合成调控机制及其与细菌耐药的关系进行综述。     

大肠埃希菌和肺炎克雷伯菌外膜蛋白与耐药机制的研究进展

细菌的膜孔蛋白及其形成的孔道是细菌与外界交流的主要途径,也是抗生素透过细菌细胞膜的重要通道。细菌膜孔蛋白合成降低或膜孔蛋白缺失可阻碍抗生素进入细菌,从而引起细菌对抗生素耐药。在细菌的耐药机制研究方面,膜孔蛋白的作用日益受到关注,文章从大肠埃希菌和肺炎克雷伯菌入手,对其膜孔蛋白的特点、构成、合成调控机制及其与细菌耐药的关系进行综述。     

院内获得性绿脓杆菌感染对抗生素敏感性的研究

目的探讨院内获得性绿脓杆菌感染特点及目前常用多种抗生素的耐药性。方法收集2009年10月-2011年5月呼吸内科合并肺绿脓杆菌感染病例117例（其中47例气管插管或气管切开接受机械通气）痰培养标本,应用微生物自动分析仪对绿脓杆菌共457株进行鉴定及药物敏感试验。结果引起院内获得性绿脓杆菌感染的457株绿脓杆菌对13种常用抗生素的平均耐药率〉30％,对阿米卡星耐药率〈30％,对喹喏酮类耐药率接近30％,对β-内酰胺类和头孢菌素类抗生素耐药率较高。结论治疗院内获得性绿脓杆菌感染,β-内酰胺酶类联合氨基糖甙类或喹诺酮类为较优化的组合;对MDR—PA可首选头孢哌酮舒巴坦与阿米卡星联合或头孢哌酮舒巴坦与环丙沙星联合。     

120株奶牛乳腺炎流行病原菌的分类和耐药谱分析

目的 通过对流行于四川成都、眉山和绵阳的奶牛乳腺炎病原菌进行分类和耐药性分析,为奶牛乳腺炎的临床合理用药提供科学依据.方法 采用K-B法测定了临床分离的120株奶牛乳腺炎病原菌对青霉素、链霉素、四环素、红霉素、庆大霉素、喹诺酮类、头孢噻吩和头孢噻肟8种抗生素的药物敏感性.结果 120株奶牛乳腺炎病原菌中91株病原菌表现为耐药,耐药率为75.8%,大部分病原菌耐受1种(34.0%)或2种抗生素(33.0%).病原菌对8种抗生素的敏感性与临床用药规律呈一定的相关性,其中分离病原菌对青霉素和链霉素的耐药率最高,分别为65.2%和64.8%;其次为四环素和红霉素,耐药率分别为26.7%和30.3%;对环丙沙星的敏感性最好,敏感率为89.2%,提示其为该地区治疗奶牛乳腺炎的有效药物.结论 该地区奶牛乳腺炎病原菌以葡萄球菌和大肠埃希菌最为常见,所试奶牛乳腺炎病原菌耐药率高,部分菌株表现为多重耐药,提示应合理规范使用抗生素,减缓耐药菌株的产生.     

Resistance to antibiotics: are we in the post-antibiotic era?

Serious infections caused by bacteria that have become resistant to commonly used antibiotics have become a major global healthcare problem in the 21st century. They not only are more severe and require longer and more complex treatments, but they are also significantly more expensive to diagnose and to treat. Antibiotic resistance, initially a problem of the hospital setting associated with an increased number of hospital-acquired infections usually in critically ill and immunosuppressed patients, has now extended into the community causing severe infections difficult to diagnose and treat. The molecular mechanisms by which bacteria have become resistant to antibiotics are diverse and complex. Bacteria have developed resistance to all different classes of antibiotics discovered to date. The most frequent type of resistance is acquired and transmitted horizontally via the conjugation of a plasmid. In recent times new mechanisms of resistance have resulted in the simultaneous development of resistance to several antibiotic classes creating very dangerous multidrug-resistant (MDR) bacterial strains, some also known as "superbugs". The indiscriminate and inappropriate use of antibiotics in outpatient clinics, hospitalized patients and in the food industry is the single largest factor leading to antibiotic resistance. In recent years, the number of new antibiotics licensed for human use in different parts of the world has been lower than in the recent past. In addition, there has been less innovation in the field of antimicrobial discovery research and development. The pharmaceutical industry, large academic institutions or the government are not investing the necessary resources to produce the next generation of newer safe and effective antimicrobial drugs. In many cases, large pharmaceutical companies have terminated their anti-infective research programs altogether due to economic reasons. The potential negative consequences of all these events are relevant because they put society at risk for the spread of potentially serious MDR bacterial infections.     

铜绿假单胞菌的耐药性及碳青霉烯类抗生素的研究进展

铜绿假单胞菌(Pseudomonas aeruginosa)是一种常见的医院内获得性感染致病菌，其耐药性强，耐药谱广。亚胺培南等碳青霉烯类抗生素是近年来治疗铜绿假单胞菌疗效较好的药物，但随着临床的广泛应用，铜绿假单胞菌对亚胺培南等产生了耐药性。铜绿假单胞菌对碳青霉烯类抗生素的耐药机制有β-内酰胺酶的水解、外膜通透性降低和主动外排系统的排出等，这些耐药机制之间相互协同作用而产生高度耐药。针对这些耐药机制，开发活性更高、安全性更好的碳青霉烯类抗生素显得极为迫切。本文对铜绿假单胞菌的耐药性及碳青霉烯类抗生素的研究进展进行了综述。     

产超广谱β-内酰胺酶细菌流行病学研究

超广谱β-内酰胺酶(ESBLs)是由质粒介导,能水解青霉素、广谱头孢菌素及单环类抗生素并产生耐药。各地区ESBLs的检出率、基因分型各不相同,细菌质粒上可以同时携带≥2种的ESBL编码基因。产ESBLs菌感染为多种危险因素所致,临床治疗产ESBLs菌感染应首选碳青霉烯类抗生素。     

幽门螺杆菌抗生素耐药率分析

目的分析本院3年中幽门螺杆茵(helicobacter pylori,Hp)抗生素耐药率,为临床根除Hp时抗生素的选择提供参考。方法选取2000年9月-2002年4月在我院行胃镜检查后活检组织作Hp培养的患者共728例,对306例活检组织Hp培养阳性者行5种抗生素(甲硝唑、阿莫西林、头孢三嗪、大观霉和呋喃唑酮)的敏感试验。结果6种抗生素的耐药率逐年上升(P<0.05)。甲硝唑的耐药率显著高于其他4种抗生素(32％,P<0.01),其余4种抗生素耐药率相比差异无显著性(P>0.05)。性别与不同年龄组的耐药率比较均无明显差异(P>0.05)。结论 随着根治Hp时抗生素的应用,Hp的抗生素耐药率逐年上升;甲硝唑的耐药率最高;性别和年龄与抗生素耐药之间没有相关性。     

Can antibiotic use be both just and sustainable... or only more or less so?

Antibiotic resistance threatens the capacity to treat life-threatening infections. If it is accepted that it will be many years (if not decades) until the production of new antibiotics overcomes current concerns with antibiotic resistance then ways to conserve the effectiveness of current antibiotics will have to be found. For many bacterial agents of infection levels of antibiotic resistance are directly dependent on the quantity of antibiotic prescribed. Antibiotics are currently underutilised in many parts of the world. If a just distribution of access to antibiotics requires equal access for individuals with equal need irrespective of wealth then responding to this requirement of justice has the potential to shorten the effective life of currently available antibiotics. Increasing the range and numbers of individuals treated with antibiotics would seem to threaten sustainability and also potentially undermine the access of future generations to cost-effective treatments for bacterial infection. The control of antibiotic resistance requires that the determinants of infectious disease transmission are addressed, such as poor housing, education and nutrition as well as the provision of antibiotics. The apparent tension between intragenerational justice and sustainability diminishes when the account of distributive justice extends beyond access to antibiotics and includes plural entitlements. Controlling antibiotic resistance requires more than the redistribution or reduction (in the overall use) of antibiotics.     

Antibiotics in the environment

Molecules with antibiotic properties, produced by various microbes, have been around long before mankind recognized their usefulness in preventing and treating bacterial infections. Bacteria have therefore been exposed to selection pressures from antibiotics for very long times, however, generally only on a micro-scale within the immediate vicinity of the antibiotic-producing organisms. In the twentieth century we began mass-producing antibiotics, mainly synthetic derivatives of naturally produced antibiotic molecules, but also a few entirely synthetic compounds. As a consequence, entire bacterial communities became exposed to unprecedented antibiotic selection pressures, which in turn led to the rapid resistance development we are facing today among many pathogens. We are, rightly, concerned about the direct selection pressures of antibiotics on the microbial communities that reside in or on our bodies. However, other environments, outside of our bodies, may also be exposed to antibiotics through different routes, most often unintentionally. There are concerns that increased selection pressures from antibiotics in the environment can contribute to the recruitment of resistance factors from the environmental resistome to human pathogens. This paper attempts to 1) provide a brief overview of environmental exposure routes of antibiotics, 2) provide some thoughts about our current knowledge of the associated risks for humans as well as ecosystems, and 3) indicate management options to reduce risks.