Overview of the epidemiological profile and laboratory detection of extended-spectrum β-lactamases
Overview of the epidemiological profile and laboratory detection of extended-spectrum β-lactamases
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DOI：
10.1086/500662
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发表时间：
2006-04-15
影响因子：
11.8
通讯作者：
Segreti, J
中科院分区：
文献类型：
--
作者：
Pfaller, MA;Segreti, J
超广谱β-内酰胺酶（ESBLs）是质粒介导的细菌酶，其赋予对广泛的β-内酰胺类的抗性。它们是由革兰氏阴性菌中发现的天然β-内酰胺酶的基因突变遗传而来，尤其是大肠杆菌和克雷伯氏菌属的感染性菌株。基因序列的修饰拓宽了酶的底物特异性，包括第三代头孢菌素，如头孢他啶。由于产ESBL菌株对多种常用抗菌药物具有耐药性，因此其增殖构成了严重的全球健康问题，使越来越多的住院患者的治疗策略变得复杂。另一种耐药机制也是肠杆菌科常见的，是由染色体或质粒来源的AmpC β-内酰胺酶的过量产生引起的。这些微生物具有与产ESBL微生物相似的抗菌药物耐药模式，但与大多数ESBL不同的是，AmpC酶不受棒菌素和类似B-内酰胺酶抑制剂的抑制。最近在检测和制定ESBL检测和确证检测统一标准方面的技术改进有望使临床实验室更容易准确鉴定产ESBL微生物。
Extended-spectrum beta-lactamases (ESBLs) are plasmid- mediated bacterial enzymes that confer resistance to a broad range of beta-lactams. They are descended by genetic mutation from native beta-lactamases found in gram-negative bacteria, especially infectious strains of Escherichia coli and Klebsiella species. Genetic sequence modifications have broadened the substrate specificity of the enzymes to include third-generation cephalosporins, such as ceftazidime. Because ESBL-producing strains are resistant to a wide variety of commonly used antimicrobials, their proliferation poses a serious global health concern that has complicated treatment strategies for a growing number of hospitalized patients. Another resistance mechanism, also common to Enterobacteriaceae, results from the overproduction of chromosomal or plasmid- derived AmpC beta-lactamases. These organisms share an antimicrobial resistance pattern similar to that of ESBL-producing organisms, with the prominent exception that, unlike most ESBLs, AmpC enzymes are not inhibited by clavulanate and similar b- lactamase inhibitors. Recent technological improvements in testing and in the development of uniform standards for both ESBL detection and confirmatory testing promise to make accurate identification of ESBL-producing organisms more accessible to clinical laboratories.