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超广谱β-内酰胺酶及其他赋予对氧亚氨基β-内酰胺耐药性的酶

Extended-spectrum beta-lactamases and other enzymes providing resistance to oxyimino-beta-lactams.

作者信息

Jacoby G A

机构信息

Edith Nourse Rogers Memorial Veterans Hospital, Bedford, Massachusetts, USA.

出版信息

Infect Dis Clin North Am. 1997 Dec;11(4):875-87. doi: 10.1016/s0891-5520(05)70395-0.

Abstract

Bacteria have once again demonstrated their remarkably versatility in meeting the introduction of new classes of beta-lactam antibiotics by modifying available plasmid mediated beta-lactamases to expand their spectrum of action and by incorporating chromosomal beta-lactamase genes onto plasmids that permit their spread to new hosts. Such resistance is more common than presently is appreciated because current NCCLS breakpoints for resistance underestimate its prevalence. A number of risk factors for acquisition of ESBL-producing K. pneumoniae have been defined, but most will be no easier to control than those for infection by MRSA or VRE. More clinical and animal model studies are needed to evaluate options for treatment. Most strains remain susceptible to imipenem and other carbapenems, but carbapenem resistance has appeared either by spread of metallo-beta-lactamase or by production of an AmpC enzyme combined with loss of an outer membrane porin channel. Attack on our adversaries' latest biological weapons is likely to require enhanced versatility on our part as well.

摘要

细菌再次展现出其非凡的适应性,它们通过修饰现有的质粒介导的β-内酰胺酶来扩大其作用谱,以及将染色体β-内酰胺酶基因整合到质粒上,使其能够传播到新宿主,从而应对新型β-内酰胺类抗生素的出现。这种耐药性比目前所认识到的更为普遍,因为当前美国国家临床实验室标准化委员会(NCCLS)的耐药性断点低估了其流行程度。已经确定了一些获得产超广谱β-内酰胺酶肺炎克雷伯菌的危险因素,但大多数因素并不比耐甲氧西林金黄色葡萄球菌(MRSA)或耐万古霉素肠球菌(VRE)感染的危险因素更容易控制。需要更多的临床和动物模型研究来评估治疗方案。大多数菌株对亚胺培南和其他碳青霉烯类药物仍敏感,但碳青霉烯类耐药性已通过金属β-内酰胺酶的传播或通过产生AmpC酶并伴有外膜孔蛋白通道缺失而出现。要对抗我们对手的最新生物武器,我们自身可能也需要增强适应性。

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