β-Lactam resistance in Staphylococcus aureus: the adaptive resistance of a plastic genome

被引：159

作者：

Fuda, CCS ^{[1
]}

Fisher, JF ^{[1
]}

Mobashery, S ^{[1
]}

机构：

[1] Univ Notre Dame, Dept Chem & Biochem, Notre Dame, IN 46556 USA

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2005年 / 62卷 / 22期

关键词：

Staphylococcus aureus; beta-lactamase; blaZ; blaI; blaR; mecR; mecI; mecA; PBP; 2a; MRSA; VRSA;

D O I：

10.1007/s00018-005-5148-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Staphylococci have two mechanisms for resistance to beta-lactam antibiotics. One is the production of beta-lactamases, enzymes that hydrolytically destroy beta-lactams. The other is the expression of penicillin-binding protein 2a (PBP 2a), which is not susceptible to inhibition by beta-lactam antibiotics. Strains of S. aureus exhibiting either beta-lactamase or PBP 2a-directed resistance (or both) have established a considerable ecological niche among human pathogens. The emergence and subsequent spread of bacterial strains designated as methicillin-resistant S. aureus (MRSA), from the 1960s to the present, has created clinical difficulties for nosocomial treatment on a global scale. The recent variants of MRSA that are resistant to glycopeptide antibiotics (such as vancomycin) have ushered in a new and disconcerting chapter in the evolution of this organism.

引用

页码：2617 / 2633

页数：17

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