期刊
MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS
卷 86, 期 2, 页码 -出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/mmbr.00159-21
关键词
Staphylococcus aureus; MRSA; MecA; antimicrobial resistance
类别
资金
- UKRI Strategic Priorities Fund [EP/T002778/1]
- EPSRC [EP/T002778/1] Funding Source: UKRI
The development of resistance to beta-lactam antibiotics has made Staphylococcus aureus, especially MRSA, a global clinical burden. The acquisition of mecA, which encodes PBP2A, allows MRSA to proliferate in the presence of beta-lactams. Further genetic adjustments are required to develop high-level resistance.
The development of resistance to beta-lactam antibiotics has made Staphylococcus aureus a clinical burden on a global scale. MRSA (methicillin-resistant S. aureus) is commonly known as a superbug. The development of resistance to beta-lactam antibiotics has made Staphylococcus aureus a clinical burden on a global scale. MRSA (methicillin-resistant S. aureus) is commonly known as a superbug. The ability of MRSA to proliferate in the presence of beta-lactams is attributed to the acquisition of mecA, which encodes the alternative penicillin binding protein, PBP2A, which is insensitive to the antibiotics. Most MRSA isolates exhibit low-level beta-lactam resistance, whereby additional genetic adjustments are required to develop high-level resistance. Although several genetic factors that potentiate or are required for high-level resistance have been identified, how these interact at the mechanistic level has remained elusive. Here, we discuss the development of resistance and assess the role of the associated components in tailoring physiology to accommodate incoming mecA.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据