Abstract
Summary Methicillin resistance in Staphylococcus aureus is due to the acquisition of an additional, low affinity penicillin binding protein, PBP2', which causes an intrinsic resistance to all β-lactams. Characteristic of methicillin resistance is its heterogenous expression, a strain specific and growth phase dependent property which can be modulated by external factors. Resistant strains segregate a small subpopulation of highly resistant clones. The resistance level is controlled by chromosomal genes and does not correlate with the amount of PBP2' produced. There is growing evidence that cell wall biosynthetic genes, as well as global regulators like sar and the stationary phase sigma sigB operon influence methicillin resistance levels.
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