Most beta-lactam antibiotics have multiple penicillin-binding-protein (PBP)targets in gram-positive bacteria. These targets are not protected by any significant impermeable barrier. Therefore, intrinsic (non-beta-lactamase-mediated) resistance can arise from alterations of the targets or under conditions in which the target is 'shifted' from multiple PBPs to a single insensitive target. This can occur in enterococci as a phenotypic adaptation to growth under suboptimal conditions or as a result of a mutation. Methicillin-resistant staphylococci have an additional beta-lactam-resistant PBP, designated PBP2a, that is entirely absent from sensitive strains. This can functionally replace all the sensitive PBPs under conditions in which these have been inhibited by beta-lactam antibiotics. Although methicillin-resistant staphylococci have reduced susceptibility to other beta-lactams besides methicillin, they are not always clinically resistant to these agents.
|Title of host publication||Current Topics in Infectious Diseases and Clinical Microbiology|
|Number of pages||4|
|Publication status||Published - 1990|
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