Altered Penicillin-Binding Proteins and Meticillin-Resistant Staphylococcus aureus
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Altered PBPs are responsible for reduced sensitivity to β-lactam agents by Strep. pneumoniae (PBP1a, PBP2b and PBP2x) and Haemophilus influenzae (PBP3a and PBP3b), but by far the most clinically significant example is MRSA.
ALTERED PENICILLIN-BINDING PROTEINS AND
METICILLIN-RESISTANT Staphylococcus Aureus
Altered PBPs are responsible for
reduced sensitivity to β-lactam agents by Strep. pneumoniae (PBP1a, PBP2b and PBP2x) and Haemophilus influenzae (PBP3a and PBP3b), but by far
the most clinically significant example is MRSA. By the early 1950s, the
acquisition and spread of plasmid-encoded β-lactamases had blunted the
effectiveness of penicillin for treating Staph. aureus infections such as boils, carbuncles,
pneumonia, endocarditis and osteomyelitis. The β-lactamase-stable agent
meticillin was introduced in 1959, but by 1960, meticillin-resistant strains
were identified. This was the result of Staph. aureus acquiring the mecA gene, which encodes an
altered PBP gene, PBP2a. The mecA gene is chromosomal and expression is either
constitutive or inducible, but not by meticillin. PBP2a has low affinity for
most β-lactam antibiotics.
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