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Emergence of antibiotic resistance is a global crisis.1,2 Approximately 2 million nosocomial infections occur in the United States each year, of which one half are caused by antibiotic-resistant organisms. Treatment failure owing to antibiotic resistance adds approximately $4.5 billion annually to health care costs in this country.
Bacteria acquire resistance through clever mechanisms of genetic engineering to survive increasing selection pressure of antibiotic use. Methicillin resistance in Staphylococcus aureus is due to the mecA gene that encodes for a surrogate penicillin-binding protein (PBP), PBP2a, which has a low affinity for β-lactam antibiotics.3 The PBP2a functions as a transpeptidase to maintain cell wall synthesis, thereby preventing β-lactams from blocking the production of peptidoglycans. All methicillin-resistant Staphylococcus aureus (MRSA) possess the mecA gene, which also conveys methicillin resistance in coagulase-negative staphylococci (CNS). MRSA first appeared in 1960, one year after introduction of β-lactamase-resistant penicillins, and now accounts for 40% of
Jones DB. Emerging Antibiotic Resistance: Real and Relative. Arch Ophthalmol. 1996;114(1):91-92. doi:10.1001/archopht.1996.01100130087016