This patient with recurrent boils and skin abscesses is likely colonized with Staphylococcus aureus, a gram-positive cocci that grows in clusters.  Methicillin-resistant strains are able to grow in the presence of oxacillin due to the acquisition of a mobile genetic element that contains the mecA gene, which encodes for penicillin-binding protein (PBP) 2a.  PBPs catalyze peptidoglycan cross-linking during cell wall synthesis; they are the target of beta-lactam medications, which bind to and irreversibly destroy the enzyme.  Unlike other PBPs, PBP 2a has a low affinity for beta-lactams and continues to cross-link peptidoglycan in the presence of oxacillin, methicillin, cephalosporins (eg, cefazolin), and other beta-lactam medications.

Therefore, treatment of methicillin-resistant S aureus (MRSA) generally requires the use of a non–beta-lactam drug.  Common medications for MRSA include trimethoprim-sulfamethoxazole (inhibits 2 steps in folate synthesis), clindamycin (inhibits bacterial protein synthesis by binding to the 50s ribosomal subunit), doxycycline (inhibits protein synthesis by binding to the 30s ribosomal subunit), or vancomycin (inhibits integration of peptidoglycan subunits) (Choices B, C, D, and E).

Educational objective:
Methicillin-resistant Staphylococcus aureus (MRSA) is resistant to most beta-lactam medications (eg, oxacillin, methicillin, cephalosporins) due to the acquisition of a mobile genetic element that contains the mecA gene.  This gene encodes for a specialized penicillin-binding protein that has low affinity for beta-lactam antibiotics.  Treatment of MRSA therefore requires a non–beta-lactam medication such as trimethoprim-sulfamethoxazole, clindamycin, doxycycline, or vancomycin.