Antibacterials (ABX) Practice Exam

MRSA’s resistance to most beta-lactams comes from PBP2a, a penicillin-binding protein with low affinity for beta-lactam antibiotics. Because beta-lactams target PBPs to stop cell wall synthesis, binding to a PBP that beta-lactams don’t effectively engage allows MRSA to continue building its cell wall. Vancomycin works by a different mechanism: it binds directly to the D-Ala-D-Ala terminus of the peptidoglycan precursors, blocking cell wall synthesis regardless of which PBP is present. That’s why vancomycin is commonly effective against MRSA. The other statements don’t fit MRSA’s resistance profile: beta-lactamase-related explanations don’t account for PBP2a-mediated resistance, altering DNA gyrase describes fluoroquinolone resistance, and beta-lactamase inhibitors don’t restore activity against PBP2a-mediated resistance.