Clinical meaning
Methicillin-resistant Staphylococcus aureus (MRSA) colonization serves as a persistent reservoir for recurrent infections because S. aureus establishes stable carriage in the anterior nares, where it adheres to nasal epithelial cells via surface adhesins (clumping factor B, wall teichoic acid) and forms biofilm communities that resist immune clearance. The anterior nares are the primary colonization site, but MRSA also colonizes the axillae, groin, perineum, throat, and chronic wound sites. Colonization precedes and predicts infection: approximately 30% of the population carries S. aureus nasally, and MRSA carriers have a 4-10 fold increased risk of subsequent MRSA infection compared to non-carriers. Decolonization protocols aim to eradicate carriage from all body sites simultaneously. Mupirocin (pseudomonic acid) is the cornerstone intranasal decolonization agent; it inhibits bacterial isoleucyl-tRNA synthetase, blocking protein synthesis at a step distinct from other antibiotic classes, providing potent activity against staphylococci including MRSA. Mupirocin is applied intranasally (2% ointment to bilateral anterior nares twice daily for 5 days), combined with chlorhexidine gluconate (CHG) 4% body washes for cutaneous decolonization. CHG disrupts microbial cell membranes through electrostatic binding to the negatively charged bacterial cell wall, and its persistent residual activity on skin provides continued antimicrobial effect for hours after application. Decolonization failure occurs with high-level mupirocin resistance (encoded by the mupA gene on transferable plasmids, conferring MICs greater than 512 mcg/mL), incomplete protocol adherence, or failure to address environmental reservoirs (shared towels, bedding, personal items). The clinician evaluates decolonization candidacy based on recurrent infection history, household transmission patterns, and pre-surgical MRSA risk, and performs post-decolonization surveillance cultures to confirm eradication.