Chlorhexidine and mupirocin susceptibilities in methicillin-resistant Staphylococcus aureus isolates from bacteraemia and nasal colonisation.

Chlorhexidine and mupirocin have been increasingly used in healthcare facilities to eradicate methicillin-resistant Staphylococcus aureus (MRSA) carriage. The aim of this study was to determine the prevalence and mechanisms of chlorhexidine and mupirocin resistance in MRSA from invasive infections and colonisation. MRSA isolates obtained from blood and nasal samples between 2012 and 2014 were analysed. Susceptibility to mupirocin was determined by disk diffusion and Etest and susceptibility to chlorhexidine by broth microdilution. The presence of mupA and qac (A/B and C) genes was investigated by PCR. Molecular typing was performed in high-level mupirocin-resistant (HLMR) isolates. Mupirocin resistance was identified in 15.6% of blood isolates (10.9% HLMR) and 15.1% of nasal isolates (12.0% HLMR). Presence of the mupA gene was confirmed in all HLMR isolates. For blood isolates, chlorhexidine minimum inhibitory concentrations (MICs) ranged from ≤0.125 to 4mg/L and minimum bactericidal concentrations (MBCs) from ≤0.125 to 8mg/L. In nasal isolates, chlorhexidine MICs and MBCs ranged from ≤0.125 to 2mg/L. The qacA/B gene was detected in 2.2% of MRSA isolates (chlorhexidine MIC range 0.25-2mg/L) and the qacC gene in 8.2% (chlorhexidine MIC range ≤0.125-1mg/L). The prevalence of qacC was 18.9% in HLMR isolates and 3.6% in mupirocin-susceptible isolates (P=0.009). Most of the HLMR isolates (97.1%) belonged to ST125 clone. These results suggest that chlorhexidine has a higher potential to prevent infections caused by MRSA. In contrast, mupirocin treatment should be used cautiously to avoid the spread of HLMR MRSA.