Servicio de Microbiología Clínica, Hospital Universitario 12 de Octubre, Madrid, Spain.
Servicio de Microbiología Clínica, Hospital Universitario 12 de Octubre, Madrid, Spain; Spanish Network for the Research in Infectious Diseases (REIPI RD12/0015), Instituto de Salud Carlos III, Madrid, Spain.
J Glob Antimicrob Resist. 2016 Mar;4:65-69. doi: 10.1016/j.jgar.2015.11.005. Epub 2015 Dec 11.
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.
氯己定和莫匹罗星已在医疗机构中越来越多地用于根除耐甲氧西林金黄色葡萄球菌（MRSA）定植。本研究旨在确定从侵袭性感染和定植分离的 MRSA 中氯己定和莫匹罗星耐药的流行率和机制。分析了 2012 年至 2014 年间从血液和鼻腔样本中获得的 MRSA 分离株。通过纸片扩散和 Etest 法测定莫匹罗星的药敏性，通过肉汤微量稀释法测定氯己定的药敏性。通过 PCR 检测 mupA 和 qac（A/B 和 C）基因的存在。在高水平耐莫匹罗星（HLMR）分离株中进行分子分型。在血液分离株中鉴定出 15.6%（10.9% HLMR）和鼻腔分离株中 15.1%（12.0% HLMR）对莫匹罗星耐药。所有 HLMR 分离株均证实存在 mupA 基因。血液分离株的氯己定最低抑菌浓度（MIC）范围为≤0.125 至 4mg/L，最低杀菌浓度（MBC）范围为≤0.125 至 8mg/L。鼻腔分离株的氯己定 MIC 和 MBC 范围为≤0.125 至 2mg/L。qacA/B 基因在 2.2%的 MRSA 分离株（氯己定 MIC 范围为 0.25-2mg/L）中检出，qacC 基因在 8.2%（氯己定 MIC 范围为≤0.125-1mg/L）中检出。HLMR 分离株中 qacC 的检出率为 18.9%，莫匹罗星敏感分离株为 3.6%（P=0.009）。大多数 HLMR 分离株（97.1%）属于 ST125 克隆。这些结果表明，氯己定在预防 MRSA 感染方面具有更高的潜力。相比之下，莫匹罗星的治疗应谨慎使用，以避免 HLMR-MRSA 的传播。
