David J Hetem1, H Charles Vogely2, Tim T Severs3, Annet Troelstra3, Johannes G Kusters3, Marc J M Bonten4. 1. Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands d.j.hetem@umcutrecht.nl. 2. Department of Orthopaedic Surgery, University Medical Center Utrecht, Utrecht, The Netherlands. 3. Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands. 4. Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands.
Abstract
OBJECTIVES: The association between mupirocin use and plasmid-based high-level resistance development mediated through mupA in CoNS has not been quantified. We determined acquisition of mupirocin resistance in Staphylococcus aureus and CoNS in surgery patients treated peri-operatively with mupirocin. PATIENTS AND METHODS: Patients admitted for surgery were treated with nasal mupirocin ointment and chlorhexidine soap for 5 days, irrespective of S. aureus carrier status. Nasal swabs were obtained before decolonization (T1) and 4 days after surgery (T2) and were inoculated onto agars containing 8 mg/L mupirocin. Staphylococci were identified by MALDI-TOF MS and mupirocin resistance was confirmed by Etest. RESULTS: Among 1578 surgical patients, 936 (59%) had nasal swabs obtained at T1 and T2; 192 (21%) patients carried mupirocin-resistant CoNS at T1 and 406 (43%) at T2 (P<0.001). Of 744 patients not colonized at T1, 277 acquired resistance (37%), corresponding to an acquisition rate of 7.4/100 patient days at risk. In all, 588 (97%) of 607 mupirocin-resistant CoNS had an MIC >256 mg/L (high level) and 381 of 383 (99.5%) were mupA positive. No acquisition of mupirocin resistance was observed in S. aureus. CONCLUSIONS: Acquisition of mupirocin resistance following decolonization was widespread in CoNS and absent in S. aureus. As almost all isolates harboured the mupA gene, monitoring resistance development in S. aureus when decolonization strategies containing mupirocin are used is recommended.
OBJECTIVES: The association between mupirocin use and plasmid-based high-level resistance development mediated through mupA in CoNS has not been quantified. We determined acquisition of mupirocin resistance in Staphylococcus aureus and CoNS in surgery patients treated peri-operatively with mupirocin. PATIENTS AND METHODS: Patients admitted for surgery were treated with nasal mupirocin ointment and chlorhexidine soap for 5 days, irrespective of S. aureus carrier status. Nasal swabs were obtained before decolonization (T1) and 4 days after surgery (T2) and were inoculated onto agars containing 8 mg/L mupirocin. Staphylococci were identified by MALDI-TOF MS and mupirocin resistance was confirmed by Etest. RESULTS: Among 1578 surgical patients, 936 (59%) had nasal swabs obtained at T1 and T2; 192 (21%) patients carried mupirocin-resistant CoNS at T1 and 406 (43%) at T2 (P<0.001). Of 744 patients not colonized at T1, 277 acquired resistance (37%), corresponding to an acquisition rate of 7.4/100 patient days at risk. In all, 588 (97%) of 607 mupirocin-resistant CoNS had an MIC >256 mg/L (high level) and 381 of 383 (99.5%) were mupA positive. No acquisition of mupirocin resistance was observed in S. aureus. CONCLUSIONS: Acquisition of mupirocin resistance following decolonization was widespread in CoNS and absent in S. aureus. As almost all isolates harboured the mupA gene, monitoring resistance development in S. aureus when decolonization strategies containing mupirocin are used is recommended.