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539 Surveillance of mupirocin susceptibility in MRSA over a 10-year period in a tertiary care hospital

Saturday, March 20, 2010
Grand Hall (Hyatt Regency Atlanta)
Dominique S. Blanc, PhD , Hospital Preventive Medicine Service, Centre hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
Laurence Senn, MD , Hospital Preventive Medicine Service, Centre hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
Immaculée Nahimana, MD , Hospital Preventive Medicine Service, Centre hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
Valérie Vogel, PhD , Hospital Preventive Medicine Service, Centre hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
Patrick Basset, PhD , Hospital Preventive Medicine Service, Centre hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
Giorgio Zanetti, MD, MS , Hospital Preventive Medicine Service, Centre hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
Background: The widespread use of intranasal mupirocin (Mup) ointment for the decolonization of methicillin-resistant Staphylococcus aureus (MRSA) prompted concerns about Mup resistance. Low-level resistance (LLR) is the result of mutations in native tRNA synthetase (IleS), whereas high-level resistance (HLR) is due to the presence of mupA gene on a plasmid. Ongoing MRSA surveillance at the University tertiary care hospital of Lausanne (Switzerland), where mupirocin is used since the beginning of the 90s, provided an opportunity to characterize Mup resistance.

Objective: To investigate Mup resistance in MRSA isolated in our hospital over a 10-year period.

Methods: Mup resistance was determined in MRSA isolated from all clinical and surveillance samples drawn from patients between 2000 and 2009 by the disk diffusion method (5 mg). MIC was performed on isolates showing an inhibition diameter <13 mm, using the Etest method.

Results: 2378 patients were found to be colonized/infected by MRSA. 556 (23%) of them had a MRSA isolate showing LLR (MIC=8-64 mg/L), and 44 (1.9%) showing HLR (MIC≥512 mg/L).

In 489/556 (88%) pts with LLR-MRSA, the first isolate drawn before any exposure to Mup already showed LLR phenotype. A majority of LLR isolates (364/556, 65%)  actually belonged to an outbreak caused by one strain (ST228-SCCmec I) between October 2008 and 2009. Sequencing of IleS gene of this strain revealed a point mutation previously described and responsible for LLR.

37/44 (84%) pts with HLR-MRSA belonged to the ST228 outbreak. PCR for mupA was positive in all but 3 HLR isolates. In the other 7 pts outside the outbreak the first MRSA isolate was phenotypically susceptible to Mup and had a genotype identical to that of its subsequent HLR counterpart.

Conclusions: Surprisingly, in our setting, LLR was found to be clonally spread instead of secondarily acquired during treatment. Moreover, an epidemic strain apparently acquired the plasmid-mediated mupA gene. It remains unclear if this occurred once or on several occasions. This illustrates the great capacity of S.aureus to quickly adapt to its environment by acquiring new genetic elements.