JAC Advance Access originally published online on September 20, 2002
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Journal of Antimicrobial Chemotherapy (2002) 50, 755-757
© 2002 The British Society for Antimicrobial Chemotherapy
Correspondence |
Molecular epidemiology of resistance to macrolides–lincosamides–streptogramins in methicillin-resistant Staphylococcus aureus (MRSA) causing bloodstream infections in patients admitted to Belgian hospitals
1 Staphylococcus Reference Laboratory, Service de Microbiologie, Université Libre de Bruxelles-Erasme Hospital, Brussels; 2 Scientific Institute of Public Health, Brussels, Belgium
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Keywords: MRSA, PFGE, macrolide–lincosamide–streptogramin resistance
Sir,
In Staphylococcus aureus, three mechanisms of resistance to macrolides, lincosamides and streptogramins (MLS) are known: target modification, active efflux and drug modification.1 Adenine-specific N-methyltransferases mediated by erm genes modify the A2058 residue of the 23S subunit of rRNA, which confers cross-resistance to macrolides, lincosamides and streptogramin B. This MLSB resistance phenotype can be either inducible or constitutive. MLS resistance is less commonly mediated by efflux systems or inactivating enzymes.1 In this study we characterized genes encoding these MLS resistance mechanisms in methicillin-resistant S. aureus (MRSA) collected in Belgium and determined the resistance gene distribution by PFGE typing profile.
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