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Journal of Clinical Microbiology, May 2007, p. 1505-1510, Vol. 45, No. 5
0095-1137/07/$08.00+0     doi:10.1128/JCM.01984-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Characterization of the Epidemic European Fusidic Acid-Resistant Impetigo Clone of Staphylococcus aureus{triangledown}

A. J. O'Neill,1 A. R. Larsen,2 R. Skov,2 A. S. Henriksen,3 and I. Chopra1*

Antimicrobial Research Centre and Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom,1 Department of Research and Development, Statens Serum Institut, Artillerivej 5, DK-2300 Copenhagen, Denmark,2 LEO Pharma, Industriparken 55, DK-2750 Ballerup, Denmark3

Received 25 September 2006/ Returned for modification 20 November 2006/ Accepted 23 February 2007

Resistance to the antibiotic fusidic acid in European strains of Staphylococcus aureus causing impetigo has increased in recent years. This increase appears to have resulted from clonal expansion of a strain we have designated the epidemic European fusidic acid-resistant impetigo clone (EEFIC), which carries the fusidic acid resistance determinant fusB on its chromosome. To understand better the properties of the EEFIC responsible for its success, we have performed detailed phenotypic and genotypic characterization of this clone. Molecular typing revealed the EEFIC to be ST123, spa type t171, and agr type IV and therefore unrelated to earlier prevalent fusB+ strains found in the United Kingdom. EEFIC strains exhibited resistance to fusidic acid, penicillin, and, in some cases, erythromycin, which are all used in the treatment of impetigo. PCR analysis of the EEFIC and complete DNA sequencing of the 39.3 Kb plasmid it harbors identified genes encoding several toxins previously implicated in impetigo (exfoliative toxins A and B and EDIN-C). The location of fusB was mapped on the chromosome and found to be associated with a novel 16.6-kb genomic island integrated downstream of groEL. Although this element is related to classical staphylococcal pathogenicity islands, it does not encode any known virulence factors and consequently has been designated SaRIfusB (for "S. aureus resistance island carrying fusB").

* Corresponding author. Mailing address: Antimicrobial Research Centre and Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom. Phone: 44 113 343 5604. Fax: 44 113 343 5638. E-mail: i.chopra{at}leeds.ac.uk

{triangledown} Published ahead of print on 7 March 2007.

Journal of Clinical Microbiology, May 2007, p. 1505-1510, Vol. 45, No. 5
0095-1137/07/$08.00+0     doi:10.1128/JCM.01984-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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