Yngvar Tveten1, Andrew Jenkins, Bjørn-Erik Kristiansen. 1. Telemark Biomedical Centre, A/S Telelab, Department of Medical Microbiology, Strømdaljordet 4, PO Box 1868, N-3703 Skien, Norway. yngvar.tveten@telelab.no
Abstract
OBJECTIVE: To investigate the possibility that the increased prevalence of fusidic acid-resistant Staphylococcus aureus in Norway is caused by clonal spread. METHODS: Fusidic acid-resistant and -susceptible clinical isolates of S. aureus from patients with skin infections in the Norwegian county of Telemark and fusidic acid-resistant isolates from other parts of Scandinavia were compared. MICs of fusidic acid for bacterial isolates and pulsed-field gel electrophoresis (PFGE) patterns were investigated. Prevalence data for fusidic acid-resistant S. aureus for the period 1992-2001 were obtained. RESULTS: The prevalence of fusidic acid resistance in S. aureus increased from 1992 to 2001. Eighty per cent of the resistant isolates investigated shared an identical PFGE pattern. The same pattern was found in fusidic acid-resistant isolates from other parts of Scandinavia. Fusidic acid-resistant S. aureus was typically found in impetigo bullosa-like skin disease in children mostly in the summer months. CONCLUSIONS: Fusidic acid resistance among S. aureus is increasing in Norway and is predominantly caused by one clone of S. aureus. The clone may spread further to other countries, and dissemination may be facilitated by extensive use of topical fusidic acid.
OBJECTIVE: To investigate the possibility that the increased prevalence of fusidic acid-resistant Staphylococcus aureus in Norway is caused by clonal spread. METHODS:Fusidic acid-resistant and -susceptible clinical isolates of S. aureus from patients with skin infections in the Norwegian county of Telemark and fusidic acid-resistant isolates from other parts of Scandinavia were compared. MICs of fusidic acid for bacterial isolates and pulsed-field gel electrophoresis (PFGE) patterns were investigated. Prevalence data for fusidic acid-resistant S. aureus for the period 1992-2001 were obtained. RESULTS: The prevalence of fusidic acid resistance in S. aureus increased from 1992 to 2001. Eighty per cent of the resistant isolates investigated shared an identical PFGE pattern. The same pattern was found in fusidic acid-resistant isolates from other parts of Scandinavia. Fusidic acid-resistant S. aureus was typically found in impetigo bullosa-like skin disease in children mostly in the summer months. CONCLUSIONS:Fusidic acid resistance among S. aureus is increasing in Norway and is predominantly caused by one clone of S. aureus. The clone may spread further to other countries, and dissemination may be facilitated by extensive use of topical fusidic acid.
Authors: Nuno A Faria; Duarte C Oliveira; Henrik Westh; Dominique L Monnet; Anders R Larsen; Robert Skov; Hermínia de Lencastre Journal: J Clin Microbiol Date: 2005-04 Impact factor: 5.948
Authors: Anne-Merethe Hanssen; Aina Fossum; Jarle Mikalsen; Dag S Halvorsen; Geir Bukholm; Johanna U Ericson Sollid Journal: J Clin Microbiol Date: 2005-05 Impact factor: 5.948
Authors: Michelle Ia Rijnders; Sita Nys; Christel Driessen; Christian Jpa Hoebe; Rogier M Hopstaken; Guy J Oudhuis; Arno Timmermans; Ellen E Stobberingh Journal: Br J Gen Pract Date: 2010-12 Impact factor: 5.386
Authors: David J Farrell; Rodrigo E Mendes; Mariana Castanheira; Ronald N Jones Journal: Antimicrob Agents Chemother Date: 2016-05-23 Impact factor: 5.191
Authors: Maike Koningstein; Leon Groen; Kathelijn Geraats-Peters; Suzanne Lutgens; Ariene Rietveld; Petr Jira; Jan Kluytmans; Sabine C de Greeff; Mirjam Hermans; Peter M Schneeberger Journal: Antimicrob Resist Infect Control Date: 2012-11-20 Impact factor: 4.887