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J. Clin. Microbiol. doi:10.1128/JCM.02280-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Association between methicillin susceptibility and biofilm regulation in Staphylococcus aureus isolates from device-related infections

UCD School of Biomolecular and Biomedical Science, Ardmore House, University College Dublin, Belfield, Dublin 4, Ireland; Department of Microbiology and Immunology, New York Medical College, Valhalla, New York 10595, USA; Department of Clinical Microbiology, Education and Research Centre, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland

^* To whom correspondence should be addressed. Email: jim.ogara{at}ucd.ie.

	Abstract

Production of icaADBC-encoded polysaccharide intercellular adhesin or poly-N-acetylglucosamine (PIA/PNAG) represents an important biofilm mechanism in staphylococci. We previously described a glucose-induced, ica-independent biofilm mechanism in four methicillin-resistant Staphylococcus aureus (MRSA) isolates. Here biofilm regulation by NaCl and glucose was characterised in 114 MRSA and 98 methicillin-sensitive S. aureus (MSSA) isolates from diagnosed device-related infections. NaCl-induced biofilm development was significantly more prevalent among MSSA than MRSA isolates, and this association was independent of the isolate's genetic background as assessed by spa sequence typing. Among MSSA isolates PIA/PNAG production correlated with biofilm development in NaCl whereas in MRSA isolates grown in NaCl or glucose PIA/PNAG production was not detected even though icaADBC was transcribed and regulated. Glucose-induced biofilm in MRSA was ica-independent and apparently mediated by a protein adhesin(s). Experiments performed with strains that were amenable to genetic manipulation revealed that deletion of icaADBC had no effect on biofilm in a further six MRSA isolates but abolished biofilm in four MSSA isolates. Mutation of sarA abolished biofilm in seven MRSA and eight MSSA isolates. In contrast mutation of agr in thirteen MRSA and eight MSSA isolates substantially increased biofilm (> 2-fold) in only 5/21 (23%) isolates or had no significant impact on biofilm in the remaining 16 isolates. We conclude that biofilm development in MRSA is ica-independent and involves a protein adhesin(s) regulated by SarA and Agr whereas SarA-regulated PIA/PNAG plays a more important role in MSSA biofilm development.

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