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Journal of Clinical Microbiology, May 2007, p. 1379-1388, Vol. 45, No. 5
0095-1137/07/$08.00+0     doi:10.1128/JCM.02280-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Association between Methicillin Susceptibility and Biofilm Regulation in Staphylococcus aureus Isolates from Device-Related Infections{triangledown} ,{dagger}

Eoghan O'Neill,1,3 Clarissa Pozzi,1 Patrick Houston,1 Davida Smyth,2 Hilary Humphreys,3 D. Ashley Robinson,2 and James P. O'Gara1*

UCD School of Biomolecular and Biomedical Science, Ardmore House, University College Dublin, Belfield, Dublin 4, Ireland,1 Department of Microbiology and Immunology, New York Medical College, Valhalla, New York 10595,2 Department of Clinical Microbiology, Education and Research Centre, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland3

Received 9 November 2006/ Returned for modification 6 December 2006/ Accepted 19 February 2007

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 characterized 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 13 MRSA and 8 MSSA isolates substantially increased biofilm (more than twofold) in only 5 of 21 (23%) isolates and 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.

* Corresponding author. Mailing address: UCD School of Biomolecular and Biomedical Science, Ardmore House, University College Dublin, Belfield, Dublin 4, Ireland. Phone: 353-1-716 1263. Fax: 353-1-716 1183. E-mail: jim.ogara{at}ucd.ie

{triangledown} Published ahead of print on 28 February 2007.

{dagger} Supplemental material for this article may be found at http://jcm.asm.org/.

Journal of Clinical Microbiology, May 2007, p. 1379-1388, Vol. 45, No. 5
0095-1137/07/$08.00+0     doi:10.1128/JCM.02280-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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