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Journal of Clinical Microbiology, February 2002, p. 382-388, Vol. 40, No. 2
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.02.382-388.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

The ica Operon and Biofilm Production in Coagulase-Negative Staphylococci Associated with Carriage and Disease in a Neonatal Intensive Care Unit

G. D. I. de Silva,1,2 M. Kantzanou,1 A. Justice,1 R. C. Massey,1 A. R. Wilkinson,2 N. P. J. Day,3 and S. J. Peacock1*

Nuffield Department of Clinical Laboratory Sciences,1 Department of Pediatrics,2 Nuffield Department of Clinical Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom3

Received 18 May 2001/ Returned for modification 15 September 2001/ Accepted 14 November 2001

Coagulase-negative staphylococci (CoNS) are a major cause of sepsis in the neonatal intensive care unit (NICU). We evaluated the hypothesis that the ica operon and biofilm production are associated with CoNS disease in this setting. CoNS associated with bacteremia or blood culture contamination and from the skin of infants with CoNS bacteremia or healthy controls were obtained during a prospective case-control study on a busy NICU. A total of 180 strains were identified, of which 122 (68%) were Staphylococcus epidermidis and the remainder were S. capitis (n = 29), S. haemolyticus (n = 11), S. hominis (n = 9), S. warneri (n = 8), and S. auricularis (n = 1). The presence of the genes icaA, icaB, icaC, and icaD was determined by PCR, and biofilm production was examined using qualitative (Congo red agar [CRA]) and quantitative (microtiter plate) techniques. There were no significant differences in the presence of the ica operon or CRA positivity among the four groups of strains. However, quantitative biofilm production was significantly greater in strains isolated from either the blood or the skin of neonates with S. epidermidis bacteremia. We conclude that the quantity of biofilm produced may be associated with the ability to cause CoNS infection. This conclusion suggests that the regulation of biofilm expression may play a central role in the disease process.

* Corresponding author. Mailing address: Department of Microbiology, Level 7, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom. Phone: 44-1865-220537. Fax: 44-1865-222195. E-mail: sharon.peacock{at}ndcls.ox.ac.uk.

Journal of Clinical Microbiology, February 2002, p. 382-388, Vol. 40, No. 2
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.02.382-388.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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