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Infection and Immunity, September 2002, p. 4987-4996, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.4987-4996.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Virulent Combinations of Adhesin and Toxin Genes in Natural Populations of Staphylococcus aureus

Sharon J. Peacock,1* Catrin E. Moore,2 Anita Justice,1 Maria Kantzanou,1 Lisa Story,1 Kathryn Mackie,1 Gael O'Neill,3 and Nicholas P. J. Day2

Nuffield Department of Clinical Laboratory Sciences,1 Nuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford,2 Central Public Health Laboratory, Colindale, London, United Kingdom3

Received 20 March 2002/ Returned for modification 3 May 2002/ Accepted 16 May 2002

Most cases of severe Staphylococcus aureus disease cannot be explained by the action of a single virulence determinant, and it is likely that a number of factors act in combination during the infective process. This study examined the relationship between disease in humans and a large number of putative virulence determinants, both individually and in combination. S. aureus isolates (n = 334) from healthy blood donors and from patients with invasive disease were compared for variation in the presence of 33 putative virulence determinants. After adjusting for the effect of clonality, seven determinants (fnbA, cna, sdrE, sej, eta, hlg, and ica) were significantly more common in invasive isolates. All seven factors contributed independently to virulence. No single factor predominated as the major predictor of virulence, their effects appearing to be cumulative. No combinations of the seven genes were either more or less likely to cause disease than others with the same number of virulence-associated genes. There was evidence of considerable horizontal transfer of genes on a background of clonality. Our findings also suggested that allelic variants of a polymorphic locus can make different contributions to the disease process, further study of which is likely to expand our understanding of staphylococcal disease pathogenesis.

* Corresponding author. Mailing address: Nuffield Department of Clinical Laboratory Sciences, Level 4, Academic Block, John Radcliffe Hospital, Headington, Oxford OX3 9DU, United Kingdom. Phone: 44 1865 220857. Fax: 44 1865 220984. E-mail: sharon.peacock{at}ndcls.ox.ac.uk.

Editor: E. I. Tuomanen

Infection and Immunity, September 2002, p. 4987-4996, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.4987-4996.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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