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Infection and Immunity, May 2007, p. 2603-2611, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.01291-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Determination of the Relationship between Group A Streptococcal Genome Content, M Type, and Toxic Shock Syndrome by a Mixed Genome Microarray{triangledown} ,{dagger}

Bart J. M. Vlaminckx,1* Frank H. J. Schuren,2 Roy C. Montijn,2 Martien P. M. Caspers,2 Ad C. Fluit,1 Wim J. B. Wannet,3 Leo M. Schouls,3 Jan Verhoef,1 and Wouter T. M. Jansen1

University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht,1 TNO Quality of Life, Business Unit Microbiology, Utrechtseweg 48, 3704 HE Zeist,2 National Institute of Public Health and the Environment (RIVM), Antonie van Leeuwenhoeklaan 9, 3721 MA Bilthoven, The Netherlands3

Received 11 August 2006/ Returned for modification 2 November 2006/ Accepted 29 January 2007

Group A streptococci (GAS), or Streptococcus pyogenes, are associated with a remarkable variety of diseases, ranging from superficial infections to life-threatening diseases such as toxic-shock-like syndrome (TSS). GAS strains belonging to M types M1 and M3 are associated with TSS. This study aims to obtain insight into the gene profiles underlying different M types and disease manifestations. Genomic differences between 76 clinically well characterized GAS strains collected in The Netherlands were examined using a mixed-genome microarray. Inter-M-type genomic differences clearly outweighed intra-M-type genome variation. Phages were major contributors to observed genome diversification. We identified four novel genes, including two genes encoding fibronectin-binding-like proteins, which are highly specific to a subset of M types and thus may contribute to M-type-associated disease manifestations. All M12 strains were characterized by the unique absence of the citrate lyase complex and reduced growth under hypoxic, nutrient-deprived conditions. Furthermore, six virulence factors, including genes encoding a complement-inhibiting protein (sic), an exotoxin (speA), iron(III) binding factor, collagen binding factor (cpa), and fibrinogen binding factor (prt2-like), were unique to M1 and/or M3 strains. These virulence factors may contribute to the potential of these strains to cause TSS. Finally, in contrast to M-type-specific virulence profiles, we did not identify a common virulence profile among strains associated with TSS irrespective of their M type.

* Corresponding author. Mailing address: University Medical Center Utrecht, Eijkman Winkler Center for Medical Microbiology and Infectious Diseases, G 04.614, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. Phone: 31-30-2508108. Fax: 31-30-2541770. E-mail: B.J.M.Vlaminckx{at}lab.azu.nl

{triangledown} Published ahead of print on 26 February 2007.

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

Editor: V. J. DiRita

Infection and Immunity, May 2007, p. 2603-2611, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.01291-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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  • Vlaminckx, B. J. M., Schuren, F. H. J., Montijn, R. C., Caspers, M. P. M., Beitsma, M. M., Wannet, W. J. B., Schouls, L. M., Verhoef, J., Jansen, W. T. M. (2007). Dynamics in Prophage Content of Invasive and Noninvasive M1 and M28 Streptococcus pyogenes Isolates in The Netherlands from 1959 to 1996. Infect. Immun. 75: 3673-3679 [Abstract] [Full Text]  


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