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Infection and Immunity, January 2004, p. 364-370, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.364-370.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Plasminogen Binding by Group A Streptococcal Isolates from a Region of Hyperendemicity for Streptococcal Skin Infection and a High Incidence of Invasive Infection

Fiona C. McKay,¹ Jason D. McArthur,^1, Martina L. Sanderson-Smith,¹ Sandra Gardam,^1, Bart J. Currie,^2,3 Kadaba S. Sriprakash,^2,3,4 Peter K. Fagan,^5, Rebecca J. Towers,^2,3 Michael R. Batzloff,⁴ Gursharan S. Chhatwal,⁵ Marie Ranson,¹ and Mark J. Walker^1*

Department of Biological Sciences, University of Wollongong, Wollongong, New South Wales 2522,¹ Menzies School of Health Research,² Cooperative Research Centre for Aboriginal and Tropical Health, Darwin, Northern Territory 0810,³ and Queensland Institute of Medical Research, Herston, Queensland 4006, Australia,⁴ German National Centre for Biotechnology, Braunschweig 38124, Germany⁵

Received 15 May 2003/ Returned for modification 10 July 2003/ Accepted 9 September 2003

Reports of resurgence in invasive group A streptococcal (GAS) infections come mainly from affluent populations with infrequent exposure to GAS. In the Northern Territory (NT) of Australia, high incidence of invasive GAS disease is secondary to endemic skin infection, serotype M1 clones are rare in invasive infection, the diversity and level of exposure to GAS strains are high, and no particular strains dominate. Expression of a plasminogen-binding GAS M-like protein (PAM) has been associated with skin infection in isolates elsewhere (D. Bessen, C. M. Sotir, T. M. Readdy, and S. K. Hollingshead, J. Infect. Dis. 173:896-900, 1996), and subversion of the host plasminogen system by GAS is thought to contribute to invasion in animal models. Here, we describe the relationship between plasminogen-binding capacity of GAS isolates, PAM genotype, and invasive capacity in 29 GAS isolates belonging to 25 distinct strains from the NT. In the presence of fibrinogen and streptokinase, invasive isolates bound more plasminogen than isolates from uncomplicated infections (P 0.004). Only PAM-positive isolates bound substantial levels of plasminogen by a fibrinogen-streptokinase-independent pathway (direct binding). Despite considerable amino acid sequence variation within the A1 repeat region of PAM where the plasminogen-binding domain maps, the critical lysine residue was conserved.

Editor: S. H. E. Kaufmann

Present address: Queensland Institute of Medical Research, Queensland 4006, Australia.

Present address: Centenary Institute, Royal Prince Alfred Hospital Grounds, Camperdown, New South Wales 2050, Australia.

Present address: Menzies School of Health Research and Cooperative Research Centre for Aboriginal and Tropical Health, Darwin, Northern Territory 0810, Australia.

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