Plasminogen binding by group A streptococcal isolates from a region of hyperendemicity for streptococcal skin infection and a high incidence of invasive infection

McKay, Fiona C., McArthur, Jason D., Sanderson-Smith, Marina L., Gardam, Sandra, Currie, Bart J., Sriprakash, Kadaba S., Fagan, Peter K., Towers, Rebecca J., Batzloff, Michael R., Chhatwal, Gursharan S., Ranson, Marie and Walker, Mark J. (2004) Plasminogen binding by group A streptococcal isolates from a region of hyperendemicity for streptococcal skin infection and a high incidence of invasive infection. Infection and Immunity, 72 1: 364-370. doi:10.1128/IAI.72.1.364-370.2004

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Author McKay, Fiona C.
McArthur, Jason D.
Sanderson-Smith, Marina L.
Gardam, Sandra
Currie, Bart J.
Sriprakash, Kadaba S.
Fagan, Peter K.
Towers, Rebecca J.
Batzloff, Michael R.
Chhatwal, Gursharan S.
Ranson, Marie
Walker, Mark J.
Title Plasminogen binding by group A streptococcal isolates from a region of hyperendemicity for streptococcal skin infection and a high incidence of invasive infection
Journal name Infection and Immunity   Check publisher's open access policy
ISSN 1098-5522
1070-6313
Publication date 2004-01
Sub-type Article (original research)
DOI 10.1128/IAI.72.1.364-370.2004
Open Access Status File (Publisher version)
Volume 72
Issue 1
Start page 364
End page 370
Total pages 7
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Formatted abstract
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.
Keyword Extracellular Cysteine Protease
Toxic-Shock-Syndrome
Molecular Epidemiology
Surface Protein
Staphylococcus-Aureus
Alpha-Enolase
Human Plasma
Streptokinase
Plasmin(ogen)
Activation
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
 
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