Publication Details

This article was originally published as McKay, FC, Plasminogen binding by group A streptococcal isolates from a tropical region with hyperendemic streptococcal skin infection and a high incidence of invasive infection, Infection and Immunity, 72(1), 2004, 364-370.


Reports of resurgence in invasive group A streptococcal (GAS) infections come mainly from affluent populations with infrequent exposure to GAS. In the tropical 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 is high and no particular strains dominate. Expression of a plasminogen-binding group A streptococcal M-like protein (PAM) has been associated with skin infection in isolates elsewhere (Bessen, D., C.M. Sotir, T.M. Readdy, and S.K. Hollingshead.1996. J. Infect. Dis. 173:896-900) 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.



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