Hostname: page-component-cd9895bd7-lnqnp Total loading time: 0 Render date: 2024-12-22T15:26:40.744Z Has data issue: false hasContentIssue false

Streptococcus pyogenes prtFII, but not sfbI, sfbII or fbp54, is represented more frequently among invasive-disease isolates of tropical Australia

Published online by Cambridge University Press:  18 July 2002

A. DELVECCHIO
Affiliation:
Menzies School of Health Research, Darwin, Australia
B. J. CURRIE
Affiliation:
Menzies School of Health Research, Darwin, Australia
J. D. McARTHUR
Affiliation:
Department of Biological Sciences, University of Wollongong, NSW, Australia
M. J. WALKER
Affiliation:
Department of Biological Sciences, University of Wollongong, NSW, Australia
K. S. SRIPRAKASH
Affiliation:
Menzies School of Health Research, Darwin, Australia Cooperative Research Centre for Aboriginal and Tropical Health, Darwin, Australia Queensland Institute of Medical Research, Brisbane, Australia
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Streptococcus pyogenes (group A streptococcus) strains may express several distinct fibronectin-binding proteins (FBPs) which are considered as major streptococcal adhesins. Of the FBPs, SfbI was shown in vitro to promote internalization of the bacterium into host cells and has been implicated in persistence. In the tropical Northern Territory, where group A streptococcal infection is common, multiple genotypes of the organism were found among isolates from invasive disease cases and no dominant strains were observed. To determine whether any FBPs is associated with invasive disease propensity of S. pyogenes, we have screened streptococcal isolates from bacteraemic and necrotizing fasciitis patients and isolates from uncomplicated infections for genetic endowment of 4 FBPs. No difference was observed in the distribution of sfbII, fbp54 and sfbI between the blood isolates and isolates from uncomplicated infection. We conclude that the presence of sfbI does not appear to promote invasive diseases, despite its association with persistence. We also show a higher proportion of group A streptococcus strains isolated from invasive disease cases possess prtFII when compared to strains isolated from non-invasive disease cases. We suggest that S. pyogenes may recruit different FBPs for different purposes.

Type
Research Article
Copyright
2002 Cambridge University Press