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BMC Microbiol. 2001;1:33. Epub 2001 Dec 17.

Mouse skin passage of a Streptococcus pyogenes Tn917 mutant of sagA/pel restores virulence, beta-hemolysis and sagA/pel expression without altering the position or sequence of the transposon.

Author information

1
Department of Microbiology and Immunology, Medical College of Ohio, Toledo, Ohio 43614, USA. teberhard@mco.edu

Erratum in

  • BMC Microbiol 2002 May 20;2(1):10.

Abstract

BACKGROUND:

Streptolysin S (SLS), the oxygen-stable hemolysin of Streptococcus pyogenes, has recently been shown to be encoded by the sagA/pel gene. Mutants lacking expression of this gene were less virulent in a dermonecrotic mouse infection model. Inactivation of the sagA/pel gene affect the expression of a variety of virulence factors in addition to the hemolysin. Insertion of a Tn917 transposon into the promoter region of the sagA/pel gene of S. pyogenes isolate CS101 eliminated expression of SLS, as well as decreased expression of the streptococcal pyrogenic exotoxin B, streptokinase and M protein.

RESULTS:

In this study a mouse skin air sac model was utilized to analyze the effect of biological pressures on expression of SLS and other sagA/pel regulated gene products. The insertion delayed the lethal effect of S. pyogenes in a mouse skin infection model. Despite this, bacteria could be cultured from the kidneys 72 hours post infection. These kidney-recovered isolates were beta-hemolytic despite the transposon being present in its original location and had equivalent virulence to the wild type isolate when re-injected into naive mice. Northern blot analysis of the kidney-recovered isolates confirmed that transcription of sagA/pel was restored; however the expression of all sagA/pel regulated genes was not restored to wild type levels.

CONCLUSIONS:

These results show that biological pressure present in the mouse can select for variants with altered expression of key virulence factor genes in S. pyogenes.

PMID:
11801184
PMCID:
PMC64569
[Indexed for MEDLINE]
Free PMC Article

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