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Abstract Background Streptolysin S (SLS), the oxygen-stable hemolysin of <it>Streptococcus pyogenes</it>, has recently been shown to be encoded by the <it>sagA/pel</it> gene. Mutants lacking expression of this gene were less virulent in a dermonecrotic mouse infection model. Inactivation of the <it>sagA/pel</it> gene affect the expression of a variety of virulence factors in addition to the hemolysin. Insertion of a Tn<it>917</it> transposon into the promoter region of the <it>sagA/pel</it> gene of <it>S. pyogenes</it> 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 <it>sagA/pel</it> regulated gene products. The insertion delayed the lethal effect of <it>S. pyogenes</it> in a mouse skin infection model. Despite this, bacteria could be cultured from the kidneys 72 hours post infection. These kidney-recovered isolates were β-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 <it>sagA/pel</it> was restored; however the expression of all <it>sagA/pel</it> 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 <it>S. pyogenes</it>.</p

bmc microbiology

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.