Complementation of a speA negative Streptococcus pyogenes with speA: effects on virulence and production of streptococcal pyrogenic exotoxin A.
We have shown previously that an isogenic SPEA-negative Streptococcus pyogenes strain did not attenuate virulence in a murine model of necrotizing fasciitis. The aim of this study was to confirm that streptococcal pyrogenic exotoxin A (SPEA) is not crucial for streptococcal invasiveness in murine invasive infection. The SPEA-negative S. pyogenes (H326) was complemented with speA extra-chromosomally to create strain H361 which produced 2.2-fold more SPEA compared with the parental speA(+)wild-type (H305). The growth phase-regulated expression of SPEA in vitro was unaffected in this strain. Complementation with speA resulted in reduced virulence and bacterial counts in invasive murine infection. SPEA production was quantitated from muscle tissue of infected mice. However, H361 did not produce more SPEA than H305 in vivo. We conclude that SPEA does not play a key role in invasive murine streptococcal infection.
Unnikrishnan
M
M
Department of Infectious Diseases, Imperial College School of Medicine, Hammersmith Hospital, Du Can Road, London W12 0NN, UK.
Cohen
J
J
Sriskandan
S
S
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D015169:Colony Count, Microbial; D004195:Disease Models, Animal; D005098:Exotoxins / Q000032:analysis / Q000096:biosynthesis*; D019115:Fasciitis, Necrotizing / Q000097:blood / Q000382:microbiology*; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D005816:Genetic Complementation Test; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D009132:Muscles / Q000382:microbiology; D013297:Streptococcus pyogenes / Q000235:genetics* / Q000472:pathogenicity*; D015996:Survival Rate; D014774:Virulence / Q000235:genetics*
D001426:Bacterial Proteins; D005098:Exotoxins; D008565:Membrane Proteins; C117980:SpeA protein, Streptococcus pyogenes; C027951:erythrogenic toxin