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Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage
Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage
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Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage
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Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage
Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage

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Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage
Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage
Journal Article

Staphylococcus aureus β-toxin Production is Common in Strains With the β-toxin Gene Inactivated by Bacteriophage

2014
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Overview
Background. Staphylococcus aureus causes life-threatening infections, including infective endocarditis, sepsis, and pneumonia, β-toxin is a sphingomyelinase encoded for by virtually all S. aureus strains and exhibits human immune cell cytotoxicity. The toxin enhances S. aureus phenol-soluble modulin activity, and its activity is enhanced by superantigens. The bacteriophage ɸSa3 inserts into the β-toxin gene in human strains, inactivating it in the majority of S. aureus donai groups. Hence, most strains are reported not to secrete β-toxin. Methods. This dynamic was investigated by examining β-toxin production by multiple donai groups of S. aureus, both in vitro and in vivo during infections in rabbit models of infective endocarditis, sepsis, and pneumonia. Results, β-toxin phenotypic variants are common among strains containing ɸSa3. In vivo, ɸSa3 is differentially induced in heart vegetations, kidney abscesses, and ischemie liver compared to spleen and blood, and in vitro growth in liquid culture. Furthermore, in pneumonia, wild-type β-toxin production leads to development of large caseous lesions, and in infective endocarditis, increases the size of pathognomonic vegetations. Conclusions. This study demonstrates the dynamic interaction between S. aureus and the infected host, where ɸSa3 serves as a regulator of virulence gene expression, and increased fitness and virulence in new enivronments.