Journal article
Staphylococcus aureus β-toxin production is common in strains with the β-toxin gene inactivated by bacteriophage
The Journal of infectious diseases, Vol.210(5), pp.784-792
09/01/2014
DOI: 10.1093/infdis/jiu146
PMCID: PMC4202305
PMID: 24620023
Abstract
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 φSa3 inserts into the β-toxin gene in human strains, inactivating it in the majority of S. aureus clonal groups. Hence, most strains are reported not to secrete β-toxin.
This dynamic was investigated by examining β-toxin production by multiple clonal groups of S. aureus, both in vitro and in vivo during infections in rabbit models of infective endocarditis, sepsis, and pneumonia.
β-toxin phenotypic variants are common among strains containing φSa3. In vivo, φSa3 is differentially induced in heart vegetations, kidney abscesses, and ischemic 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.
This study demonstrates the dynamic interaction between S. aureus and the infected host, where φSa3 serves as a regulator of virulence gene expression, and increased fitness and virulence in new environments.
Details
- Title: Subtitle
- Staphylococcus aureus β-toxin production is common in strains with the β-toxin gene inactivated by bacteriophage
- Creators
- Wilmara Salgado-Pabón - Department of Microbiology, University of Iowa Carver College of Medicine, Iowa CityAlfa Herrera - Department of Microbiology, University of Iowa Carver College of Medicine, Iowa CityBao G Vu - Department of Microbiology, University of Iowa Carver College of Medicine, Iowa CityChristopher S Stach - Department of Microbiology, University of Iowa Carver College of Medicine, Iowa CityJoseph A Merriman - Department of Microbiology, University of Iowa Carver College of Medicine, Iowa CityAdam R Spaulding - Department of Microbiology, University of Iowa Carver College of Medicine, Iowa CityPatrick M Schlievert - Department of Microbiology, University of Iowa Carver College of Medicine, Iowa City
- Resource Type
- Journal article
- Publication Details
- The Journal of infectious diseases, Vol.210(5), pp.784-792
- Publisher
- United States
- DOI
- 10.1093/infdis/jiu146
- PMID
- 24620023
- PMCID
- PMC4202305
- ISSN
- 0022-1899
- eISSN
- 1537-6613
- Grant note
- T32AI007511 / NIAID NIH HHS T32 AI007511 / NIAID NIH HHS
- Language
- English
- Date published
- 09/01/2014
- Academic Unit
- Molecular Physiology and Biophysics; Microbiology and Immunology; Internal Medicine
- Record Identifier
- 9984001135802771
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