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Published online ahead of print on 29 October 2009 as doi:10.1099/mic.0.030304-0
Microbiology (2009), DOI 10.1099/mic.0.030304-0
© 2009 Society for General Microbiology
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Microbiology 0 (2009), mic.0.030304; DOI  10.1099/mic.0.030304-0
© 2009 Society for General Microbiology

Epidemiology, variable genetic organisation and regulation of the EDIN-B toxin in Staphylococcus aureus from bacteraemic patients

Gefion C. Franke1, Alexandra Böckenholt1, Motoyuki Sugai2, Holger Rohde1 and Martin Aepfelbacher1,3

1 Universitätsklinikum Hamburg-Eppendorf;
2 Hiroshima University Graduate School of Biomedical Sciences

EDIN-B (Epidermal cell Differentiation INhibitor-B; also termed C3Stau) is an exotoxin of S. aureus which ADP-ribosylates and inactivates Rho GTP-binding proteins. The EDIN-B gene (edin-B) and the gene for exfoliative toxin D (etd) make up the central part of a recently described pathogenicity island. Here we evaluated the prevalence and genetic organisation of the edin-B/etd pathogenicity island in invasive S. aureus isolates and characterized edin-B transcription and EDIN-B production using artificial constructs transduced in S. aureus strains RN6390 and -Newman. We found that 8 out of 121 (7 %) S. aureus blood culture isolates harbour edin-B which is organised in three novel variants of the original edin-B/etd pathogenicity island. In the serum of patients infected with edin-B positive S. aureus significant titres of anti-EDIN-B antibodies could be detected. Regulation of edin-B transcription depended on the sarA- but not on the agr regulatory system. Furthermore, retrieval of EDIN-B protein secreted by S. aureus RN6390 required the presence of {alpha}2-macrogobulin to inhibit the activity of extracellular proteases. These data suggest that the EDIN-B toxin is produced during human infection, is part of a highly variable pathogenicity island and can be controlled by the sarA gene regulon and secreted bacterial proteases.

3 E-mail: m.aepfelbacher{at}uke.uni-hamburg.de






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