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Microb Pathog. 2008 Jan;44(1):84-8. Epub 2007 Aug 14.

CAMP factor is not essential for systemic virulence of Group B Streptococcus.

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Division of Pediatric Pharmacology and Drug Discovery, School of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0687, USA.


The Gram-positive pathogen Group B Streptococcus (GBS) is the leading cause of bacterial pneumonia, sepsis, and meningitis in human newborns. GBS elaborates a pore-forming toxin known as CAMP factor that synergizes with Staphylococcus aureus beta-toxin, generating a co-hemolytic reaction useful in identification of GBS in the clinical laboratory. To evaluate the indirect evidence implicating CAMP factor in GBS pathogenesis, the cfb gene encoding the pore-forming cytotoxin was deleted by precise allelic replacement. The virulence properties of the CAMP factor mutant were then explored by a series of in vitro and in vivo assays. Compared to wild-type, the isogenic GBS Deltacfb mutant demonstrated equivalent phagocyte resistance and endothelial cell invasiveness and also retained full virulence in a mouse model of infection. Our data suggest that CAMP factor expressed in its native context is not essential for systemic virulence of GBS.

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