Journal
MICROBIAL PATHOGENESIS
Volume 44, Issue 1, Pages 84-88Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.micpath.2007.08.005
Keywords
Bacterial infection; Streptococcus agalactiae; Pore-forming toxin; Hemolysin
Categories
Funding
- American Heart Association Established Investigator Award
- American Lung Association Career Investigator Award
- NIH [HD051796, NS051247]
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD051796] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [K08AI001451] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS051247, R56NS051247] Funding Source: NIH RePORTER
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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 Delta cfb mutant demonstrated equivalent phagocyte resistance and endothelial cell invasiveness and also retained full virulence in a mouse model of infection. Our data suggest that CAM P factor expressed in its native context is not essential for systemic virulence of GBS. (C) 2007 Elsevier Ltd, All rights reserved.
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