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A Murine Model of Group B Streptococcus Vaginal Colonization
Published on: November 16, 2016
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Phenotypic and molecular characterization of hyperpigmented group B Streptococci
Agnese Lupo1, Corinne Ruppen1, Andrew Hemphill2
1Institute for Infectious Diseases, University of Bern, Bern, Switzerland.
International Journal of Medical Microbiology : IJMM
|June 17, 2014
Summary
Group B Streptococcus (GBS) virulence is linked to its β-hemolysin/cytolysin. Mutations in the CovS/R system affect pigment and hemolytic activity in clinical GBS isolates, suggesting other pathways influence virulence factor production.
Area of Science:
- Microbiology
- Molecular Biology
- Infectious Diseases
Background:
- Group B Streptococcus (GBS) causes severe infections in vulnerable populations.
- The β-hemolysin/cytolysin, encoded by the cyl operon, is a key GBS virulence factor.
- Hyperpigmented GBS isolates are often hyperhemolytic, with altered virulence gene expression linked to the CovS/R regulatory system.
Purpose of the Study:
- To investigate the role of the CovS/R regulatory system in virulence factor production in clinical GBS isolates.
- To correlate pigment production and hemolytic activity with molecular and transcriptional changes in GBS.
Main Methods:
- Prospective collection and analysis of 10 hyperpigmented GBS isolates from clinical samples (2008-2012).
- Phenotypic characterization including spectrophotometry for pigment analysis and hemolytic activity assays.
- Molecular analysis of the cyl operon and covR gene sequence.
- Transcriptional analysis of virulence factors.
Main Results:
- Spectrophotometry data for pigment absorbance peaks significantly correlated with hemolytic activity.
- The cyl operon was conserved across all isolates.
- Mutations in the covR gene were identified in five isolates, with one mutation abrogating the CovR binding site to cylX.
- Results support previous findings on CovR-deficient mutants but indicate potential alternative pathways for virulence factor production.
Conclusions:
- The CovS/R system plays a role in regulating GBS virulence factors, including β-hemolysin/cytolysin and CAMP factor.
- Mutations in covR can lead to altered pigment and hemolytic activity.
- Other molecular pathways, beyond the CovS/R system, may contribute to virulence factor production in some clinical GBS isolates.
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