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Updated: Dec 14, 2025

A Murine Model of Group B Streptococcus Vaginal Colonization
Published on: November 16, 2016
Exposure to Moderate Glycosuria Induces Virulence of Group B Streptococcus
Preeti P John1, Brady C Baker1, Santosh Paudel1
1Department of Biology, University of Louisiana at Lafayette, Lafayette, Louisiana, USA.
Abstract:
To explore whether glycosuria induces virulence of uropathogens, in turn facilitating urinary tract infection (UTI), we exposed group B Streptococcus (GBS) strain 10/84 to human urine plain or with 300 mg/dL glucose (mimicking moderate glycosuria). Exposure to moderate glycosuria significantly augmented bacterial growth, kidney bacterial burden in a mouse model of ascending UTI, and virulence characteristics and expression of corresponding genes. Exposure to glycosuria increased GBS adherence to human bladder epithelial cell line and expression of corresponding PI2a fimbrial gene, antimicrobial peptide LL-37 resistance and bacterial surface charge modulating dltA, and GBS hemolytic ability and expression of genes encoding pore-forming toxins.
Insights
Glycosuria, or high blood sugar, enhances the virulence of group B Streptococcus (GBS), increasing the risk of urinary tract infections (UTIs). This study shows glycosuria boosts bacterial growth and infection severity.
Area of Science:
- Microbiology
- Infectious Diseases
- Urology
Background:
- Urinary tract infections (UTIs) are common bacterial infections.
- Glycosuria, characterized by glucose in the urine, is often associated with diabetes.
- The link between glycosuria and uropathogen virulence is not fully understood.
Purpose of the Study:
- To investigate if glycosuria promotes the virulence of uropathogens, thereby facilitating UTIs.
- To determine the effect of glycosuria on the growth and pathogenic characteristics of group B Streptococcus (GBS).
Main Methods:
- Group B Streptococcus (GBS) strain 10/84 was exposed to human urine with and without added glucose (300 mg/dL) to mimic moderate glycosuria.
- Bacterial growth, kidney bacterial burden in a mouse model of ascending UTI, and virulence factors were assessed.
- Gene expression related to adherence, antimicrobial peptide resistance, and hemolytic activity was analyzed.
Main Results:
- Exposure to glycosuria significantly increased GBS growth and kidney bacterial burden in a mouse UTI model.
- Glycosuria enhanced GBS adherence to bladder epithelial cells, mediated by PI2a fimbrial gene expression.
- Increased resistance to antimicrobial peptide LL-37 and enhanced hemolytic activity were observed, linked to dltA and pore-forming toxin gene expression.
Conclusions:
- Moderate glycosuria significantly augments GBS virulence.
- Glycosuria promotes key pathogenic traits in GBS, including enhanced growth, adherence, antimicrobial resistance, and cytotoxicity.
- These findings suggest glycosuria may play a crucial role in facilitating UTIs caused by GBS.
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