Glycosuria exposure increased Group B Streptococcus growth and adherence to human epithelial cells, according to the results of a study published in The Journal of Infectious Diseases.

Healthy women donated urine at the University of Louisiana. Human urine (HU) aliquots from 3 to 5 donors were prepared in sterile tryptic soy broth. Group B Streptococcus strain 10/84 pellets were resuspended in broth; plain HU (HU); or HU supplemented with glucose 50 mg/dL (HU50), 300 mg/dL (HU300), or 1000 mg/dL (HU1000). Blood agar plates were assessed for bacterial colony-forming units.

Female C57B16 mice were assessed for Group B Streptococcus infection after transurethral catheterization with broth, HU, or HU300. Epithelial monolayers were overlaid with Roswell Park Memorial Institute (RPMI) media, HU, or HU300, and were exposed to GBS. Alterations to gene expression were assessed.


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Group B Streptococcus strain 10/84 was observed to grow slowly in the nutrient-poor HU environment (td, 182±65 min). Growth was accelerated with the addition of glucose, in which growth increased in the low glycosuria HU50 environment (td, 54±7 min) and the intermediate glycosuria HU300 environment (td, 48±4 min), and was most rapid in the high glycosuria HU1000 environment (td, 40±1.1 min).

Adherence of Group B Streptococcus was similar in broth control, plain HU, and low glycosuria scenarios. In the intermediate- and high-glycosuria experiments, Group B Streptococcus adherence increased 4- to 6-fold.

At 24 hours after infection, mice exposed to HU300 had significantly more colony- forming units per mL in kidneys compared with mice exposed to broth (P =.007) or HU(P =.029).

For the epithelial monolayers, exposure to Group B Streptococcus caused pore-forming toxins β-H/C (cylE), CAMP factor B (cfb), PI2a fimbrial protein, antimicrobial peptide resistance protein (dltA), and cov 2-component system response regulator (covR) to be downregulated and oxidative stress response protein (adh) to be upregulated in the HU-exposed monolayer. For the HU300 monolayer, cylE, cfb, and adh were upregulated. Together these findings suggested that glycosuria induced Group B Streptococcus virulence genes.

The study authors concluded that a glycosuria urinary environment may augment the virulence of uropathogens, likely contributing to the increase in urinary tract infections observed in individuals with diabetes. These findings should be confirmed in diabetic mouse models.

Reference

John PP, Baker BC, Paudel S, Nassour L, Cagle H, Kulkarni R. Exposure to moderate glycosuria induces virulence of group B Streptococcus. J Infect Dis. 2021;223(5):843-847. doi:10.1093/infdis/jiaa443

This article originally appeared on Infectious Disease Advisor