Poster Presentation 20th Lancefield International Symposium on Streptococci and Streptococcal Diseases 2017

Erythritol, a polyol (sugar alcohol), enhances Group B Streptococcus virulence (#135)

Maram J Hulbah 1 , Gregory Tyrrell 1 2 3
  1. Laboratory Medicine and Pathology, University of Alberta, EDMONTON, Alberta, Canada
  2. Division of Diagnostic and Applied Microbiology, University of Alberta, EDMONTON, Alberta, Canada
  3. Provincial Laboratory for Public Health (Microbiology), University of Alberta, EDMONTON, Alberta, Canada

Group B streptococci (GBS) causes’ invasive disease in neonates and adults. A cofactor we hypothesize to be associated with GBS virulence in neonates are polyols. Polyols (of which erythritol is a member) are sugar alcohols that have been found in the amniotic fluids of humans. The effect erythritol has on GBS virulence was investigated. GBS were grown in varying concentrations of erythritol (0%, 1%, 2% and 4%), bacteria, harvested and a collection of virulence phenotypes assayed. The expression of phosphoglycerate kinase (PGK – a plasminogen binding protein on the surface of GBS) was determined by ELISA. Antiphagocytic activity of GBS was measured by assaying the bacteria’s ability to multiply in fresh human blood and the effect erythritol on the invasion by GBS of HeLa 229 cells was also assayed.

GBS showed no significant difference in growth in the various concentrations of erythritol used (P=0.69 with 1%, P=0.63 with 2% and P=0.51 with 4%). GBS growth in the presence of 1%, 2% and 4% erythritol enhanced the expression of GBS-PGK compared to 0% erythritol (120%, 122 and 134%, respectively). The antiphagocytic activity of GBS in 1%, 2% and 4% erythritol was significantly increased compared to 0% (P=0.026, P=0.019 and P=0.0002, respectively). Also, GBS invaded the HeLa cells at a higher rate (164%) in 1% erythritol than in 0% erythritol.

In summary, the presence of erythritol (a polyol) in culture media enhances the virulence of GBS. This suggests that erythritol may play a role in GBS pathogenesis during neonatal infection.