Mutated Group B Streptococcus Causes Neonatal Sepsis

They performed whole-genome comparison of 47 GBS samples from 19 mother-child pairs uncovered 21 single nucleotide polymorphisms (SNPs) and seven insertions/deletions. Within the detected SNPs, 16 appear to have been fixed in the sampled population, whereas five mutations were found to be polymorphic. In the infant strains, 14 mutations were detected, including two independently fixed variants affecting the response regulator CovR (covRS) locus, known to encode a major regulatory system of virulence.

A one-nucleotide insertion was also identified in the promoter region of the highly immunogenic surface protein ribbon gene (Rib). Gene expression analysis after incubation in human blood showed that these mutations influenced the expression of virulence-associated genes. Additional identification of three mutated strains in the mothers' milk raised the possibility of the newborns also being a source of contamination to their mothers.

The scientists found that in five out of the 19 sampled newborns, mutations with a potential role in promoting virulence had occurred in GBS. Philippe Glaser, PhD, the group leader said, “In most cases, GBS is just naturally virulent in neonates. The genomic changes in GBS that were found only in a few cases were genetically identical in most of the mother-infant pairs analyzed.” The study was published on August 17, 2015, in the Journal of Bacteriology.

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