Following maternal transmission, group B strep mutates to sicken infants


Group B streptococcus (GBS), a mostly benign inhabitant of healthy adults, is one of the leading causes of neonatal sepsis and meningitis. Researchers from the Institut Pasteur and Inserm have now shown that these pediatric cases might occur when the bacteria mutates within the infant following transmission from the mother. The research appeared August 17 in the Journal of Bacteriology, a publication of the American Society for Microbiology.

In the study, the investigators compared for the first time samples of GBS from pairs of infected newborns and their mothers. They found that in five out of the 19 sampled newborns, mutations with a potential role in promoting virulence had occurred in GBS.

The researchers suggest that these mutations take hold in neonates after their first few days of life, as their immunological defenses develop, applying selective pressure on any GBS strains that have a fitness advantage. For example, they might help the mutated strain evade the host's immune defenses. “The mechanism that encourages these virulence mutations is still to be discovered,” said Claire Poyart, MD, PHD, Director of the Barriers and Pathogens Inserm team at the Institut Cochin and the Centre National de Reference des Streptococques, Paris.

However, these genomic changes were found only in a few cases, as in most of the mother-infant pairs analyzed, GBS were genetically identical. “In most cases, GBS is naturally virulent in neonates,” said Philippe Glaser, PhD, head of the Bacterial Genomes and Evolution team, within the Biology of Gram positive Pathogens unit, at the Institut Pasteur, Paris.

GBS is a benign inhabitant bacterium of the gastrointestinal tract and the genitourinary tract of an estimated 10-30 percent of humans. The leading cause of early onset GBS infections in infants is thought to be aspiration of GBS-contaminated amniotic or vaginal fluid, leading to pneumonia or sepsis. Later onset cases, which develop after 2-3 weeks, may result in meningitis. A higher number of early onset pairs were studied in this work, but a greater proportion of late onset strains were found to be genetically different.

“There is an urgent need for better therapeutic interventions against neonatal GBS infections,” said Poyart.


Whole-genome comparison uncovers genomic mutations between group B streptococci sampled from infected newborns and their mothers, Journal of Bacteriology, August 17, 2015
Alexandre Almeida (1, 2, 3), Adrien Villain (4,*), Caroline Joubrel (5, 6, 7, 8, 9,*), Gérald Touak (5, 6), Elisabeth Sauvage (1, 2), Isabelle Rosinski-Chupin (1, 2), Claire Poyart (5, 6, 7, 8, 9, #), Philippe Glaser (1, 2, 4, #)
1 - Institut Pasteur, Unité de Biologie des Bactéries Pathogènes à Gram-positif, Paris, France;
2 - CNRS UMR3525, Paris, France;
3 - Université Pierre et Marie Curie, Paris, France;
4 - Institut Pasteur, Plateforme de Bio-Analyse Génomique, Paris, France;
5 - Service de Bactériologie, Centre National de Référence des Streptocoques, Groupe Hospitalier Paris Centre Cochin-Hôtel Dieu-Broca, Assistance Publique Hôpitaux de Paris, France;
6 - DHU “Risques et Grossesse”, Assistance Publique Hôpitaux de Paris;
7 - INSERM, U1016, Paris, France;
8 - CNRS (UMR 8104), Paris, France;
9 - Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
* These authors contributed equally to this work.
# Corresponding authors

Mis à jour le 31/08/2015


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