Streptococcus agalactiae (GBS) is the leading cause of neonatal septicaemia, meningitis, and pneumonia in the industrialized world. Early onset (EOD) and late onset (LOD) diseases are defined in neonates by their occurring within or after the first week of life, respectively. Molecular epidemiological studies have identified a capsular serotype III clone, referred to as CC-17 by Multi Locus Sequence Typing, as accounting for the vast majority of neonatal invasive diseases and for almost all cases of meningitis in LOD.

The investigators working hypothesis is that host-environmental interactions may contribute to the colonization and persistence of the hypervirulent CC-17 GBS in the neonate. In this project the investigators will determine if reciprocal interactions between the intestinal microbiota and the innate and adaptive immune system may specifically facilitate the colonization of the neonate by the hypervirulent GBS CC-17 clone.

Four specific tasks will be addressed to:

(i) Understand whether and how the gut microbiota may influence growth and colonization of GBS CC-17 within the intestine of neonates.

(ii) Study the contribution of different diets and immune system constituents enabling the persistence of GBS CC-17 in the gut of neonates.

(iii) Determine whether the adaptive immune response elicited by maternal GBS colonization and transmitted to the infant is different for GBS CC-17 versus non-CC-17 GBS.

(iv) Determine whether or not GBS strains isolated from the mothers and from their babies are identical and whether the environment (ie. the vagina or the milk for the mother, the intestine or the oral cavity for the baby) influence the expression of specific virulence factors of CC-17.

Inclusion criteria:

• Patient having a negative vaginal swab for GBS at 35-37 weeks
• Patient aged over 18 years
• Patient who received information and agreeing to sign informed consent
• Patient affiliated or beneficiary of an insurance

Exclusion criteria:

• Patient does not speak and does not understand French