Asmaa Tazi1,2,3,4, Céline Plainvert1,2,3, Olivia Anselem2,4,5, Morgane Ballon2,6, Valérie Marcou2,4,7, Aurélien Seco2,6, Fatma El Alaoui8, Caroline Joubrel1,2,4, Najoua El Helali9, Emile Falloukh10, Amandine Frigo1,2, Josette Raymond1,2,4, Patrick Trieu-Cuot11, Catherine Branger8,12, Alban Le Monnier13, Elie Azria2,4,6,7, Pierre-Yves Ancel2,4,6,9, Pierre Henri Jarreau2,4,14, Laurent Mandelbrot2,15,16,12, François Goffinet2,4,5,6, Claire Poyart1,2,3,4. 1. Department of Bacteriology, University Hospitals Paris Centre-Cochin, French National Center for Streptococci, Assistance Publique - Hôpitaux de Paris (AP-HP). 2. Département Hospitalo-Universitaire Risks and Pregnancy. 3. Team Barriers and Pathogens of Cochin Institute, Institut National de la Santé et de la Recherche Médicale (INSERM) U1016 - Unité Mixte de Recherche Centre National de la Recherche Scientifique (UMR CNRS) 8104. 4. Paris Descartes University. 5. Department of Obstetrics and Gynecology, Port-Royal Maternity, University Hospitals Paris Centre Cochin Port Royal, AP-HP. 6. Obstetrical, Perinatal and Pediatric Epidemiology Research Team (Epidémiologie Périnatale, Obstétricale et Pédiatrique), INSERM UMR 1153. 7. Maternity Unit, Paris Saint Joseph Hospital. 8. Department of Microbiology, Louis Mourier Hospital, AP-HP. 9. Unité de Recherche Clinique-Centre d'Investigation Clinique P1419, University Hospitals Paris Centre Cochin Port Royal, AP-HP. 10. Department of Neonatal Medicine, Louis Mourier Hospital, AP-HP. 11. Biology of Gram-Positive Bacterial Pathogens Unit, CNRS Equipe de Recherche Labellisée, Pasteur Institute, Paris. 12. Infection Antimicrobials Modelling Evolution, INSERM UMR1137, France. 13. Department of Microbiology, Saint Joseph Hospital, Paris. 14. Department of Neonatal Medicine, Cochin-Port Royal Hospital, AP-HP. 15. Department of Obstetrics and Gynecology, Louis Mourier Hospital, AP-HP. 16. Paris Diderot University.
Abstract
BACKGROUND: In infants, the mode of acquisition of CC17 group B Streptococcus (GBS), the hypervirulent clone responsible for late-onset disease (LOD), remains elusive. METHODS: In a prospective multicenter study in France, we evaluated GBS colonization in mother-baby pairs with 2 months of follow-up between 2012 and 2015. Criteria included positivity for GBS colonization at antenatal screening or at delivery. Maternal vaginal samples and infant oral cavity and stool samples were analyzed at delivery, 21 ± 7 days (D21), and 60 ± 7 days (D60) post-delivery. RESULTS: A total of 890 mother-baby pairs were analyzed. GBS colonized 7%, 21%, and 23% of the infants at birth, D21, and D60, respectively, of which 10%, 11%, and 13% were identified as CC17 GBS. Concordance between maternal and infant GBS type was 96%. At D21, the main risk factors for infant colonization by GBS were simultaneous maternal colonization of the vagina (odds ratio [OR], 4.50; 95% confidence interval [CI], 1.69-15.61) and breast milk (OR, 7.93; 95% CI, 3.81-17.14). Importantly, 38% (95% CI, 23%-56%) of infants colonized by CC17 GBS appeared colonized for the first time at D60 vs 18% (95% CI, 14%-24%; P < .049) of infants colonized by non-CC17 GBS. Multivariate analysis showed a higher risk for de novo infant colonization by CC17 at D60 than by other GBS (OR, 2.45; 95% CI, 1.02-5.88). CONCLUSIONS: The high incidence of CC17 GBS in LOD is likely due to an enhanced post-delivery mother-to-infant transmission.
BACKGROUND: In infants, the mode of acquisition of CC17 group B Streptococcus (GBS), the hypervirulent clone responsible for late-onset disease (LOD), remains elusive. METHODS: In a prospective multicenter study in France, we evaluated GBS colonization in mother-baby pairs with 2 months of follow-up between 2012 and 2015. Criteria included positivity for GBS colonization at antenatal screening or at delivery. Maternal vaginal samples and infant oral cavity and stool samples were analyzed at delivery, 21 ± 7 days (D21), and 60 ± 7 days (D60) post-delivery. RESULTS: A total of 890 mother-baby pairs were analyzed. GBS colonized 7%, 21%, and 23% of the infants at birth, D21, and D60, respectively, of which 10%, 11%, and 13% were identified as CC17 GBS. Concordance between maternal and infantGBS type was 96%. At D21, the main risk factors for infant colonization by GBS were simultaneous maternal colonization of the vagina (odds ratio [OR], 4.50; 95% confidence interval [CI], 1.69-15.61) and breast milk (OR, 7.93; 95% CI, 3.81-17.14). Importantly, 38% (95% CI, 23%-56%) of infants colonized by CC17 GBS appeared colonized for the first time at D60 vs 18% (95% CI, 14%-24%; P < .049) of infants colonized by non-CC17 GBS. Multivariate analysis showed a higher risk for de novo infant colonization by CC17 at D60 than by other GBS (OR, 2.45; 95% CI, 1.02-5.88). CONCLUSIONS: The high incidence of CC17 GBS in LOD is likely due to an enhanced post-delivery mother-to-infant transmission.
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