Cervicovaginal Microbial-Immune State and Group B Streptococcus Colonization in Pregnancy.


Journal

American journal of perinatology
ISSN: 1098-8785
Titre abrégé: Am J Perinatol
Pays: United States
ID NLM: 8405212

Informations de publication

Date de publication:
09 Aug 2023
Historique:
medline: 10 8 2023
pubmed: 10 8 2023
entrez: 9 8 2023
Statut: aheadofprint

Résumé

 Maternal colonization with Group B  This was a secondary analysis of a prospective cohort study of pregnant individuals with singleton pregnancies who had CV microbiota specimens analyzed at 16 to 20, 20 to 24, and 24 to 28 weeks' gestation, along with a third trimester GBS rectovaginal (RV) culture (  Of 492 individuals, 34.3% were GBS RV + . Compared with individuals with CST I at 16 to 20 weeks, individuals with CST IV-A and CST II had a significantly elevated relative risk of subsequent GBS RV+ status. When stratified by high and low β-defensin-2 levels, β-defensin-2 was found to be an effect modifier of the association between CST IV-A and GBS RV+ status. In individuals with low β-defensin-2 levels, CST VI-A was associated with GBS RV+ status, but among individuals with high β-defensin-2 levels, there was no such association (interaction  Pregnant individuals with CV microbiota characterized by CST IV-A and CST II had significantly elevated risk of GBS RV colonization in the third trimester compared with those with CST I, and β-defensin-2 was an effect modifier of the association between CST IV-A and GBS RV+ status. Future research should investigate if manipulation of the CV microbiota can prevent GBS colonization, thereby reducing intrapartum antibiotic prophylaxis and the risks of neonatal GBS infection. · The relationship between the CV microbiota and GBS RV colonization is unknown.. · A Lactobacillus-deficient, anaerobic rich vaginal community, CST IV-A, is associated with increased risk of GBS RV colonization.. · β-defensin-2 is an effect modifier of the association between CST IV-A and GBS RV+ status..

Identifiants

pubmed: 37557898
doi: 10.1055/s-0043-1772226
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NINR NIH HHS
ID : R01 NR014784
Pays : United States

Informations de copyright

Thieme. All rights reserved.

Déclaration de conflit d'intérêts

None declared.

Auteurs

Jennifer A McCoy (JA)

Department of OB/GYN, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Heather H Burris (HH)

Department of OB/GYN, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.

Kristin D Gerson (KD)

Department of OB/GYN, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Clare McCarthy (C)

Department of OB/GYN, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Jacques Ravel (J)

Department of Microbiology and Immunology, Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, Maryland.

Michal A Elovitz (MA)

Department of Obstetrics, Gynecology and Reproductive Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.

Classifications MeSH