Prenatal antibiotics may be linked to higher newborn risk of group B streptococcus.

A Swedish registry-based study reported prenatal antibiotic exposure was associated with a 29% higher adjusted risk of early-onset group B Streptococcus in newborns, with overall incidence 0.71 per 1,000 live births.

A Swedish population-based cohort study published in the Journal of Infection examined whether prenatal antibiotic exposure is associated with early-onset group B Streptococcus (GBS) disease in newborns. Researchers used four national registries to review all singleton live births in Sweden from 2006 to 2016. Sweden implemented intrapartum antibiotic prophylaxis in 2008 to reduce GBS transmission during delivery, but GBS continued to cause a substantial share of severe early-onset infections. The study reports an observed association between prenatal antibiotic exposure and higher newborn GBS risk, and the authors cautioned that causal links are not established. Key findings: - The analysis included 1,095,644 singleton live births; 24.5% had recorded prenatal antibiotic exposure. - The overall incidence of GBS disease was 0.71 per 1,000 live births; incidence within four weeks postpartum was 0.86 per 1,000 for exposed newborns versus 0.66 per 1,000 for unexposed, corresponding to an adjusted 29% higher risk (aOR 1.29). - The association was strongest for early third-trimester antibiotic exposure (aOR 1.67); among pregnancies without recorded GBS risk factors the aOR was 1.34, and no association was observed for pregnancies with at least one risk factor (aOR 0.91). - The authors stated it is too early to conclude causation, suggested antibiotic-related disruption of the maternal microbiota (including declines in Lactobacillus) as a possible mechanism, and called for studies with detailed intrapartum antibiotic data and dose-response analyses. Summary: The study identified an association between prenatal antibiotic exposure and increased early-onset GBS risk in newborns, reporting an adjusted 29% higher risk. Authors emphasized that causation is unproven and recommended further research to confirm the finding and to investigate mechanisms and more detailed antibiotic exposure data.