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Updated: Jun 19, 2025
Assessment of Intestinal Transcytosis of Neonatal Escherichia coli Bacteremia Isolates
Published on: February 17, 2023
Neonatal intestinal colonization of Streptococcus agalactiae and the multiple modes of protection limiting
Kara G Greenfield1, Olivia S Harlow1, Lila T Witt1
1Department of Immunology, Mayo Clinic, Rochester, MN, USA.
Insights
Maternal milk
Area of Science:
- Neonatal immunology
- Microbiology
- Infectious diseases
Background:
- Group B Streptococcus (GBS) is a leading cause of neonatal sepsis.
- GBS can colonize the infant gut, potentially leading to late-onset sepsis.
- Understanding GBS colonization in neonates is crucial for prevention.
Purpose of the Study:
- To investigate Group B Streptococcus (GBS) colonization dynamics in premature neonates.
- To explore the relationship between maternal factors and GBS intestinal colonization.
- To evaluate the impact of maternal vaccination on GBS colonization and neonatal outcomes.
Main Methods:
- Collected stool and milk samples from premature neonates and their mothers.
- Utilized a murine model to study GBS transmission and colonization.
- Assessed maternal immunoglobulin A (IgA) levels and GBS colonization.
- Evaluated the efficacy of maternal vaccination against GBS.
Main Results:
- GBS colonization was observed in 10% of the premature neonate cohort.
- Infant GBS abundance negatively correlated with maternal milk IgA levels.
- Maternal vaccination induced IgA responses, reducing GBS colonization and mortality in offspring.
- Both vertical and oral transmission led to intestinal GBS colonization in mice, with limited translocation.
Conclusions:
- Maternal milk IgA may play a protective role in limiting GBS intestinal colonization in neonates.
- Maternal vaccination is a potential strategy to enhance infant immunity against GBS.
- Further research is needed to elucidate the mechanisms of IgA-mediated protection against GBS.
Abstract:
Streptococcus agalactiae, also known as Group B Streptococcus (GBS), is a predominant pathogen of neonatal sepsis, commonly associated with early-onset neonatal sepsis. GBS has also been associated with cases of late-onset sepsis potentially originating from the intestine. Previous findings have shown GBS can colonize the infant intestinal tract as part of the neonatal microbiota. To better understand GBS colonization dynamics in the neonatal intestine, we collected stool and milk samples from prematurely born neonates for identification of potential pathogens in the neonatal intestinal microbiota. GBS was present in approximately 10% of the cohort, and this colonization was not associated with maternal GBS status, delivery route, or gestational weight. Interestingly, we observed the relative abundance of GBS in the infant stool negatively correlated with maternal IgA concentration in matched maternal milk samples. Using a preclinical murine model of GBS infection, we report that both vertical transmission and direct oral introduction resulted in intestinal colonization of GBS; however, translocation beyond the intestine was limited. Finally, vaccination of dams prior to breeding induced strong immunoglobulin responses, including IgA responses, which were associated with reduced mortality and GBS intestinal colonization. Taken together, we show that maternal IgA may contribute to infant immunity by limiting the colonization of GBS in the intestine.
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