P-1545. Impact of Perinatal Exposure and Colonization by Drug-resistant Enterobacterales on Infant Gut Microbiota

TL;DR

The study examines how exposure to drug-resistant bacteria during birth affects the development of an infant's gut microbiome.

Contribution

It identifies that perinatal colonization with beta-lactamase-resistant Enterobacterales leads to early gut microbiome differences in infants.

Findings

Infants colonized with beta-lactamase-resistant Enterobacterales showed distinct gut microbiome structures early in life.

Escherichia coli prevalence and abundance varied over time, with notable differences between resistant and non-resistant samples.

Early life microbial diversity differences were more pronounced in infants colonized with drug-resistant bacteria.

Abstract

Antibiotic-resistant Enterobacterales, including beta-lactamase producing (BL-E) and ceftriaxone resistant (CefR-E) strains, are prevalent in the U.S. and globally. Our objective was to assess the impact of resistant Enterobacterales exposure and perinatal colonization on infant microbiota development in healthy parent-infant dyads.Table 1.Demographics and clinical dataFigure 1.Enterobacterales species prevalence and relative abundance in maternal and infant samples

Demographics and clinical data

Enterobacterales species prevalence and relative abundance in maternal and infant samples

Pregnant women were enrolled during labor at a high-volume hospital in Chicago, IL. Exclusion criteria were delivery < 35 weeks gestation, fever, scheduled cesarean, and NICU admission. Maternal rectal swabs were collected prior to delivery, and infant stool was collected at 1-2 days (timepoint1), 7-10 days (t2), 2 months (t3), and 8 months of life (t4). Clinical data were obtained from the medical record and parental survey. Samples were plated on MacConkey + ceftriaxone and underwent shotgun next generation sequencing. Shotgun sequencing results were decontaminated and processed to obtain microbial taxonomic profiling and BL gene identification. CefR culture-based and metagenome-based results were combined to identify each sample’s beta-lactamase status (BL-E negative or positive). Whole genome sequencing was performed for ceftriaxone resistant (CefR) isolates.Figure 2.Prevalence and relative abundance of Escherichia coli in mother and infant gut microbiomeFigure 3.Beta diversity of infant gut microbiome over time grouped by BL-E status combining culture- and metagenome-based identificationKruskal-Wallis test p < 0.01; post hoc pairwise comparisons using Wilcoxon rank sum test p < 0.01 between all timepoints for infant samples

Prevalence and relative abundance of Escherichia coli in mother and infant gut microbiome

Beta diversity of infant gut microbiome over time grouped by BL-E status combining culture- and metagenome-based identification

Kruskal-Wallis test p < 0.01; post hoc pairwise comparisons using Wilcoxon rank sum test p < 0.01 between all timepoints for infant samples

Sixty-one dyads were enrolled 2/2022-1/2023 [Table 1], with 57 parent and 185 infant stool samples (t1=46, t2=50, t3=46, t4=43). CefR-E was identified in 15 parent and 13 infant samples over the study period. Not all infants with CefR-E had CefR-E cultured at subsequent timepoint. Among the 35 Enterobacterales species identified, Escherichia coli showed the highest prevalence and relative abundance [Fig 1]. Infant E. coli relative abundance decreased over time. Infant E. coli prevalence showed an increasing trend over time, with a distinct difference between BL-E positive and negative samples [Fig 2]. Difference in infant microbial community structure and beta diversity between BL-E positive and negative samples was larger for early time points (t1 and t2) compared to later time points (t3 and t4) [Fig 3].

Maternal and perinatal colonization with beta-lactamase resistant Enterobacterales leads to gut microbiome differences in early infancy. The impact of these early life alterations in E. coli and diversity warrants further investigation.

All Authors: No reported disclosures

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