Characteristics and environmental susceptibility of first-pass meconium microbiota in neonates with congenital intestinal atresia.

PURPOSE: Whether congenital gastrointestinal atresia (atresia) specifically affects the meconium microbiota because of an altered intrauterine intestinal environment remains unclear. Therefore, we aimed to characterize the meconium microbiota of neonates with congenital anomalies, specifically atresia.

METHODS

Meconium samples were collected from healthy term neonates (control), neonates with congenital malformations other than atresia (other anomalies), and those with atresia who were admitted to the growing care unit or obstetrics ward. Alpha-diversity (Shannon index and observed features) and beta-diversity (principal coordinate analysis) were assessed through 16S rRNA gene sequencing. The microbial composition was examined at the phylum and genus levels, and stratified by delivery mode and mother's antibiotic exposure.

RESULTS

The study included 20 controls, 37 neonates with other anomalies, and 11 with atresia, including esophageal, duodenal, small intestinal, and colonic atresia. Alpha-diversity was the lowest in atresia, particularly with cesarean delivery or maternal antibiotic exposure (p < 0.05). Beta-diversity analysis demonstrated that the distribution of microbial profiles significantly differed between the control and atresia groups (p < 0.05). At the phylum level, atresia had a high proportion of Bacteroidetes, whereas Firmicutes and Proteobacteria were reduced. Several genera that were abundant in the control were markedly reduced in atresia (p < 0.001 vs. control; p < 0.01, among 3 groups), with higher Pseudomonas but lower Staphylococcus (p < 0.05, vs. control and other anomalies) and Escherichia (p < 0.05 vs. other anomalies).

CONCLUSION

Congenital gastrointestinal atresia demonstrated unique meconium microbiota profiles compared with those of healthy neonates and other congenital anomalies. This suggests differences in the intraintestinal environment during the fetal period.

LEVEL OF EVIDENCE: Ⅱ.