Background: Escherichia coli occupies a paradoxical niche in the human gut microbiome, owing to its exceptional genomic plasticity it sustains the dual identity of a commensal as well as a versatile pathogen. It has diverged into eight phylogenetic lineages whose ecological functions differ substantially. Phylogroups A and B1 are primarily adapted for intestinal commensalism, attracting increasing interest as probiotic candidates. Groups B2, C, D, E, F and G carry expanded virulence determinant arrays along with an arsenal of ARGs that underlie their established roles in bacteraemia, sepsis and neonatal meningitis. E. coli is acquired within hours of birth, establishing itself as a founding flora of the gut microbiome during the neonatal period, a window of vulnerability during which immune maturation and metabolic programming are simultaneously being established, with perturbations carrying systemic health consequences extending into adulthood. In this context, the identity or characteristics of the microbial lineages that colonize the neonatal gut becomes a critical determinant. While maternal microbiota transmission has long been recognised as the primary seed of initial neonatal gut colonization, this study reflects that ecological factors like hospital environment compounded by antibiotic selection pressure, might have an upper hand. Whether commensals persist under these pressures, or if pathogenic lineages with higher fitness outcompete them, is unknown. Further, as most studies have documented the role of E. coli phylogroups in the context of disease, their distribution in healthy neonates remain poorly understood. This study therefore characterized the E. coli phylogenetic landscape and antibacterial susceptibility patterns in healthy mother–infant pairs to uncover early colonization trends.

Method: Stool specimens were collected from healthy mother-infant pairs admitted to a hospital. Bacterial strains were isolated following standard stool culture procedure. Identification and antibiotic susceptibility profiles for bacterial strains were carried out by VITEK® 2 compact system. For all identified E. coli, PCR-based phylogroup detection was performed using the revised Clermont quadruplex PCR method, which targets the genes arpA, chuA, yjaA, and TspE4.C2.

Result: Among the identified E. coli strains (n=62), 38 were isolated from mothers and 24 from neonates. Phylogroup A was most abundant (42.1%) in maternal strains, followed by B1, B2 and D, each comprising 15.7%. Single isolates belonged to C, E, and F. Among neonates, phylogroup A was most frequent (37.5%), followed by D (29.1%), B2 (16.6%), and C (8.3%). Single strains of B1 and F were also identified. The distribution of some phylogroups varied between mothers and infants. Across both maternal and neonatte strains, resistant patterns were concentrated in B2, D, and F, with a trend of elevated resistance to β-lactam antibiotics and fluoroquinolones. In neonates, phylogroups B2, D, and F demonstrated the highest levels of resistance across β-lactams and fluoroquinolones. B2 and F exhibited 75–100% nonsusceptibility to these classes, while D showed variable resistance (16.7– 83.3%). Among maternal isolates, phylogroups D and F were 100% resistant to third-generation cephalosporins and ciprofloxacin, and B2 showed 50–83.3% nonsusceptibility across the same classes. Notably, commensal A displayed moderate to high nonsusceptibility in both mothers (31.3– 75%) and neonates (up to 77.8%). Multidrug resistance (MDR) was restricted to B2, D, and F in both maternal and infant populations.

Conclusion: The phylogenetic landscape of E. coli showed non-overlapping distributions between maternal and infant strains, indicating that early gut colonization is governed by ecological pressures. The presence of B2, D, and F, marked by MDR in healthy infants, signified the silent transmission of high-risk strains. However, the finding that phylogroup A, already harbours up to 75% nonsusceptibility to critically important antibiotics in both maternal and neonatal compartments fundamentally reframes the concept of “commensal” in clinical microbiology. Hence, this study calls for early phylogenydriven microbial surveillance and integrative microbiome stewardship.