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Updated: Jul 2, 2026

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
Molecular determinants of Escherichia coli causing neonatal invasive infection following vertical transmission
Liang Gao1,2, Jia Yin Wu3, Xue Rong Huang1,2
1Department of Neonatology, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Background:
Escherichia coli (E. coli) is a leading cause of life-threatening neonatal invasive infections via vertical transmission. However, the bacterial molecular features that distinguish invasive infection from asymptomatic colonization following vertical transmission remain unclear in genomically confirmed mother-neonate pairs.
Methods:
A single-center retrospective case-control study enrolled 43 mother-neonate pairs with genome sequencing-confirmed clonal E. coli vertical transmission (average nucleotide identity, ANI ≥99.99%) between January 2020 and June 2025. Pairs were stratified into an invasive infection group (n = 27) and a colonization group (n = 16) based on neonatal clinical outcomes. Genomic characterization, including multilocus sequence typing (MLST), serotyping, and virulence gene profiling, was performed on maternal E. coli isolates. The Boruta algorithm was used for feature selection, and a Bayesian logistic regression model was constructed to identify independent predictors of invasive infection.
Results:
No significant differences were observed in baseline clinical characteristics between the two groups. ST95 was exclusively detected in the invasive infection group (29.6% vs. 0%, P = 0.018). The virulence genes neuA (63% vs. 13%), neuS (59% vs. 13%), iutA (78% vs. 38%), and kpsMT II (93% vs. 63%) were significantly more prevalent in the invasive infection group (all raw P < 0.05). Bayesian modeling identified four independent predictors: ST95 [odds ratio (OR) = 6.05, 90% credible interval (CrI): 0.82-66.7, posterior probability P(OR>1) = 0.85], neuA (OR = 4.95, 90%CrI: 1.65-16.44, P(OR>1) = 0.96), kpsMT II (OR = 4.48, 90%CrI: 1.35-16.44, P(OR>1) = 0.95), and iutA (OR = 3.32, 90%CrI: 1.22-9.03, P(OR>1) = 0.93). Notably, all ST95 isolates (100%) co-harbored neuA, kpsMT II, and iutA, forming a distinct "clonal virulence complex." The model exhibited good predictive performance (AUC = 0.847, 95%CI: 0.727-0.954), while the composite virulence burden score showed no intergroup difference (P = 0.208).
Conclusion:
The ST95 E. coli clonal virulence complex (co-harboring neuA/kpsMT II and iutA) is strongly associated with invasive infection following vertical transmission. This signature represents a potential candidate marker for clinical risk stratification of neonates at high risk of E. coli invasive infection, with potential implications for precision monitoring and intervention in perinatal care.
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