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Updated: Sep 26, 2026

Assessment of Intestinal Transcytosis of Neonatal Escherichia coli Bacteremia Isolates
Published on: February 17, 2023
Escherichia coli in infants' intestinal microflora: colonization rate, strain turnover, and virulence gene carriage
Forough Nowrouzian1, Bill Hesselmar, Robert Saalman
1Department of Clinical Bacteriology, Sahlgrenska University Hospital, Göteborg, Sweden. forough.nowrouzian@microbio.gu.se
Insights
Escherichia coli colonization in infants is delayed and strain turnover is slow, suggesting reduced exposure. Virulence factors like P fimbriae aid E. coli persistence in the infant gut microbiome.
Area of Science:
- Microbiology
- Pediatrics
- Human Microbiome
Background:
- Escherichia coli colonization patterns in infants may be changing due to modern lifestyles.
- Understanding early-life gut microbial colonization is crucial for infant health.
Purpose of the Study:
- To characterize Escherichia coli (E. coli) colonization and strain dynamics in healthy Swedish infants.
- To identify factors influencing E. coli persistence and virulence gene prevalence.
Main Methods:
- Longitudinal study of 70 infants over the first year of life.
- E. coli isolation from rectal swabs and fecal samples.
- Strain typing via random amplified polymorphic DNA and virulence gene identification using multiplex PCR.
Main Results:
- Late colonization by E. coli observed, with only 61% positive by 2 months.
- Slow strain turnover rate (1.5 strains/infant over 6 months).
- Genes for type 1 fimbriae, P fimbriae, and hemolysin were more common in persistent strains.
Conclusions:
- Swedish infants show late E. coli colonization and low strain turnover, indicating limited exposure.
- Virulence factors, particularly P fimbriae, facilitate E. coli persistence in the infant gut.
- Presence of pets, specifically cats, correlated with a higher prevalence of P-fimbrial adhesin genes in E. coli strains.
Abstract:
Colonization by Escherichia. coli in infants might have decreased in the last decades, owing to changes in hospital routines and family lifestyle. In this study, the E. coli flora was characterized in 70 healthy Swedish infants followed for the first year of life. E. coli was isolated from rectal swabs obtained at 3 d of age and quantified in fecal samples collected at 1, 2, 4, and 8 wk of age and at 6 and 12 mo of age. Strains were typed using random amplified polymorphic DNA, and their virulence factor genes were identified by multiplex PCR. Colonization by E. coli occurred late; only 61% of the infants were positive by 2 mo of age. The turnover of individual strains in the microflora was slow (1.5 strains per infant during 6 mo, 2.1 during 1 y). Environmental factors, such as siblings, pets, or feeding mode, did not influence colonization kinetics or strain turnover rate. Genes encoding type 1 fimbriae, P fimbriae, and hemolysin were significantly more common in E. coli strains persisting for at least 3 wk in the microflora than in transient strains. The P-fimbrial class III adhesin gene was more common in E. coli from children who had a cat in their homes than in E. coli from children without pets (p = 0.01); this adhesin type is common in E. coli from cats. The late colonization and low E. coli strain turnover rate suggest limited exposure of Swedish infants to E. coli. Our results confirm that P fimbriae and other virulence factors facilitate persistence of E. coli in the human colonic microflora.
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