DOI 10.1097/inf.0000000000005360
Early-Life Antibiotic Exposure Disrupts Bifidobacterium in Infants: A qPCR-Based Cohort Study.
Аннотация
BACKGROUND
Early infancy represents a critical window for establishing the gut microbiome, during which Bifidobacterium species dominate and play essential roles in metabolic, immune and intestinal maturation. Antibiotic exposure during this sensitive period may disrupt microbial development, yet quantitative data on its longitudinal impact remain limited. To evaluate the effect of systemic antibiotic exposure during the first 6 months of life on the abundance of Bifidobacterium using quantitative real-time polymerase chain reaction in a prospective infant cohort.
METHODS
Seventy healthy term infants were enrolled at birth and followed at 1, 3 and 6 months. Stool samples were analyzed using quantitative real-time polymerase chain reaction targeting genus-level Bifidobacterium. Infants were categorized into antibiotic-exposed (n = 27) and nonexposed (n = 43). Demographic and clinical variables were compared, and longitudinal and multivariate analyses were used to assess factors associated with Bifidobacterium abundance.
RESULTS
No significant baseline differences were observed between groups. Antibiotic-exposed infants demonstrated significantly lower Bifidobacterium levels at all measured time points (P < 0.001). Nonexposed infants showed the expected rise in Bifidobacterium from 1 to 3 months, whereas exposed infants exhibited a significant decline from 1 to 6 months (P = 0.009). Multivariate regression analysis indicated that clinical factors, such as delivery mode, feeding type, gestational age and maternal intrapartum antibiotics, were not significant predictors of Bifidobacterium levels among exposed infants.
CONCLUSIONS
Antibiotic exposure in the first 6 months leads to persistent suppression of Bifidobacterium, disrupting normal microbiome maturation. These findings underscore the importance of cautious antibiotic use in early infancy and highlight the need for strategies to restore microbial balance following antibiotic therapy.
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