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Updated: Oct 16, 2025
Quantitative Polymerase Chain Reaction-based Analyses of Murine Intestinal Microbiota After Oral Antibiotic Treatment
Published on: November 17, 2018
Early-life formula feeding is associated with infant gut microbiota alterations and an increased antibiotic
Katariina M M Pärnänen1, Jenni Hultman1, Melina Markkanen1
1Department of Microbiology, University of Helsinki, Helsinki, Finland.
Insights
Formula feeding in infants is linked to a higher burden of antibiotic resistance genes (ARGs) in the gut microbiome. This finding suggests that feeding practices significantly impact infant gut health and the development of antibiotic resistance.
Area of Science:
- Microbiology
- Pediatrics
- Genetics
Background:
- Infants face high mortality risks from infections, necessitating effective antibiotics.
- Infant gut microbiomes harbor numerous antibiotic resistance genes (ARGs), contributing to high mortality rates from resistant infections.
- While antibiotic impact on infant resistome is studied, other factors influencing gut ARG burden remain unclear.
Purpose of the Study:
- To investigate the effect of early formula exposure on ARG load in preterm and full-term neonates and infants.
- To test the hypothesis that infant diet influences gut microbial communities and that formula feeding increases ARG-carrying taxa.
Main Methods:
- Utilized cross-sectionally sampled gut metagenomes from 46 neonates.
- Developed a generalized linear model to assess diet's impact on neonatal ARG loads.
- Cross-validated the model using public neonate metagenomes and a custom statistical pipeline.
Main Results:
- Formula-fed neonates showed increased abundances of opportunistic pathogens like Staphylococcus aureus and Klebsiella pneumoniae.
- The relative abundance of ARGs was 69% higher in formula-fed infants compared to those exclusively fed human milk.
- Formula-fed infants exhibited reduced levels of beneficial bacteria, such as Bifidobacteria.
Conclusions:
- Formula exposure correlates with an elevated neonatal ARG burden.
- Feeding mode should be considered alongside antibiotic use to mitigate antibiotic-resistant gut bacteria proliferation in infants.
Background:
Infants are at a high risk of acquiring fatal infections, and their treatment relies on functioning antibiotics. Antibiotic resistance genes (ARGs) are present in high numbers in antibiotic-naive infants' gut microbiomes, and infant mortality caused by resistant infections is high. The role of antibiotics in shaping the infant resistome has been studied, but there is limited knowledge on other factors that affect the antibiotic resistance burden of the infant gut.
Objectives:
Our objectives were to determine the impact of early exposure to formula on the ARG load in neonates and infants born either preterm or full term. Our hypotheses were that diet causes a selective pressure that influences the microbial community of the infant gut, and formula exposure would increase the abundance of taxa that carry ARGs.
Methods:
Cross-sectionally sampled gut metagenomes of 46 neonates were used to build a generalized linear model to determine the impact of diet on ARG loads in neonates. The model was cross-validated using neonate metagenomes gathered from public databases using our custom statistical pipeline for cross-validation.
Results:
Formula-fed neonates had higher relative abundances of opportunistic pathogens such as Staphylococcus aureus, Staphylococcus epidermidis, Klebsiella pneumoniae, Klebsiella oxytoca, and Clostridioides difficile. The relative abundance of ARGs carried by gut bacteria was 69% higher in the formula-receiving group (fold change, 1.69; 95% CI: 1.12-2.55; P = 0.013; n = 180) compared to exclusively human milk-fed infants. The formula-fed infants also had significantly less typical infant bacteria, such as Bifidobacteria, that have potential health benefits.
Conclusions:
The novel finding that formula exposure is correlated with a higher neonatal ARG burden lays the foundation that clinicians should consider feeding mode in addition to antibiotic use during the first months of life to minimize the proliferation of antibiotic-resistant gut bacteria in infants.
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