The Surprising Link Between Antibiotics and Your Baby’s Microbiome

Prefer a less clinical read? This article covers the underlying research and mechanisms in full. If you’d rather start with the lived experience, what this actually looks and feels like, and what it means for your child — my Substack article may suit you better. Read it on Escape the Eczema Trap →

In the hours after birth, something remarkable begins. A newborn’s gut, until that moment essentially sterile, starts to fill with microbial life. Within days, trillions of bacteria have taken up residence, organising themselves into a community that will go on to shape almost every aspect of the child’s health: digestion, metabolism, and, as a growing body of research now shows, the skin.

This is a colonisation event. It happens only once, during a narrow window in early infancy, and the order in which species arrive matters almost as much as which species arrive at all. For most babies, the process unfolds naturally. But for a substantial number of infants, those who receive antibiotics in the first days or weeks of life, for all the right reasons including a suspected infection, a Caesarean delivery, or a Group B Streptococcus (GBS) swab that came back positive during labour, that colonisation event is interrupted before it has properly begun.

This article looks at what happens when it is interrupted. Specifically, it examines the growing evidence that early antibiotic exposure disrupts the infant gut microbiome in a way that is increasingly linked to a child’s risk of developing atopic dermatitis (eczema) and a cluster of related immune conditions.

An ecosystem under construction

Think of the infant gut, in those first weeks, less as a finished structure and more as a building site. The bacteria arriving are not simply passing through, they are laying down infrastructure that the immune system will rely on for years.

Among the earliest and most important arrivals is a genus called Bifidobacterium. In a healthy, breastfed infant, Bifidobacterium species dominate the gut for the first months of life, feeding on components of breast milk that the baby itself cannot digest. In return, they produce compounds that strengthen the gut lining and, crucially, help train a population of immune cells called regulatory T cells, the cells responsible for teaching the immune system not to overreact to harmless things: pollen, food proteins, a baby’s own skin.[1,2]

This is the gut-skin axis in its simplest form. What colonises the gut in the first weeks of life calibrates how the immune system responds to the world for years afterwards, and it is a process that, by its nature, can only happen once, in sequence, at the right time.

THE CRITICAL WINDOW The first two weeks of life appear to be the most consequential. Antibiotics given intravenously in hospital during this period consistently cause greater disruption, and disruption that lasts longer, than antibiotics given during labour or later in infancy. The earlier the interruption arrives relative to this first wave of colonisation, the further the gut’s development drifts from its intended course.

What happens when antibiotics arrive early

When antibiotics are given in the first weeks of life, the effect on this developing ecosystem is profound. Studies from Finland, Russia, South Korea and elsewhere have each found that early antibiotic exposure reduces the overall diversity of the gut microbiome, sometimes for a year or more.[3,4,5]

Diversity matters in much the same way it matters in any ecosystem: a gut populated by many species is more resilient, more functionally complete, and better able to recover from future disturbances than one dominated by a small number of species.

One large 2025 study found minimal disruption following antibiotic exposure[7], but on closer inspection, this cohort received antibiotics predominantly after four months of age, well outside the most vulnerable window. If anything, this reinforces my initial point: timing is everything.

The survivors of an early antibiotic course are not necessarily the strains you would choose. Bifidobacterium, the genus doing so much of the immune-training work described above, is consistently among the casualties. Following antibiotics given during labour for GBS, the expected colonisation by Bifidobacterium is delayed, with longer courses producing longer delays.[6] Following antibiotics given directly to newborns, the intravenous antibiotics often started within hours of birth if sepsis is suspected, the depletion can be more severe and more persistent: one German study found a particular species, B. longum, still suppressed at both one month and one year after antibiotics given during labour,[8] while a Finnish cohort found Bifidobacterium species still reduced at two years of age following neonatal antibiotics.[5]

Into the space left behind moves a different cast of characters: a family of bacteria called Enterobacteriaceae, which includes species such as E. coli. To be clear, these are not inherently harmful, they are part of a normal gut community in small numbers, but when they expand to fill a gap left by Bifidobacterium, they bring something with them. Their outer membrane is studded with a molecule called lipopolysaccharide, or LPS, which the immune system reads as a signal of danger.

Where Bifidobacterium tends to produce calming, anti-inflammatory compounds, an Enterobacteriaceae-dominated gut tends to produce the opposite. One study found this shift detectable from three weeks of age and still present at one year, and more pronounced in formula-fed infants than breastfed ones.[9]

This is the signature that recurs across the literature: less Bifidobacterium, more Enterobacteriaceae. Less calm, more alarm, at precisely the moment the immune system is supposed to be learning the difference between the two.

Recovery and the role of breastfeeding

For most infants exposed to antibiotics during labour, the gut finds its way back towards a typical trajectory within six to twelve weeks.[6,11] For infants exposed to antibiotics directly after birth, recovery can take longer, up to a year for some markers,[9] up to two years for others.[5]

One factor consistently speeds this recovery: breastfeeding. Across multiple cohorts, breastfed infants who had received antibiotics recovered a more typical gut microbiome roughly two weeks faster than formula-fed infants, with lower levels of the Enterobacteriaceae described above.[9] In a process that otherwise unfolds largely outside anyone’s control, this is one of the few levers available and one that is worth being aware of.

From the gut to the skin

The connection between gut bacteria and skin disease might sound unlikely, until you look at the largest study to test it directly.

Hoskinson and colleagues followed more than 3,400 Canadian infants from birth to age five.[1] Children who had received systemic antibiotics during their first year were 81% more likely to be diagnosed with atopic dermatitis at five years old, and the risk rose further with each additional course of antibiotics.[1]

What makes this study unusual is that the researchers did not stop at the association. They had also collected stool samples at one year, and when they analysed them, they found a familiar signature: more of a bacterium called Tyzzerella nexilis, less Bifidobacterium, less of the fermentative activity that produces calming gut compounds.

This signature, the same one that follows early antibiotic exposure, accounted for around 39% of the link between antibiotics and eczema.[1] In other words, approximately two-fifths of the increased risk could be traced through the gut.

THE HEADLINE FINDING In the largest study of its kind, infants given antibiotics in their first year were 81% more likely to develop eczema by age five, and around two-fifths of that increased risk could be traced directly to changes in their gut bacteria.

Not every study agrees. One retrospective US study found the opposite: that antibiotics in the first month of life were associated with a slightly lower rate of eczema.[12] But that study relied on diagnosis codes rather than physician assessment, collected no microbiome data at all, and could not account for the ways in which infants prescribed antibiotics for an early fever might differ, in all sorts of unmeasured ways, from infants who were not. This study carries considerably less weight than Hoskinson’s prospective design, physician-confirmed diagnoses, and paired microbiome data.

It is worth pointing out, however, that no study has yet measured the skin itself. Transepidermal water loss, skin pH, the lipid layers that make up a healthy barrier in infants carrying this gut signature, have not been monitored. The chain runs convincingly from antibiotics, to gut bacteria, to eczema diagnosis. What is happening at the skin’s surface while all this unfolds has not yet been directly observed.

Beyond the skin

The same gut signature shows up, with remarkable consistency, in other corners of a child’s health.

In a study of more than 2,600 Canadian children, those given antibiotics in their first year were nearly twice as likely to develop asthma, and again, part of the effect ran through reduced gut microbiome diversity.[2] One Canadian study also linked Enterobacteriaceae overgrowth following early antibiotics to food sensitisation, the early immune misfires that can precede food allergy, at one year of age.[14]

A SURPRISING FINDING The consequences of early gut disruption are not confined to skin and airways. A 2025 study in Nature found that infants with lower Bifidobacterium levels after neonatal antibiotic exposure produced measurably weaker antibody responses to their childhood vaccinations, including the pneumococcal and six-in-one vaccines, six months later.[13]

In the Netherlands, researchers found that neonatal antibiotics left a measurable signature in infants’ circulating immune markers a full year later.[15] In Germany, antibiotics given during labour were linked to a more inflammation-prone profile of T-helper cells, also measured at one year.[8]

All of these individual studies and findings describe the same story from different angles: an immune system that, having missed part of its early training, leans towards reactivity rather than tolerance, in the gut, in the lungs, in response to vaccines, and, the evidence increasingly suggests, in the skin.

What we don’t yet know

It is worth being precise about where the evidence is available and where it is not.

The link between early antibiotics and gut microbiome disruption is well established, replicated across countries, populations, and methods. The signature itself, less Bifidobacterium and more Enterobacteriaceae, is one of the most consistent findings in this entire field.

The link between that signature and atopic dermatitis rests, for now, on one exceptionally well-designed study.[1] It is a strong study, but it is one study, and its eczema diagnoses were made at age five, leaving the years in between as an open question. What happens to a child’s skin and immune system between one and five years old? Do dietary changes, illnesses, or environmental exposures during that gap modify the trajectory one way or the other? We do not yet know.

And the most direct test of all, measuring an infant’s actual skin barrier function against their gut microbiome profile, has simply not been done and, for the moment, can’t be done.

Until it becomes possible, the chain from gut to skin remains one of strong inference rather than direct proof.

What this means in practice

A NOTE ON ANTIBIOTICS None of this is an argument against giving antibiotics to infants who need them. Suspected sepsis, confirmed infection, and GBS prophylaxis remain clearly necessary for an antibiotic prescription, and that decision should never be complicated by microbiome considerations. What this evidence points to is something that happens after the antibiotics, a recovery period that, for most families, isn’t being focused on at the moment.

A few things follow from this.

Timing is information. An infant who received intravenous antibiotics in the first two weeks of life has, on the evidence so far, undergone a more significant disruption than one exposed only to antibiotics during labour. That history is worth knowing, and worth factoring into how much attention the recovery period gets. What kind of support can be put in place to help the microbiome recover?

Breastfeeding helps, and is worth actively supporting through and after any antibiotic course, where possible. I don’t mean this as a moral position, but because the evidence shows it measurably speeds the gut’s return towards a typical trajectory.[9]

The Bifidobacterium gap is specific enough to target. Given how consistently B. longum and B. bifidum are the species depleted by early antibiotics,[5,8] strain-specific probiotic support in the weeks and months following an antibiotic course has a clearer evidence-based rationale than generic, multi-strain products.

Diet matters early. Human milk oligosaccharides for breastfed infants, and a gradually widening diversity of fibre as weaning begins, both support the return of Bifidobacterium populations, and this is squarely within the scope of nutritional support.

The aim isn’t to second-guess an antibiotic prescription, which was undoubtedly important. What it does is open up a second decision, to support the recovery of the microbiome, that is rarely discussed, and that the evidence suggests is worth doing.

For a more personal read on this subject, head over to my Substack — Escape the Eczema Trap.

References

1. Hoskinson C, Medeleanu M, Reyna M, et al. Antibiotics within first year are linked to infant gut microbiome disruption and elevated atopic dermatitis risk. Journal of Allergy and Clinical Immunology. 2024.
2. Sbihi H, Patrick D, Dai DLY, et al. Early-life antibiotic exposure, the gut microbiome, and the risk of childhood asthma. Environmental Epidemiology. 2019.
3. Yassour M, Vatanen T, Siljander H, et al. Natural history of the infant gut microbiome and impact of antibiotic treatments on strain-level diversity and stability. Science Translational Medicine. 2016.
4. Uzan-Yulzari A, Turta O, Belogolovski A, et al. Neonatal antibiotic exposure impairs child growth during the first six years of life by perturbing intestinal microbial colonization. Nature Communications. 2021.
5. Stearns J, Simioni JC, Gunn E, et al. Intrapartum antibiotics for GBS prophylaxis alter colonization patterns in the early infant gut microbiome of low risk infants. Scientific Reports. 2017.
6. Teuscher JL, Lupatsii M, Graspeuntner S, et al. Persistent reduction of Bifidobacterium longum in the infant gut microbiome in the first year of age following intrapartum penicillin prophylaxis for maternal GBS colonization. Frontiers in Immunology. 2025.
7. Daele EV, Kamphorst K, Vlieger A, et al. Effect of antibiotics in the first week of life on faecal microbiota development. Archives of Disease in Childhood. 2022.
8. Nguyen AT, Aquino M. Association between early life antibiotic exposure and development of early childhood atopic dermatitis. Pediatrics. 2023.
9. Ryan F, Clarke M, Lynn M, et al. Bifidobacteria support optimal infant vaccine responses. Nature. 2025.
10. Yasmin F, Tun H, Konya T, et al. Cesarean section, formula feeding, and infant antibiotic exposure: separate and combined impacts on gut microbial changes in later infancy. Frontiers in Pediatrics. 2017.