Nobody Told Me That the Antibiotics for the Infected Eczema Might Make the Next Infection More Likely

This article is part of the Nella Vosk Complete Guide to Baby Eczema for Australian Families — everything parents managing atopic dermatitis need to know about triggers, management, and the skin barrier.

This article is part of Nella Vosk’s Nobody Told Me series — a growing collection of posts written for the parent who has been trying everything and still feels like they’re failing their child. Every post in this series starts from a moment a parent wasn’t given information they needed, and works back through what the evidence actually says. You can find the full series at nellavosk.com.au/pages/nobody-told-me.

Nobody told me that the antibiotics for the infected eczema might make the next infection more likely.

We had been through the cycle enough times that I knew the pattern by heart. The eczema would flare. The scratching would open the skin. Within days there would be the honey-coloured crusting, the increased warmth, the skin that wouldn’t settle. We would go to the GP. We would leave with antibiotics. The infection would clear. The eczema would settle, briefly. And then, six or eight or ten weeks later, it would start again.

Nobody had explained to me that each round of antibiotics, while necessary and appropriate for the immediate infection, was also disrupting something in my son’s skin that made the next infection more likely. Nobody had told me about the skin microbiome, or about Staphylococcus aureus, or about why the cycle of infection and treatment tends to repeat in eczema-prone children rather than resolving over time.

Understanding that dynamic didn’t make the antibiotics wrong — they were the right treatment for confirmed bacterial infection, and they still are. But it changed what I did between courses, and it gave me a framework for thinking about long-term eczema management that I hadn’t had before.

The Skin Microbiome and Why It Matters for Eczema

Healthy skin is not sterile. It hosts a complex community of bacteria, fungi, and other microorganisms — collectively the skin microbiome — that plays an active role in immune regulation, barrier function, and protection against pathogenic invasion. In healthy skin, this community is diverse: hundreds of species occupying different ecological niches, competing with each other, producing antimicrobial compounds, and maintaining a dynamic equilibrium.

In eczema-prone skin, that equilibrium is disrupted. Research consistently shows that the skin of people with atopic dermatitis has significantly reduced microbial diversity — and that Staphylococcus aureus, a bacterium that is present in low levels on most people’s skin without causing harm, is present in dramatically elevated concentrations. In babies and children with eczema, more than 90% show evidence of S. aureus colonisation on affected skin, compared to around 30% of people without eczema.

S. aureus is not just a passive coloniser. It actively worsens eczema. Toxins produced by S. aureus penetrate the already-compromised skin barrier and trigger an immune response that drives inflammation — the same inflammation that characterises eczema flares. S. aureus colonisation is associated with increased eczema severity, more frequent flares, and a higher risk of secondary bacterial infection. Managing S. aureus colonisation is, for many children with moderate to severe eczema, central to managing the condition itself.

Can Antibiotics Make Eczema Worse?

The short answer is: sometimes, indirectly, and through a specific mechanism that is worth understanding.

Oral antibiotics prescribed for infected eczema work by targeting the bacterial infection — typically a S. aureus strain — and clearing it. They do this job effectively. The problem is that broad-spectrum antibiotics don’t only target the pathogenic bacteria causing the infection. They also reduce the populations of commensal bacteria that were providing protective competition against S. aureus. In a diverse, healthy skin microbiome, multiple species produce antimicrobial compounds — including compounds that specifically suppress S. aureus. When antibiotics reduce the diversity of the skin microbiome, they can temporarily eliminate some of this competitive suppression.

The result, in some children, is that S. aureus returns after the antibiotic course in higher concentrations than before — because the ecological competition that was keeping it in check has been reduced. The infection clears, but the underlying colonisation problem worsens. This is one mechanism by which repeated antibiotic courses can, paradoxically, contribute to a pattern of recurrent infection rather than resolving it.

There is also the antibiotic resistance dimension. S. aureus is highly capable of developing resistance to antibiotics — including the antibiotics most commonly prescribed for eczema-related skin infections. Repeated courses of the same antibiotic create selection pressure that favours resistant strains. Methicillin-resistant S. aureus (MRSA) is an extreme example of this process, but resistance can develop at lower levels of clinical severity. A child who has had multiple courses of the same antibiotic for recurrent eczema infections may develop a S. aureus colonisation pattern that is more resistant to standard treatment, making future infections harder and more complex to manage.

Do Antibiotics Make Eczema Worse in Every Case?

No — and this is an important distinction. Antibiotics for confirmed bacterial infection in eczema are the appropriate treatment, and withholding them out of concern for microbiome disruption is not clinically appropriate. When infection is present — identified by the characteristic signs of honey-coloured crusting, weeping, increased warmth, or a child who is unwell — antibiotics prescribed by a GP are the right intervention and should be taken as directed.

The concern is not with any single course of antibiotics. It is with the pattern of recurrent courses without addressing the underlying S. aureus colonisation and skin barrier factors that are driving the cycle. A child who has had three or more courses of antibiotics for eczema-related skin infections in a year is a child whose underlying eczema management warrants review, not just whose infections warrant treatment.

What Actually Reduces S. Aureus Colonisation

The most effective long-term strategy for reducing S. aureus colonisation in eczema is not antibiotics — it is consistent, sustained skin barrier repair that changes the environment in which S. aureus thrives. A compromised, dry, inflamed skin barrier is the ideal habitat for S. aureus colonisation. A well-moisturised, less-inflamed skin barrier is a less hospitable one.

Consistent emollient use: Twice-daily application of a thick, fragrance-free emollient — applied immediately after bathing to slightly damp skin — is the single most evidence-based intervention for reducing the frequency of eczema-related S. aureus infections. The emollient layer reduces transepidermal water loss, supports barrier repair, and reduces the cracking and fissuring that gives S. aureus easy entry points.

Dilute bleach baths: For children with recurrent bacterial infections, GPs and dermatologists sometimes recommend dilute bleach baths as part of an ongoing management strategy. The concentration used is approximately equivalent to a swimming pool. When prepared and used correctly under medical guidance, they are safe and may reduce S. aureus surface colonisation without the systemic effects of oral antibiotics. These should only be used as recommended by a healthcare provider, not self-prescribed.

Scratch protection: Every scratch in eczema-prone skin breaks the skin barrier and creates an entry point for S. aureus. Reducing scratching — through consistent overnight scratch protection, temperature management in the bedroom, and addressing the underlying itch with appropriate topical treatment — directly reduces infection risk. This is one of the strongest arguments for taking nighttime scratch protection seriously as a clinical management strategy rather than a comfort measure.

Addressing the eczema severity itself: S. aureus colonisation is strongly correlated with eczema severity. Children with mild eczema have significantly lower rates of recurrent infection than children with moderate to severe eczema. Achieving better overall eczema control — through the stepped treatment approach we covered in the staging post — reduces the infection-prone skin environment that drives the cycle.

A Note on Probiotics

The connection between the gut microbiome, skin microbiome, and eczema has generated significant research interest in probiotics as a potential intervention. The evidence to date is mixed — some strains of lactobacillus and bifidobacterium show modest benefit in some populations in some studies, while others show no significant effect. The research is not yet at a point where a specific probiotic recommendation for eczema can be made with confidence.

What the research does suggest is that a diverse gut microbiome in early infancy appears to be protective against atopic sensitisation, and that early antibiotic use — particularly in the first year of life — is associated with higher rates of eczema and atopic conditions. This is a population-level observation rather than a mandate to avoid medically necessary antibiotics. But it does support the principle of using antibiotics judiciously and only when clinically indicated, rather than as a routine first response to any eczema flare.

What to Say at the GP

If your child has had recurrent bacterial infections on top of eczema, it is entirely appropriate to raise this pattern explicitly at a GP appointment: ‘My child has had [X] courses of antibiotics in the past year for infected eczema. I’d like to discuss whether there are strategies we can put in place to reduce the frequency of infection, and whether a referral to a dermatologist might be appropriate.’ The infected eczema post in our eczema cluster covers the signs of infection and when to seek treatment in detail. This post is about the longer-term pattern — and the conversation that needs to happen after the third or fourth course, not just the first.

Related Reading

Infected Eczema in Babies: Signs, Symptoms & When to Act

NTM-2-14: Nobody Told Me There Was a Staging System

Wet Wrapping for Eczema: How It Works, When to Use It

How to Stop Baby Scratching at Night

NTM-2-12: Nobody Told Me the Cream I Was Using Could Be Triggering the Eczema

ABOUT THE AUTHOR
Kelly Northey is a Certified Postpartum Nutrition Professional (CPPNP) and founder of Nella Vosk, the parent company of the Bamboo Bubby range. She has spent fourteen years working with Australian families navigating baby and child eczema — the sleepless nights, the skin that won’t heal, and the guilt of feeling like you should be doing more. The Bamboo Bubby range exists because of those families.
Learn more about Kelly.