Paediatric food allergy and atopic march

Paediatric food allergy: the Australian guide for parents and GPs

Australia has among the world's highest rates of childhood food allergy — around 10% of Melbourne 12-month-olds have confirmed IgE-mediated food allergy. Common triggers include peanut, tree nuts, egg, cow's milk, wheat, soy, fish, shellfish, and sesame.

ASCIA guidelines recommend introducing allergens — including peanut and egg — before 12 months for all infants. The LEAP trial showed early peanut introduction reduces allergy by around 80%.

Anaphylaxis treatment is intramuscular adrenaline (EpiPen or Anapen), not antihistamines. Every at-risk child needs two auto-injectors, an ASCIA Action Plan, and referral to a paediatric allergist.

Why Australia leads the world in childhood food allergy

Australia has one of the highest rates of childhood food allergy globally — and it is not fully understood why. The HealthNuts study, conducted in Melbourne, found that approximately 10% of 12-month-old infants had challenge-confirmed IgE-mediated food allergy. Among those at highest risk — infants with moderate or severe eczema — the rate of peanut allergy approached 30% in some birth cohorts.

These numbers have important practical consequences. For parents, the prospect of anaphylaxis is frightening. For GPs, the consultation burden around allergy education, EpiPen prescribing, action plans, school liaison, and referral coordination is substantial. This article addresses all of it: prevention, recognition, diagnosis, anaphylaxis management, and the Australian healthcare pathways.

The central story of the last decade is this: the biology of food allergy prevention has been reversed. We used to be told to delay allergenic foods to protect babies. The opposite is true. Early introduction prevents allergy from developing.

A. Core clinical — the Australian general practice framework

Understanding the atopic march

The atopic march describes the natural progression of allergic disease through childhood:

  1. Atopic dermatitis (eczema) — typically begins at 3–6 months of age, driven by skin-barrier dysfunction (often associated with filaggrin gene variants that disrupt the epidermal barrier)
  2. IgE-mediated food allergy — develops in the context of a disrupted skin barrier that allows transcutaneous allergen sensitisation
  3. Asthma — typically emerges in the toddler to preschool period
  4. Allergic rhinitis — usually preschool to school age

The causal link between eczema and food allergy is the dual-allergen exposure hypothesis (Lack 2008): when an infant has disrupted skin (eczema) and encounters allergen through inflamed skin before encountering it orally, the immune system tends toward sensitisation rather than tolerance. Early oral introduction — before cutaneous sensitisation becomes established — supports oral tolerance. This mechanistic understanding underpins the ASCIA early introduction guidelines.

Aggressive eczema control — regular emollients, topical corticosteroids for flares — is therefore not only treating a skin condition but is one of the foundations of food allergy prevention, by restoring skin-barrier integrity.

The big 9 allergens and their natural history

The foods responsible for over 90% of IgE-mediated food allergy in Australian children:

FoodCommon presentationTypically outgrown?
PeanutOften severe; common cause of anaphylaxis~20% outgrow
Tree nuts (cashew, walnut, almond, pistachio, Brazil nut, hazelnut, pecan, macadamia)Cashew often severeMostly persistent
EggCommon in infancy; baked egg often tolerated earlier~70% outgrow by 6 years
Cow’s milkIgE-mediated and non-IgE forms (distinct)~80% outgrow by 5 years
WheatDistinct from coeliac disease~65% outgrow by adolescence
SoyOften co-exists with cow’s milk allergy~80% outgrow by school age
FishSpecies-specific reactivity possibleMostly persistent
Shellfish (crustacean and mollusc)Adult-onset also commonMostly persistent
SesameIncreasing prevalence in AUMostly persistent

Prevention: early introduction

The LEAP trial (Du Toit et al, NEJM 2015) was paradigm-shifting. High-risk infants (with severe eczema or existing egg allergy) randomised to consume peanut from 4–11 months had an 81% relative risk reduction in peanut allergy at age 5, compared to those who avoided peanut. The LEAP-On extension confirmed that sustained protection required continued ingestion.

The PETIT trial (Natsume et al, Lancet 2017) showed a 79% reduction in egg allergy at 12 months with heated egg introduction from 6 months in infants with eczema.

ASCIA 2020 guidelines now recommend for all Australian infants:

  • Introduce solid foods around 6 months of age, when the infant shows signs of developmental readiness (never before 4 months)
  • Introduce common allergenic foods — including peanut, cooked egg, cow’s milk in dairy products, fish, wheat, soy, sesame — before 12 months of age
  • After successfully introducing a food, continue to offer it regularly (several times per week) to maintain tolerance
  • For high-risk infants (severe eczema, or established egg allergy) — consider GP or allergist review before first peanut introduction, as skin-prick testing may be warranted

Maternal dietary restriction during pregnancy and breastfeeding is not recommended — multiple trials and NHMRC review have found no benefit for allergy prevention and potential harms from nutritional restriction.

Recognising anaphylaxis

ASCIA / WAO definition — anaphylaxis is present when any ONE of these criteria is met:

  1. Acute onset of skin or mucosal involvement (hives, flushing, swelling) AND either respiratory compromise or cardiovascular compromise
  2. Two or more of these after likely allergen exposure: skin/mucosal features, respiratory symptoms, cardiovascular symptoms, persistent gastrointestinal symptoms
  3. Reduced blood pressure after exposure to a known allergen

Practical Australian approach (RCH Melbourne CPG): any acute respiratory or cardiovascular symptoms following suspected allergen exposure should be treated as anaphylaxis until proven otherwise → use adrenaline immediately.

Antihistamines and corticosteroids do not treat anaphylaxis — they are adjuncts only, after adrenaline. Delay to adrenaline is associated with worse outcomes. The instinct to “start with antihistamine and see how it goes” is incorrect and potentially dangerous.

Anaphylaxis management

Lay the child flat — do not allow them to stand or sit upright. Postural hypotension can cause sudden cardiac arrest in anaphylaxis. If pregnant: left lateral tilt.

Adrenaline intramuscular (IM) into the anterolateral mid-thigh — the preferred site in children because of reliable absorption from thigh muscle:

WeightDeviceDose
<7.5 kgDraw up from ampoule0.05 mg (0.5 mL of 0.1 mg/mL adrenaline)
7.5–20 kg (~1–5 years)EpiPen Jr / Anapen 1500.15 mg
20–50 kgEpiPen / Anapen 3000.3 mg
>50 kgEpiPen / Anapen 500 (available in AU)0.3–0.5 mg

Repeat adrenaline every 5 minutes if no response. Call 000. Transfer all children with anaphylaxis to an emergency department for at least 4 hours’ observation — biphasic reactions (a second wave of anaphylaxis) occur in approximately 5% of cases, sometimes hours after the initial event.

Diagnosing food allergy

Skin-prick testing (SPT) — performed in-clinic by an allergist or immunologist. A small drop of allergen extract is placed on the skin and a lancet is pressed through it. A wheal (raised area) of ≥3 mm above the saline control at 15 minutes indicates sensitisation. A large wheal (e.g. >8 mm to peanut in an infant <2 years) has high positive predictive value. Antihistamines must be stopped 5 days beforehand.

Specific IgE (sIgE) blood testing — useful when SPT is not feasible (severe eczema covering the skin, dermographism, antihistamine use, very young infant). MBS-rebated under defined criteria. Component-resolved diagnostics — such as Ara h 2 for peanut (high-risk storage protein associated with severe reactions) — provide more nuanced risk stratification.

Oral food challenge — the gold standard. Performed under specialist supervision with resuscitation facilities, in incremental doses over hours. Used to confirm or exclude allergy when history and testing are equivocal, or to confirm that a child has outgrown their allergy.

Avoid panel testing — ordering broad allergen panels without clinical correlation produces false positives, unnecessary food avoidance, nutritional deficiency in infants, family anxiety, and potential loss of oral tolerance through avoidance of a food the child could actually eat safely. Test targeted to the clinical history.

IgG and IgG4 food testingASCIA explicitly recommends against these tests. They detect normal immune exposure to food, not allergy. They are unvalidated, misleading, and increasingly marketed in Australia; they should not guide dietary decisions.

B. Evidence highlights

The landmark prevention evidence is the LEAP trial and PETIT trial, as described above — the highest quality prevention evidence in food allergy. Both confirmed early oral introduction as the primary prevention strategy; both shifted international guidelines.

Aggressive infant eczema treatment is supported biologically and by observational evidence, though the BEEP trial (2020) showed that emollient alone from birth did not prevent eczema or food allergy development. The implication is that treating established eczema (with topical corticosteroids as indicated) matters more than prophylactic emollient before eczema begins.

Maternal dietary restriction during pregnancy and breastfeeding is not supported — Cochrane review and NHMRC review found no benefit and potential nutritional harms. This recommendation applies to restriction intended for allergy prevention; separate guidance applies if the infant has confirmed FPIAP (where maternal cow’s milk elimination can help the breastfed infant with blood in stools).

C. Non-IgE-mediated food allergy disorders

FPIES (Food Protein-Induced Enterocolitis Syndrome) causes profuse, repetitive vomiting 1–4 hours after ingestion of a trigger food, with pallor, lethargy, and sometimes hypotension. There are no hives, no throat symptoms. Common triggers in Australian infants include cow’s milk formula, soy, rice, oat, fish, and egg. Acute FPIES can mimic sepsis and frequently presents to the emergency department. Adrenaline is not the treatment. Acute management is IV fluid resuscitation; ondansetron reduces vomiting. Most children outgrow FPIES by school age.

FPIAP (Food Protein-Induced Allergic Proctocolitis) presents in otherwise well infants with streaky or mucousy blood in stools. It most commonly occurs in breastfed infants reacting to cow’s milk protein in maternal breastmilk. The infant is well, gaining weight, without anaemia or systemic illness. Management is maternal cow’s milk elimination (with dietitian guidance to ensure calcium adequacy) or switching to an extensively hydrolysed formula. Most resolve by 12 months.

Eosinophilic oesophagitis (EoE) presents with dysphagia, food impaction, vomiting, and feeding difficulty, often with atopic background. Diagnosis requires endoscopy and biopsy (≥15 eosinophils per high-power field). Treatment includes proton pump inhibitors (response in ~30%), topical swallowed corticosteroids (budesonide or fluticasone), and in some cases dupilumab (PBS-listed under criteria for EoE). Refer to paediatric gastroenterology and allergy.

D. Australian operations — prescribing and pathways

EpiPen prescribing on the PBS

Adrenaline auto-injectors (EpiPen Jr, EpiPen, Anapen 150/300/500) are PBS Authority Required. Prescribe two devices — one for home, one for school or childcare. PBS Authority criteria require either confirmed anaphylaxis (to food, insect, or drug) or high risk (established IgE-mediated food allergy with asthma, or history of a severe allergic reaction). Document the indication clearly in the medical record. Authority codes change; confirm current codes in the PBS online database.

ASCIA Action Plans

Every child with confirmed or high-risk food allergy needs a personalised ASCIA Action Plan. This is a one-page document specifying: the confirmed allergens, symptoms requiring adrenaline (vs antihistamine alone), weight-appropriate device and dose, and who to call. The plan goes to the school, childcare centre, sports coaches, and other carers. Victorian Ministerial Order 706 mandates anaphylaxis policies in schools; similar requirements exist in other states.

School and childcare

  • School must receive the ASCIA Action Plan and a named EpiPen for the child
  • Schools are also recommended to hold a general-use EpiPen (Emergency Anaphylaxis Kit)
  • Staff require twice-yearly anaphylaxis management training
  • No food sharing; hand washing after eating; regular label checking; known allergen risk minimisation in food preparation areas

MBS items

Standard GP consultations MBS items 23, 36, 44; Aboriginal and Torres Strait Islander children item 715; 4-year-old health assessment [item 701/703/707]; GP management plan and team care arrangement [items 721/723 and 731/732] for complex multi-food allergy requiring multidisciplinary coordination (GP, allergist, paediatric dietitian).

Referral pathways

Refer to a paediatric allergist for:

  • Any child with confirmed anaphylaxis to food
  • Multi-food allergy (two or more foods)
  • Suspected FPIES or EoE
  • High-risk infants needing SPT before first peanut introduction
  • Any child whose allergy status is uncertain and needs an oral food challenge

Public hospital allergy clinics have long waitlists (often 12–18 months in metropolitan areas). Private paediatric allergist waitlists are typically 2–6 months. For a child with anaphylaxis who requires specialist review while awaiting appointment, ensure a current ASCIA Action Plan and two EpiPens are in place in the interim.

E. Special populations

High-risk infants (severe eczema defined as eczema covering >10% of body surface, or established egg allergy) — these are the group most likely to develop peanut allergy, and the group for whom peanut skin-prick testing before the first home introduction is recommended. GP or allergist-guided SPT identifies those with large peanut wheals (often requiring first ingestion under supervised clinic conditions) vs those who can proceed with home introduction.

Aboriginal and Torres Strait Islander children — lower observed rates of food allergy in some cohorts, though access barriers to diagnosis mean under-ascertainment is likely. Use MBS item 715 for comprehensive paediatric health assessment. Connect with Aboriginal Community Controlled Health Organisations (ACCHOs) for culturally appropriate care.

Immigrant and culturally diverse families — cultural foods may include sesame, fish, and various nuts as part of traditional early infant feeding; these families may inadvertently be doing early allergen introduction. ASCIA resources are available in multiple languages via the National Allergy Council.

Children with multiple atopic conditions — eczema, food allergy, asthma, and allergic rhinitis frequently co-exist. Coordinating care across skin (dermatology), allergy (allergist), and lung (paediatric respiratory/GP) is important. Some children meet criteria for dupilumab (biologic treatment for severe atopic dermatitis and/or EoE) — PBS-listed under specialist-initiated authority.

When to escalate

Call 000 immediately when anaphylaxis occurs — any acute respiratory or cardiovascular symptoms after allergen exposure. Give adrenaline IM before calling if the device is immediately available; do not delay adrenaline to call first.

Same-day or emergency department review:

  • Suspected anaphylaxis that resolved but no EpiPen was given
  • FPIES episode with dehydration, pallor, or collapse
  • A child with known high-risk allergy who has ingested an allergen, even without symptoms yet (biphasic risk)

Within one week:

  • New urticaria after a specific food — needs allergy workup and interim safety plan

Routine referral:

  • Confirmed food allergy for specialist review, oral food challenge planning, and ongoing monitoring

What this article is and is not

This article provides general health information drawn from ASCIA guidelines, NHMRC Infant Feeding Guidelines, eTG Allergy and Immunology, RCH Melbourne CPGs, National Allergy Council, and the LEAP and PETIT trials. It is not personal medical advice. Food allergy diagnosis and management — particularly anaphylaxis risk assessment, EpiPen prescribing, and decisions about oral food challenges — should be guided by your GP and a paediatric allergist.

For crisis support: Lifeline 13 11 14, Beyond Blue 1300 22 4636. For anaphylaxis emergency: call 000.

For AU consumer information: Allergy and Anaphylaxis Australia, HealthDirect — Food allergies in children, Better Health Channel — Food allergy, National Allergy Council.


Sources cited

  1. ASCIA — Food Allergy
  2. ASCIA Infant Feeding and Allergy Prevention Guidelines 2020
  3. ASCIA Anaphylaxis Action Plans
  4. NHMRC — Infant Feeding Guidelines
  5. Therapeutic Guidelines (eTG) — Allergy and Immunology
  6. RCH Melbourne CPG — Anaphylaxis
  7. National Allergy Council Australia
  8. Allergy and Anaphylaxis Australia
  9. PBS — Adrenaline auto-injector listings
  10. MBS Online
  11. RACGP Red Book
  12. Du Toit G et al — LEAP trial (NEJM 2015)
  13. Natsume O et al — PETIT trial (Lancet 2017)
  14. HealthDirect — Food allergies in children
  15. Better Health Channel — Food allergy

Frequently asked questions

  • When should I introduce peanut and egg to my baby?

    Current ASCIA (Australasian Society of Clinical Immunology and Allergy) guidelines recommend introducing peanut, egg, and other common allergens to all infants around the time other solids are started — from around 6 months of age, not before 4 months. This applies regardless of whether there is a family history of allergy. Early introduction, and then continuing to offer the food regularly (at least several times a week), is the most evidence-based strategy to reduce the risk of developing allergy. For high-risk infants — those with severe eczema or an existing egg allergy — your GP may recommend a skin-prick test before the first peanut introduction. Peanut for infants is offered as smooth peanut butter stirred into puree, peanut powder dissolved in formula, or commercial peanut puff products — never whole peanuts or chunks, which are choking hazards before 3 years.

  • What is the difference between a food allergy and a food intolerance?

    An IgE-mediated food allergy involves the immune system and causes symptoms within minutes to two hours of eating — hives, vomiting, lip and throat swelling, difficulty breathing, or anaphylaxis. It can be life-threatening. A food intolerance does not involve the immune system and causes digestive symptoms (bloating, loose stools, discomfort) that are unpleasant but not dangerous. Lactose intolerance is the classic example — it is not an allergy. Non-IgE-mediated disorders (FPIES, eosinophilic oesophagitis) sit between these poles — they involve immune mechanisms but not IgE. The distinction matters for management: food allergies require formal diagnosis, an ASCIA Action Plan, and often an adrenaline auto-injector; intolerances require dietary modification.

  • My child had hives after eating — does this mean they have a food allergy?

    Hives (urticaria) after eating suggest an IgE-mediated allergic reaction but are not the same as anaphylaxis. A reaction that stays skin-only — hives or mild swelling — is concerning and needs investigation, but is generally less immediately dangerous than a reaction involving the throat, breathing, or collapse. Write down exactly what was eaten, how much, and when symptoms appeared. See your GP as soon as practicable. They can order skin-prick testing or specific IgE blood tests, and if the result supports allergy, refer to a paediatric allergist. In the meantime, your GP may prescribe an adrenaline auto-injector if they assess the child to be at risk of a more severe reaction next time. Hives from viral illness are also extremely common in children and are not food allergy — the context matters.

  • How do I use an EpiPen and when?

    Use the EpiPen for any anaphylaxis — any reaction involving the airways (throat tightening, hoarseness, wheeze, difficulty breathing, stridor) or cardiovascular symptoms (pallor, collapse, loss of consciousness) after contact with a suspected allergen. Do not wait to see if it gets worse. Technique: remove the blue safety cap; press the orange tip firmly against the outer thigh (can be given through clothing); hold for 10 seconds; remove and rub the site. Lay the child flat (do not let them stand up — sudden death can occur from postural hypotension). Call 000 immediately even if the EpiPen improves things rapidly, because biphasic reactions (a second wave) occur in about 5% of anaphylaxis episodes, sometimes hours later. Give a second EpiPen after 5 minutes if there is no improvement or the reaction returns. Every family managing anaphylaxis should practice with a trainer device; your GP or pharmacist can show you.

  • Will my child outgrow their food allergy?

    It depends on the food. Egg and cow's milk allergies are frequently outgrown — about 70% of egg-allergic children and 80% of cow's-milk-allergic children no longer have allergy by school age. Wheat and soy allergy similarly often resolve. Peanut, tree nut, fish, and shellfish allergies are more likely to persist into adulthood — only about 20% of peanut-allergic children outgrow their allergy. A paediatric allergist will monitor your child's allergy over time with periodic skin-prick or specific IgE testing, and arrange an oral food challenge under supervised conditions when they assess the allergy may have resolved. Do not trial reintroduction of a food that has caused anaphylaxis at home without specialist guidance.

  • What is FPIES and how is it different from a typical food allergy?

    FPIES (Food Protein-Induced Enterocolitis Syndrome) is a non-IgE-mediated food allergy that causes profuse, repetitive vomiting starting 1–4 hours after eating a trigger food, accompanied by pallor, lethargy, and sometimes collapse. Unlike typical food allergies, there are no hives, no throat symptoms, and no breathing problems. Common triggers include cow's milk formula, soy, rice, oat, and fish. FPIES can look like sepsis or gastroenteritis and often presents to emergency departments with the first episode. The adrenaline auto-injector is not the treatment for FPIES (because it is not IgE-mediated); acute management is intravenous fluids and sometimes ondansetron. FPIES is managed by trigger avoidance and specialist review; most children outgrow it by school age.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.