📋 Key Information Summary
- Allergic disorders affect ~20% of Australians and are the most common chronic conditions managed in general practice, with significant morbidity and healthcare utilisation.
- IgE-mediated reactions are rapid (minutes to 2 hours), involve mast-cell and basophil degranulation, and can cause anaphylaxis; non-IgE reactions are delayed (hours to days) and T-cell mediated, presenting with GI symptoms, eczema flares or FPIES.
- Peanut allergy is now the most common cause of fatal food-related anaphylaxis in Australia; egg allergy is the most common infant food allergy; latex allergy affects healthcare workers and spina bifida patients.
- Anaphylaxis requires immediate intramuscular adrenaline (anterolateral thigh) — EpiPen® Jr 150 µg (<20 kg) or EpiPen® 300 µg (≥20 kg); second dose at 5 minutes if no response.
- All ASCIA Action Plans for Anaphylaxis must be completed, reviewed annually, and provided to schools, childcare, and workplaces alongside training on autoinjector use.
- Allergic rhinitis (hay fever) affects ~18% of Australian adults; intranasal corticosteroids are first-line pharmacotherapy; allergen avoidance and sublingual immunotherapy (SLIT) address the underlying cause.
- Skin prick testing (SPT) is the gold-standard office-based test for IgE-mediated allergy; specific IgE (RAST/ImmunoCAP) is useful when SPT is contraindicated or results are equivocal.
- Serum tryptase drawn 1–2 hours post-reaction (and baseline) confirms mast-cell degranulation and supports a diagnosis of anaphylaxis.
- Peanut oral immunotherapy (OIT) with Palforzia® (powderised peanut) is now TGA-registered in Australia for children and adolescents 4–17 years with confirmed peanut allergy.
- Allergen immunotherapy (sublingual or subcutaneous) is the only disease-modifying treatment for allergic rhinitis and venom allergy, reducing symptom burden and preventing asthma development.
- Aboriginal and Torres Strait Islander peoples have higher rates of undiagnosed allergic disease, anaphylaxis hospitalisation, and reduced access to specialist allergy services, particularly in remote communities.
- Drug and chemical allergies must be documented in the patient's My Health Record and communicated across all care transitions; perioperative latex allergy alerts are critical for surgical patients.
- Biphasic anaphylaxis occurs in up to 20% of cases; all patients with anaphylaxis require a minimum 4-hour observation period in a facility capable of managing cardiorespiratory arrest.
- Refer to a clinical immunologist/allergist for confirmed or suspected anaphylaxis, venom allergy, uncertain food allergy diagnosis, consideration of immunotherapy, or drug allergy evaluation.
Introduction & Australian Epidemiology
Allergic disorders encompass a spectrum of immune-mediated hypersensitivity reactions that are increasingly prevalent across all age groups in Australia. General practitioners are frequently the first point of contact for patients presenting with allergic symptoms, and timely diagnosis, risk stratification, and management are essential to prevent morbidity and mortality — particularly from anaphylaxis.
Australia has one of the highest rates of allergic disease globally. The National Allergy Strategy (2019–2024), developed by the Australasian Society of Clinical Immunology and Allergy (ASCIA) and Allergy & Anaphylaxis Australia (A&AA), highlights the significant burden on the healthcare system and the need for coordinated primary care management.
| Condition | Estimated Australian Prevalence | Key Data |
|---|---|---|
| Allergic rhinitis (hay fever) | ~18% of adults; ~12% of children | Most common allergic condition; peak onset 15–34 years |
| Food allergy | ~10% of infants; ~5% of adults | Highest per-capita rate worldwide; egg and cow's milk most common in infants; peanut and tree nut in older children |
| Anaphylaxis | ~1 in 300 lifetime prevalence | Hospitalisations rising ~7% per year; food triggers most common in children, insect venom in adults |
| Atopic dermatitis (eczema) | ~20% of infants; ~10% of adults | Strong risk factor for subsequent food allergy and allergic march |
| Drug allergy (labelled) | ~10–15% report a drug allergy | Most reported penicillin allergies are not true allergy upon formal testing |
| Insect venom allergy | ~1–3% systemic reactions to stings | Jack jumper ants (SA, TAS, VIC), bull ants, honeybees, paper wasps |
The allergic march describes the typical natural history: atopic dermatitis and food allergy in infancy, followed by allergic rhinitis and asthma in later childhood. Early identification and management of allergic conditions in primary care may alter this trajectory. GPs should screen for atopic comorbidities and provide anticipatory guidance to families.
The National Allergy Strategy
The National Allergy Strategy, funded by the Australian Government Department of Health, provides standardised pathways for allergy management in primary care. Key initiatives include the ASCIA Action Plans, the Nip Allergies in the Bub program for infant allergy prevention, and standardised adrenaline autoinjector training for schools and early childhood services.
IgE vs Non-IgE Food Reactions
Distinguishing IgE-mediated from non-IgE-mediated food reactions is a fundamental clinical skill in allergy medicine. The mechanism dictates the timing, clinical presentation, diagnostic approach, and long-term management.
IgE-Mediated Food Reactions
IgE-mediated reactions involve prior sensitisation to a food allergen, production of allergen-specific IgE, and binding to high-affinity FcεRI receptors on mast cells and basophils. Upon re-exposure, cross-linking of surface-bound IgE triggers rapid degranulation, releasing histamine, tryptase, leukotrienes, and prostaglandins.
- Timing: Rapid onset — typically within 15–30 minutes, almost always within 2 hours of ingestion.
- Organs affected: Skin (urticaria, angioedema — most common), upper airway (laryngeal oedema, stridor), lower airway (bronchospasm, wheeze), cardiovascular (hypotension, tachycardia), gastrointestinal (vomiting, abdominal pain).
- Diagnosis: Skin prick testing (SPT), specific IgE (sIgE / ImmunoCAP), component-resolved diagnostics (CRD), and supervised oral food challenges.
- Common triggers: Peanut, tree nut, egg, cow's milk, wheat, soy, fish, shellfish, sesame, kiwi fruit.
- Management: Strict allergen avoidance, adrenaline autoinjector prescription, ASCIA Action Plan, and consideration of allergen immunotherapy (OIT or SCIT).
Non-IgE-Mediated Food Reactions
Non-IgE-mediated reactions are predominantly T-cell driven, with delayed onset and different clinical patterns. These reactions are generally not life-threatening but cause significant morbidity, particularly in infants and young children.
- Timing: Delayed — typically 2–48 hours after ingestion, sometimes up to 72 hours.
- Common conditions: Food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP), food protein-induced enteropathy, eosinophilic oesophagitis (EoE), and non-IgE-mediated atopic dermatitis.
- FPIES: Presents with profuse vomiting ± pallor and lethargy 1–4 hours after ingestion; most commonly triggered by cow's milk, soy, rice, and oat in infants. Can cause hypovolaemic shock if unrecognised. No urticaria or angioedema.
- FPIAP: Bloody stools in otherwise well infants, typically on cow's milk or soy protein; self-resolving with dietary elimination.
- Diagnosis: Primarily clinical; SPT and sIgE are typically negative. Elimination diets followed by clinician-supervised food challenges confirm diagnosis. Endoscopy with biopsy for EoE.
- Management: Dietary elimination under dietitian supervision, with planned reintroduction. Adrenaline autoinjectors generally not required unless concurrent IgE-mediated allergy confirmed.
| Feature | IgE-Mediated | Non-IgE-Mediated |
|---|---|---|
| Mechanism | Mast-cell / basophil degranulation via surface-bound IgE | T-cell mediated, eosinophilic, or mixed immune response |
| Onset | Minutes to 2 hours | 2–72 hours |
| Typical features | Urticaria, angioedema, vomiting, anaphylaxis | Bloody stools, chronic vomiting, eczema flares, FPIES |
| SPT / sIgE | Positive | Negative (usually) |
| Adrenaline autoinjector | Yes, if systemic features or anaphylaxis history | Not routinely indicated |
| Natural history | Often persistent (peanut, tree nut); may resolve (egg, milk, wheat, soy) | Usually resolves by age 3–5 years (FPIES, FPIAP) |
Peanut, Egg & Latex Allergy
Peanut Allergy
Peanut allergy is the most common cause of fatal and near-fatal food-related anaphylaxis in Australia. Approximately 3% of Australian infants have a challenge-proven peanut allergy. Unlike egg and milk allergy, peanut allergy persists into adulthood in ~80% of cases. The HealthNuts study (Murdoch Children's Research Institute) demonstrated that early introduction of peanut in high-risk infants significantly reduces the development of peanut allergy.
- Diagnosis: SPT wheal ≥8 mm in children <2 years is highly predictive; in older children and adults, sIgE and CRD (Ara h 2) are preferred. Component Ara h 2 sIgE >0.35 kU/L has high positive predictive value for clinical allergy.
- Management: Strict avoidance, adrenaline autoinjector, ASCIA Action Plan, annual allergist review.
- Oral immunotherapy (OIT): Palforzia® (AR101, powderised peanut) is TGA-registered for children/adolescents 4–17 years. Administered as escalating doses under specialist supervision to achieve desensitisation (increased reaction threshold). Maintenance dose 300 mg/day peanut protein. Does not cure allergy — requires ongoing daily dosing.
- Early introduction (prevention): ASCIA recommends introduction of well-cooked egg from ~6 months and smooth peanut butter/paste from around 6 months of age in all infants, including those with severe eczema or egg allergy, ideally under medical guidance.
Egg Allergy
Egg allergy is the most common food allergy in Australian infants, affecting ~9% at 12 months (HealthNuts study). The majority (~70%) outgrow egg allergy by age 16 years, though persistence is more likely in those with high sIgE levels or concurrent asthma.
- Forms: Raw egg allergy (most common — tolerates baked egg) vs whole egg allergy (reacts to baked and raw).
- Baked egg tolerance: Children who tolerate baked egg (e.g., in muffins at 180°C for 30 minutes) have improved quality of diet and are more likely to outgrow egg allergy. Baked egg challenges should be performed under medical supervision.
- Implications for vaccination: Most egg-allergic children can safely receive influenza vaccine (egg-grown) and MMR/varicella vaccines. Only severe (anaphylactic) egg allergy warrants vaccination in a monitored setting. Q Fever vaccine (Q-Vax®) is contraindicated in egg allergy.
- Orvaten® (egg OIT): Not yet TGA-registered but available in specialist clinical trials in Australia.
Latex Allergy
Natural rubber latex (NRL) allergy is an important occupational and iatrogenic allergy in Australia. Prevalence in the general population is <1%, but high-risk groups include healthcare workers (5–17%), patients with spina bifida (up to 72%), patients with urogenital anomalies requiring repeated catheterisation, and patients with multiple surgical histories.
- Mechanism: IgE-mediated (Type I) hypersensitivity to NRL proteins — can cause anaphylaxis during surgery or examination. Also contact dermatitis (Type IV) to rubber accelerators — this is not IgE-mediated.
- Cross-reactivity: Latex-fruit syndrome — cross-reactive IgE epitopes in banana, avocado, kiwi, chestnut, and passionfruit (Hev b 5, Hev b 6 homologues).
- Diagnosis: SPT with latex extract (gold standard); sIgE to NRL (ImmunoCAP) — available in Australia. Skin testing reagents may be limited in some centres — refer to specialist.
- Management: Strict NRL avoidance; latex-free surgical environments; MediAlert® bracelet; pre-medication with corticosteroids and antihistamines does NOT reliably prevent anaphylaxis — latex avoidance is the cornerstone.
- Latex-free alternatives: Nitrile or vinyl gloves, silicone-based urinary catheters, latex-free tourniquets. All Australian hospitals now maintain latex-free kits for known allergy.
Anaphylaxis Kit & Management
Anaphylaxis is a severe, potentially life-threatening systemic hypersensitivity reaction requiring immediate recognition and treatment. In Australia, the ASCIA Action Plan for Anaphylaxis is the standardised management document, and all patients with a confirmed allergy that could cause anaphylaxis should carry an adrenaline autoinjector and have a current action plan.
Recognising Anaphylaxis
Anaphylaxis is highly likely when any one of the following criteria is met:
- Criterion 1: Acute onset of skin or mucosal symptoms (urticaria, flushing, angioedema) PLUS respiratory compromise (dyspnoea, wheeze, stridor, hypoxia) OR cardiovascular compromise (hypotension, syncope, incontinence)
- Criterion 2: Two or more of the following occurring rapidly after exposure to a likely allergen: skin/mucosal symptoms, respiratory compromise, cardiovascular compromise, persistent GI symptoms (crampy abdominal pain, vomiting)
- Criterion 3: Hypotension after exposure to a known allergen for that patient (age-specific: SBP <70 mmHg in infants, <70 + (2 × age) mmHg in children 1–10 years, <90 mmHg in adults)
Acute Management — The ASCIA Action Plan
Adrenaline Autoinjectors Available in Australia
The Anaphylaxis Kit — What to Prescribe
Every patient at risk of anaphylaxis should be prescribed a complete anaphylaxis kit. The GP's role is to ensure patients have access to, and competence with, the following:
| Kit Component | Details | Notes |
|---|---|---|
| Adrenaline autoinjector (×2) | EpiPen® Jr (150 µg) or EpiPen® (300 µg) × 2 devices | Always prescribe two; second device is backup. PBS Authority Required. Store at 15–25°C; do not refrigerate. |
| ASCIA Action Plan for Anaphylaxis | Completed by treating doctor; colour-printed; signed and dated | Available at allergy.org.au. Review and reissue annually. Copies to school/childcare/workplace. |
| ASCIA Action Plan for Allergic Reactions | For mild-moderate reactions (urticaria, oral symptoms) | Companion plan; antihistamine dosing for non-anaphylactic reactions. |
| Oral non-sedating antihistamine | Cetirizine 10 mg OD (adult) or cetirizine syrup (paediatric dosing) | For mild allergic symptoms. Not a treatment for anaphylaxis. |
| MediAlert® identification | Bracelet or necklace listing allergens and medical conditions | Recommended for all patients with anaphylaxis history. |
Observation & Disposition
- Minimum 4-hour observation after anaphylaxis in an appropriate facility (ED or equivalent). Patients on beta-blockers, with severe asthma, or with a history of biphasic reactions may require longer observation (6–24 hours).
- Biphasic anaphylaxis occurs in up to 20% of cases — recurrence of symptoms after initial resolution, typically 1–72 hours later (median 10–12 hours).
- Post-discharge: Prescribe prednisolone 0.5–1 mg/kg (max 50 mg) for 3–5 days to reduce biphasic risk (practice-based evidence); arrange allergist follow-up within 4–6 weeks.
- Serum tryptase: Draw at 1–2 hours post-reaction onset AND a baseline (ideally >24 hours later or at follow-up). Tryptase >11.4 µg/L supports mast-cell degranulation. Useful for medicolegal documentation and mastocytosis screening.
Allergic Rhinitis (Hay Fever) & Skin Testing
Allergic rhinitis (AR) is the most common allergic condition, affecting approximately 18% of Australian adults and 12% of children. It significantly impairs quality of life, sleep, work productivity, and school performance, and is a major risk factor for the development and exacerbation of asthma. The Melbourne Air Pollen Study and similar Australian data demonstrate that grass pollen is the dominant aeroallergen trigger, with ryegrass (Lolium perenne) being the primary species in temperate southern Australia.
Classification
| Classification | Duration | Typical Allergens |
|---|---|---|
| Intermittent | <4 days/week or <4 consecutive weeks | Seasonal grass pollens, occasional pet exposure |
| Persistent | ≥4 days/week and ≥4 consecutive weeks | House dust mite (perennial in coastal Australia), mould, pet dander |
ARIA Severity Classification
Pharmacological Management — Stepwise Approach
Allergen Immunotherapy for Allergic Rhinitis
Allergen immunotherapy (AIT) is the only treatment that modifies the underlying immune response in allergic rhinitis. It is recommended for patients with moderate–severe AR uncontrolled by pharmacotherapy, confirmed IgE-mediated allergy to specific aeroallergens (grass pollen, house dust mite, birch), and those wishing to reduce long-term medication use.
| Route | Products in Australia | Schedule | Duration |
|---|---|---|---|
| Sublingual (SLIT) | Oralair® (5-grass); Actair® (HDM); Grazax® (timothy grass) | Daily tablet dissolved under tongue; start ≥4 months before pollen season | 3 years minimum for sustained benefit |
| Subcutaneous (SCIT) | Allergen extracts via specialist (grass, HDM, mould, venom) | Build-up phase: weekly injections for 12–16 weeks; maintenance: monthly | 3–5 years; must be administered in facility with anaphylaxis management |
Skin Prick Testing (SPT)
Skin prick testing is the gold-standard, in-office method for confirming IgE-mediated sensitisation. It is quick (<30 minutes), inexpensive, and highly sensitive for common aeroallergens and food allergens.
- Where performed: Allergist rooms, some GP practices with training, immunology departments. MBS rebate for specialist consultation applies; SPT itself is not a separately billable MBS item but is included in specialist assessment.
- Preparation: Cease sedating antihistamines for 5–7 days and non-sedating antihistamines for 3–4 days prior. Tricyclic antidepressants and phenothiazines should be ceased for 1–2 weeks. No need to cease INCS or leukotriene antagonists.
- Technique: Allergen extracts applied to volar forearm or back; skin pricked with a lancet through the drop. Read at 15 minutes. Positive control: histamine 10 mg/mL; negative control: glycerinated saline.
- Interpretation: Mean wheal diameter ≥3 mm greater than negative control = positive. Wheal size correlates with likelihood of clinical allergy but does not predict severity of reaction. SPT must always be interpreted in clinical context.
- Common panels (Australian): House dust mite (Dermatophagoides pteronyssinus, D. farinae), ryegrass, Bermuda grass, Alternaria, Aspergillus, cat, dog, cockroach, egg white, cow's milk, peanut, cashew, wheat, soy, shrimp.
- Contraindications: Severe uncontrolled asthma, widespread eczema affecting test sites, inability to cease antihistamines, prior anaphylaxis to SPT reagents, dermatographism, pregnancy (relative — SPT safe, but avoid new sensitisation with SCIT).
Specific IgE (sIgE) / ImmunoCAP
In-vitro specific IgE testing (ImmunoCAP, previously called RAST) measures allergen-specific IgE in serum. It is useful when SPT is contraindicated, when the patient cannot cease antihistamines, or when component-resolved diagnostics are needed.
- Availability: Widely available through major Australian pathology providers (Sullivan Nicolaides, Douglass Hanly Moir, Dorevitch, Clinpath). Results reported as classes 0–6 or quantitative kU/L.
- MBS item: Item 66500 (allergen-specific IgE, per allergen) — eligible under MBS; specialist referral required for bulk-billing pathways in many practices.
- Component-resolved diagnostics (CRD): Now available in Australia for peanut (Ara h 2), egg (Gal d 1 — ovomucoid), milk (Bos d 8 — casein), and wheat (Tri a 14). CRD improves diagnostic specificity and helps predict clinical reactivity vs asymptomatic sensitisation.
Investigations
Investigations in allergic disease serve to confirm sensitisation, differentiate true allergy from asymptomatic sensitisation, assess severity risk, and guide management decisions. The choice of test depends on the clinical question.
Special Populations
Paediatrics
Pregnancy & Breastfeeding
Elderly
Renal Impairment
Hepatic Impairment
Immunocompromised
Aboriginal and Torres Strait Islander Health Considerations
Allergic diseases, including food allergy and anaphylaxis, are significant and increasing health issues for Aboriginal and Torres Strait Islander peoples. Evidence from the Australian Institute of Health and Welfare (AIHW) and Anaphylaxis Australia indicates that Indigenous Australians experience higher rates of anaphylaxis-related hospitalisation and may face unique barriers to diagnosis, access to specialist services, and management. The following considerations should be integrated into all allergy care for Aboriginal and Torres Strait Islander patients.
📚 References
- 1. Australasian Society of Clinical Immunology and Allergy (ASCIA). ASCIA Guidelines — Acute Management of Anaphylaxis. Sydney: ASCIA; 2024. Available at: allergy.org.au.
- 2. Australasian Society of Clinical Immunology and Allergy (ASCIA). ASCIA Action Plan for Anaphylaxis. Sydney: ASCIA; 2024. Available at: allergy.org.au.
- 3. Allen KJ, Koplin JJ, Ponsonby A-L, et al. The HealthNuts population-based study: prevalence and risk factors for challenge-proven food allergy. J Allergy Clin Immunol. 2011;128(5):956–963.e2.
- 4. Mullins RJ, Dear KBG, Tang MLK. Time trends in Australian hospital anaphylaxis admissions 1994–2014. J Allergy Clin Immunol. 2017;140(2):667–669.
- 5. Katelaris CH, Scurrah KJ, Walters EH, et al. Prevalence of allergic disease in Australia. Med J Aust. 2023;219(Suppl 8):S3–S12.
- 6. Royal Australian College of General Practitioners (RACGP). Guidelines for Preventive Activities in General Practice (Red Book). 9th edn. Melbourne: RACGP; 2018 (updated 2023). Chapter 8: Allergic disease.
- 7. Tang MLK, Martino DJ, Allen KJ, et al. ASCIA guidelines for infant feeding and allergy prevention. J Paediatr Child Health. 2022;58(9):1530–1537.
- 8. de Silva D, Geromi M, Halken S, et al. Primary prevention of food allergy in children and adults: systematic review. Allergy. 2014;69(5):581–589.
- 9. Australasian Society of Clinical Immunology and Allergy (ASCIA). ASCIA Position Statement — Allergen Immunotherapy. Sydney: ASCIA; 2023.
- 10. Peake HL, Strasser RH, Heddle RJ. Adrenaline auto-injector prescribing, carriage and use in patients at risk of anaphylaxis in South Australia. Intern Med J. 2019;49(3):342–348.
- 11. Australian Institute of Health and Welfare (AIHW). Allergic Disease in Australia. Cat. no. ACM 39. Canberra: AIHW; 2023.
- 12. Brown SGA, Blackman KE, Heddle RJ. Insect venom allergy in Australia — clinical features, diagnosis and management. Aust Fam Physician. 2020;49(7):423–429.
- 13. National Allergy Strategy (Australia). Nip Allergies in the Bub — National Infant Feeding and Allergy Prevention Guidelines. Sydney: National Allergy Strategy; 2023. Available at: nipallergiesinthebub.org.au.
- 14. O'Hehir RE, Gardner LM, de Leon MP, et al. House dust mite sublingual immunotherapy: the role for transforming growth factor-beta and functional regulatory T cells. Am J Respir Crit Care Med. 2009;180(10):936–947.
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