Paeds Vivas · allergy-and-immunology
Egg, wheat, soy, fish and shellfish allergy: Viva
Branching structured oral on paediatric egg, wheat, soy, fish and shellfish allergy: distinguishing IgE from non-IgE mechanisms, the signature allergen proteins and heat-stability, skin-prick and specific-IgE interpretation, component-resolved diagnostics, the baked-egg ladder, anaphylaxis treatment with intramuscular adrenaline, and the prognosis separating childhood-outgrown from lifelong allergens.
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Target exams
Branch 1: Recognising and treating the acute event
The candidate should immediately recognise this as food-induced anaphylaxis. The rapid onset of urticaria with wheeze and hypotension minutes after eating a known allergen meets the clinical criteria for anaphylaxis, and the first action is intramuscular adrenaline into the anterolateral thigh. The single most important teaching point is that adrenaline must not be delayed for antihistamines, bronchodilators or observation, and that the combination of food allergy with uncontrolled asthma marks this boy as high-risk for a fatal outcome. [2]
The dose is the weight-appropriate autoinjector dose: at 14 years he is likely over 20 kg, so the 0.3 mg device is used, repeated after five minutes if there is no response. Adjuncts include high-flow oxygen, an inhaled bronchodilator for persistent wheeze, intravenous isotonic fluid for shock, and supine positioning with legs raised. The candidate should state that he needs hospital observation for a biphasic reaction, which can recur four to thirty hours later, and discharge with an adrenaline autoinjector, an action plan and allergy follow-up. [2]
Branch 2: The diagnostic reasoning for fish allergy
The examiner will ask why fish allergy is severe and persistent. The candidate should name parvalbumin (Gad c 1) as the major fish allergen and explain that it is heat-stable and highly cross-reactive across bony fish species, which is why the boy reacted to well-cooked grilled fish and why a child reactive to one fish is often reactive to others. This contrasts with the heat-labile proteins of egg and milk that may be tolerated when extensively baked. [1]
The candidate should describe the diagnostic approach. A skin-prick test of 3 mm or more and a raised fish-specific IgE confirm sensitisation, and parvalbumin-specific IgE confirms genuine cross-reactive allergy. The oral food challenge is the gold standard but is often unnecessary when the history and tests are concordant. The candidate should note that fish and shellfish allergy typically persist for life, unlike egg, wheat and soy, which are usually outgrown, and that shellfish shares tropomyosin with dust mite (the mite-shrimp syndrome), which can produce a first-exposure shellfish reaction in a dust-mite-sensitised child. [3]
Branch 3: Across the five allergens and their mechanisms
The examiner will broaden to the five foods. The candidate should be able to name the signature allergen for each: ovomucoid (Gal d 1) and ovalbumin (Gal d 2) for egg, omega-5-gliadin (Tri a 19) for wheat, the storage proteins Gly m 5 and Gly m 6 for soy, parvalbumin for fish and tropomyosin (Pen a 1) for shellfish. The practical consequence is heat-stability: heat-stable proteins survive cooking and provoke reactions in any form, whereas heat-labile proteins may be tolerated baked, which is the basis of the baked-egg ladder. [1]
The candidate should also separate the IgE-mediated immediate reactions from the non-IgE cell-mediated syndromes. Egg, wheat and soy can trigger FPIES, with delayed profuse vomiting and pallor two to four hours after exposure and a normal specific IgE, and they can contribute to eosinophilic oesophagitis. Coeliac disease, the key wheat differential, is an autoimmune enteropathy against gluten confirmed by tissue transglutaminase IgA, not an IgE reaction. Knowing the mechanism selects the right test and the right diet. [2]
Branch 4: Long-term management and prognosis
The examiner will ask about the long-term plan. The candidate should describe the three pillars: allergen avoidance with dietetic support, active tolerance induction where appropriate, and a safety-net of an action plan and adrenaline. For fish and shellfish the plan is lifelong avoidance and safety-netting, because these usually persist; for egg, wheat and soy the plan includes periodic re-testing and supervised re-challenge to detect resolution, because these are usually outgrown. [1]
The candidate should be explicit about the high-risk features that shape the plan. Asthma optimisation is essential because uncontrolled asthma plus food allergy is the highest fatal-anaphylaxis profile. Adolescents need a transition plan that ensures they carry and can use the autoinjector, read labels, and manage restaurants, parties and travel. An adrenaline autoinjector is prescribed for any systemic reaction or co-existing asthma, and the family, school and carers are trained in its use and in recognising early reactions. [2]
Branch 5: The prevention and early-introduction evidence
The examiner may close on prevention. The candidate should cite the LEAP trial, which showed that early peanut consumption in high-risk infants reduced peanut allergy by about 80 per cent and prompted the 2017 NIAID addendum recommending early introduction. The same principle of early allergen introduction has been extended toward egg, though the evidence is less conclusive than for peanut. The HealthNuts cohort provides the population prevalence and resolution data for egg allergy that underpin current practice, confirming that roughly half of egg allergy resolves by age six and that baked-egg tolerance predicts faster resolution. [1]
References
- [1]Sicherer SH, Sampson HA Food allergy: Epidemiology, pathogenesis, diagnosis, and treatment. J Allergy Clin Immunol, 2014.PMID 24388012
- [2]Boyce JA, Assa'ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol, 2010.PMID 21134576
- [3]Sicherer SH, Munoz-Furlong A, Sampson HA Prevalence of seafood allergy in the United States determined by a random telephone survey. J Allergy Clin Immunol, 2004.PMID 15241360