Oral allergy syndrome and pollen-food syndrome — branching viva

Stem

The examiner moves from a definition, to the cross-reactive mechanism, to diagnostics, and finishes on the management fork and the lipid-transfer-protein phenotype. [1] [2]

Branch 1 — Definition and the "raw not cooked" clue

Examiner: A nine-year-old with birch hayfever gets oral tingling within a minute of a raw apple, yet tolerates baked apple. What is this, and why is the cooked form tolerated? [1]

Strong answer: This is pollen-food allergy syndrome (oral allergy syndrome). She is sensitised to birch pollen (Bet v 1), and the raw apple carries the homologous PR-10 protein Mal d 1, which cross-links IgE on her oral mast cells. The protein is heat-labile and digestion-labile, so cooking denatures it and the cooked apple is tolerated — that single fact defines the syndrome and explains why the reaction usually stays local. [1] [7]

Branch 2 — Phenotype classification

Examiner: How do you classify the pollen-food phenotypes, and which one is the systemic-risk outlier? [2]

Strong answer: Sort by the responsible protein family and by protein stability. PR-10 (birch) and profilin families are labile — local, cooked tolerated. Ragweed and mugwort syndromes track the weed season and are usually local. The outlier is lipid transfer protein (Pru p 3 in peach): it is heat-stable and digestion-stable, so it is absorbed intact and can cause anaphylaxis. LTP allergy is regarded as a separate phenotype, not classic PFAS. [2] [10]

Branch 3 — Diagnostics

Examiner: How do you confirm the diagnosis, and which test sorts the phenotypes? [4]

Strong answer: The history leads — raw but not cooked, in a pollen-sensitised child. Commercial skin-prick extracts are often falsely negative for labile proteins, so I use the fresh-food prick-prick test. Component-resolved diagnostics sorts the phenotypes: rBet v 1 and rMal d 1 indicate low-risk labile cross-reactivity; rBet v 2 flags wide profilin cross-reactivity; rPru p 3 flags systemic-risk LTP. I apply it within the EAACI Molecular Allergology User's Guide framework, and I remember that a positive test without a reaction history is sensitisation, not allergy. [4] [7]

Branch 4 — The management fork

Examiner: Outline the management for the low-risk labile phenotype and for the systemic-risk LTP phenotype. [12]

Strong answer: For the low-risk labile phenotype, avoid the raw trigger, keep cooked, baked, canned or peeled forms, and give a non-sedating oral antihistamine for breakthrough local reactions — without over-restricting tolerated foods. For the systemic-risk LTP phenotype, avoid the trigger in all forms, provide a written anaphylaxis action plan (ASCIA/BSACI/FARE) with the child's photo and allergen, prescribe two weight-banded adrenaline autoinjectors, train the family and school, and review periodically. The fork turns on a single question: is this local-only, or is there any systemic feature? [12] [10]

Branch 5 — The systemic-risk scenario

Examiner: A fourteen-year-old collapses with urticaria and wheeze after a peach at a picnic, having taken ibuprofen and gone for a run. What is your first action, and what changes in her long-term plan? [13]

Strong answer: This is anaphylaxis — a clinical diagnosis. Give IM adrenaline into the anterolateral thigh first, roughly 0.01 mg/kg of 1:1000 (a 0.30 mg autoinjector at her weight); call for help; lie flat, oxygen and IV fluids for shock, bronchodilator adjunctive; repeat adrenaline at five minutes if no response; observe at least six hours and admit. Long term, this is an LTP phenotype with cofactors: avoid peach in all forms, confirm with rPru p 3, prescribe two adrenaline autoinjectors and an action plan, educate her and the school about NSAID and exercise cofactors, and review with a view to specialist immunotherapy referral. [13] [10]

Examiner extras

• A positive skin-prick or IgE with no reaction history is sensitisation, not allergy — do not over-restrict the diet on testing alone. [12]
• PFAS is uncommon in toddlers because it needs prior pollen sensitisation; in a young child, reconsider a primary food allergy. [1]
• Birch drives apple, hazelnut and cherry; ragweed drives melon, banana and cucumber; mugwort drives celery and the celery-mugwort-birch-spice syndrome. [2]
• Latex-fruit syndrome (kiwi, banana, avocado, chestnut) is the look-alike to exclude by confirming latex sensitisation. [12]