A. Case study
B. More information
C. Editors' comments
D. References
E. CPD questions (South Africa, Australia



A. Case study

A 15-year-old girl presented with swelling of the tongue and slight swelling of the throat soon after ingestion of various types of food. The girl listed apple, carrot, banana, peach and tomato as the offending foods. Her mother had a severe peanut allergy. Because the mother experienced the first symptoms of anaphylaxis to peanut as being swelling of the throat and tightness of the chest, every time her daughter would start experiencing swelling of the tongue and throat, the mother would encourage her to take an antihistamine. The symptoms would then disappear within minutes.

The clinical history revealed that the daughter had a history of hay fever as a result of pollens. The pollen allergy started to present at age 7 when their neighbours planted olive trees in their garden. The suspicion of pollen allergy was arrived at by the child's mother because her daughter's symptoms would appear specifically when the olive trees were pollinating. She also sometimes experienced hay fever when she visited an area for the first time. Sometimes olive trees were found to be present and other times not. She took antihistamines to treat her hay fever as she needed to. A doctor or allergist was never consulted about this. The girl started developing reactions to foods later in life, when she was about 12 years old. She decided to seek professional help when she started to react to more and more of her favorite foods.

Upon further questioning, the girl related that her throat started to itch just before it would start to swell. She never experienced any difficulty breathing or any other symptoms such as urticaria or eczema after eating the offending foods.

This type of reaction is more likely to be an allergy than an intolerance. What type of allergy reaction could this be?
a. Start of an anaphylactic reaction
b. Contact urticaria/angioedema due to the offending food
c. Contact urticaria/angioedema due to something else that was present in her mouth with the food, e.g., cutlery
d. Oral allergy syndrome

a. Although swelling of the throat is often one of the first symptoms of an anaphylactic reaction, this was probably not the case here. If the reaction was the start of anaphylaxis, taking antihistamines would probably have little effect on the progression of the symptoms. The symptoms also never got worse than a slight swelling of the throat, even after eating large amounts of the offending food.
b. The symptoms she described sounded similar to urticaria or angioedema. Although contact allergy to these foods is possible, the girl did not experience any swelling after contact of food with any other part of her body.
c. The foods that would elicit a reaction were all eaten with her hands or with cutlery. The cutlery was used to eat all her other food, without symptoms.
d. The typical characteristics of oral allergy syndrome are:

i. Localized oropharyngeal symptoms: These were present.
ii. Concomitant sensitization to a respiratory allergen: This was present (olive tree pollen).
iii. Reproducible symptoms with repeated contact with a particular food. The patient was asked the following questions: Did she always react to a specific food whenever she ate it, without exception? Did she sometimes react to raw but not cooked food? Was she eating the foods on their own or mixed with other food?

Trying to determine the foods that caused her symptoms, she had tried all the suspect foods by themselves. The child reacted to all the foods every time she ate them, except carrot and tomato. She was unsure whether she would react to the foods if they were cooked, as she ate most of them raw. However, she had picked up before that she reacted to carrot only when eaten raw. She was not sure whether tomato was cooked or uncooked when she reacted to it.

It was thus clear that she was reacting to at least one heat-labile allergen.

Is there a common allergen in these foods that was causing them to cross-react with each other? And is this allergen heat-labile?

Profilin, a heat-labile panallergen, was found to be present in all of the foods that she listed. (Panallergens are allergens that are present in a number of plants, including pollens. The plants are not necessarily related to each other by family. Each panallergen performs a specific function in the various plants.) This would explain why she did not react to carrot when it was eaten cooked. All of the other foods were generally eaten raw. A possible reason for her uncertainty about when she reacted to tomato is that tomato can be eaten raw or cooked and she had not picked up an association. In general, her experience suggested that a sensitivity to profilin was causing her symptoms.

If this were oral allergy syndrome, one would expect the same allergen to be present in the pollen that was causing the respiratory symptoms (hay fever, in her case). It was determined that profilin is also present in olive tree pollen. It was thus clear that the girl was experiencing oral allergy syndrome to apple, carrot, banana, peach and tomato, which can be concomitant with respiratory allergy to olive tree pollen.

Oral allergy syndrome rarely causes symptoms more severe than slight swelling of the throat, but if the patient wanted to avoid this reaction, she would have to avoid eating these foods, or she would have to cook them before she ate them. She was also informed of other pollens, containing profilin that she might react to, such as Bermuda grass, common silver birch tree, date palm tree, European chestnut tree, hazelnut tree, Johnson grass, mugwort, ragweed, Timothy grass and white ash tree.

TIP for Allergy Advisor users:
When entering the offending foods into the pattern search function of Allergy Advisor, a common constituent, profilin, a panallergen, is identified. (The panallergen search function can also be used.) When clicking on the word, a window will open and allow the user to read more about profilin, including that it is heat labile and that it can be associated with oral allergy syndrome. Clicking on the "Cross-reactions" tab along the top of the window, one will find details of cross-reactions between these profilin-containing foods. Under the "Management menu", one can find a list of foods that have been associated with oral allergy syndrome (click the "Differential Diagnosis Lists" button).

B. More information:

What is Oral Allergy Syndrome?
Oral allergy syndrome (OAS) is an IgE-mediated reaction to a certain food (or foods that all contain a similar allergen), affecting the oropharyngeal mucosa of sensitized individuals.1 Symptoms include itchiness (pruritus) and swelling of the lips, tongue, palate and throat.2,3

What causes OAS?
OAS is caused by various types of fruit, vegetables and nuts. But what makes this syndrome so distinctive is that it is always seen in individuals with co-existing sensitization to inhaled allergens, usually tree, weed or grass pollens. If symptoms to inhaled allergens are experienced, they are most often those of hay fever.3,4 It should be noted that there have been reports of OAS symptoms without a concomitant sensitization to an inhaled allergen. But there is a question whether these cases should be referred to as OAS or as "OAS-like symptoms," as true OAS according to the definition is the combination of allergy to food and to an inhalant allergen.

How common is it?
OAS appears to be more common in adults than children.5 Atopic individuals are more prone to OAS, especially those who are sensitive to pollens.6 It has been reported to occur in up to 35-75% of patients with pollen allergy.7,8,9,10,11


What is the association between pollen allergy and allergy to fruit and vegetables?
This is explained by cross-reacting allergens, which means that the same allergen is present in both pollen and fruit and/or vegetables, even though they may not belong to the same botanical family. The hypothesis is that a patient becomes sensitized to an airborne pollen allergen (by gradually building up IgE antibodies to these allergens over time) and then becomes capable of reacting to the same allergen that is present in various foods.2,11,12,13,14

A number of allergens have been associated with OAS, including lipid transfer protein (heat-stable) and the profilin family (heat-labile), including Bet v1 and Art v1.11 These are all panallergens and, as indicated, are either heat-stable or heat-labile. Patients affected by a heat-labile allergen may be able to tolerate the foods containing it when these are cooked.2,11

Many panallergens are defense-related proteins, which provide a plant with resistance to stresses (e.g., infections/viruses, harsh growing conditions and exposure to some types of chemicals). Under stress conditions, the defense-related proteins increase. Agriculturally, this property in a plant could be quite valuable. Less toxic substances that cause crops to express defensive proteins are being investigated as a new type of agrochemical. This has important implications for the allergenicity of future plants, as increasing the defense-related proteins means that panallergen concentration also increases.15

A fairly well-known example of another panallergen, which is not involved in OAS, is chitinase. It is present in latex and foods such as kiwi and mango and is responsible for the cross-reactivity between them.16

Patterns between food and pollen allergies that have been recorded include:
Birch: Almond, apple, apricot, carrot, celery, cherry, fennel, hazelnut, kiwi, nectarine, parsley, parsnip, peach, pear, plum, potato, prune and walnut
Ragweed: Banana, chamomile tea, cantaloupe, cucumber, dandelion tea, honey dew, watermelon and zucchini
Mugwort: Apple, carrot, celery, coriander, fennel, melons, pepper and sunflower
Grass: Melons, orange and tomato6

Other food and airborne allergens associated with OAS include:

  • Allergy to ingesting various kinds of pork (salami, bacon and both raw and cooked ham), associated with an inhaled allergy to horse dander. This person could, however, tolerate cooked pork (chops and sausages). The allergy was due to a heat-labile allergen.17

  • Allergy to uncooked mushroom in a patient allergic to mold11
  • Allergy to pistachio nut and Parietaria (a type of weed)18

  • OAS after the ingestion of salami in a patient with sensitization to dust mite allergens3
  • Allergy to fig,19 jackfruit,20 spinach,21 shell-fish, egg22 and chicken meat23

  • The type of concomitant pollen and food sensitivity a person might experience is mainly dependant on the immediate environment. For example, in Italy, where grass pollen is a common cause of hay fever, one would expect OAS to be more often associated with food allergy to tomato, melon, watermelon and orange, all of which are widely consumed in that country.24

    Different panallergens tend to be associated with different types of reactions. A person reacting to Bet v1, for example, is likely to experience OAS alone. Those sensitive to LTPs frequently experience both OAS and systemic symptoms after eating an offending food.25

    Symptoms associated with OAS
    Symptoms present during or within 5-30 minutes of oral contact with the culprit food and generally resolve rapidly (within ½ - 1 hour).24

    Local symptoms include itching of the lips, mouth or pharynx and angioedema (swelling) of the lips, tongue, palate and throat. Blisters may also appear in the oral area. (These must be distinguished from apthous ulcers, which are not associated with OAS.) In severe cases, edema of the glottis may occur. This occurs frequently in patients with OAS due to celery.26 More and more cases of severe reactions to celery are occurring, so much so that some European countries consider it to be a major allergen.

    Although OAS symptoms are considered to be a distinct entity, they can extend beyond oropharyngeal manifestations to systemic reactions in some individuals, especially those who continue to ingest the offending food. Symptoms include urticaria, angioedema, conjuctivitis, rhinitis, asthma, nausea, vomiting and anaphylaxis. Anaphylaxis has been reported in approximately 2% of patients with OAS. Foods implicated in anaphylaxis associated with OAS include lentils, tomatoes, apricot, peach, pear, cherry, apple, walnut and hazelnut.27

    A thorough clinical history is the best tool to diagnose OAS. As mentioned in the case study, the typical symptoms are:

  • reproducible with repeated contact with a particular food.

  • localized to the mouth, lips, pharynx and glottis.

  • accompanied by sensitization to an inhaled allergen.2
  • The clinical history may be supported by allergy tests. The value of skin prick tests is often limited in OAS, as the proteins (allergens) in commercial extracts that are used (e.g., fruit extract) degrade easily, leading to significant loss in potency and diagnostic sensitivity and sometimes resulting in false negatives.2,14 This tends to be due to factors in the preparation of the extract, such as heat. As discussed above, many patients who suffer from OAS can tolerate cooked food but not the raw form.28 The efficiency of skin prick and blood tests as predictors of clinical food reactivity varies depending on the type of food. Although sometimes impractical and perhaps risky (because of the chance of anaphylaxis), skin prick tests with fresh foods may have greater diagnostic sensitivity.2,14

    When fresh fruits or vegetables are used, characteristics of the food may, however, influence the sensitivity of the skin prick test. For example, the allergenic potency may increase during the food's maturation, as shown for Golden Delicious apples.29 Also, one should ensure that the patient does not react to other compounds that are present in the extract. A example of this is a histamine-sensitive individual who could show a reaction (non-allergic reaction but similar to an allergic reaction) to fresh tomato extract, which naturally contains histamine.

    Another aid in the diagnosis of OAS is to challenge the patient with the suspected food. The results can then be compared to the characteristic symptoms of OAS (listed above). The challenge should be done with the natural form of the food. It must not be dried or given in capsule form.

    The easiest, safest and cheapest treatment is avoidance of the food. If the symptoms are due to a heat-labile allergen such as profilin, the patient may tolerate cooked or canned food. Many of the panallergens involved in OAS are found predominantly or exclusively in the skins of the offending foods. Some persons may therefore prevent a reaction by removing the skins. However, this is not an absolute guarantee of safety, as the act of cutting or peeling may shift the proteins in the skin to the flesh of the food.6 If a person does not wish to avoid one or more foods, an antihistamine could suppress the resultant reactions.

    The patient should be warned of other foods and airborne allergens that may affect him or her due to the presence of the same allergen (as was done in the case study). For example, an apple-allergic individual living in the Southern Hemisphere, where there are very few birch trees (which cross-react with apple), should be warned of the presence of these trees when visiting Europe. Airborne allergens that affect the patient can be avoided by visiting certain areas at the times of the year when there is a low pollen count. With regard to foods, one must keep in mind that people may not react in the same way to all the foods containing the same allergen.

      compiled by Karen du Plessis B.Sc. Diet.
    Food & Allergy Consulting & Testing Services (FACTS)
    PO Box 565
    Milnerton 7435
    South Africa

    C. Comments by our editor

    Prof Janice M. Joneja Ph. D., RDN
    OAS is becoming increasingly recognized as an allergic disease distinct from anaphylaxis. The increased incidence of OAS may be a result of better methods of diagnosis, or, as some researchers suggest, a symptom of an increase in pathogenesis-related proteins, which are important allergens common to trees and food plants involved in the aetiology of OAS. Pathogenesis-related proteins tend to be expressed by trees and plants under "stress" as a result of pollution and other environmental agents that could potentially harm the plant, and are thought to be a response to the noxious chemicals that seem to be increasing in the urban environment.

    The specific foods responsible for triggering OAS are sometimes difficult to identify because they often do not elicit a typical response in skin tests, as a result of the use of inappropriate allergen preparations. A method of skin testing that is frequently employed in order to avoid the false negative results common with commercial allergen extracts, is the prick-to-prick method. In this test, a sterile needle is inserted into the fresh, raw food, and then inserted into the patient's skin. This transfers non-denatured antigen and is more likely to elicit a positive response than a commercial extract of the same food. However, even the prick-to-prick test is not highly accurate, and diagnosis of the culprit food/pollen combination in OAS must be confirmed by challenge. An obvious danger of the prick-to-prick test is when the OAS is in fact part of an anaphylactic reaction that has been misdiagnosed as OAS. Transferring a raw antigen into the skin in an anaphylactic patient can be fatal, so great care must be taken to avoid using this test indiscriminately.

    Dr. Harris Steinman M.B.Ch.B.
    Individuals suffering with OAS should remember that they are more prone to developing symptoms of hayfever when going on holiday to other parts of the world where specific trees (whose pollen shares cross-reacting allergens) are more prevalent.

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    D. References
    1. Amlot PL, Kemeny DM, Zachary C, Parks P, Lessof MH. Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy 1987; 17:33-38.
    2. Ortolani G, Ispano M, Pastorello EA, Ansaloni R, Magri A. Comparison of results of skin prick tests (with fresh foods and commercial extracts) and RAST in 100 patients with oral allergy syndrome. J Allergy Clin Immunol 1989; 83: 683-690.
    3. Liccardi G, D'Amato M, D'Amato G. Oral allergy syndrome after ingestion of salami in a subject with monosensitization to mite allergens. J Allergy Clin Immunol 1996;98:850-2.
    4. Helbling A. [Important cross-reactive allergens] Schweiz Med Wochenschr. 1997 Mar 8;127(10):382-9.
    5. Kivity S, Dunnerk K, Marian Y. The pattern of food hypersensitivity in patients with onset after 10 years of age. Clin Exp Allergy 1994; 24:19-22.
    6. Sloane D, Sheffer A. Oral allergy syndrome. Allergy Asthma Proc. 2001 Sep-Oct;22(5):321-5.
    7. Bircher AJ, Van Melle G, Haller E, Curty B, Frei PC. IgE to food allergens are highly prevalent in patients allergic to pollens, with and without symptoms of food allergy. Clin Exper Allergy 1994; 24:367-374.
    8. Pastorello EA, Ispano M, Pravettoni V et al. Clinical aspects of food allergy. Proc XVI European Congress of Allergology and Clinical Immunology 1995; 883-888.
    9. Eriksson NE. Birch pollen allergy associated with food hypersensitivity. An enquiry study Nordic Aerobiology 1984; 66-69.
    10. Ebner C, Birkner T, Valenta R et al. Common epitopes of birch pollen and apples. Studies by Western and Northern blot. J Allergy Clin Immunology 1991; 88:588-595.
    11. Dauby PL, Whisman BA, Hagan L. Cross-reactivity between raw mushroom and molds in a patient with oral allergy syndrome. Ann Allergy Asthma Immunol 2002;89:319-21.
    12. Eriksson NE. Clustering of foodstuffs in food hypersensitivity. An enquiry study in pollen allergic patients. Allergol Immunopathol 1984; 12:28-32.
    13. De Martino m, Novembre E, Cozza G, et al. Sensitivity of tomato and peanut allergens in children monosensitized to grass pollen. Allergy 1988; 43: 206-213.
    14. Anhoj C, Backer V, Nolte H. Diagnostic evaluation of grass- and birch-allergic patients with oral allergy syndrome. Allergy 2001;56:548-52.
    15. Yagami T. Allergies to cross-reactive plant proteins. Latex-fruit syndrome is comparable with pollen-food allergy syndrome. Int Arch Allergy Immunol. 2002 Aug;128(4):271-9.
    16. Brehler R,Theissen U,Mohr C, Luger T. "Latex-fruit syndrome": frequency of cross-reacting IgE antibodies. Allergy 1997;52(4):404-10.
    17. Asero R, Mistrello G, Falagiani P. Oral allergy syndrome from pork. Allergy 1997;52:694-6.
    18. Liccardi G, Mistrello G, Noschese P, D'Amato M, D'Amato G. Oral allergy syndrome (OAS) in pollinosis patients after eating pistachio nuts. Two cases with two different patterns of onset. Allergy 1996;51:919-22.
    19. Antico A, Zoccatelli G, Marcotulli C, Curioni A. Oral allergy syndrome to fig. Int Arch Allergy Immunol 2003;131(2):138-42.
    20. Wutrich B, Borga A, Yman L. Oral allergy syndrome to jackfruit (Artocarpus integrifolia). Allergy 1997;52:428-31.
    21. Sanchez I, Rodriguez F, Garcia-Abujeta JL, Fernandez L, Quinones D, Martin-Gil D. Oral allergy syndrome induced by spinach. Allergy 1997;52:1245-6.
    22. Joneja JM. Oral allergy syndrome, cross-reacting allergens and co-occurring allergies. Journal of Nutritional & Environmental Medicine 1999;9:289-303.
    23. Vila L, Barbarin E, Sanz ML. Chicken meat induces oral allergy syndrome: a case report. An Allergy Asthma Immunol 1998;80:195-6.
    24. Ortolani C, Ispano M, Pastorello EA, Bigs A, Ansaloni R. The oral allergy syndrome. Ann Allergy 1988; 61: 47-52.
    25. Asero R. Detection and clinical characterization of patients with oral allergy syndrome caused by stable allergens in Rosaceae and nuts. Ann Allergy Asthma Immunol 1999;83(5):377-83 (Asero 1999 ref.2598 4)
    26. Pauli G, Bessot JC, Braun PA, Dietermand-Molard A, Kopferschmidt-Kuber MC. Celery allergy: clinical and biological study of 20 cases. Ann Allergy 1988; 60: 243-246.
    27. Ortolani G, Pastorello EA, Farioli L et al. IgE mediated allergy from vegetable allergens. Ann Allergy 193; 83: 683-690.
    28. Wutrich B, Staeger J, Johansson SGO. Celery allergy associated with birch and mugwort pollinosis. Allergy 1990; 45: 566-571.
    29. Vieths S, Jankiewicz A, Schoning B, Aulepp H. Apple allergy: the IgE binding potency of apple strains is related to the occurrence of the 18-kD allergen. Allergy 1994; 49:262-271.

    E. CPD Questions (For South African dietitians only. Australian dietitians: where you have relevant learning goals, CPD hours related to this resource can be included in your APD log.)

    You can obtain 2 CPD points for reading this newsletter and answering the accompanying questions. This newsletter with questions has been accredited for dietitians.
    CPD reference number: DT03/3/087/13

    1. Complete your personal details below.
    2. Read the newsletter and answer the questions.
    3. Indicate your answers to the questions by making a "X" in the appropriate block.
    4. You will earn 2 CPD points if you answer more than 75% of the questions correctly. If you score is between 60 and 75%, 1 CPD point will be allocated. A score of less than 60% will unfortunately not earn you any CPD points.
    5. Make a photocopy for your own records in case your answers do not reach us.
    6. Cut and paste the area indicated below into a e-mail message and e-mail it to to be received no later than 31 October 2003. Answer sheets received after this date will not be processed.

    (There is only one correct answer per question.)
    1. What type of reaction is Oral allergy syndrome (OAS)?
    (a.) IgE-mediated
    (b.) Non-IgE-mediated
    (c.) Intolerance
    (d.) Toxic reaction

    2. Which of the following panallergens would not be tolerated when cooked?
    (a.) Profilin
    (b.) Bet v1
    (c.) Art v1
    (d.) Lipid transfer protein

    3. Plant defense-related proteins provide protection against which of the following?
    (a.) Plant infections/viruses
    (b.) Harsh growing conditions
    (c.) Exposure to chemicals
    (d.) All of the above

    4. Which one of the following is not a typical example of allergens that would be concomitantly involved in OAS?
    (a.) Birch, apple and celery
    (b.) Ragweed, plum and apricot
    (c.) Mugwort, apple and celery
    (d.) Grass, melon and tomato

    5. Which of the following is true regarding the onset and resolution of OAS symptoms?
    (a.) Onset: 5-30 minutes; Resolution: ½ - 1 hour
    (b.) Onset: 1 hour; Resolution: 2-4 hours
    (c.) Onset: 2 hours; Resolution: 5-10 hours
    (d.) Onset: 1 day; Resolution: 2-2.5 days

    6. Which of the following does not fit the TYPICAL presentation of OAS?
    (a.) The symptoms are reproducible with repeated contact with a particular food.
    (b.) The symptoms are localized to the mouth, lips, pharynx and glottis.
    (c.) Sensitization to an inhaled allergen is present.
    (d.) Systemic manifestations are present.

    7. True or false: The value of skin prick tests with commercial extracts is limited in the diagnosis of OAS, as the proteins (allergens) degrade easily.
    (a.) True
    (b.) False

    8. True or false: The easiest, safest and cheapest treatment of OAS is with antihistamines.
    (a.) True
    (b.) False

    Cut and paste this section below into an e-mail message

    Oral Allergy Syndrome
    CPD Reference number: DT03/3/087/13

    HPCSA number: DT
    Surname as registered with the HPCSA:
    E-mail address:

    Please make an "X" in the appropriate block for each question

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