A. Case study
B. More information
C. Editors' comments
E. CPD questions (South Africa, Australia)
A. Case study
An 11-month-old boy was seen for eczema. Since birth he had been given
cow's milk-based formula, until he developed eczema at the age of 3
months. He was put onto a soya formula, and his symptoms resolved. The
mother began to give him solid foods at age 5 months. She started him
on rice and maize cereals and gradually introduced a variety of fruits
and vegetables, as well as rice, potato, chicken and beef. At the age
of 9 months, he developed severe eczema again. He was drinking about
800ml of soya formula per day at this stage. The general practitioner
requested some blood tests, with the following results (in KU/L):
Total IgE: 300 (High)
Soya: 9.47 (Class 3)
Rice: 0.39 (Class 1)
Maize: <0.35 (Class 0)
Potato: <0.35 (Class 0)
Phadiatop: 0.46 (Class 1)
(This last is a
screening test that measures the level of IgE to a combination of the
common inhalant allergens. A positive result indicates that the subject
is sensitized to 1 or more of these inhalants, but does not indicate
which. From there one can test for specific allergens.)
The mother was asked
to stop feeding with the soya formula, but the symptoms improved only
slightly. (She was, importantly, sent to a dietitian to ensure that
the child's diet would be nutritionally adequate.) The mother returned
to the doctor when the child was 11 months old. He still had chronic
eczema, but he also seemed to have severe "flare-ups" now
and again. The mother could not establish what the cause was.
Apart from reacting to something in his everyday environment or diet
that produced constant eczema, the child must have been exposed to something
causing the "flare-ups." What were the possibilities?
a. He was reacting to something (environmental or dietary) that he was
exposed to only occasionally.
b. He was sometimes being exposed to a higher dose of the allergen (environmental
or dietary) that was causing his constant eczema.
c. He was reacting to varying "hidden" sources of cow's milk
and/or soya in his diet.
d. In a patient with eczema, one should consider stress and other non-food
factors (e.g., exposure to house dust mite, pets, smoke, perfumes and
fabric softeners) that could aggravate eczema.
a-b. These will be discussed below.
c. A detailed dietary history was taken to determine whether hidden
allergens were present. But because the mother was very careful, she
gave only plain food (no processed foods or added flavorants). No hidden
allergens could be identified.
d. Even though the serum-specific IgE to Phadiatop was quite low, the
child could have been reacting to an environmental allergen not tested
for in the Phadiatop mix. No association could, however, be drawn between
any environmental allergen and his symptoms. The boy was not exposed
to smoke, perfumes or fabric softeners, and stress was not a factor.
What could be the next step?
a. Do more serum-specific IgE tests to other foods.
b. Ask the mother to keep a food-symptom diary.
c. Do an elimination diet and oral challenges.
a. There was no clear indication of which food could be a cause of the
reaction, and it would therefore have been difficult to suggest which
foods to test for. But testing for the most common allergens can be
helpful in such circumstances, as the chance of a child reacting to
one of these is better than to uncommon foods. The tests were done and
b. The purpose of keeping a diary is to detect a pattern in what is
eaten and the development of symptoms. Because the child experienced
constant eczema, the diary would probably not have assisted in identifying
the general cause; but it was potentially helpful for identifying the
allergen causing the "flare-ups." But it was decided to do
an elimination diet with challenges, which could be useful in both areas.
c. Because there was no clear indication of which food could be the
cause of the reaction, an elimination diet was singled out as an approach.
The mother was asked to allow only rice and rice products, maize and
maize products, potato (as the IgE levels of all of these were 0 or
low), banana, pear and chicken (as these are low-allergenic foods) in
her son's diet. The plan was to keep him on this diet until his symptoms
disappeared, and then challenge him with the foods that were excluded,
to see which provoked a reaction. After 1.5 weeks, the symptoms had
not improved. The mother did, however, pick up that her son's symptoms
got worse ("flared up") after he ate sweet corn. She was asked
to exclude all sources of maize, including the maize cereal, while still
following the rest of the elimination diet. This was done, and his symptoms
improved dramatically. Upon a rechallenge (with a double-blind method),
the symptoms flared again. This supports a recent finding that skin-specific
IgE and serum-specific IgE to maize have little, if any, clinical significance
for most patients studied (discussed below).
The other foods
were put back into his diet without adverse effects.
|TIP for Allergy
Allergy Advisor contains a guide to elimination diets under
the "Assessment" bar, under "Assessment Forms
& Guides". It contains examples of few foods diets
for different age groups as well as a step-by-step guide to
oral challenges. The "Challenge Vehicles" provides
ideas for vehicles that can be used to disguise foods during
B. More information:
Mango is not one of the "big eight" allergens (milk, peanut,
wheat, seafood, fish, soya, tree nuts, and egg), and therefore not as
much is known about it. But there are compelling reasons to study less
common allergens to the extent possible. One is that they may be "emerging"
allergens, as mango is (see immediately below). Incidence of an allergy
may rise significantly in a short time, leaving many clinicians unprepared.
Furthermore, knowledge of less common allergens is important not only
in terms of the allergies patients may have, but those they DON'T have.
Self-diagnosis is probably more common in allergy than in any other
area of healthcare, and patients are certainly not restricted mainly
to the "big eight" in their incorrect ideas about adverse
reactions they are experiencing. For any reported adverse reaction,
a clinician needs both the means to assemble solid evidence about the
nature of the reaction, and also a theoretical framework within which
to reason. Without, for instance, a range of suspicions of cross-reactions,
based on, for example, botanical relationship or the presence or the
type of a panallergen, diagnosis and management will be incomplete.
In the recent past,
the import and consumption of exotic foods have increased substantially.
Parallel to this rise, there has been an increase in the number of persons
experiencing adverse reactions to these products.1 These foods are
referred to as "emerging allergens". One of the foods is mango.
Adverse reactions to mango have been reported from tropical and subtropical
areas throughout the world, including the Philippines, Argentina, the
West Indies, the East Indies, India, Japan, and Florida. During mango's
fruiting season, it is the most common cause of plant dermatitis in
Hawaii.2 The frequency of adverse reactions to mango may be underestimated
because of the low consumption of this fruit in the Northern Hemisphere.
It is likely that, with wider consumption of mango in the West, an increased
frequency of reported adverse reactions will be seen.3,4
Mango's Latin botanical
name is Mangifera indica, and it belongs to the Anacardiaceae family,
which includes cashew nuts, pistachio nuts, "sweet pepper",
hog plum, Jamaican plum, sumac, poison ivy and poison oak.2,4,5,6 (Mangifera is a combination of the common name "mango" and
fero ("to bear" in Latin). Indica means "of India",
which is where the mango plant originates.2)
Mango is commonly
eaten peeled and raw. Green or unripe mango has many uses in the cuisines
of India, Malaysia and Thailand. It is used in various vegetable and
lentil dishes, as a meat tenderizer, and in recipes for chutney, pickles
stem sap may contaminate the peel, forming bleached, varnished or blackened
patches. This occurs because of the self-melanizing urushiol (going
black on contact with air), a substance present in members of the Anacardiaceae
mango pollen7, as well as to mango seed8 and mango fruit, has been
documented.9 Commercial products derived from the mango plant, such
as mango wood and sawdust (the timber is used commercially for items
such as boats and furniture) are potential causes of dermatitis.2
In some fruits,
such as apple, some strains or varieties are more allergenic (e.g.,
Granny Smith and Golden Delicious) than others (e.g., Jamba, Gloster,
Boskop); the latter being tolerated without or with moderate symptoms.
World-wide mango is cultivated in approximately 1000 strains even though
only a few are sold commercially, of which the Tommy Atkins variety
is the most popular. It has, however, been demonstrated that the allergenic
potencies of the four most consumed mango strains in Europe are very
reactions to mango fruit
reactions can occur after ingestion of or contact with the fruit.
The reactions that have been reported are facial erythema,4
urticaria,2,4,11,12 angioedema,11 periorbital
oedema,4 rhinoconjunctivitis,3 nausea, vomiting
and abdominal cramps,1 dyspnoea.3,4 cough,3
asthma and rhinitis after eating the fruit2,12 as well
as from mango tree pollen,13,14 anaphylaxis,15,16
burning sensation in the mouth,1 swelling of the lips,
face and tongue,1 pruritis of the eyes and/or mouth,
oral allergy syndrome,3 and contact dermatitis.17
syndrome is an IgE-mediated reaction that occurs to a number of
foods that all contain a similar allergen, affecting the oropharyngeal
mucosa of sensitized individuals.17 The main symptoms
include itchiness (pruritus) and swelling of the lips, tongue,
palate and throat.19,20 (Also
see the Educational Review of September 2003.)
is sometimes limited to vesicles at the angles of the mouth, and/or
the buccal mucosa, but it usually affects the entire periorbital region,
and eruptions may become generalised.2,21 Even the ingestion
of mango skin has induced erythematous vesicular eruptions of the lips
and face, and contact dermatitis has also occurred after climbing mango
An interesting finding
regarding sensitisation to mango was that mango dermatitis seems to
be more common in visitors to Hawaii, and in those who have moved there
from the United States mainland, than in those born locally. A possible
explanation is that those born on the islands are immunologically tolerant
to urushiol (3'5'-pentadecylcatechol), a substance known to sensitize
an individual upon exposure. Urushiol is found in the leaves, bark,
stems, tree latex and skin (pericarp) of the mango and also in other
plants of the Anacardiaceae family.2,3,5,6,22,23 It is proposed that
when primary exposure to urushiol is through the skin, allergic contact
dermatitis can result, but that when initial exposure occurs through
ingestion, the substance is presented to the gut-associated lymphoid
tissue, resulting in specific immunological tolerance. Mainland-born
people experience primary exposure to urushiol through the skin from
contact with poison ivy and poison oak, which induce delayed hypersensitivity.
Poison ivy and oak are not found on the Hawaiian Islands. An islander's
first contact with the antigen is typically through the ingestion of
mango at an early age, which results in the induction of specific immunological
tolerance.2,5,22,24 Mango dermatitis presents as very similar to dermatitis
caused by cashew and poison ivy. This is probably due to the urushiol
present in these foods. Urushiol dermatitis caused by plants of the
Anacardiaceae family is thought to be the most common cause of acute
allergic contact dermatitis.25,26 Immediate hypersensitivity to mango
is much less common, though it does occur. It is most commonly found
in atopic individuals.2,5,22,24
What is the mechanism
Adverse reactions to mango are probably IgE-mediated, as positive skin
prick tests and IgE RAST tests to mango have been documented. Another
possible mechanism of less severe reactions, such as contact urticaria,
is an IgG-mediated response.3
One would expect an extensive cross-reactivity among the different
individual species of the genus (e.g., mango, cashew and pistachio
nut), but this, in fact, does not occur frequently.27
Cross-reactivity has been found among pistachio nut, cashew nut,
and mango seed, but this cross-reactivity did not extend to mango
pulp. It is possible that pistachio and cashew nut-sensitive patients
may tolerate mango since only the pulp is usually consumed. However,
more studies are needed to completely understand the cross-reactivity
between mango fruit and nuts of this family.1,8
many other foods, contains more than one allergen, some of which
have been identified and others not. If an allergen belongs to
a panallergen family, there is a higher risk that the mango-allergic
individual will react to other foods as well (i.e., the cross-reacting
foods). Each panallergen in mango is associated with a different
group of foods that mango is likely to cross-react with. Some
examples are discussed below.
are allergens present in a number of plants, including their pollens.
The plants are not necessarily related to each other by family.
Each panallergen performs a specific function in the various plants.
Many panallergens are defense-related proteins, which provide
a plant with resistance to stresses such as infections, harsh
growing conditions and exposure to some types of chemicals. Under
stress conditions, the defense-related proteins increase.28)
between the so-called "celery-mugwort-spice syndrome"
and allergy to mango fruit has been described in the literature.
This syndrome involves cross-reactions among mango fruit, mugwort
pollen, birch pollen, celery, and carrot and cannot be explained
as a sensitization connected by botanic relation, as these plants
belong to different botanical families. It is, however, posited
that the association is based on allergens related to Bet v 1
and Art v 1, the major allergens of birch and mugwort pollen respectively.9,29,30
Of birch pollen-allergic
individuals, 10-15% may also be allergic to mango and other foods
such as litchi, banana, orange, apple, pear and carrot. This can
be attributed to an allergen that is common to these foods and
birch pollen. This is thought to be a 35kDa minor birch pollen
is one of the important panallergens that contribute to latex-fruit
syndrome. Latex-allergic individuals are at a high risk of having
a concominant allergy to foods such as mango, papaya, avocado,
banana, chestnut, passion fruit, fig, melon, kiwi, pineapple,
peach and tomato.13 An allergy to mango as a result
of cross-reactivity to latex has been more frequently reported
than an allergy to mango alone.3,4 It has been suggested
that putative class I chitinases, specifically, are the proteins
responsible for these cross-reactions.31 Chitinases
are defense proteins, i.e., they are usually activated by stress
to the plant. They break down chitin, the structural components
of insect exoskeletons and cell walls of fungi. Considering the
high degree of structural similarity among chitinases from different
plant species, one would suspect individuals with this syndrome
to be sensitized to most foods containing class I chitinases.
However, this is not the case for foods such as legumes and cereal
flours. They are rarely associated with latex allergy.32
This may be due to the fact that these foods are usually heated
before being consumed: it has been found that the allergic activity
of class I chitinases is lost by heating (i.e., they are heat-labile).32
been a report of an allergy to mango and latex in the same individual,
without there being any cross-reactivity. The person was allergic
to different allergens present in latex and mango respectively.3
mango allergy diagnosed?
A diagnosis of mango allergy is normally made quite easily through
a dietary history. The fruit is usually eaten on its own and is
unlikely to be mistaken for another food. However, skin prick
tests have been successfully performed using fresh mango juice4
and fresh mango pulp.3 Accurate skin tests are more
frequently performed using the fresh fruit than using extracts,
because of the lability of the antigen involved. Also, the fruit
pulp is more suitable for skin testing than the peel.1
RAST tests are also available.3 Because the diagnosis
is usually quite straightforward, there is generally little need
for oral challenges.
Avoiding mango in the diet is usually quite easy, barring a few sources
of hidden allergens such as meat tenderizers and some oriental dishes.
But mango-allergic individuals should be warned about possible cross-reactivity.
They may become sensitized to cross-reacting foods and other substances
such as latex.
||compiled by Karen du Plessis
Food & Allergy Consulting & Testing Services (FACTS)
PO Box 565
Comments by our editors
Janice M. Joneja Ph. D., RDN
study introduces an aspect of food allergy that is very inadequately
understood, and where more research is required, namely the possible
role of cell-mediated Type IV hypersensitivity. The fact that
the patient experienced a reaction localized in oral tissues,
which at first glance seems to indicate a diagnosis of oral allergy
syndrome, but in which there is no history of pollinosis, suggests
a Type IV hypersensitivity contact allergy rather than the IgE-mediated
Type I hypersensitivity characteristic of oral allergy syndrome.
Urushiol dermatitis is known to be a Type IV reaction, and the
fact that mango and other foods containing urushiol can cause
a contact allergy provides further evidence for this reaction
mechanism in the case presented.
A very interesting aspect of Type IV reactions is that in some
cases desensitization to the allergen can be achieved by the oral
route. This has been documented in several examples of Type IV
hypersensitivity, including nickel contact dermatitis (1,2), and
urushiol contact dermatitis (3). A further interesting observation
about Type IV contact allergy to urushiol is that development
of tolerance to contact with the allergen from one source can
lead to tolerance to the allergen in another: A article from 1989
reported that workers allergic to poison ivy/poison oak by contact,
lost their reactivity after working in a cashew nut shell oil
factory for several months (4).
Type IV hypersensitivity reactions are readily diagnosed by skin
patch tests, however, in some cases the reaction is delayed and
normally the patch is left in place for up to 72 hours before
a negative response is recorded.
DL. Intradermal testing and sublingual desensitization for nickel.
Cutis. 1998 Mar;61(3):129-32
2. Panzani RC, Schiavino D, Nucera E, Pellegrino S, Fais G, Schinco
G, Patriarca G. Oral hyposensitization to nickel allergy: preliminary
clinical results. Int Arch Allergy Immunol. 1995 May-Jun;107(1-3):251-4.
3. Ikeda Y, Yasumo H, Sato A, Kawai K. Oral and epicutaneous desensitization
in urushiol contact dermatitis in guinea pigs sensitized by 2
methods of different sensitizing potency. Contact Dermatitis 1998
4. Reginella, RF, Fairfield JC, Marks JG Jr. Hyposensitization
to poison ivy after working in a cashew nut shell oil processing
factory. Contact Dermatitis 1989 22(3):192
more information on this subject and other allergy and intolerance related
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1. Jansen A, de Lijster de Raadt J, van Toorenenbergen AW, van Wijk
RG. Allergy to pistachio nuts. Allergy Proc. 1992;13(5):255-8.
2. McGovern TW, LaWarre S. Botanical briefs: the mango tree--Mangifera
indica L. Cutis. 2001;67(5):365-6.
3. Duque S, Fernandez-Pellon L, Rodriguez F. Mango allergy in a latex-sensitized
patient. Allergy. 1999;54(9):1004-5.
4. Miell J, Papouchado M, Marshall AJ. Anaphylactic reaction after eating
a mango. BMJ. 1988;297(6664):1639-40
5. Geroso AM, Elpern DJ. Some observations on mango and mokihana dermatitis
from Hawaii. Contact Dermatitis. 1992;26(5):346-7
6. Garcia F, Moneo I, Fernandez B, Garcia-Menaya JM, Blanco J, Juste
S, Gonzalo MA. Allergy to Anacardiaceae: Description of cashew and pistachio
7. Vargas Correa JB, Sanchez Solis L, Farfan Ale JA, Noguchi H, Moguel
Banos MT, Vargas de la Pena MI. Allergological study of pollen of mango
(Magnifera indica) and cross reactivity with pollen of piru (Schinus
molle). [Spanish] Rev Alerg. 1991;38(5):134-8
8. Fernandez C, Fiandor A, Martinez-Garate A, Martinez Quesada J. Allergy
to pistachio: crossreactivity between pistachio nut and other Anacardiaceae.
Clin Exp Allergy. 1995;25(12):1254-9.
9. Paschke A, Kinder H, Zunker K, Wigotzki M, Steinhart H, Wessbecher
R, Vieluf I. Characterization of cross-reacting allergens in mango fruit.
10. Kinder et al. IgE-Binding Patterns and Allergenicity of Mango Fruit
Varieties. Internet Symposium on Food Allergens 1999;1(2):43-49.
11. Goldberg LC. Mango dermatitis. J Am Med Assoc. 1954;156(10):954
12. Kahn IS. Fruit sensitivity. South Med 1942;35:858-859
13. Brehler R, Theissen U, Mohr C, Luger T. "Latex-fruit syndrome":
frequency of cross-reacting IgE antibodies. Allergy. 1997;52(4):404-10
14. Pumhirun P, Towiwat P, Mahakit P. Aeroallergen sensitivity of Thai
patients with allergic rhinitis. Asian Pac J Allergy Immunol. 1997;15(4):183-5.
15. Dang RW, Bell DB 2nd. Anaphylactic reaction to the ingestion of
mango. Case report. Hawaii Med J. 1967;27(2):149-50
16. Rubin J, Shapiro J, Muehlbauer P, Grolnick M. Shock reaction following
ingestion of mango. JAMA 1965;193:391-398
17. Lampe KF. Dermatitis-producing Anacardiacea of the Caribbean area.
Clin Dermatol 1986;4:171-182
18. 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.
19. 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.
20. 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.
21. Zakon SJ. Contact dermatitis due to mango. JAMA 1939;113:1808
22. Hurtado I. Poisonous Anacardiaceae of South America. Clin Dermatol
23. Folster-Holst R, Hausen BM, Brasch J, Christophers E. Contact allergy
caused by poison ivy (Toxicodendron spp.) [German] Hautarzt. 2001;52(2):136-42.
24. Ippen H. Contact allergy to Anacardiaceae. A review and case reports
of poison ivy allergy in central Europe. [German] Derm Beruf Umwelt.
25. Rosen T, Fordice DB. Cashew nut dermatitis. South Med J 1994;87(4):543-546.
26. Marks JG Jr, DeMelfi T, McCarthy MA, Witte EJ, et al. Dermatitis
from cashew nuts. J Am Acad Dermatol 1984;10(4):627-631.
27. Yman L. Botanical relations and immunological cross-reactions in
pollen allergy. 2nd ed. Pharmacia Diagnostics AB. Uppsala. Sweden. 1982:
28. 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.
29. Wellhausen A, Schoning B, Petersen A, Vieths S. IgE binding to a
new cross-reactive structure: a 35 kDa protein in birch pollen, exotic
fruit and other plant foods. Z Ernahrungswiss. 1996 Dec;35(4):348-55
30. Wüthrich B, Hofer T. Food allergy: the celery-mugwort-spice
syndrome. Association with mango allergy? [German] Dtsch Med Wochenschr.
1984 Jun 22;109(25):981-6
31. Diaz-Perales A, Collada C, Blanco C, Sanchez-Monge R, Carrillo T,
Aragoncillo C, Salcedo G. Cross-reactions in the latex-fruit syndrome:
A relevant role of chitinases but not of complex asparagine-linked glycans.
J Allergy Clin Immunol. 1999;104(3 Pt 1):681-7.
32. Sanchez-Monge R, Blanco C, Perales AD, Collada C, Carrillo T, et
al. Class I chitinases, the panallergens responsible for the latex-fruit
syndrome, are induced by ethylene treatment and inactivated by heating.
J Allergy Clin Immunol 2000;106(1 Pt 1):190-5.
Questions (For South African dietitians only. Australian
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ALL THE QUESTIONS
(There is only
one correct answer per question.)
1. To which part of mango can one become sensitized?
(a.) Mango pollen
(b.) Mango seed
(c.) Mango fruit
(d.) All of the above
2. True or false:
Adverse reactions can occur after ingestion of but not on contact with
3. What type of
symptoms have been associated with mango allergy?
(a.) Skin manifestations
(b.) Intestinal symptoms
(c.) Respiratory symptoms
(d.) All of the above
4. What possible
explanation is given for mango dermatitis being more common in visitors
to Hawaii, and in those that moved there from the United States mainland,
than in those born locally?
(a.) The locally born are immunologically tolerant to urushiol.
(b.) The locally born have early contact with poison ivy and poison
(c.) The mainland-born have early oral contact with mango.
(d.) None of the above
5. Which is the
proposed mechanism of action of severe mango allergic reactions?
(a.) IgE-mediated reaction
(b.) Non-IgE-mediated reaction
(c.) IgG-mediated reaction
(d.) Intolerance reaction
6. Where symptoms
occur after oral ingestion of mango: which of the following groups is
mango fruit least likely to cross-react with?
(a.) Cashew and pistachio nuts
(b.) Celery, mugwort and carrot
(c.) Birch pollen, litchi and banana
(d.) Latex, papaya and avocado
7. True or false:
An allergy to mango as a result of cross-reactivity to latex has been
less frequently reported than an allergy to mango alone.
8. Which of the
following is true regarding diagnosis of mango allergy?
(a.) Fresh mango juice and fresh mango pulp can be used in skin prick
(b.) Accurate skin tests are more frequently performed using mango extracts
than when using the fresh fruit.
(d.) Mango peel is more suitable for skin testing than mango pulp.
(e.) There is no mango RAST test.
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