1. THE subject of food poisoning was once largely a series of disconnected observations
and records of outbreaks ; but during the last three decades the facts have been
associated and the discrepancies and fallacies removed. For example, the old
expression ‘ptomaine poisoning' has been shown to be without meaning and entirely
incorrect. Now it is possible to give a clear account of food poisoning, including the
various causal agencies, the paths of infection and the reservoirs of the various bacteria
responsible. In the first edition in 1943, the author of the book under notice gave a
clearly written account of the subject, and the second edition has brought it up to date.
The first edition dealt very inadequately with staphylococcus food poisoning ; but this
has now been remedied by the addition of a new, separate chapter of 22 pages on this
subject which gives all the essential facts. An additional section (appendix I) on
laboratory investigation of food poisoning cases is of doubtful utility, as this very
technical subject is mainly of interest to the laboratory worker, and for him the account
is barely adequate and is available elsewhere.
Abstract
Food poisoning is encountered throughout the world. Many of the toxins responsible for specific food
poisoning syndromes are no longer limited to isolated geographic locations. With increased travel and the
ease of transporting food products, it is likely that a patient may present to any emergency department
with the clinical effects of food poisoning. Recognizing specific food poisoning syndromes allows
emergency health care providers not only to initiate appropriate treatment rapidly but also to notify health
departments early and thereby prevent further poisoning cases. This article reviews several potential
food-borne poisons and describes each agent's mechanism of toxicity, expected clinical presentation, and
currently accepted treatment.
Abstract
Although food allergy can have serious health consequences, little is currently known about people’s
perceptions of food allergy. The present study examined the differences in awareness and perceptions of
food allergy and anxiety between young people with and without a food allergy. Participants completed a
questionnaire which asked about their perceptions and knowledge of allergies, perceived health
competence and anxiety. Of the 162 participants 24 reported they were allergic to at least one food; these
people perceived that their allergy had significantly less of an impact on their lives than others believed it
would. Allergy status interacted with perceived health competence to affect anxiety. People with an
allergy and with high health competence reported the greatest anxiety levels. Very few of the sample
knew the meaning of the term ‘anaphylaxis’. Findings are discussed in terms of health education
implications and possibilities.

2. Educators
http://jaa.sagepub.com/
Journal of Asthma & Allergy
http://jaa.sagepub.com/content/3/4/172
The online version of this article can be found at:
DOI: 10.1177/2150129711431888
Journal of Asthma & Allergy Educators 2012 3: 172 originally published online 28 December 2011
Stephanie E. Hullmann, Elizabeth S. Molzon, Angelica R. Eddington and Larry L. Mullins
Dating Anxiety in Adolescents and Young Adults With Food Allergies: A Comparison to Healthy Peers
Published by:
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On behalf of:
Association of Asthma Educators
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Journal of asthma & allergy educators August 2012
Research Article

3. Abstract: The present study sought to examine dating
anxiety and problems in social relationships and healthrelated quality of life in adolescents and young
adults
with food allergies compared with their healthy peers.
It was hypothesized that individuals with food allergies
would experience greater dating anxiety and poorer social
functioning and physical and mental health–related
quality of life than their healthy peers. Participants with
food allergies were age, gender, and ethnicity matched to
young adults without a history of allergies or any other
chronic illness for analyses. The majority of adolescents and
young adults with food allergies reported that their allergies
interfere with physical intimacy with their current partner.
Results further revealed that adolescents and young adults
with food allergies reported greater dating anxiety and fear
of negative evaluation than healthy peers. No differences
were observed between the groups on physical or mental
health–related quality of life or social functioning. For both
groups, dating anxiety was a significant predictor of mental
quality of life and social functioning.
Keywords: food allergy; dating anxiety; quality of life
A
pproximately 150 individuals (adults and children) die
annually due to adverse reactions to food.1
These adverse
food reactions are often caused by food allergies, which affect

4. 6% to 8% of children and 2% of adults in the United States.1
Adverse food reactions are characterized by an immunological
IgE reaction to the proteins on the food, with the 8 most
common food allergies being fish, peanut, egg, soy, wheat,
shellfish, tree nut, and cow’s milk.1
Individuals with food
allergies are faced with considerable uncertainty. The severity
of an allergic reaction to food can be unpredictable and
depends on several factors, including an individual’s sensitivity,
the type of food, and amount of food eaten.1
Exposure to
food proteins can occur without an individual’s knowledge
and without consuming the food. For example, individuals
with peanut allergies may not be aware when peanut oil has
been used in cooking, or they may have an allergic reaction
to the peanut oils from peanut shells and skins that have been
thrown on a restaurant floor. There is also evidence to suggest
that engaging in physically intimate behaviors with a partner
who has recently consumed the allergen can cause an allergic
reaction.2
Peanut allergens can remain in salvia for over an
hour, even after an individual has brushed his/her teeth or used
mouthwash.3
Notably, research suggests that kissing can allow
for the transfer of allergens through the skin, oral mucosa, or

5. saliva.2,3 As such, adults with food allergies must be diligent to
avoid exposure, inquire about ingredients and food preparation
when they have not prepared the food themselves, and
communicate about their allergies with their partner.
Whereas allergies have traditionally been thought of simply
as a nuisance disease with little impact on an individual’s
psychosocial functioning,4
recent research has demonstrated
the mental health implications associated with having allergies.
Specifically, adolescents and young adults with allergies
experience higher rates of depressive and anxious symptoms
and poorer mental and physical health–related quality of life
(HRQOL) than their healthy peers.5
Women with allergies have
also demonstrated increased levels of state and trait anxiety
when compared with healthy controls.6
Additionally, researchers
have examined the difference between healthy controls and
individuals with allergies to understand the impact the disease
has on HRQOL. Researchers have found that individuals with
allergies have significantly lower HRQOL when compared with
healthy controls.7,8 In an interesting allergen exposure task,
DOI: 10.1177/2150129711431888. From the Department of Psychology, Oklahoma State University,
Stillwater, Oklahoma. The author(s) declared no potential conflicts
of interest with respect to the research, authorship, and/or publication of this article. Address
correspondence to: Stephanie E. Hullmann, MS, 116 North Murray Hall,

6. Oklahoma State University, Stillwater, OK 74078; e-mail: stephanie.hullmann@okstate.edu.
For reprints and permissions queries, please visit SAGE’s Web site at
http://www.sagepub.com/journalsPermission.nav.
© 2011 The Author(s)
Dating Anxiety in Adolescents and Young Adults
With Food Allergies
A Comparison to Healthy Peers
stephanie e. hullmann, ms, elizabeth s. molzon, Ba, angelica r. eddington, ms, and larry l. mullins, Phd
Downloaded from jaa.sagepub.com by guest on August 25, 2013

7. IMP
Food Allergy Seminar.Lecture.ClassPresentation Transcript
1. Food Allergy Update: Overview for SCAFP Suzanne S. Teuber, M.D.
[email_address] Professor of Medicine Training Program Director, Allergy
and Immunology
2. Sometimes tough to avoid…
3. Definitions
4. Adverse Food Reactions Bacterial food poisoning Heavy metal
poisoning Scombroid fish poisoning Caffeine Alcohol Histamine Toxic /
Pharmacologic Non-Toxic / Intolerance Non-immunologic Lactase
deficiency Galactosemia Pancreatic insufficiency Gallbladder / liver
disease Hiatal hernia Gustatory rhinitis Anorexia nervosa Idiosyncratic
Adapted from Sicherer S, Sampson H. J Allergy ClinImmunol
2006;117:S470-475.
5. Adverse Food Reactions Systemic (Anaphylaxis) Oral Allergy Syndrome
Immediate gastrointestinal allergy Asthma/rhinitis UrticariaMorbilliform
rashes and flushing Contact urticariaEosinophilic esophagitis Eosinophilic
gastritis Eosinophilic gastroenteritis Atopic dermatitis IgE-Mediated (most
common) Non-IgE Mediated Cell-Mediated Immunologic Protein-Induced
Enterocolitis Protein-Induced EnteropathyEosinophilicproctitis Dermatitis
herpetiformis Contact dermatitis Sampson H. J Allergy ClinImmunol
2004;113:805-9, Chapman J et al. Ann Allergy Asthma &Immunol
2006;96:S51-68.
6. Pathophysiology
7. Allergens Proteins or glycoproteins (not fat or carbohydrate as primary
immunogens) Generally heat resistant, acid stable Major allergenic foods

8. (>85% of allergy) Children: milk, egg, soy, wheat, peanut, tree nuts Adults:
peanut, tree nuts, shellfish, fish , fruits and vegetables commonly stated
that “ 90% of food allergies are caused by the “Big 8 ””, this was true for
children with atopic dermatitis, not the general population with anaphylaxis.
ER studies in US: FRUITS and VEGGIES same % as peanut, crustaceans
highest
8. Emergency Department Visits for Food Allergy (Clark et al. JACI
2004;113:347) Crustaceans: 19% Peanuts: 12% Fruits and Veggies: 12%
Are these counted in food allergy prevalence estimates? -NO
9. CASE: Crustacean Allergy: IgE Towards Protein in the Food, NOT
Iodine 79 year old man had anaphylaxis to shrimp at age 20, 25 Doctors
told him he was allergic to iodine in seafood Avoided seafood, iodized salt
for years Age 70: retirement dinner, hostess picked shrimp out of his
portion and gave it to him --- ER visit for anaphylaxis At age 79, specific
IgE measurement extremely high to shrimp: >100 kU/L On follow-up after
education on avoidance, happily consuming foods with iodized salt
because he didn’t have to screen salt source any more
10. Pan-allergens Proteins in food, pollen or plants that possess
homologous IgE binding epitopes across species Tropomyosins:
crustacea, dust mites, cockroach, mollusks Storage mites in flour:
anaphylaxis reported! Parvalbumins: fish Bovine IgG: beef, lamb, venison,
cow’s milk Lipid transfer protein: fruits (peach, apple), vegetables, peanut,
tree nuts Profilin: fruits, vegetables Class 1 chitinases: fruits, wheat, latex
11. Immune Mechanisms IgE-Mediated IgE-receptor Histamine Protein
digestion Antigen processing Some Ag enters blood Mast cell APC B cell T
cell TNF- IL-5 Non-IgE Mediated
12. Risk Factors
13. Risk Factors for Development of Food Allergy Chapman J et al. Ann
Allergy Asthma &Immunol 2006;96:S51-68. Local Factors (Rodent Models)

9. Pepsin digestion Gastrointestinal infections? Malabsorption Rate of
absorption Antigen processing Nature and dose of Ag Transdermal
exposure Host Factors Age (esp neonates) Genetic susceptibility FHx of
atopyFHx of food allergy Atopic dermatitis Transdermal food exposure
(peanut)
14. Food Allergy Disorders
15. Anaphylaxis Syndromes Food-induced anaphylaxis Food allergy = #1
cause of anaphylaxis in the ED Rapid-onset, up to 30% biphasic May be
localized (single organ) or generalized Potentially fatal Do DNA Allergy
Relief Treatments for these high risk foods: peanut, tree nut, seafood
(cow’s milk and egg in young children) Food-dependent, exercise-induced:
2 forms Specific foods (wheat, celery most common) Any food (post-
prandial)
16. Fatal Food Anaphylaxis Frequency: ~ 150 deaths / year Clinical
features: Biphasic reaction can contribute –initially better, then recurs
Cutaneous symptoms may not be present Respiratory symptoms
prominent Risk factors : Underlying asthma – Delayed epinephrine
Symptom denial – Previous severe reaction Adolescents, young adults
History: known food allergen Key foods: peanuts and tree nuts dominate
(~90% of fatalities) , fish,crustaceans, few milk, few misc. Most events
occurred away from home Bock SA, et al. J Allergy ClinImmunol
2001;107:191-3.
17. Cutaneous Reactions Acute urticaria/angioedema – common Contact
urticaria - common Food allergy rarely causes chronic
urticaria/angioedema 1/3 of kids with moderate to severe atopic dermatitis
may have food allergy (especially cow’s milk, egg, soy, wheat). Morbilliform
rashes may be seen in these children upon food challenge. Contact
dermatitis (food handlers)
18. Respiratory Responses Upper and lower respiratory tract symptoms
may be seen (rhinoconjunctivitis, laryngeal edema, asthma) Rarely

10. isolated, usually accompany skin and GI symptoms Inhalational exposure
may cause respiratory symptoms that can be severe Occupational
Restaurants Kitchen/Home Example: crabs to be boiled
19. Pollen-Food Syndrome or Oral Allergy Syndrome Clinical features:
rapid onset oral pruritus, rarely progressive Epidemiology: prior
sensitization to pollens Key foods: raw fruits and vegetables Allergens:
Profilins and pathogenesis–related proteins Heat labile (cooked food
usually OK) Cause: cross reactive proteins pollen/food Birch Apple, carrot,
celery, cherry, pear, hazelnut Ragweed Banana, cucumber, melons Grass
Melon, tomato, orange Mugwort Melon, apple, peach, cherry
20. GI Syndromes of Children and Adults: Celiac Disease (Gluten-sensitive
enteropathy) In children: FTT, or weight loss Malabsorption, diarrhea,
abdominal pain May be subtle In adults, average 10 years of nonspecific
symptoms: Diarrhea, abdominal pain GERD Malabsorption May present
atypically with osteoporosis, infertility, neurologic sx Pathophysiology: an
immune-mediated enteropathy triggered by gluten peptides in genetically
predisposed patients (DQ2 or DQ8) Lymphocytic infiltration of small bowel
Villus atrophy
21. Celiac Disease (Gluten-sensitive enteropathy) Cont’d: Diagnosis
~1/133 people in US have celiac disease – many are currently
undiagnosed IgA anti-tissue transglutaminase (IgG if IgA-deficient), anti-
endomysialAb, little role for anti-gliadinAb currently due to poor specificity
Upper endoscopy with biopsy; Management Strict, lifelong, gluten
avoidance (wheat, barley, rye) Rare risk of GI lymphoma Oats almost
always OK Link with resources: dietician, local support groups, national
organizations (listed at www.celiac.nih.gov)
22. GI Syndromes of Children and Adults Gastrointestinal Anaphylaxis or
Immediate Gastrointestinal Allergy IgE-mediated Acute
emesis/diarrhea/abdominal pain Can present without other signs or
symptoms of an allergic reaction to food

11. 23. GI Syndromes of Children and Adults Eosinophilic Gastrointestinal
Disorders: eosinophilic esophagitis/gastritis/gastroenteritis Prevalence
increasing, eosinophilic esophagitis is the most common syndrome, all rare
in adults Symptoms Post-prandial N/V/D/abdominal pain, weight loss FTT
in infants and young children, irritability, sleep disturbance GER, often
refractory, may be seen In teens/adults: dysphagia, food impaction
24. Eosinophilic Gastrointestinal Disorders: eosinophilic
esophagitis/gastritis/gastroenteritis cont’d: Diagnosis Biopsy: eos infiltration
(mucosa serosa): >15/HPF Presence of eos doesn’t necessarily invoke
food allergy May affect esophagus to rectum Response to specific food
elimination found in a subset of patients (especially eosinophilic
esophagitis): can screen for food allergy with prick/in vitro IgE, patch
testing with food is currently under investigation
25. Disorders Not Proven to be Related to Food Allergy Migraines
Behavioral / Developmental disorders Arthritis Seizures Inflammatory
bowel disease
26. Prevalence and Natural History
27. Prevalence of Food Allergy Perception by public: 20-25% Confirmed
allergy (oral challenge) Adults: 3-4% Infants/young children: 6-8% Specific
Allergens Dependent upon societal eating and cooking patterns
Prevalence higher in those with: Atopic dermatitis Certain pollen allergies
Latex allergy Prevalence seems to be increasing
28. Estimated Prevalence of Food Allergy Sampson H. J Allergy Clin
Immunol;113:805-19. Food Children (%) Adults (%) Cow’s milk 2.5 0.3 Egg
1.3 0.2 Soy 0.3-0.4 0.04 Peanut 0.8 0.6 Tree nut 0.2 0.5 Crustaceans Fish
0.1 0.1 2.0 0.4
29. Prevalence of Clinical Cross Reactivity Among Food “Families” Food
Allergy Prevalence of Allergy to > 1 Food in Family Fish 30% -100% Tree

12. Nut 15% - 40% Grain 25% Legume 5% Any 11% Sicherer SH. J Allergy
ClinImmunol. 2001 Dec;108(6):881-90.
30. Natural History Dependent on food &immunopathogenesis ~ 85% of
cases of cow milk, soy, egg and wheat allergy remit by age 3 yrs –
numbers may be worse now for milk and egg Declining/low levels of
specific-IgE favorable IgE binding to conformational epitopes favorable
Non-IgE-mediated GI allergy Infant forms resolve in 1-3 years Toddler /
adult forms more persistent
31. Natural History (cont’d) Allergies to peanuts, tree nuts, seafoods, and
seeds typically persist ~20% of cases of peanut allergy resolve by age 5
years. Prognostic factors include : PST <6mm ≥ 2 years avoidance History
of mild reaction Few other atopic diseases Low levels of peanut-specific
IgE Rarely re-develop allergy: role for regular ingestion?
32. Diagnosis and Management
33. Evaluation: History & Physical Exam History: most important
Symptoms, timing, reproducibility, treatment and outcome Concurrent
exercise, NSAIDs, EtOH Diet details / symptom diary Subject to recall “
Hidden” ingredient(s) may be overlooked Physical exam: assess for other
allergic and alternative disorders Identify general mechanism Allergy vs
intolerance IgE versus non-IgE mediated
34. Evaluation of Food Allergy Suspect IgE-mediated Panels/broad
screening should NOT be done without supporting history because of high
rate of false positives. Prick skin tests (prick-prick with fresh food if pollen-
food syndrome) In vitro tests for food-specific IgE Suspect non-IgE-
mediated Consider biopsy of gut, skin Suspect non-immune, consider:
Breath hydrogen Sweat test Endoscopy
35. Interpretation of Laboratory Tests Positive prick test or specific IgE
Indicates presence of IgE antibody NOT clinical reactivity ~90% sensitivity
~50% specificity ~ 50% false positives Larger skin tests/higher

13. IgEcorrelates with likelihood of reaction but not severity Negative prick test
or specific IgE Essentially excludes IgE antibody (>95% specific)
36. Unproven/Experimental Tests Intradermal skin test with food Risk of
systemic reactions and death Not predictive (high false positive rate)
Provocation/neutralization, cytotoxic tests, applied kinesiology (muscle
response testing), hair analysis, electrodermal testing, food-specific IgG or
IgG4 (IgG “RAST”) Note: industry/restaurants have no way of ascertaining
whether a consumer was “diagnosed” by these methods or has a true food
allergy. Science does not enter until a lawsuit is filed….
37. Diagnosis: Elimination Diets & Food Challenges Elimination diets (1 - 6
weeks) most useful for chronic disease ( eg. AD, GI syndromes) Eliminate
suspected food(s) or Prescribe limited “eat only” diet or Elemental diet Oral
challenge testing (MD supervised, emergency meds available) Open
Single-blind Double-blind, placebo-controlled (DBPCFC)
38. Diagnostic Approach: IgE-Mediated Allergy If test for specific-IgE
antibody is Negative: reintroduce food* Positive: start elimination diet If
elimination diet is associated with No resolution: reintroduce food*
Resolution Open / single-blind challenges to “screen” DBPCFC for
equivocal open challenges * Unless convincing history warrants supervised
challenge
39. Treatment of Food Allergy Complete avoidance of specific food trigger
Ensure nutritional needs are being met Education Anaphylaxis Emergency
Action Plan if applicable most accidental exposures occur away from home
This frozen dessert could have peanut, tree nut, cow’s milk, egg, wheat
40. Peanut allergen exposure through saliva: assessment and
interventions to reduce exposure. Maloney JM et al. JACI 2006:118:719-24
. In our UC Davis group of patients with severe tree nut or peanut allergy,
5.3% volunteered that they had a reaction from kissing, sometimes several
hours after partner had eaten food. 1/3 in dating situation . This study:
Waiting 60 min, then brushing still did not remove peanut allergen

14. completely Authors suggest waiting several hours and ingesting a peanut-
free meal to be more effective than tooth-brushing or gum-chewing.
41. Treatment: Dietary Elimination Education Hidden ingredients in
restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”,
changes, errors) Cross contact (shared equipment) Seeking assistance
Food allergy specialist Registered dietitian: (www.eatright.org) Food
Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and
local support groups
42. Treatment: Dietary Elimination Education Hidden ingredients in
restaurants/homes (peanut in sauces,egg rolls) International products
Restaurants: outsourced dressings/desserts a problem Woman with near-
fatal reaction after patisserie cake Secret ingredients
43. FALCPA won’t help this: “No Nuts in It!” swore the chef -- Meal served.
Told specifically that there were no nuts in it 36 yr old woman with tree nut
allergy – peanuts OK Upscale bistro; chef in charge Told waitress of life-
threatening allergy – asked to check with chef to make sure dishes she
was ordering were safe. Was told, “No problem.” Highly Educated Expert
Chef
44. Ate a few bites and started to have tingling in the mouth Called the
waitress over and asked if there was any way there were nuts in the dish –
was told “No” Reaction progressed over minutes, trouble breathing and
speaking, used her Epi-Pen, 911 called Hospitalized Jambalaya
45. After discharge, she spoke to the chef, who repeatedly denied to her
that there were nuts in the dish Important to find out the cause, because if
it was a new allergy she would have to track it down to avoid it in future
along with tree nuts Threatened a lawsuit Chef only then disclosed ground
cashews were used as a secret ingredient
46. “ Didn’t know it could be so serious” The chef maintained that he had
been residing on planet earth despite an address in San Francisco

15. 47. Hospitality literature Wait staff: majority thought it was OK to pick an
allergen off a dish and serve it to the customer 80% of managers said they
were familiar with food allergy but only about 50% could define it. Others
gave examples of things like spoiled food.
48. Treatment: Dietary Elimination Education Hidden ingredients in
restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”,
changes, errors) Cross contact (shared equipment) Seeking assistance
Food allergy specialist Registered dietitian: (www.eatright.org) Food
Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and
local support groups
49. Contain cow’s milk: Artificial butter flavor, butter, butter fat, buttermilk,
casein, caseinates (sodium, calcium, etc.), cheese, cream, cottage cheese,
curds, custard, Half&Half ® , hydrolysates (casein, milk, whey),
lactalbumin, lactose, milk (derivatives, protein, solids, malted, condensed,
evaporated, dry, whole, low-fat, non-fat, skim), nougat, pudding, rennet
casein, sour cream, sour cream solids, sour milk solids, whey (delactosed,
demineralized, protein concentrate), yogurt. MAY contain milk : brown
sugar flavoring, natural flavoring, chocolate, caramel flavoring, high protein
flour, margarine, Simplesse ® . AS of January 1, 2006, all food containing
“Big Eight Allergens” (cow’s milk, peanut, tree nut, hen’s egg, soy, wheat,
fish, crustacean) in the U.S. MUST declare the ingredient on the label in
COMMON language. Does NOT apply to non-Big 8 allergens (e.g.,
sesame). Label reading used to be very challenging Example: Cow’s Milk
Food Allergen Labeling and Consumer Protection Act of 2004 (P.L. 108-
282) (FALCPA)
50. Geographic Unit United States (U.S. Public Law 2004) European Union
(European Commission 2003) Australia-New Zealand (Australia New
Zealand Food Authority 2001) Canada (pending law, Health Canada 2008)
Japan (Ministry of Health 2001) Cow’s milk √ √ √ √ √ Hen’s egg √ √ √ √ √
Wheat √ √ √ √ √ Soy √ √ √ √ Peanut √ √ √ √ √ Tree nuts √ √ √ √ Fish √ √ √ √

16. Crustacean √ √ √ √ Molluscs √ √ Sesame √ √ √ Mustard seed √ celery √
buckwheat √
51. Undeclared food (allergens) Current laws don’t help people with allergy
to less common food allergens that are present in small amounts.
Example: spices. UCD: personally have patients with oregano, cumin,
garlic allergy. Virtually any food can be an allergen Prefer not to
experiment with finding a threshold in an uncontrolled setting! FULL
disclosure of all ingredients would be helpful Gets back to fact that we
need more data on meaningful thresholds for a reaction E.g., soy lecithin
52. May Contain.. FDA mandated to publish results of follow-up studies on
utility and consumer preferences for “may contain” labeling. Should be
available soon. Consumers “hate it” As detection kits improve, can the use
of these terms decrease? Need thresholds
53. Treatment: Dietary Elimination Education Hidden ingredients in
restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”,
changes, errors) Cross contact (shared equipment) Seeking assistance
Food allergy specialist Registered dietitian: (www.eatright.org) Food
Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and
local support groups
54. Cross-Contact We need to do a better job teaching patients And
restaurant staff Utensils Surfaces Pans/pots Deep fryers Scatter No need
to “eliminate” allergens when there is a “safe” area for all and
knowledgeable staff.
55. Treatment: Dietary Elimination Education Hidden ingredients in
restaurants/homes (peanut in sauces,egg rolls) Labeling issues (“spices”,
changes, errors) Cross contact (shared equipment) Seeking assistance
Food allergy specialist Registered dietitian: (www.eatright.org) Food
Allergy & Anaphylaxis Network (www.foodallergy.org; 800-929-4040) and
local support groups

17. 56. Emergency Treatment: Anaphylaxis Epinephrine: drug of choice Self-
administered epinephrine readily available at all times If administered, seek
medical care IMMEDIATELY Train patients, parents, contacts:
indications/technique Anti-histamines: secondary therapy only: WILL NOT
STOP ANAPHYLXAXIS Written Anaphylaxis Emergency Action Plan
Schools, spouses, caregivers, mature sibs / friends Emergency
identification bracelet
57. MYTH: Prior Episodes Predict Future Reactions No predictable pattern
Severity depends on: Sensitivity of the individual Dose of the allergen
Other factors (e.g., food matrix effects, exercise, concurrent medications,
airway hyperresponsiveness) Must always be prepared for an emergency .
58. Patients with severe food allergy may not receive education on
avoidance, self-injectable epinephrine or referral to an allergist at
emergency department visits. It is imperative for primary care doctors and
allergists to recognize the risks and help patients avoid a future accident.
Emergency Department Management of Food Allergy Clark S, et al. J
Allergy ClinImmunol 2004;113:347-352.
59. Future Immunomodulatory Therapies Recombinant anti-IgE antibody
Mutated B-cell epitopes Minimal T-cell epitopes Immune-modulating
adjuvants (ISS) Probiotics T lymphocyte manipulation to induce tolerance
Heat-killed E. coli encoding mutated allergens Chinese herbal remedies
(Food Allergy Herbal Formula) Oral tolerance induction
60. Induction of tolerance after establishment of peanut allergy by the food
allergy herbal formula-2 is associated with up-regulation of IFN- γ .Qu et al.
CEA 2007;37:846 . Murine model of peanut anaphylaxis Treatment by
gavage bid x 6 weeks started AFTER mice allergic completely blocks
reactions Still blocked reactions to peanut 4 weeks after treatment stopped
IL-4, IL-5, IL-13 significantly decreased in mesenteric lymph nodes of
treated mice IFN- γ significantly increased in mesenteric lymph nodes of

18. treated mice An apparently synergistic combination of phytochemicals is
present
61. Phamacological and immunological effects of individual herbs in the
Food Allergy Herbal Formula-2 (FAHF-2) on peanut allergy. Kattan JD et
al. Phytotherapy Res 2008;epub ahead of print 4/08 The nine separate
“herbs” were individually tested as in the previous studies in the murine
model No single herb offered full protection One offered statistically signif
(but only 4 mice) protection (only ¼ mice had a reaction to peanut): Huang
Bai: Phellodendron bark Huang Bai also reduced plasma histamine levels,
but no change in IgE or specific IgG2a levels, whereas FAHF-2 results in
decreased IgE and increased IgG2a Tried a simplified formula with only
Huang Bai and 2 other “herbs”, but 2/5 mice had anaphylactic reactions to
peanut Best results with full formula
62. Food Allergy Initiative and NIH-NIAID Food Allergy Consortium
Funding to Xiu-Min Li and Hugh Sampson at Mt. Sinai. Food Allergy Herbal
Formula 2 is a bitter-tasting decoction/tea. Now, a tablet form has been
developed (12 small tablets tid is the human dose). Phase I trial scheduled
to start now – announced that patients were now being enrolled at 2008
AAAAI meeting: just tolerability/safety. They plan to seek FDA approval via
Phase II, III trials.
63. If the safety profile is good, since it is an herbal supplement, it could be
available OTC with no health claims by the end of 2008 according to a
recent Food Allergy Initiative mailer. This needs to be thought through very
carefully though Knock-offs could proliferate with claims for all kinds of
allergies Lead, arsenic, cadmium, adulteration (remember
Zencor/sildenafil??) Takes time for FTC to catch up with those who illegally
make claims
64. A randomized, double-blind, placebo-controlled study of Milk Oral
Immunotherapy (MOIT) for cow’s milk allergy. Skripak JM et al. JACI
2008;S137 20 randomized to milk or placebo (2:1 ratio) after baseline

19. studies Build up day: started with 0.4 mg milk protein, final dose 50 mg
Daily dosing with eight weekly dose increases to maintenance of 500 mg
Continued daily for 3-4 mo 11 completed, 5 active, 6 placebo Baseline
OFC: all 11 reacted to 40 mg milk protein (the initial dose)
65. Cont’d: MOIT Post OFC active group: cumulative median dose to elicit
reaction in active group: 5,140 mg (range 2,540 – 6,140) 1 patient tolerated
final dose of 8,140 mg with no symptoms. Post OFC placebo group: still
reactive at 40 mg 968 total active MOIT doses: 9.9% local reactions, 3.8%
systemic, epi given in 2 reactions 994 placebo doses: 11.3% local
reactions, 1.2% systemic, no epi given.
66. Rush specific oral tolerance induction in peanut allergic patients at high
risk of anaphylactic reactions. Blumchen K et al. JACI 2008:S136 . 6
children, ages 3-10 Peanut ImmunoCAP range 85->100 kU/l, median >100
All asthmatic, all “high risk” DBPCFC median provoking dose 470 mg
peanut Inpatient rush protocol, allergic symptoms appeared at 96 mg to
480 mg, 3/6 had lower respiratory symptoms, multiple reactions requiring
treatment Discharged after 6 days: on maintenance doses from 24 mg to
160 mg of peanut NOT protective doses! Conclusion: not a good approach
for this type of pt.