Small and Large Animal Dermatology

Allergic Skin Diseases

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Allergic Skin DiseasesAtopic dermatitis – Dogs

A. General Considerations:

1. Atopy is defined as an inherited predisposition to develop IgE antibodies to environmental allergens, which are normally innocuous substances.

2. Atopic dermatitis is a disease syndrome wherein an atopic individual develops hypersensitivity to such environmental allergens, and cutaneous signs result.

3. Atopy and atopic dermatitis are often used interchangeably in animals.

4. Next to flea allergy, atopic dermatitis is the second most common allergic skin disease of dogs and is seen frequently in small or mixed animal practices.

5. Reported incidence are:

a. 15% of canine population.

b. 3 – 8% of skin disorders at a university practice.

c. 30% of skin disorders at a private specialty practice.

B. Etiology and Pathogenesis:

1. The pathogenesis of atopic dermatitis is complex and new concepts are still emerging.

2. Atopic dermatitis is thought to be mainly a true Type I hypersensitivity reaction (IgE mediated).

3. Dogs inhale, or absorb percutaneously various allergens that induce the production of greater than normal amounts of allergen-specific IgE antibodies.

4. Allergen-specific IgE fixes to mast cells and basophils.

5. Up to this stage is the sensitization phase.

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6. When allergen penetrates the body again (by respiratory or percutaneous route) and cross-links cell-fixed IgE, mast cells and basophils degranulate. A number of pharmacologically active compounds are released and clinical signs of atopic dermatitis occur.

7. Total serum IgE levels are significantly higher in people with atopy.

8. Total serum IgE levels are not significantly higher in atopic dogs compared with normal dogs. However, serum allergen-specific IgE levels of dogs with atopic dermatitis are higher than the levels of normal dogs.

9. Other antibody classes may be involved in the pathogenesis of atopic dermatitis (short-term sensitizing IgG or IgGd).

10. The route of allergen penetration is controversial. In pets, the respiratory route has been historically considered the mode of environmental allergens penetration (inhalation). However, this route of exposure is the subject of investigation.

11. The percutaneous route is a plausible mode of allergen exposure in dogs with atopic dermatitis, since the most commonly affected sites (muzzle, feet, flexor and extensor sites) are likely to come into contact with environmental allergens and are subject to continuous minor trauma.

12. Recent research findings suggest the participation of T-cells in the pathogenesis of atopic dermatitis (possible type-IV component):

a. Presence of high affinity IgE receptors on Langerhans cells which will bind IgE.

b. Percutaneous absorption of allergens.

c. Allergen-Langerhans cells complex presents allergens to T-cells.

Important Facts

Atopic dermatitis is an inhered predisposition for the development of IgE antibodies to innocuous environmental allergens, which will result in cutaneous signs.

Sensitizing allergens are inhaled by the animal and/or penetrate the body through the skin.

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C. Allergens Involved in Canine Atopy:

1. Pollens (glycoprotein antigens):

a. Somewhat regional.

b. Season varies with the pollen; trees pollinate first, then grasses and weeds.

2. House Dust (most common allergen in humans and perhaps in dogs):

a. Complex substances consisting of breakdown products from clothing, furniture, animal and human dander, molds, insect parts, and house dust mites.

b. Dermatophagoides pteronyssinus and Dermatophagoides farinae are the most common dust mite in the Midwest. They are extremely potent allergens.

c. Mostly nonseasonal allergens.

3. Molds:

a. Found in all areas of the U.S. in soil and decaying organic matter, damp basements, etc.

b. Peak in U.S. depends on weather, but usually is in June through September. Some indoor molds can be present year-round.

c. Dogs are very seldom positive to mold allergens on most allergy tests, leading to speculation that mold allergies are not very important in dogs (as opposite to humans, where they are quite common).

4. Epidermal Antigens (cat, horse, etc) – less common allergens:

a. Hair is not a major antigen; rather, it is the dander (desquamated epidermal cells) and dried saliva that has high concentrations of substances to which allergy develops. Animals do not appear to be often allergic to other animals or to humans.

b. Feathers (pillows, birds).

c. Wool.

5. Miscellaneous – less common:

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a. Household insects.

b. Furniture stuffings.

b. Tobacco

Important Facts

Allergens commonly involved in canine atopic dermatitis are pollens, house dust, and molds.

D. Historical Findings in Atopic Dermatitis:

1. A detailed history is the single most important factor in the diagnosis and management of an atopic case.

2. History of Pruritus:

a. The historical hallmark of canine atopy is pruritus, initially unassociated with lesions.

b. Pruritus almost always starts at 1 to 3 years of age, but onset can be from 6 months to 6 years of age. After 3 years of age the incidence of atopy decreases and, it is infrequently diagnosed in dogs older than 6 years of age.

c. Pruritus can be seasonal or nonseasonal. Most initially seasonal cases progress to a year-round condition after 3 to 4 years.

d. Pruritus generally worsens from year to year.

3. Breed Predisposition:

a. Atopic dermatitis can be recognized in any dog of any breeding, but because of the genetic predisposition, the disorder is recognized more frequently in certain breeds or families.

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b. Breeds with reported higher incidence: Boston Terrier, Cairn Terrier, English Bulldog, Miniature Schnauzer, Pug, Wirehaired Fox Terrier, West Highland White Terrier, Golden and Labrador Retrievers, Lhasa Apso, Dalmatian, Irish and English Setter.

4. Historically, atopic dermatitis responds well to corticosteroid therapy.

Important Facts

A thorough history is the single most important factor in the diagnosis and treatment of canine atopy.

The historical hallmark of canine atopic dermatitis is pruritus.

Signs typically start at 1 to 3 years of age, but onset can be from 6 months to 6 years of age.

Clinical signs can be seasonal or nonseasonal.

Because of the genetic predisposition, the disorder is recognized more frequently in certain breeds or families.

E. Physical Examination Findings in Atopic Dermatitis:

1. Animals are pruritic

2. Where are they pruritic?

a. Face (periocular and perioral pruritus).

b. Feet licking and chewing.

c. Axilla, ventrum, lateral thorax, flanks.

d. Chronic pruritic otitis with inflamed pinnae (often recurrent).

3. What lesion do we see?

a. Rarely a primary lesion (erythematous papules) is associated with atopic dermatitis. Most dermatologists believe that there are no primary lesions with atopy. The disease causes only pruritus; any lesions seen are secondary to the dog’s scratching or to complicating diseases such as pyoderma, seborrhea, malassezia dermatitis.

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b. Lesions secondary to self-trauma:

1. Erythema.

2. Excoriations from scratching.

3. Alopecia: related to pruritus and secondary complications, but can be remarkably symmetrical.

4. Hyperpigmentation and lichenification: chronic cases.

c. Secondary staphylococcal pyoderma is VERY common in canine atopy.

1. Papules, pustules, yellowish crusts, epidermal collarettes, moth-eaten-alopecia are all signs of staphylococcal pyoderma.

2. Predisposing factors for the development of secondary pyoderma:

a. Keratinocytes of atopic dogs bind more Staphylococcus organisms.

b. Allergic skin is inflamed and warmer.

c. Hyperhydrosis occurs in approximately 10% of the cases and it increases skin moisture.

d. Increased sebaceous secretions provide nutrients for Staphylococcus.

e. Excoriation damages the epidermis to allow bacterial colonization.

d. Secondary seborrhea is also commonly seen in atopic dogs.

1. Scale is the hallmark sign of seborrhea. If scale is associated with excessive sebum secretion, it is a case of seborrhea oleosa. If scale is not associated with excessive sebum secretion, it is a case of seborrhea sicca.

2. Seborrhea oleosa occurs more often in canine atopic dermatitis.

e. Secondary Malassezia dermatitis is commonly seen in atopic dogs.

1. Clinical signs are variable.

2. Lichenified plaques with erythema, alopecia and scales.

3. Ventral neck, axillary regions, inguinal area and interdigital spaces.

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4. It is intensively pruritic.

5. Be suspicious of secondary Malassezia dermatitis if a dog is chewing (not licking) at his feet.

6. Malassezia dermatitis is often associated with Staphylococcus pyoderma.

f. Other Facts:

1. Recurrent otitis externa is common in atopic dogs (it can rarely be the sole sign of atopic dermatitis).

2. Recurrent “hot spots” can be a manifestation of atopy.

3. Ocular signs can be present in some cases (conjunctivitis, lacrimation, rubbing at eyes).

4. Respiratory signs are rare in dogs.

5. Anal pruritus can be a sign of atopic dermatitis.

Important Facts

Pruritus is typically localized to the face, axilla, ventrum, lateral thorax and feet.

Otitis externa is common in atopic dogs.

Rarely atopic dermatitis will be associated with primary lesions; any lesions seen are secondary to the dog’s scratching or to complicating diseases such as pyoderma, seborrhea, malassezia dermatitis.

Secondary staphylococcal pyoderma, secondary seborrhea and secondary malassezia dermatitis are VERY common in atopic dogs and these secondary complications often aggravate the pruritus primarily related with atopy.

F. Differential Diagnosis and Diagnosis in Atopic Dermatitis:

1. Differential diagnosis for pruritus without primary lesions:

a. Atopy.

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b. Food allergy.

c. Primary seborrhea/keratinization defects.

2. Differential diagnosis for pruritus with papules in dogs:

a. Pyoderma (+/- atopy, food allergy, etc.).

b. Flea allergy.

c. Sarcoptic mange.

d. Other ectoparasites (lice, cheyletiella).

e. Dermatophytosis.

f. Demodicosis.

g. Contact allergy.

h. Drug eruption.

i. Pemphigus foliaceous.

3. Diagnosis:

a. There is no perfect test for diagnosing atopic dermatitis.

b. A good history is extremely important !

1. Signalment (breed, age of onset).

2. Seasonal or non-seasonal pruritus.

3. Itch before rash:

a. The pyoderma can cause pruritus, which would present with a rash before the itch.

b. Treat pyoderma if it is present.

4. Atopic dermatitis should be responsive to anti-inflammatory doses of corticosteroids.

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c. Rule out food allergy. Atopy and food allergy can look exactly the same.

d. If the clinical signs are compatible with atopy, intradermal skin testing is the best diagnostic test.

e. Intradermal Skin Testing (IDST):

1. Intradermal skin testing is currently the accepted “gold standard” for diagnosis of atopic dermatitis in animals, though this may change with the improvement in other tests.

2. Allergen is injected intradermally and if allergen-specific IgE is present in the skin and bound to mast cells, the allergen will cross link the IgE leading to mast cell degranulation and a wheal and flare response.

3. Use aqueous extracts. Do not use glycerinated extracts.

4. Allergens are tested at 1,000 PNU’s (protein nitrogen units) or 1:1000 W/V. Approximately 0.05 ml is injected.

5. A positive control (histamine) and a negative control (saline) should always be used.

6. A positive skin test reaction is greater in size than the saline reaction, and is accompanied by erythema. It is graded subjectively on a scale of 0-4.

7. Animals are skin tested in lateral recumbency. An area over the lateral thorax is clipped and allergens are injected intradermally.

8. If sedation is needed, xylazine is the sedative of choice for a dog and IV ketamine is often used for a cat. Ketamine and valium can also be used in dogs. Other sedatives may decrease the wheal and flare response.

9. A number of factors may affect skin test reactivity.

a. Reasons for false negative reactions:

1. Improper technique.

2. Old antigens.

3. Improper antigen concentration.

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4. Allergens mixes.

5. Anergy (testing during peak of hypersensitivity reaction).

6. Drugs: glucocorticoids, progestogens, antihistamines, tranquilizers (acepromazine), any drug that lowers blood pressure significantly.

7. Severe stress (severe disease, struggling, fright).

8. Insufficient fixed IgE.

9. Estrus, pregnancy, pseudopregnancy.

10. Off-season testing (testing more than one to two months after clinical signs have resolved).

b. Reasons for false-positive reactions:

1. Improper technique (trauma).

2. Reactive skin (saline negative control may react).

3. Irritating antigens (house dust, wool, feathers and kapok antigens can act as primary irritants. May need to use them diluted to 500 or 250 PNU/ml instead.

10. Drug withdrawal prior to skin testing:

a. Antihistamines should be discontinued 10 to 14 days prior to skin testing.

b. Injectable corticosteroids should be discontinued 6 to 8 weeks prior to skin testing.

c. Oral prednisone should be discontinued at least 3 to 4 weeks.

d. Topical glucocorticoids can have a profound effect on skin test results and should be stopped 3 to 4 weeks depending on the strength of the steroid.

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f. In vitro allergy testing:

1. Radioimmunoassay procedures (Radio-Allergo-Sorbant_test or RAST) and enzyme-linked immunosorbent assays (ELISA) both measure allergen-specific IgE and IgGd levels in serum.

2. Advantages:

a. Little patient preparation (only requires serum sample).

b. No training.

c. Useful for those that can not be skin tested.

d. Fewer false negatives from exogenous drugs (though one company is recommending steroid withdrawal).

3. Disadvantages:b

c a. Many companies use grouped allergen.

d b. Poor correlation with intradermal skin test.

e c. High incidence of false positive reactions.

f d. Not reproducible.gh e. Response to hyposensitization vaccine therapy using a recipe from

i a serum allergy test is less (50% response) compared to the response using a vaccine recipe based on a skin test (70% response).

g. Skin Biopsy:

1. Non-specific results.

2. Superficial perivascular dermatitis – eosinophils are usually absent.

h. When should you consider diagnostic testing for atopy:

1. After ruling out other differentials.

2. When medical management is unsatisfactory.

3. If owner is willing to hyposensitize the animal.

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4. An animal is older than 1 year (experienced all seasons).

5. Clinical signs are present for more than 3 months each year.

6. Animal who can tolerate the hyposensitization injection schedule.

Important Facts

There is no perfect test for diagnosing atopic dermatitis.

Other causes of pruritic dermatitis that can appear similar to atopy should be ruled out: food allergy, contact allergy, sarcoptic mange, cheyletiellosis, flea allergy and pruritic pyoderma.

A good history and thorough examination are extremely important!

Atopic dermatitis should respond to anti-inflammatory doses of corticosteroids.

Intradermal skin testing is currently the accepted “gold standard” for the diagnosis of the specific allergens associated with atopy in animals.

Be sure to have the animals off of corticosteroids and antihistamines before testing to prevent false negative results.

Serum-based RAST or ELISA testing for IgE require little patient preparation, no restraint, and are an option for patients that can not be skin tested.

However, these tests are associated with high rate of false positive reactions (nonallergic dogs can be positive on these tests).

G. Treatment:

1. Canine atopic dermatitis is a complex, lifelong disease with many potential manifestations, and many possible modes of treatment. Every patient is different!

2. Client education is strongly advised upon initial diagnosis of atopy, particularly in a young dog. Owners must know what to expect!

a. Atopic dermatitis is a lifelong disease.

b. A controllable, but not curable disease.

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c. Relapses and secondary problems (mainly Staphylococcus pyoderma) are to be expected periodically.

d. No one treatment is universally effective.

3. The “Pruritic Threshold” concept in managing atopic disease:

a. Every animal will tolerate a certain amount of pruritic stimulus without scratching. Once this threshold is exceeded, clinical signs result.

b. Therefore, all possible contributing pruritic stimuli must be evaluated in each patient, and treated as necessary. Examples:

1. Secondary complications: staphylococcal pyoderma, seborrhea, Malassezia dermatitis, etc. VERY important!

2. Are Concurrent food allergies present?

3. Is Concurrent flea allergy dermatitis present?

4. Personality of the animal may influence mode and response to treatment.

5. Treatment may vary with time of the year.

4. Avoidance is possible for some allergens (examples: avoiding wool, limiting outdoor time in pollen-sensitive animals, various manipulations to keep dust mite populations down) but most times is impractical.

5. Medical Management of Atopic Dermatitis:

a. Antihistamines. Not always effective in dogs (perhaps more effective in cats) but always worth a try. Do an antihistamine trial using several and ask the owner to determine which one worked the best, if any. It has been reported to be useful in 10 to 20% of the cases.

1. Hydroxyzine (Atarax) 2.2 mg/kg TID.

2. Diphenhydramine (Benadryl) 2.2 mg/kg TID.

3. Chlorpheniramine 0.5 to 2 mg/kg BID.

4. Clemastine (Tavist) 0.05 mg/kg or 0.5 to 2.0 mg/dog BID.

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5. Amitriptyline (Elavil) 2.2 mg/kg BID – may cause arrhytmias – check heart first.

b. Omega-3 fatty acids:

1. Includes eicosapentanoic acid (EPA), docosapentanoic acid, docosahexanoic acid.

2. Inhibits production of pro-inflammatory mediators PG2 series and LT4 series.

3. Derm Caps which also contains omega-6 fatty acids, decreased pruritus by > 50% in up to 33% of atopic dogs; 18% did not require additional treatment.

4. Dose of EPA in one study was 180 mg/10 lbs of body weight – watch for diarrhea.

5. It may take up to 2 months before any result can be seen.

6. It works synergistically with antihistamines and steroids.

c. Glucocorticoids:

1. Inhibits inflammation, edema, pruritus.

2. Good efficacy for most atopic dogs, but many will develop adverse effects eventually.

3. For year-round scratchers, this would be the treatment of LAST resort.

4. Corticosteroids may be very appropriate lifelong therapy if the animal has signs for only a few months out of every year and if the pet owner can tolerate the side effects!

5. Drug of choice is prednisone, alternate-day therapy. Avoid the use of more potent drugs.

6. Starting dose is 0.5 to 1.0 mg/kg/day of prednisone PO, daily until remission (7 to 10 days) then 0.25 to 0.5 mg/kg every-other-day.

7. Injectable glucocorticoids should not be used in the dog.

8. Glucocorticoids may be combined with antihistamines and/or fatty acid supplements; this will sometimes decrease the required dose of prednisone.

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9. Before considering the use of glucocorticoids to manage atopic dogs, look for and treat any staphylococcal and malassezia infections if they are present. These secondary infections usually aggravate the pruritus primarily caused by atopy. Glucocorticoid therapy may be unnecessary if you successfully resolve the infections.

10. Always perform a chemistry profile, urinalysis and urine culture at least once a year if corticosteroids will be used as maintenance therapy.

d. Immunotherapy (also called hyposensitization or desensitization):

1. Treatment of choice for animals with a prolonged seasonal or perennial dermatitis.

2. Most authors report 60 to 70% response in dogs, if response is defined as at least a 50% improvement in clinical signs. About 15% of atopic dogs become normal with hyposensitization therapy (though it must be given lifelong).

3. The 30 to 40% of atopic animals that do not respond to hyposensitization must then be managed by medical therapy (antihistamines, corticosteroids).

4. Mechanism of action: extracts of the offending allergens are injected in gradually-increasing amounts, starting with tiny amounts and working up to large doses. Mechanisms in man include:

a. Developing of serum IgG “blocking antibody”. With successive allergen injections, an IgG titer is built up. IgG combines with the allergen in the circulation and ties it up before it can react with IgE bound to mast cells.

b. Stimulation of certain classes of T-lymphocytes, which via cytokine regulation reduce IgE production and increase IgG production.

5. Selection of allergens:

a. In general, no more than 12-15 aqueous allergens are included in a vaccine.

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b. In a dog with numerous strong positive reactions, select those allergens that are most prevalent in dog’s environment and that agree with seasonality of clinical signs.

c. More than one vaccine can be administered to a dog.

d. Molds are high in proteases and may inactivate other allergens. They should probably be placed in separate vaccine. This is currently up for debate!

6. Interval between injections may be modified depending upon the dog’s response.

7. In general, with aqueous extracts, a response is not seen before 3 months, and may not be observed until 9 to 12 months.

8. If vaccine helps it must be continued for life.

9. Additional therapy (glucocorticoids, antihistamines, essential fatty acids, topical therapy) is often necessary to control pruritus while waiting for hyposensitization to work.

10. Adverse reactions:

a. Mild reactions occur in approximately 10% of the patients. They include: intensification of clinical signs for a few hours, local edema or pruritus at the injection site.

b. Anaphylaxis occur in less than 1% of the dogs treated. Signs in dogs are generally depression, vomiting, diarrhea, weakness, collapse. Facial swelling and hives can also be seen.

c. If signs of anaphylaxis occur, for the next and subsequent injections, pretreat with 2 mg/kg of oral diphenhydramine, one dose 1 to 2 hours prior to injection.

d. After the initial episode, the next few injections should be given in the veterinarian’s office (with diphenhydramine pretreatment) and the dog observed for one hour after the injection.

11. Nonmedical adjunctive therapy:

a. Electrostatic air filters are excellent.

b. Air conditioning can be helpful.

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Important Facts

Treat every case as a single patient!

Remember to tell your client that atopy can not be cured but only controlled with continuous or intermittent therapy.

Staphylococal pyoderma, malassezia dermatitis and seborrhea often aggravate the pruritus associated with atopy. So, identify and treat them appropriately!

The only mode to treat atopy specifically is the hyposensitization therapy.

Response to hyposensitization vaccine therapy using a recipe from a serum allergy test (RAST or ELISA) is less (50% response) compared to the response using a vaccine recipe based on a skin test (70% response).

In general, results are not observed before 3 months of therapy, and may not be noted until 9 to 12 months.

Medical therapy should be instituted if the animal is not a candidate for hyposensitization therapy, when waiting for the hyposensitization to work, or if the animal does not respond to hyposensitization therapy.

Medical therapy include antihistamines, fatty acid supplements, corticosteroids and medicated shampoos and conditioners.

Always do an antihistamine trial to determine the best one to be used as maintenance therapy.

Antihistamines and essential fatty acids work synergistically.

Treat the secondary complications (pyoderma, malassezia dermatitis and seborrhea) before considering the use of corticosteroids.

Do not use injectable steroids in dogs!

The maintenance dose of corticosteroids should not exceed 0.5 mg/kg given every-other-day.

Always perform a chemistry profile, urinalysis and urine culture at least once a year if corticosteroids will be used as maintenance therapy.

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References

1. Scott, Miller, Griffin: Immunologic Skin Diseases. In: Small Animal Dermatology, 5th ed, W.B. Saunders, Philadelphia, PA, 1995, p 500 – 518.

2. Reedy, Miller, Willemse: Urticaria, Angioedema, and Atopy. In: Allergic Skin Diseases of Dogs and Cats, 2nd ed, W.B. Saunders, Philadelphia, PA, 1997, p 33 – 49.

Learning Objectives

1. Define the pathogenesis of atopic dermatitis.

2. Describe the historical and clinical features of canine atopic dermatitis.

3. Describe the principles, advantages and disadvantages of the different ways allergy testing can be performed.

4. How do you manage atopic dermatitis with medical therapy?

5. What are the principles and procedure for hyposensitization therapy for atopic dermatitis?

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Allergic Skin DiseasesAtopic Dermatitis – Feline

A. General Considerations:

1. Although there are increasing reports about “Atopic dermatitis – like problems" in cats, it remains unclear exactly what feline atopy is.

2. Cats with various cutaneous disorders have shown skin test reactivity to aeroallergens, among which house dust mites are most common.

B. Cause and Pathogenesis:

1. Feline atopy is caused by an exaggerated or inappropriate response of the affected cat to environmental allergens.

2. The most common environmental allergens are nonseasonal.

3. A study of 10 atopic cats showed 100% reactivity to the house dust mite, Dermatophagoides farinae.

4. The pathogenesis of the inappropriate response is unknown, though it is believed that a reaginic antibody is present in the skin.

5. That a reaginic antibody exists and resembles IgE is supported not just by the positive intradermal test but also by other studies, which showed that:

a. Positive skin test reactions in normal and atopic cats can be passively transferred to normal cats, and this reaction is heat labile (IgE is destroyed by heat).

b. The reaginic antibody cross-reacts with canine IgE.

c. Hyposensitization is effective in the management of atopic cats.

C. Clinical Signs:

1. The clinical manifestation of atopy in cats is not as clear cut as it is in the dog.

2. Atopic cats can show lesional and nonlesional pruritus.

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3. Clinical signs are variable and include:

a. Miliary dermatitis.

b. Head and neck pruritus with or without rhinitis or conjunctivitis.

c. Traumatic alopecia mimicking psychogenic alopecia.

d. Generalized pruritus.

e. Lesions of the eosinophilic granuloma complex.

f. Facial excoriations.

g. Generalized exfoliative dermatitis.

4. If lesions of the eosinophilic granuloma complex are present, they usually occur with other skin lesions, especially those of the miliary dermatitis.

5. The age of onset is very variable ranging from 6 months to 8.5 years, with most cases below the age of 2 years.

6. No sex predilection has been mentioned.

7. As in dogs, pruritus seems to be a hallmark for atopy-like problems in cats.

8. Atopic cats can exhibit their symptoms seasonally or perennially.

9. Since severely pruritic cats will mutilate their bodies, they are often presented to veterinary dermatologists early in the course of the disease so the true seasonality can be difficult to determine.

D. Diagnosis:

1. The diagnosis is usually based on:

a. Compatible history and physical examination.

b. Results of skin tests.

c. Response to glucocorticoids.

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d. Skin biopsy (histopathologic findings does not reliably distinguish between the lesions of flea allergy, atopy, or food allergy).

e. Exclusion of other cutaneous diseases such as food hypersensitivity, dermatophytosis, parasitic diseases, and flea allergy.

2. Skin scrapings, fecal flotations, and fungal cultures should be run in all cases.

3. The next step depends on the clinical presentation and history.

4. Where appropriate, flea bite allergy should be excluded by an extensive flea control program and dietary allergy should be investigated by a dietary restriction.

5. Although skin testing is commonly performed in cats, there are various problems in testing this species.

6. Skin reactions are difficult to interpret and are inconsistent, and stress influences skin test reactivity considerably.

7. Serologic testing has not been properly evaluated in this species. Hence, its diagnostic value is questionable.

E. Treatment:

1. Hyposensitization therapy is an option available in cases for which intradermal allergy testing has determined what the cats are specifically allergic to.

2. The same protocol used for the dog is most often used for cats.

3. No placebo controlled studies have been performed to evaluate the success rate of hyposensitization therapy in cats.

4. Glucocorticoids are the mainstay therapy in atopic cats.

5. Methylprednisolone acetate is given SQ or IM at the dose of 20 mg/car or 4 to 5 mg/kg. It can be given as needed but not more frequently than every 8 weeks and preferably every 12 weeks.

6. Oral prednisone or prednisolone can also be used. The initial dose is 2.2 mg/kg q 24h until the patient is in remission (5 to 10 days), followed by an alternate-day regimen.

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7. Be sure to perform a chemistry profile, urinalysis and urine culture if the animal is to be maintained on steroid therapy.

8. Antihistamines are also effective in cats. Cats are relatively sensitive to antihistamines and those other than chlorpheniramine (2 mg/cat BID) and clemastine (0.67 mg/cat BID) should be used with caution.

9. Fatty acid supplements have been reported to be beneficial in the management of atopy in cats. It will work better when given in association with antihistamines.

10. Remember to tell the owner that atopy can not be cured but only controlled with continuous or intermittent use of medications.

Important Facts

The pathogenesis of feline atopy is not well understood.

Inappropriate response to innocuous environmental allergens will induce the production of a reaginic antibody similar to IgE.

Clinical signs of atopy in cats are quite variable.

The most important rule outs are food allergy, flea bite allergy, dermatophytosis, demodicosis, self-inflicted alopecia.

Diagnosis is based on history, clinical signs and the exclusion of other pruritic dermatosis.

A positive skin test is not required for the diagnosis, however, it will identify the allergens which the animal is allergic to.

Treatment includes hyposensitization therapy, glucocorticoids, antihistamines and fatty acid supplements.

Most cases are well controlled with periodic injections of methylprednisolone acetate.

Do not administer it more often than every 8 to 12 weeks.

Monitor for side effects with a chemistry profile, urinalysis and urine culture at least once a year if the animal will be maintained on corticosteroid therapy.

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References

1. Scott, Miller, Griffin: Immunologic Skin Diseases. In: Small Animal Dermatology, 5th ed, W.B. Saunders, Philadelphia, PA, 1995, p 518 – 522.

2. Reedy, Miller, Willemse: Urticaria, Angioedema, and Atopy. In: Allergic Skin Diseases of Dogs and Cats, 2nd ed, W.B. Saunders, Philadelphia, PA, 1997, p 44 – 45.

Learning Objectives

1. Describe the historical and clinical features of feline atopy.

2. Define how to diagnose feline atopy.

3. Describe how to manage atopy with medical therapy in cats.

4. Describe the principle and procedure for hyposensitization for atopy.

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Allergic Skin DiseasesAtopy – Horses

A. General Considerations:

1. Atopy is an inherited predisposition to form sensitizing antibodies to environmental antigens, such as pollens of grasses, weeds, and trees, molds and dust.

2. Atopy has not been conclusively documented in large animals.

3. However, it is well known that IgE, reaginic antibodies, and Type I hypersensitivity reactions occur in horses, cattle, sheep, swine, and goats. Thus, all these species would appear to be capable of developing atopy.

4. The disease has been more extensively studied and better documented in horses.

B. Pathogenesis:

1. Sensitizing antibodies (usually IgE) bind to mast cells in the skin or respiratory tract – antigen cross-links IgE, resulting in mast cell release of inflammatory mediators.

2. Release of these mediators and their effects on other cells culminate in pruritus.

C. Clinical Signs:

1. Clinical characteristics of atopy in horses are still not well defined.

2. Pruritus may be seasonal or year-round, depending on the allergens to which the animal is allergic.

3. Pruritus and secondary lesions of alopecia, excoriation, lichenification, and hyperpigmentation may be present on the face, ears, ventrum and legs.

4. Clinical signs may resemble insect bite hypersensitivity.

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5. In some horses, pruritus may be accentuated in areas not typical for insect hypersensitivity, making differentiation of the two disorders easier.

6. Some horses seem to have pruritus that results from both pollens and mold allergies and insect hypersensitivity.

7. Some cases develop long-term recurrent urticaria, which may or may not be pruritic.

8. There is conflicting evidence about the role of atopy in chronic obstructive pulmonary disease (COPD).

9. A subset of horses with COPD seem to be truly atopic, based on intradermal skin testing, response to challenge with allergens, and response to hyposensitization.

D. Diagnosis:

1. Diagnosis is based on history, physical findings, ruling out other differentials, and intradermal skin testing.

2. Intradermal skin testing remains the diagnostic test of choice for atopy.

3. The value of RAST or ELISA testing in the diagnosis of equine atopy has not been documented in peer-reviewed literature.

4. There are several reasons why the intradermal skin test may be more valid than blood testing:

a. The skin test assesses tissue-fixed IgE, the IgE that actually mediates the disease.

b. It also assesses the complete mast cell response to a specific allergen.

c. No data are available to suggest that there is a direct correlation between antigen-specific IgE in tissue and that in blood.

d. In fact, tissue IgE may be high without the parallel increase in blood IgE.

e. A mechanism was recently suggested by which mast cells can augment B-cell production of antigen-specific IgE in tissues without blood levels being significantly elevated.

f. Mast cells can produce IL-4, and they express the ligand for CD40, two signals that the B-cell requires for IgE production.

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g. B-cells could then contact their local mast cell for stimulation bypassing the need for T-helper cells (this mechanism works for previously activated B cells, not naïve cells).

h. The clinical implication is that an intradermal skin test could pick up this elevation in IgE, but that the blood test could not.

i. Studies have demonstrated that local production of allergen-specific IgE can increase in COPD without a concomitant increase in blood levels.

5. Unfortunately, access to intradermal skin testing in horses is very restricted.

6. Remember! A positive skin test reaction tells us that the animal can make antigen-specific IgE and that the IgE is present in the skin; it does not tell us that the antigen in question causes the disease.

7. False-positive reactions and false-negative reactions can occur with intradermal skin testing.

8. Skin testing requires that the animal receive no antihistamines for at least 2 weeks.

9. Ideally, glucocorticoids should also be withdrawn, although anecdotal reports suggest that horses can be successfully skin tested when taking daily or every-other-day doses of 250 mg prednisone for 30 days or more.

10. The same technique described for testing dogs can be used in horses. Fractious animals can be sedated with xylazine hydrochloride (Rompun). The skin over the lateral neck (horse) is the preferred test site. The hair is gently clipped with a No. 40 blade.

11. The results of an intradermal skin test must be interpreted in the light of the history and physical examination. If a horse is not pruritic at the time a plant pollinates, then the positive skin test reaction to that plant is not relevant to the horse’s disease and should not be included in a hyposensitization vaccine.

E. Treatment:

1. The ideal treatment of allergies is avoidance of the allergens identified on the intradermal skin test.

2. Unfortunately, avoidance of allergens is frequently impossible or impractical.

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3. If avoidance is not an option, the treatment of choice is hyposensitization with the environmental antigens to which the horse is allergic.

4. Hyposensitization has been performed successfully in horses; an experienced

allergist can assist you in developing the treatment plan.

5. Testimonial evidence suggests that horses respond well to hyposensitization therapy. However, no placebo-controlled studies have been conducted to confirm this belief.

6. Non-specific therapy such as glucocorticoids and/or antihistamines can be used as adjunctive or alternative therapy if hyposensitization didn’t work or hasn’t been an option.

7. Prednisone or prednisolone and dexamethasone are the glucocorticoids used more often to manage equine pruritic dermatoses.

8. Daily induction doses are needed to stop the disease process and then a tapering process is attempted to arrive at a safer alternate-day maintenance.

9. Most induction periods range from 7 to 14 days, followed by a tapering period of 2 to 5 weeks.

10. Induction anti-inflammatory doses of prednisone or prednisolone are 0.5 to 1.5 mg/kg/day, with maintenance doses at 0.2 to 0.5 mg/kg every 48 hours.

11. Some cases will be resistant to prednisone or prednisolone and may respond to either oral or injectable dexamethasone.

12. Often an initial loading dose of dexamethasone at 0.02 to 0.1 mg/kg can produce immediate remission, which can be followed by a oral maintenance dose of 0.01 to 0.02 mg/kg every 48 to 72 hours.

13. Antihistamines have fewer side effects than corticosteroids and provide an alternative for horses that cannot tolerate corticosteroids.

14. Hydroxyzine hydrochloride has been reported to be the most effective antihistamine to manage both urticaria and allergic hypersensitivities in horses.

15. It is given at a dose of 1 to 1.5 mg/kg every 8 to 12 hours. It generally is more effective for urticaria than for pruritus.

16. Other less effective antihistamines are: diphenhydramine (0.75 to 1 mg/kg), doxepin hydrochloride (0.5 to 0.75 mg/kg), and chlorpheniramine (0.25 mg/kg ) every 12 hours.

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17. The only side effects observed with antihistamines are occasional episodes of sedation or personality changes.

18. Atopy has a reasonable prognosis, if specific allergens can be diagnosed. If glucocorticoids are used as the sole treatment, they may become ineffective over time, requiring higher doses to be administered.

19. The owner should be aware that the allergic tendency is an inherited trait; however, the specific genetic mechanisms have not been elucidated in the horse.

20. The owner should also be aware that this is a manageable condition, not a curable disease.

Important Facts

Atopy has been diagnosed in horses, however, there is still a lot to learn about this disease in horses.

Pruritus can be seasonal or year-round.

Pruritus and secondary lesions of alopecia, excoriation, lichenification, and hyperpigmentation may be present on the face, ears, ventrum and legs.

Clinical signs can mimic insect hypersensitivity.

Diagnosis is based on history, clinical signs, exclusion of other pruritic dermatoses and intradermal skin testing.

The value of RAST or ELISA in the diagnosis of equine atopy is not known at the present time.

Treatment includes one or more of the following: avoidance (often impractical); hyposensitization therapy based on the intradermal skin test results; corticosteroids and antihistamines which can be used as the sole therapy or in association with hyposensitization to improve response.

Explain to the owner that this disease is inherited and it can not be cured but only controlled with continuous or intermittent uses of medications.

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References

1. Scott, D.W.. Immunologic Diseases. In: Large Animal Dermatology. 1st ed., W.B. Saunders, Philadelphia, PA, 1988, p 294-300.

2. Fadok, V.A. Overview of Equine Pruritus. In: Veterinary Clinics of North America: Equine Practice, W.B. Saunders, Philadelphia, PA, 1995, p 1-10.

Learning Objectives

1. Describe the pathogenesis of atopy.

2. How can atopy manifest clinically in horses?

3. How is atopy diagnosed in horses?

4. How is atopy managed in horses?

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Allergic Skin DiseasesFood Allergy – Dogs and Cats

A. General Considerations:

1. Food allergy is an uncommon NONSEASONAL pruritic dermatosis of dogs and cats.

2. Estimates of disease prevalence vary from 1 % to 10% of all pruritic diseases.

3. Most people agree that it is more common in cats than in dogs.

B. Cause and Pathogenesis:

1. Pathogenesis is still not well understood. It may involve a Type I (immediate, IgE mediated), Type III (immune complex mediated) or Type IV (delayed, cell mediated) hypersensitivity to an ingested allergen.

2. It may occur with a new diet or after being on the same diet for years. It rarely occurs after a change in diet.

3. Offending allergens are: beef, dairy products, wheat, soy, and fish and chicken (cats).

C. Clinical Signs:

1. Canine:

a. They are pruritic!

b. Where are they pruritic?

1. No “classical” set of cutaneous signs.

2. Face, feet, axillary pruritus – atopic-like.

3. Tail base – flea allergy – like.

4. “Ears and Rears” – recurrent otitis and perianal dermatitis.

5. Ventrum – scabies – like.

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6. Atopy, food allergy, and scabies can look exactly the same.

7. Concurrent GI signs may be seen alone or in conjuction to dermatologic signs (vomiting, diarrhea, colic, excessive flatulence).

c. What lesions do we see?

1. 50% have primary papular eruption.

2. Urticaria and angioedema.

3. Lesions secondary to self-trauma:a. alopecia, crusts, scales

b. Lichenification and hyperpigmentation (signs of chronicity).

4. Secondary staphylococcal pyoderma which can present as papules, pustules, crusts, moth-eaten alopecia and epidermal collarette.

5. Secondary seborrhea, which will present as scales with or without excessive sebum production.

d. Age:

1. It can occur from 2 to 3 months to more than 10 years of age.

2. Many cases occur in young dogs and may raise the index of suspicion above that of atopic disease when pruritus occurs in dogs under 6 months of age.

2. Cats:

a. They are pruritic too!

b. Where are they pruritic?

1. Face

2. Head and neck

3. Generalized

4. Pruritic otitis externa.

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c. What lesions do we see?

1. Miliary dermatitis (widespread papulocrustous dermatitis).

2. Alopecia from excessive grooming (mimic psychogenic alopecia).

3. Self-trauma induced lesions such as excoriations, crusts, alopecia.

4. Eosinophilic plaque.

5. GI signs are uncommon.

D. Diagnosis:

1. History and physical findings.

2. The only reliable method of testing for food allergy is an elimination diet trial.

3. Elimination Trial:

a. Feed a single source of protein and carbohydrate that the animal hasn’t received previously, for 8 to 10 weeks.

b. Again, feed food items the dog or cat has not been exposed to previously.

c. Feeding a carefully selected home-prepared diet is preferred over feeding a commercially prepared limited protein source diet. A huge disadvantage is client compliance; with the advent of good commercially-prepared limited protein source diets, many clients now prefer to use these.

d. To select the diet to be used on the trail, be sure to get a complete diet history from the owner. A totally novo protein and carbohydrate sources should be selected for the trail.

e. Switching brands is not helpful, as all commercial foods contain similar ingredients.

f. Protein sources that can be used include venison, rabbit, white fish, tofu and in some cases lamb. Potatoes can be substituted for rice.

g. For cats, lamb, venison, pork or rabbit can be used.

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h. Small dogs and cats can be fed Gerbers lamb and baby food.

i. If you are going to use a commercially prepared protein limited diet, it is critical to understand that the reliability of virtually none of these diets has been confirmed in known food-allergic dogs or cats. Under treatment, you will find names of commercially available diets, which can be used during the food elimination trial. The newly available truly hypoallergenic diets are probably the best commercial diets to be used in the trial.

j. Be sure owners discontinue any treats, table scraps Pet-tabs, filaribits, or chewable heartgard during trial. Use DEC or non-chewable heartgard for heartworm preventative.

k. At least 50% decrease in pruritus is considered a positive test. Many

animals start to show improvement after about 2 weeks.

l. Diagnosis is confirmed by feeding the animal its regular diet and seeing the pruritus recur within 14 days (dietary challenge). Usually signs recur after 3 to 72 hours of challenging.

4. Intradermal skin testing, RAST, and ELISA are not good diagnostic tests for food allergy.

E. Treatment:

1. Be sure to identify and treat any secondary problems such as staphylococcal pyoderma, seborrhea and/or malassezia dermatitis.

2. Dietary avoidance.

3. Possible Commercial Diets for Dogs:

a. Hill’s prescription diets dry D/D.

b. Nature’s Recipe®.

c. Eukanuba Response Formula® – fish and potato.

d. Innovative Veterinary Diets®: duck and potato, rabbit and potato, venison and potato.

e. These diets can be used as trial diets or as maintenance diets.

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4. Commercial Hypoallergenic Diets (Dogs):

a. Purina HA Diet® – this diet can be used as trial or maintenance diet.

b. DVM Exclude – this diet is currently recommended as trial diet only because of the expense.

c. The protein contained in these 2 diets are processed to small molecular weight products which can not stimulate the immune system. Thus, these diets are considered truly hypoallergenic diets.

5. Commercial single protein diets:

a. Alpo® chicken.

6. Possible Commercial Diets for Cats:

a. Feline d/d® (canned, lamb and rice).

b. Nature’s Recipe®.

c. Walthan Selected Protein® (dry – duck and rice).

d. IVD Limited Diet (venison or duck). Not very palatable.

e. Lamb baby food.

f. Cooked ground lamb or leg of lamb.

g. These diets can be used as trial or maintenance diets.

7. Home-Prepared Diets:

a. These diets are usually not adequately balanced and, in young growing animals, should not be fed without supplements.

b. Because the calcium content of such diets is particularly low, a nondairy calcium source as well as vitamins and essential fatty acids, at the minimum, should be added to the diet.

c. Home-prepared diets are the ideal ones to be used during the food elimination trial. However, a well-balanced home-cooked diet can also be used as maintenance if the owner is willing to prepare it.

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Important Facts

Food allergy is a Type I, Type II or Type IV hypersensitivity to an ingested allergen.

Pruritus is the hallmark of food allergy.

Clinical signs in dogs and cats can be quite variable.

Food allergy and atopy can look exactly the same.

Be suspicious of food allergy if an animal show clinical signs before 1 year of age!

Intradermal skin testing, RAST or ELISA are not good diagnostic tests for food allergy.

Elimination trial diet is the only reliable method of testing for food allergy.

Feed a single and novo protein and carbohydrate source, exclusively, for 8 to 10 weeks.

A decrease in pruritus of at least 50% is considered a positive test.

Diagnosis is then confirmed by feeding the animal its regular diet and seeing the pruritus recur within 14 days.

Ideally, a home-cooked diet should be provided during the trial.

The same diet used during the trial can usually be provided as maintenance diet.

Be sure to identify and treat any secondary problem such as staphylococcal pyoderma, malassezia dermatitis and seborrhea.

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References

1. Scott, Miller, Griffin: Immunologic Skin Diseases. In: Small Animal Dermatology, 5th ed, W.B. Saunders, Philadelphia, PA, 1995, p 528 – 536.

2. Reedy, Miller, Willemse: Urticaria, Angioedema, and Atopy. In: Allergic Skin Diseases of Dogs and Cats, 2nd ed, W.B. Saunders, Philadelphia, PA, 1997, p 173– 188.

Learning Objectives

1. Describe the pathogenesis of food allergy.

2. List the different ways food allergy can manifest in dogs and cats.

3. List all the steps involved (diets used, duration of the trial etc) in doing an elimination diet trial (be able to explain that well to your client).

4. What is the next step if the animal’s pruritus decreases at least 50% during the elimination trial?

5. How do you manage food allergy?

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Allergic Skin DiseasesFood Intolerance – Large Animals

A. General Considerations:

1. Food intolerance is a rarely reported cause of pruritic skin disease in large animals.

2. It has been rarely described in horses, cattle and swine.

3. Incriminated substances have included:

a. Horses: wheat, oats, concentrates, barley, bran, alfalfa, and tonics.

b. Cattle: wheat, maize, soybeans, rice bran, and clover hay.

c. Swine: pasture plants.

B. Pathogenesis:

1. These animals can have an allergic or idiosyncratic reaction to the above described food stuffs.

2. Allergic reactions to foods are believed to be caused by multiple immunologic mechanisms, including Type I (immediate, IgE mediated), Type III (immune complex mediated) and, Type IV (delayed, cell mediated) hypersensitivity reactions.

3. Idiosyncratic reactions could result from nonimmunologic triggering of mast cell release or from mechanisms that are unknown.

C. Clinical Signs:

1. Food allergy classically is considered a non-seasonal pruritic dermatosis; however, it may be seasonal if the animal is receiving the offending substance at one particular time of the year.

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2. Horses:

a. Urticaria (hives) or pruritus and alopecia, which are sometimes, but not always, restricted to the tail.

b. In some cases pruritus is present on parts of the body less likely to be affected in insect hypersensitivity, such as the lateral caudal thorax and flanks. This makes differentiating the two conditions easier.

c. The differential diagnosis should include the other causes for urticaria, insect hypersensitivity, ectoparasites, and possibly atopy.

d. For pruritus restricted to the tail, one should also consider pinworm infestation (oxyuriasis), pediculosis, chorioptic mange and stable vice.

3. Cattle:a. Generalized pruritus with or without plaques, or pruritic urticaria.

4. Swine:a. Generalized erythema has been reported in cases in which food allergy

was suspected.

D. Diagnosis:

1. History and clinical signs.

2. Ruling out of other possible diagnoses by laboratory tests.

3. Diagnosis can only be made reliably by elimination diet testing.

a. The animals are fed a restricted diet for a period of 3 to 4 weeks.

b. Restricted diets should be individualized for each patient, based on careful dietary history.

c. Eliminate first all supplements and concentrates for 3 to 4 weeks.

d. If no clinical changes, take off any sweet feed and/or grain and feed a grass hay only.

e. If some type of grain is necessary in addition to the hay, the owner can switch from a sweet-mixed feed to a pure grain, such as oats or corn.

f. Which grain is used will depend on the contents of the original diet.

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g. No treats (horses mainly) or supplements should be given during this time.

h. The owner should watch for a decrease in pruritus during the 3 to 4 weeks the animals are on the elimination diet.

i. If improvement is observed, the owner should feed the suspected foodstuff for 3 to 7 days.

j. If that food is the allergen, pruritus should recur.

4. The serologic tests, RAST or ELISA or the intradermal skin test, are not accurate to diagnose food allergy.

E. Treatment:

1. The treatment for food allergy is to remove the offending food, supplement, or additive from the diet.

2. Glucocorticoids may be palliative in cases which hypoallergenic diets are not feasible.

Important Facts

Allergic reactions to foods are believed to be caused by multiple immunologic mechanisms, including Type I, Type III, and Type IV hypersensitivity.

Clinical signs are classically year-round but, they can be seasonal if the animal is receiving the offending substance at one particular time of the year.

In horses with tail rubbing the differential diagnosis should include insect hypersensitivity, chorioptic mange, pinworm infestation, lice and stable vice.

Definitive diagnosis can only be made by performing an elimination trial diet.

A restricted diet, prepared based on a careful dietary history, should be fed for periods of 3 to 4 weeks.

If a significant decrease in pruritus is noted during the trial, the animal should be fed the suspected foodstuff for 3 to 7 days.

If that food is the allergen, pruritus should recur.

Treatment consists of removing the offending food, supplement, or additive from the diet.

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References

1. Scott, D.W.. Immunologic Diseases. In: Large Animal Dermatology. 1st ed., W.B. Saunders, Philadelphia, PA, 1988, p 301-302.

2. Fadok, V.A. Overview of Equine Pruritus. In: Veterinary Clinics of North America: Equine Practice, W.B. Saunders, Philadelphia, PA, 1995, p 1-10.

Learning Objectives

1. Describe the clinical signs associated with food allergies in large animals.

2. Define the rule-outs for tail rubbing in horses.

3. List all the steps involved in performing a food elimination trial in large animals.

4. Describe how to manage food allergy.

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Allergic Skin DiseasesFlea Bite Allergy – Dogs and Cats

A. General Considerations:

1. Flea allergy dermatitis (FAD) is the most common pruritic skin disease of dogs and cats.

2. It arises as a result of a hypersensitivity reaction to the bite of the flea.

3. FAD is an extremely important disease in small and mixed-animal practice. Unfortunately, it is all too often ineffectively managed.

4. Be sure to know how to treat it!

Important Facts

Flea allergy is the most common pruritic dermatosis of dogs and cats.

Be sure to know how to treat it!

B. Cause:

1. Fleas are small, brown wingless ectoparasitic bloodsucking insects belonging to the order Siphonaptera. There are several types of fleas:

a. Ctenocephalides felis – most common flea of dogs and cats.

b. Ctenocephalides canis – appears to be endangered if not extinct in USA.

c. Echidnophaga gallinacea – stick tight flea of poultry. It can be a problem in southeast US – March, April, October, and November.

d. Pulex irritans – human flea. It may be found on dogs in the southeastern US.

e. Any of the above fleas may also parasitize man under the right conditions; i.e. if no dogs or cats are around!

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Important Facts

Ctenocephalides felis is the most common flea of dogs and cats.

2. Life Cycle:

a. The stages of the life cycle are eggs ---- 3 larval stages ---- Pupa ---- Adult.

b. Length of the life cycle depends on environmental conditions.

1. The entire life cycle usually takes 3 to 4 weeks.

2. It can be completed in as little as 12 to 14 days.

3. It can take as long as 6 months.

4. Optimum conditions are 65 to 80 F, with high humidity.

5. Fleas do not live at altitudes over 5000 ft.

c. Adult fleas spend most of their time wandering around on the pet. Once they hatch, they must find a host within 1 to 2 weeks (adult C. felis are permanent ectoparasites). Actively feeding cat fleas removed from their host do not survive longer than 3 to 4 days.

d. However, adult fleas only represent about 1% of the total infestation!

e. The biggest problem with fleas is massive environmental contamination with eggs, larvae and pupae, not the adults on pets!

f. Female fleas can produce up to 40 to 50 eggs per day (average 27/day).

g. Female fleas can lay over 2000 eggs during their life.

h. No life cycle stage can survive freezing (10 days at 3 C or 5 days at 1 C).

i. Adult fleas may survive over the winter by “hitchhiking” on wild animals (raccoons, opossums).

j. The female Echidnophaga gallinacea flea burrow into the host’s skin to lay eggs. Larvae drop off the skin into the environment.

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Important Facts

Actively feeding Ctenocephalides felis will not survive outside the host for longer than 3 to 4 days. It is a permanent ectoparasite.

The biggest problem with fleas is massive environmental contamination with eggs, larvae and pupae, not the adult on pets!

Optimum environmental conditions are 65 to 80 F and high humidity.

C. Pathogenesis:

1. When fleas bite, their mouthparts release saliva, which contains anticoagulants and pruritogenic enzymes. This accounts for the immediate itch associated with the bite.

2. Some of the salivary components are antigenic and evoke hypersensitivity response in the host, which is responsible for the majority of the clinical signs.

3. Flea Antigen:

a. Flea saliva contains multiple (at least 15) substances to which dogs and cats develop sensitivity. The pattern of sensitivity (which substances the animal is sensitive to) appears to vary substantially between individuals.

4. The Host Hypersensitivity Response to Fleas:

a. Involves several different types of immunity. Any one type or any combination of types may be present, depending on the animal.

b. Classical Type I (immediate, IgE-mediated) and Type IV (delayed-type, cell-mediated).

1. Most dogs have both.

2. 30% have only delayed.

c. Late onset IgE mediated response.

d. Cutaneous basophil hypersensitivity.

5. Hypersensitivity state is maintained for years.

6. Nonreactivity to flea bites involves immunologic tolerance rather than hyposensitization.

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7. Dogs and cats don’t achieve natural desensitization.

8. Factors which favor the development of flea allergy:

a. Intermittent exposure to fleas.

b. First exposure to fleas later in life.

c. Atopic dogs.

Important Facts

Most flea allergic dogs and cats develop a Type I (immediate, IgE mediated) and Type IV (delayed, cell mediated) hypersensitivity to multiple antigens present in the flea saliva.

Intermittent exposure to fleas and first exposure to fleas later in life are factors, which predispose animals to the development of flea allergy.

D. Clinical Signs:

1. Dogs:

a. They are pruritic!

b. DISTRIBUTION IS VERY TYPICAL:

1. Dorsal lumbo-sacral area.

2. Base of the tail.

3. Medial and caudal hindlimbs.

4. Abdominal and inguinal areas.

5. May generalize.

c. What lesions do we see?

1. Primary papular eruption.

2. Self-trauma secondary to pruritus:

a. Crusting, scaling.

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b. Alopecia.

c. Lichenification.

d. Hyperpigmentation.

e. “Hot spots” – acute moist pyotraumatic dermatitis.

3. Secondary pyoderma – papules, pustules, crusts, epidermal collarettes.

4. Secondary seborrhea.

5. Worn incisors.

d. Any age. However, the most common age of onset is 3 to 5 years.

2. Cats:

a. They are pruritic too!

b. Where are they pruritic?

1. Distribution is similar to dogs. Lumbo-sacral area, base of the tail. It can extend to the neck.

2. What lesions do we see?

a. Crusted papules – “miliary dermatitis”. FAD is the most common cause of the clinical syndrome of “feline miliary dermatitis”.

b. Self-inflicted hair loss.

Important Facts

Clinical signs of flea allergy are very typical!

Dogs and cats will develop alopecia, papules and crusts localized to the lumbo-sacral region, base of the tail, caudal aspects of hind legs and medial thighs.

In cats, the papule-crust lesions are called “miliary dermatitis", and flea allergy is the

most common cause of this clinical syndrome in cats.

Pruritus is usually severe!

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E. Diagnosis:

1. Usually made on the basis of history and clinical signs, as distribution of lesions and pruritus is nearly pathognomonic, especially if fleas and/or flea stool is found.

2. Examine animals carefully for fleas and flea feces. Always use a flea comb to do this! Feces appear as small, dry, black, often comma-shaped specks that release a reddish-brown color when placed on moistened white paper.

3. Fleas and/or flea feces are often, though not always, evident on the animal. ABSENCE OF FLEAS OR FLEA FECES DOES NOT RULE OUT DIAGNOSIS.

4. Intradermal testing is one way to definitively demonstrate hypersensitivity to flea saliva. Not all sensitive animals will have a positive immediate reaction, because of the multiple types of hypersensitivity present, but most will.

5. The intradermal test is more an aid to client compliance than a necessity to making the diagnosis.

6. Screening tests with in-office “quick kits” that detect IgE against flea allergen may also be a useful client aid (Heska – ELISA test).

Important Facts

Diagnosis is usually based on history and clinical signs.

The presence of fleas and/or flea stools strongly supports the diagnosis, however, do not rule out flea allergy if you don’t find any flea and/or flea feces on the animal!

F. Treatment: General

1. General Principles of Treatment :

a. CLIENT EDUCATION is the single most important factor in successful treatment of FAD.

1. Increase client’s awareness of the pathogenesis – they have to realize that even one flea can cause damage on a sensitive dog or cat!

2. Increase client’s knowledge of flea control measures.

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3. Make clients aware of important factors in flea control:

a. Largest numbers of eggs are found where pet spends most of its time.

b. Larva will migrate under furniture.

c. Pupal stage is difficult to kill and results in continued emergence of fleas (“pupal window effect” – new adult fleas are seen 3 to 4 weeks after treating the environment).

d. Preventive flea control is more successful than waiting until a flea population is established.

e. Inhibiting development of larva with insect growth regulators is essential to a successful flea control program.

4. Compliance is critical!

2. General procedures that must be followed :

a. Eliminate ALL fleas in the environment.

b. Provide treatment to control secondary problems such as pyoderma, seborrhea, or pyotraumatic dermatitis.

c. In many cases, brief courses of oral corticosteroids are used to suppress the allergic response and provide immediate comfort.

3. The traditional “three-pronged” approach :

a. Treat the house.

b. Treat the yard.

c. Treat ALL pets in the household.

4. Always use a combination of an adulticide chemical (to kill existing fleas) and an insect growth regulator (to interrupt the life cycle thus preventing a continuous new crop of adults).

5. Flea control must be individualized to each client to an extent. It is extremely helpful and timesaving to design a client education sheet for your practice. Train your receptionists and technicians to answer common questions.

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6. Attempts to use Immunotherapy (hyposensitization) with flea extracts have been unsuccessful to date. Newer “hi-tech” approaches to procedure recombinant flea allergen, etc. may hold promise in the future.

7. Corticosteroid use in FAD :

a. Use as a temporary measure only, while flea control is underway.

b. Do not use if significant pyoderma is present; in this case use antibiotics instead of corticosteroids.

c. Prednisolone, 0.5 mg/kg orally once or twice daily for 4 to 7 days, then the same dose every-other-day for 10 days should suffice.

d. There is no justification for repeated use of injectable long-acting corticosteroids to control FAD in dogs, since such use may lead to iatrogenic hyperadrenocorticism.

G. Treatment: Specifics of Flea Control

1. Two options: Move to Denver or Chemical Warfare.

2. Hundreds of products are on the market, but many of these are ineffective in severe flea areas.

3. Read labels for ingredients. You only need a limited number of products, but know how to use them properly.

4. How to select products to your practice and for individual clients – consider:

a. Efficacy – must kill fleas! Fleas have long become resistant to most “grocery store” products.

b. Safety – to owner and pet.

c. Convenience of application and owner preferences.

d. Cost.

e. Species of pets and ages.

f. Environment – are pets indoors, outdoors, both? Fenced yard, city apartment, or 40 acres?

g. Geographic are: warmer climate = worse problems.

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5. Chemicals used: Adulticides

a. Organophosphates:

1. Cholinesterase inhibitors with good efficacy and residual action.

2. Not for use on cats!

3. Examples: phosmet (Paramite), chlorpyrifos (Dursban), malathion, fenvalerate, supona, cythioate (Proban), fenthin (ProSpot), Propetamphos (Safrotin), diazinon.

b. Carbamates:

1. Cholinesterase inhibitors with variable efficacy and residual action.

2. Can be used on cats.

3. Kills adults and larvae (if you are lucky!).

4. Examples: carbaryl (Sevin), propoxur (Baygon), and bendiocarb (Ficam).

c. Pyrethrins:

1. Pyrethrins are generally considered safe, even for very young animals. Rapid metabolism by mammals, insects are unable to detoxify. They break down very fast in the environment. They are present in many flea products.

2. Pyrethroids have greater stability and residual action, but also increased mammalian toxicity. Example: permethrin.

3. Microencapsulation is used to prolong action and decrease toxicity (microencapsulated pyrethrin, Sectrol).

4. Kill adult fleas and larvae.

5. Not cholinesterase inhibitors; frequently used along with organophosphates and carbamates in combination products.

6. Generally contain a synergist (piperonyl butoxide or one of the “MGK” –series).

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d. Imidacloprid (Advantage). From a new class of insecticides termed either “heterocyclic nitromethylenes” or “chloronicotinyl nitroguanidines”.

1. Not cholinesterase inhibitor, very low mammalian toxicity, use on dogs and cats.

2. Mechanism of action: binds to postsynaptic nicotinergic Ach receptors. Some insects (e.g. fleas) have a lot of these receptors, and the receptors are important to them. Other creatures (e.g ticks) have fewer, so the compound is not effective against ticks. Mammalian nicotinergic receptors are not as numerous or are of different function, so that the compounds are relatively low in mammalian toxicity.

3. Supplied as a pour-on formula. Apply to the dorsum, spreads in sebum layer. It lasts for 4 weeks. Unaffected by rain/wetting.

e. Fipronil (Frontline). A phenylpyrrazole (new class of insecticides).

1. Not cholinesterase inhibitor, very low mammalian toxicity; use on dogs and cats. Kill both fleas and ticks.

2. Mechanism of action: interferes with GABA- regulated chloride channels in the nervous system.

3. Supplied as a spray, but animal must be “doused” with quite a lot of the spray until really wet (almost like a rinse). Also supplied as “TopSpot”, a squeeze-on liquid formulation that is preferred by some owners.

4. Long residual effect – lasts 4 to 8 weeks even with shampooing (concentrates in hair follicles and thus continually “reapplies” as sebum is secreted).

6. Chemicals used: Insect Growth Regulators (IGRs)

a. Juvenile Hormone Analogues:

1. Prevent larvae from pupating.

2. Ovicidal.

3. No effect on adult fleas or developing pupae!

4. Virtually nontoxic to mammals; very safe.

5. Very long residual action – months.

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6. Examples: Methoprene (Siphotrol, Ovitrol); pyriproxifen (Nylar – newest, most potent and UV light stable).

7. Chitin Synthesis Inhibitors:

a. Inhibit development of chitin exoskeleton and “egg tooth” of flea during all immature stages of life cycle.

b. Lufenuron (Program) – currently the only licensed product in the USA.

1. Low oral toxicity in cats and dogs; long residual action (stored in adipose tissue and released slowly into bloodstream).

2. Adult fleas that bite dogs or cats are not killed, but are sterile.

3. Adult fleas also excrete feces, which is food for larvae; larvae die out when ingest feces containing lufenuron.

4. Problem remains: fleas still have to bite dog to ingest it!

8. Repellents – of very limited efficacy!

a. Brewer’s yeast – ineffective orally.

b. Pennyroyal, eucalyptus, garlic – not effective.

c. Ultrasonic room devices or collars – unproved efficacy.

d. Avon Skin-So-Soft bath oil – an effective repellent (1/5 oz/gallon water, can be mixed with flea dip).

9. The Three Most Common Reasons for Failure of Flea Control.

a. Failure to treat environment adequately

1. The inside premises – very important!

a. Mechanical control procedures in infested environments.

1. Wash pet’s bedding.

2. Vaccum thoroughly – dispose of bag.

3. Steam-clean carpets.

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b. Use sprays or exterminator with IGR such as methoprene (Precor), or pyriproxifen (Nylar) and an adulticide.

c. Do twice at 2 week intervals and then every 2 months during flea season.

d. Start next year one month before season starts and then do every 2 months as before. May only need IGR.

e. Sodium polyborate brushed into carpet is another alternative.

2. The yard.

a. Spray with malathion, chlorpyrifos or microencapsulated Diazinon every 2 to 4 weeks during season.

b. Concentrate on areas protected from direct sunlight.

c. Steinernema carpocapsae, nematode that infects flea larvae, is a nonchemical alternative.

d. Keep in mind that very hot dry summers or very wet times will decrease your outside flea burden.

b. Poor selection of products.

1. Use of chemicals to which fleas are resistant.

2. Use of chemicals with poor residual effects.

3. Failure to use combination of adulticide and IGR.

c. Failure to treat all animals in contact with household.

10. Cats require some special considerations:

a. Cats do not like baths.

b. Cats are very sensitive to organophosphate toxicity – be cautious with Dursban in environment.

c. Cats salivate profusely when alcohol based products are used.

d. Recommendations for cats:

1. Frontline.

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2. Advantage.

3. Program.

4. Nylar flea collars.

Important Facts

Client education is very important in successful treatment of flea allergy!

Clients have to realize that even one flea can induce clinical signs on an allergic animal.

So, it is necessary to eliminate ALL fleas in the environment!

For success it is important to treat the house, treat the yard and treat all animals in the household.

Always use a combination of an adulticide chemical (to kill existing fleas) and an insect growth regulator (to interrupt the life cycle thus preventing a continuous new crop of adults).

Flea control must be individualized to each client to an extent.

Provide treatment to control secondary problems such as pyoderma, seborrhea, or pyotraumatic dermatitis.

In many cases, brief courses of oral corticosteroids are used to suppress the allergic response and provide immediate comfort.

Hyposensitization therapy using flea extracts have been unsuccessful to date.

Client compliance is critical, so be sure to educate your client well!

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References

1. Scott, Miller, Griffin. Small Animal Dermatology. In: Immunologic Skin Diseases. W. B. Saunders, Philadelphia, PA, 1995, p 536 – 542.

2. Reedy LM, Miller WH. Allergic Skin Diseases of Dogs and Cats. W.B. Saunders, Philadelphia, 1997, p 202 – 225.

Learning Objectives

1. Describe the life cycle and living habits of the flea, and how this influences flea control methods.

2. Define the pathogenesis of flea allergy dermatitis.

3. What are the clinical signs of flea allergy in dogs and cats, and how is it treated?

4. List the general principles of flea control.

5. Define the specific chemicals that are contained in flea control products, the mechanism of action of each, and the possible role of each in a flea control program.

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Allergic Skin DiseasesContact Allergy – Small and Large Animals

A. General Considerations:

1. Contact hypersensitivity is rare in domestic animals.

2. Haircoat provides protection from offending substances.

3. Rarely the sensitizing substance is something new in the animal’s environment.

4. Moisture is an important predisposing factor because it decreases the effectiveness of the normal skin barrier and increases the intimacy of contact between the agent and the skin surface.

5. It seems that animals are inherently “resistant” to allergic contact dermatitis.

6. It is also possible that this condition is underdiagnosed because of the difficulties in performing an accurate diagnostic test.

Important Facts

Contact dermatitis is uncommon in domestic animals.

In rare cases the offending substance is something new in the animal’s environment.

B. Pathogenesis:

1. A Type IV (delayed, cell mediated) hypersensitivity reaction, usually to a simple chemical.

2. The chemical is usually a hapten, which becomes a complete antigen upon union with epidermal protein or Langerhans cell.

3. Prior sensitization is required.

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4. After sensitized, reaction time (period of time between exposure to the antigen and onset of clinical signs) is 12 to 72 hours.

5. Potential allergens for dogs and cats include :

a. Grass and plant oleoresins, polishes, waxes, cleansing agents, dyes and other chemicals used in carpets.

b. Flea collars, rubber of vinyl mats, plastic food bowls were often incriminated in the past, but the incriminated chemicals have been taken out of these plastics so this is rare nowadays.

c. Most common allergens are medications! Neomycin (topicals and otic products) and others.

d. Pine needles, cedar chips, deck stains, concrete have also been incriminated.

6. Potential allergens for large animals :

a. The most commonly incriminated contact sensitizers in horses include pasture plants, bedding, soaps, insect repellents, topical medications, and tack items (dyes and preservatives).

Important Facts

Contact allergy is a Type IV (delayed, cell mediated) hypersensitivity usually to a simple chemical.

Common allergens for dogs and cats include: medications, grass and plant oleoresins, polishes, waxes, cleansing agents, dyes and other chemicals used in carpets.

Common allergens for large animals include: pasture plants, bedding, soaps, insect repellents, topical medications, and tack items (dyes and preservatives).

C. Clinical Signs:

1. Small Animals:

a. Mild to moderate pruritus – not as intense as the lesions might suggest.

b. Areas involved:

1. “Contact areas”.

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2. Hairless parts of the body are often involved: ventral abdomen, scrotum, volar aspect of the feet, axilla, groin, and brisket area. This distribution can mimic atopic dermatitis and food allergy. However, primary lesions are not or, are rarely seen with these conditions.

3. Internal aspect of the pinna usually from topical medications.

c. What are the lesions?

1. Primary papular eruption.

2. Secondary changes from self-trauma: crusting, lichenification, and hyperpigmentation.

3. Secondary pyoderma.

2. Large Animals:

a. Contact hypersensitivity has been reported to occur more often in horses than other large animal species.

b. Pruritus is variable.

c. The area of the body affected often suggests the contactant:

1. Face, ears, and neck: insect repellents and sprays.

2. Muzzle and extremities: pasture and bedding.

3. Face and trunk: tack.

d. Because of the horse’s ability to sweat profusely, contactants have access to the skin even in heavily haired areas.

e. What are the lesions?

1. Acute lesions: erythema, exudation, papules or vesicles.

2. Chronic lesions: alopecia, lichenification, hyperpigmentation.

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Important Facts

Pruritus is always present but, its intensity can be variable.

Primary lesions such as papules and/or vesicles initially develop on contact areas.

In dogs and cats hairless parts of the body are commonly affected.

However, because of the horse’s ability to sweat profusely, contactants have access to the skin even in heavily haired areas in this species.

D. Diagnosis:

1. Clinical signs are suggestive (contact areas involved).

2. Detailed history is extremely important. Remember! Most allergies occur to substances that are not new in the environment.

3. Rule out other causes for a ventrally distributed papular eruption. Major differential diagnosis include food allergy, scabies, pyoderma and atopy.

4. Biopsy is not useful unless done within 12 hours of exposure: changes are too nonspecific.

5. Isolation and provocative testing – most practical.

a. Change environment for 7 to 10 days (board, hospitalize, etc) and observe signs abate.

b. Re-expose to original environment and see signs worsen after 48 to 72 hours.

c. Isolation and provocative test is time-consuming, requires a patient, dedicated owner, and frequently is impossible to undertake.

d. Additionally, isolation and provocative testing does not differ between

allergy and irritant contact dermatitis.

6. The patch test is the only test for documenting contact hypersensitivity.

a. Potential allergens must be held in close contact with a shaved area for 48 hours.

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b. It is difficult to perform in animals but it can be done on a referral basis.

Important Facts

History and clinical signs may be highly suggestive.

A positive isolation and provocative testing will only indicate that the animal developed either an allergy or irritant dermatitis to a substance present on the animal’s environment (it won’t differentiate between an allergic or irritant reaction).

The patch test is the only test for documenting contact allergy, but it can be very difficult to perform.

E. Treatment:

1. Avoidance is the ideal mode of therapy.

2. Topical or systemic corticosteroids, temporarily.

3. Pentoxifylline (Trental) has been recently reported to be effective in the treatment of contact dermatitis in dogs (it does have an antiinflammatory effect). This medication can be toxic for cats.

Important Facts

Avoidance is the best treatment for contact allergy.

Topical or systemic corticosteroids can be used, temporarily, to relieve signs.

Pentoxifylline can be a treatment option for dogs.

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References

1. Scott, Miller, Griffin. Small Animal Dermatology. In: Immunologic Skin Diseases. W. B. Saunders, Philadelphia, PA, 1995, p 523 – 528.

2. Reedy LM, Miller WH. Allergic Skin Diseases of Dogs and Cats. W.B. Saunders, Philadelphia, 1997, p 189 – 201.

3. Scott, DW. Large Animal Dermatology. In: Immunologic Diseases. W.B. Saunders, Philadelphia, PA, 1988, p 300 – 301.

Learning Objectives

1. List the pathogenesis of contact allergy.

2. Describe the clinical signs of contact allergy and the potential sensitizing substances for small and large animals.

3. How do you diagnose and treat contact allergy?

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Allergic Skin DiseasesInsect Hypersensitivity – Horses

A. General Considerations:

1. Insect hypersensitivity is the most common cause of equine pruritus.

2. It is a seasonal, highly pruritic dermatosis caused by the salivary antigens of biting insects.

3. Although insect hypersensitivity is defined as a seasonal condition, in warmer climates it can be a year-round problem.

4. There is evidence that a hereditary predisposition to develop the hypersensitivity occurs.

5. The condition seems to worsen with age.

6. In the horse, the greatest loss caused by insect hypersensitivity dermatitis is an aesthetic rather than economic value. There are monetary losses to show or performance animals that can not function as a result of their dermatitis.

Important Facts

Insect hypersensitivity is the most common cause of pruritus in horses.

It is usually a seasonal problem but, it can be year round in warmer places.

The disease is a recurrent one and it becomes progressively worse with age.

The predisposition to develop hypersensitivity to insect bites is hereditary.

B. Cause:

1. The insects most frequently involved are: Culicoides spp, Simulium spp., Haematobia irritans, and Stomoxys calcitrans.

2. Occasionally, hypersensitivity can be seen with other parasites of the horse, including mosquitoes, horse flies, and Onchocerca cervicalis.

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C. Pathogenesis:

1. Insect hypersensitivity is classically thought as a Type I hypersensitivity, which is mediated by IgE antibodies.

2. The ability to respond to antigens by the production of IgE is largely inherited.

3. Type IV (delayed, cell mediated) hypersensitivity may also play a role.

Important Facts

It is primarily a Type I (immediate, IgE mediated) hypersensitivity. However, a Type IV (delayed, cell mediated) may also play a role.

D. Clinical Signs:

1. Since the disease is allergic in nature, its occurrence is sporadic, i.e. usually only one animal out of a stable or pasture will be affected.

2. The disease is rare or nonexistent in horses under one year of age.

3. There is no apparent breed or sex predilection.

4. Most insect hypersensitivities are of a seasonal nature (first appearing in the spring, worse in the summer,and regressing in the fall).

5. The condition is a recurrent one and with each succeeding year the signs become more severe and the season gets longer.

6. The seasonality directly corresponds to the activity levels of the ectoparasites.

7. In northern climates where there is a marked difference in ambient temperature, the “allergy season” is distinct.

8. In southern climates where there is not a distinct cold winter, the flies and therefore the hypersensitivity dermatitis are present year round.

9. The lesions result from the severity of the pruritus and include excoriations, alopecia, lichenification, pigment disturbances, a “rat tail” and a “buzzed off” mane.

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10. The distribution of lesions can vary as follows:

a. “Classic” dermatitis occurs on the dorsal surface of the animal (base of the tail, rump, back, withers, crest, poll and ears).

b. Ventral distribution: legs, groin, axillac, intermandibular space, ventralthorax and ventral abdomen.

c. Combination: features of dorsal and ventral surface.

d. Generalized disease.

e. In some cases the lesions are pretty well delimited to the mane and withers region.

11. Kicking at flies or running off can lead to injury to horse and owner.

12. Horses and mules can lose up to 10 to 15% of their body weight during an outbreak of stable flies.

Important Facts

The condition is rare or non existent in horses less than one year of age.

It typically affects one animal out of a stable or pasture supporting its allergic nature.

The lesions result from the severity of the pruritus and include excoriations, alopecia, lichenification, pigment disturbances, a “rat tail” and a “buzzed off” mane.

Base of the tail, rump, back, withers, crest, poll and ears are classically affected. However, ventral distribution with or without involvement of the mane and tail can also be seen.

Lesions can be generalized.

E. Diagnosis:

1. History and clinical signs are very characteristic.

2. Intradermal skin testing is helpful to identify what the animal is specifically allergic. Reactions should, ideally, be read at 30 minutes and 4 hours after the test.

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3. It has been suggested that high concentrations of black fly antigen may be a primary irritant in the horse.

4. Skin biopsies can also be a useful diagnostic aid.

5. Histopathology most often demonstrates a superficial and deep perivascular dermatitis with eosinophils and mononuclear cells. This pattern is suggestive of insect hypersensitivity but not diagnostic for it.

6. Differential diagnosis for tail rubbing include: food allergies, tail pyoderma, pinworms, lice or mange, vice and drug eruption.

Important Facts

Diagnosis of insect hypersensitivity is usually based on history, clinical findings, biopsy results and intradermal skin testing.

F. Treatment:

1. The primary objective in treating insect hypersensitivity dermatitis is avoidance of exposure to insects.

2. Reduction of exposure can be attempted in a few ways:

a. Application of residual insecticides (must be used frequently and religiously): Pyrethroids, Avon-Skin-So-Soft.

b. Stabling during peak feeding times of the insects: e.g.: from dusk till dawn (the feeding hours for Culicoides spp.).

c. Elimination of larval development areas: compost, standing water, understory of brush).

d. Separation of cattle and equids.

3. When avoidance is not practical or the offending agent is not known, antihistamines and/or systemic glucocorticoid therapy can be instituted.

4. Antihistamine: Hydroxyzine at the dose of 200 to 400 mg orally BID.

5. Glucocorticoid: Prednisone or prednisolone at the dose of 1 mg/kg orally and daily should be given until pruritus and secondary self trauma are controlled,

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then the dosage should be tapered to the least amount that will control the disease when given every other day.

6. Hyposensitization is indicated when avoidance of the allergen is impossible and systemic glucocorticoid therapy is contraindicated.

7. Horses with hypersensitivity to either mosquitoes or the black fly only have responded favorably to hyposensitization.

8. Hyposensitization to Culicoides hypersensitivity has been ineffective (however, the value of hyposensitization for Culicoides hypersensitivity should not be ruled out – reported cases have been treated for only 5 to 6 months, and a minimum of one year should be tried before considering failure).

9. If the horse does not show any response after 12 months of treatment, hyposensitization will probably not work.

10. It is important to know that at the present time, Culicoides antigen is not commercially available; however, Greer Laboratories may have one available in the near future.

Important Facts

The primary objective in treating insect hypersensitivity dermatitis is avoidance of exposure to insects.

When avoidance is not practical or the offending agent is not known, antihistamines and/or systemic glucocorticoid therapy can be instituted.

Hyposensitization is indicated when avoidance of the allergen is impossible and systemic glucocorticoid therapy is contraindicated.

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References

1. Scott, DW. Large Animal Dermatology. In: Immunologic Diseases. W.B. Saunders, Philadelphia, PA, 1988, p 300 – 301.

2. Fadok, V.A. The Veterinary Clinics of North America. In: Parasitic Dermatoses that Cause Pruritus in Horses. W.B. Saunders, Philadelphia, PA, 1995, p 11 – 28.

Learning Objectives

1. Define the pathogenesis of insect hypersensitivity in horses.

2. List the insects most commonly involved in equine insect hypersensitivity.

3. Describe the classical history and clinical signs associated with insect hypersensitivity in horses.

4. List the limitations of the skin biopsy and intradermal skin testing as diagnostic tools in the diagnosis of insect hypersensitivity.

5. Define the measurements involved in controlling flies.

6. How would you use and when would you use antihistamines and glucocorticoids to manage this condition?

7. Identify the odds of using hyposensitization therapy to manage these cases.

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Allergic Skin DiseasesUrticaria – Small and Large Animals

A. General Considerations:

1. Urticaria is a variably pruritic, edematous skin disorder.

2. It is often, although not always, associated with a Type I (immediate, IgE mediated) hypersensitivity but, it can also be nonimmunologic in nature.

3. Urticaria can occur in any species, but it is most commonly seen in horses and dogs.

Important Facts

Urticaria can occur in any species but, it is most commonly seen is horses and dogs.

B. Cause and Pathogenesis:

1. Immunologic mechanisms involved in the pathogenesis of urticaria include a Type I (most common) and Type III hypersensitivity reactions.

2. Nonimmunologic factors that may precipitate or intensify urticarial reaction are cold, heat, sunlight, exercise, stress, genetic influences and various drugs and chemicals (e.g. aspirin, narcotics, foods, food additives).

3. Factors reported to have caused urticaria are various:

a. Drugs: antibiotics; phenothiazines (thibendazole, acepromazine); local anesthetics; nonsteroidal anti-inflammatory drugs (phenylbutazone).

b. Some are feed related (grain, hay, or chemical additives).

c. Some are inhalant – allergen related (pollen, grain dust, etc.).

d. Some are envenomation – related (snake or insect bites).

e. Some are plant – related (nettle, buttercup).

f. Some are vaccine – related.

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Important Facts

Urticaria can result from immunologic (most common) and nonimmunologic stimuli.

Immunologic cases are often associated with a Type I hypersensitivity reaction.

Nonimmunologic factors that may precipitate or intensify urticarial reaction are cold, heat, sunlight, exercise, stress, genetic influences and various drugs and chemicals (e.g. aspirin, narcotics, foods, food additives).

Urticaria can be caused by drugs, foods, inhalant allergens, snake or insect bites, plants and vaccines.

C. Clinical Signs:

1. Clinical signs are similar in all species and will be discussed together.

2. In general, no age, breed or sex predilections have been reported for urticaria.

3. Reactions are characterized by localized or generalized wheals, which usually do not exhibit serum leakage or hemorrhage.

4. Characteristically, the wheals are evanescent lesions, with each lesion persisting less than 24 hours.

5. Urticarial lesions may occasionally assume bizarre patterns (serpentiginous, linear, arciform, annular, papular). Hair may appear raised in these areas.

6. Pruritus may or may not be present.

Important Facts

No age, sex or breed predilections have been reported.

Reactions are characterized by localized or generalized wheals, which usually do not exhibit serum leakage or hemorrhage.

Urticarial lesions may occasionally assume bizarre patterns (serpentiginous, linear, arciform, annular, papular). Hair may appear raised in these areas.

Pruritus may or may not be present.

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D. Diagnosis:

1. Diagnosis is made on the basis of history and typical clinical findings.

2. The difficult part is finding the substance responsible. You may only have 50% chance in doing so.

3. Take a careful drug history.

4. Hypoallergenic diet trial for 8 to 10 weeks, then challenge with the original diet.

5. Intradermal skin testing for inhalant allergens may be indicated in some cases.

Important Facts

Diagnosis is based on a careful history and clinical signs.

It may be very difficult to find the substance responsible.

E. Treatment:

1. Elimination and avoidance of known etiologic factors, if possible.

2. Symptomatic treatment with systemic glucocorticoids.

a. Large animals – 0.1 mg/kg dexamethasone, IV or IM, or 1 mg/kg predinosone or prednisolone, IV or IM.

b. Small animals – prednisone or prednisolone at 2 mg/kg PO, IM or IV.

3. Antihistamines are usually used to prevent future reactions.

4. Epinephrine may be lifesaving in severe angioedematous reactions.

a. Large animals: 3 to 5 ml of a 1:100 solution, SQ or IM.

b. Small animals: 0.1 to 0.5 ml of a 1:1000 solution SQ or IM.

5. Drug – related urticarias usually respond poorly to steroids and can persist for several months after the last administration of the drug (though most do not).

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Important Facts

Elimination and avoidance of known etiologic factors, if possible.

Symptomatic therapy with glucocorticoids and antihistamines.

Epinephrine may be lifesaving in severe angioedematous reactions.

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References

1. Scott, DW. Large Animal Dermatology. In: Immunologic Diseases. W.B. Saunders, Philadelphia, PA, 1988, p 292 – 294.

2. Scott, Miller, Griffin. Small Animal Dermatology. In: Immunologic Skin Diseases. W. B. Saunders, Philadelphia, PA, 1995, p 497 – 500.

Learning Objectives

1. Can urticaria be precipitated by immunologic and nonimmunologic factors?

2. Identify the types of hypersensitivity involved in the immunologically induced urticaria.

3. What are the causes and various factors that precipitate and/or aggravate urticaria?

4. Define the clinical manifestation of urticaria.

5. Describe how you would diagnose and treat cases of urticaria.

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