Differential diagnoses for the itchy and scratchy (Proceedings)


Pruritus is the sensation to lick, itch, scratch or chew.

I. Introduction

Pruritus is the sensation to lick itch scratch or chew. The most common causes for pruritus in small animal medicine are ectoparasites and allergies. Very rarely do infections from fungus and bacteria cause pruritus. Each of the different causes for pruritus has different clinical presentations. It is important to be familiar with the various clinical presentations and diagnostic tests that are useful for determining a definitive diagnosis so that the animal can be appropriately treated.

II. Common Ectoparasites That Cause Pruritus

A. Sarcoptic Mange (canine scabies)

1. Etiology and Pathogenesis

a. Sarcoptes scabiei var. canis

b. Mites burrow into the stratum corneum

c. Females lay eggs in burrows

d. Life cycle takes about 21 days

e. Mites can live off of the host and can be a source of reinfestation

f. Considered to be host specific, but can affect other species including human beings, cats, and foxes.

g. A hypersensitivity reaction may develop to the mites or their by-products

2. Historical findings

a. Common in young and old animals (immune systems probably compromised). Animals at any age may develop scabies but it is more common in ones that are on corticosteroids, stressed or their immune system is suppressed.

b. Other animals within the household or human beings may be affected. It is possible for one dog in a household has scabies and the other dog in the same household does not have scabies.

c. Non-seasonal from the onset

d. Marginal response to anti-inflammatory corticosteroids

3. Clinical findings

a. INTENSE pruritus (non-seasonal). These dogs are so itchy that they usually keep the owners up at night with their itching.

b. The classic presentation is ears (especially the margins), elbows and hocks, ventral abdomen, chest and proximal limbs. One or more of these locations may be affected.

c. Papules, pustules, excoriations, crusts, scale, and alopecia in any combination may occur

d. Chronic cases may develop lichenification with hyperpigmentation

e. Pinnal-pedal reflex is present in many of these cases (about 90%)

f. Peripheral lymphadenopathy may be present

4. Differential diagnosis of sarcoptic mange

a. Food allergy

b. Non-seasonal atopy

c. Allergic contact or irritant contact dermatitis

d. Dermatophytosis

e. Pyoderma

f. Other parasitic causes: Pelodera strongyloides, hookworm dermatitis, demodicosis (much less pruritic though)

5. Diagnosis

a. Multiple (Multiple!) superficial skin scrapings. Collect keratin debris over large areas, shave hair if necessary. Always scrape ear margins, elbows, hocks, sternum and papules. The mites are difficult to find on skin scrapings (only about 30% of the time do you find an egg or mite). One egg or mite is diagnostic.

b. Positive pinnal-pedal reflex (90% of the cases). This procedure involves firmly rubbing the edge of the ear with your thumb and index finger. The rear leg on the same side that you are rubbing on will scratch the dog's ventrum. Be careful, dogs with inflamed or chronic ear infections may also give you a positive pinnal-pedal reflex (false positive).

c. Distribution pattern of pruritus (ear margins, elbows, entire ventrum, hocks)

d. Involvement of other animals

e. History of possible exposure

f. Intensity of pruritus (itchy). Very few dermatologic infections cause a dog to itch and scratch in the exam room. If this occurs, then scabies should be on your differential diagnoses list. The only other dermatologic problem that cause dogs to be intensely pruritic in the exam room are severely flea allergic dogs. If you think it might be scabies, you are justified in making a tentative diagnosis based on index of suspicion and response to therapy.

6. Treatment

a. Treat all contact animals and refer humans to a dermatologist if they are affected.

b. Parasiticidal dips

a. Organophosphate dips (Paramite® ) once weekly for 4-6 weeks. Resistance is common and this product is not recommended.

b. Lime Sulfur dips (LymDyp® ) once weekly for 4-6 weeks. Safe for puppies or debilitated animals. This treatment has the added advantage of being anti-pruritic. The main disadvantage is smell and that it will stain white hair coated animals yellow. Also, this dip will stain jewelry so the pet owner should wear gloves if doing these dips themselves.

c. Amitraz (Mitaban® ) mixed at bottle dosage, once every 2 week s for 3-4 treatments. This product is not approved as a scabicidal agent and should not be used on dogs less than 12 weeks old.

c. Topical products that are not dips

a. Selamectin (Revolution® ) every 2 to 4 weeks. This is a topical flea control product similar to Advantage or Frontline. The hair is parted and the contents of the vial are applied to the skin. The active ingredient, selamectin, is absorbed into the bloodstream.

d. Systemic products

a. Ivermectin (Ivomec 1%® ), 200-300 µg/kg subcutaneously, every 14 days for 2 to 3 treatments. This product is not approved for use in dogs or cats but it has been used in veterinary medicine for many years. Ivermectin has been approved for treatment of scabies in people. It is contraindicated for Collie, Sheltie, Border Collie, Australian Shepherd, or Old English Sheepdog breeds. It should not be used for dogs less than 12 weeks of age. Potential side effects of this treatment include: dilated pupils, walking into walls (acting blind), ataxia, and coma. Although these side effects are uncommon, the owners need to be aware this medication is associated with neurologic signs when it is administered at this dosage.

e. Treat secondary pyoderma or seborrhea

f. The dogs will usually get more pruritic 1 week after treating scabies. Benadryl (diphenhydramine) at a dosage of 2.2 mg/kg TID, PO may be required to make the dog less itchy and/or to sedate the dog.

g. Dispose of bedding, thoroughly vacuum environment and dispose of the bag. Environmental treatment with organophosphates or environmental flea control products may be needed in cases of severe infestation.

B. Notoedric Mange (feline scabies)

1. Etiology and Pathogenesis

a. Notoedres cati

b. Life cycle similar to sarcoptes

c. Host specific but may affect human beings, foxes, rabbits, dogs.

d. Few endemic areas within the U.S.A. (Baltimore, Hawaii, Corpus Christi, San Antonio)

2. Historical findings

a. Similar to sarcoptes

3. Clinical findings

a. Intense pruritus of the head, neck and ear regions, rarely feet or perineum.

b. Severe crusting with alopecia, excoriations, and lichenification

c. Peripheral lymphadenopathy may be present

d. Secondary infection may be present

4. Differential diagnosis

e. Dermatophytosis

f. Food allergy

g. Atopy

h. Flea allergy

i. Ear mites (Otodectes)

j. Pemphigus foliaceus

5. Diagnosis

a. Multiple superficial skin scrapings. Many mites are usually identified.

Involvement of other members of the household

b. Distribution pattern of lesions

6. Treatment

k. Treat all contact animals

l. Bathe to remove crusting using a sulfur based shampoo. Sedation may be indicated.

m. Parasiticidal dips

i. Lime Sulfur (LymDyp® ) once weekly for 4-6 weeks. Do not allow the cat to groom while the dip is wet.

ii. Amitraz (Mitaban® ) used at ( strength every 2 weeks until remission. This product is not approved and toxicity studies indicating safety or efficacy have not been performed. I do not routinely recommend this product for cats.

d. Ivermectin (Ivomec1%® ) 200-300 µg/kg subcutaneously, every 14 days for 3 treatments. This product is not approved for use in cats. Fatal toxicity has been noted with the above dosages, so caution is indicated. Also, do not use on kittens less than 12 weeks of age.

i. Treat secondary skin infections. Secondary dermatophytosis may be present as well.

ii. Prednisolone 1mg/lb once daily (orally) for 2-3 days may be needed to reduce severe pruritus.

iii. Environmental control may be needed.

C. Feline Demodicosis

1. Etiology and Pathogenesis

a. Several different kinds of demodex infest the cat (Demodex cati, Demodex gatoi and undescribed Demodex sp). Only one species Demodex gatoi is consistently known to be pruritic.

b. Demodex gaoti is the only contagious form of demodex.

c. Food allergy has also been seen in association Demodex gaoti.

2. Historical findings

a. Alopecia which is mostly commonly non-pruritic but may be pruritic (see comments about Demodex gatoi). Demodex may be seen in any breed of cat but appears to be more common in purebred Siamese and Burmese cats.

b. Demodex cati most commonly is associated with an underlying medical condition (ie diabetes mellitus, feline leukemia virus infection, feline immunodeficiency virus infection, lupus erythematosus, hyperadrenocorticism, or cancer (ie squamous cell carcinoma in situ). In some cases, no underlying cause can be found.

c. Demodex gatoi has been found to be potentially contagious to other cats. In some cats, the presence of Demodex gatoi has also been noted with an underlying food allergy.

3. Physical examination

a. Skin lesions may occur anywhere on the body. Some reports suggest that skin lesions most commonly occur on the head. However, others have reported skin lesions on the neck, trunk and limbs. The alopecia may be focal or multifocal. Generalized demodicosis in cats is rare. Other types of skin lesions that may be present include: macules, scaling, erythema, hyperpigmentation, and crusting.

b. Alopecia is the most common skin lesion present. Other types of skin lesions that can occur include: macules, scaling, erythema, hyperpigmentation and crusting. One or more of these types of skin lesions may be present.

4. Differential diagnoses

a. Bacterial skin infection

b. Dermatophytosis

c. Notoedres (if pruritic and lesions are on the face)

d. Psychogenic alopecia

e. Flea allergy

f. Food allergy

g. Atopy

h. Contact allergy

5. Diagnosis

a. Skin scraping is the only way to rule out feline demodex. Demodex cati looks similar to the canine demodex mite whereas the other two mites are short and blunted. The unnamed demodex mite looks similar to the Demodex gatoi but is larger and posses other anatomical differences.

b. Other underlying conditions (see above in the historical section) need to be ruled in or out depending on which species of demodex is present.

6. Treatment

a. Lime sulur dip (Lym dyp® ) is the preferred treatment for feline demodex. This treatment does NOT work for canine demodex. It is thought that one of the reasons that this dip works in cats is that the mite is more superficial in location than it is in dogs. This dip is used weekly for 4 to 6 weeks.

b. Amitraz (Mitaban® ) dips at concentrations of 125 to 250 ppm have been used but many have had problems with SIDE EFFECTS. I do NOT recommend using amitraz in cats.

D. Flea Allergy Dermatitis (FAD)

1. Definition: A hypersensitivity disorder of animals sensitized to allergens in flea saliva

a. Etiology and Pathogenesis

i. Type I hypersensitivity (immediate)

1. Reactions occur 15-30 minutes post exposure

2. Proteins in flea saliva are antigenic by themselves

3. Predominantly IgE mediated

ii. Type IV hypersensitivity (delayed)

1. Reactions occur 24-48 hours post exposure

2. Haptens in flea saliva combine with dermal collagen to form a complete antigen.

iii. Late phase IgE reaction and cutaneous basophil reaction

1. Reactions occur 15-48 hours post exposure

2. Only reported in dogs

iv. Histamine like compounds and enzymes that are proteolytic, anticoagulant, and cytolytic. These substances are pruritogenic and cause local irritation and inflammation.

v. One flea bite every 10-14 days may be sufficient to keep an allergic patient symptomatic.

b. Historical findings

i. Age of onset is usually less than 3 years of age but may occur at any age depending on flea exposure.

ii. One or few animals within the household may be affected.

iii. Exposure to fleas and inadequate flea control are sometimes more important than the presence of fleas.

iv. Usually there is a history of warm weather seasonal pruritus but can present as non seasonal pruritus in some environments. Reduced humidity is the limiting factor in flea survival.

v. Dogs with atopy are predisposed to development of flea allergy.

b. Clinical Findings (Dogs)

i. Chief complaint is pruritus of the posterior 1/3 of the body including tail head, rump, caudal thighs, inguinal, abdominal, and dorsal lumbar regions.

ii. The primary lesion is the papule

iii. Secondary excoriations, crusts, superficial moist dermatitis (hot spots) and alopecia may be present. With chronicity, lichenification and hyperpigmentation can occur.

iv. Secondary pyoderma of the inguinal and abdominal region is common.

v. The intensity of pruritus is second only to sarcoptic mange

vi. Clinical manifestations depend on the host reactivity to the flea saliva. Therefore, the flea burden does not always correlate with the severity of symptoms.

vii. Severe self mutilation may result in a classic alopecic wedge along the dorsal lumbar region.

c. Clinical Findings (Cats)

i. Chief complaint can be trauma induced alopecia due to overzealous grooming or the presence of erythematous papular eruptions (miliary dermatitis).

ii. Pruritus is localized to the posterior 1/3 of the body, and/or the head and neck regions.

iii. Cats may present with alopecia and no skin lesions

iv. Cats may present with eosinophilic plaques, recurrent indolent ulcers, miliary lesions, bilaterally symmetrical alopecia, facial pruritus or erratic behavior.

d. Differential Diagnoses

i. Atopy

ii. Food allergy

iii. Sarcoptic mange and Notoedric mange

iv. Allergic contact or irritant contact dermatitis

v. Dermatophytosis

vi. Pyoderma

e. Diagnosis

i. Based on distribution pattern of pruritus and the presence or absence of fleas. It is essential that other differential diagnoses are ruled out.

ii. A positive flea antigen intradermal skin test

iii. The presence of Dipylidium segments within the feces indicates exposure to fleas when they are not readily visible. Dead fleas may also be identified.

f. Treatment: Effective treatment of flea allergy involves strict flea avoidance for the rest of the pet's life. It is essential that our clients understand the flea life cycle for extermination to be successful.

i. Environment

1. The most important target area because >90% of fleas are not on the patient.

2. Vacuum all floor surfaces including tile and hardwood and dispose of the bag. Resist the temptation to place moth balls or flea collars in the bag as human safety has not been evaluated.

a. Removes some eggs and flea feces

b. Stimulates pre-emergent adults to hatch

3. Wash all bedding, rugs, etc., that the animals have contact with. Steam cleaning may be helpful but do not be overconfident in its efficacy.

4. Premise treatment--must treat the entire house.

a. Hand spray cracks and baseboards and areas that the animals spend the most time visiting.

b. Spray appropriate floor surfaces following application guidelines.

c. If foggers are selected, one per room is needed. Remember that they do not get under furniture very well.

d. Take precautions with fish tanks and pet birds

5. Outside environment

a. Only shaded and protected areas need to be treated.

b. Use only approved products and follow strict application guidelines.

c. Depending on the weather, every 30 day treatment should be sufficient.

6. Professional exterminators may be more cost effective.

a. Find a good one by asking important questions

b. Must treat specifically for fleas, both adult and pre-adult stages

c. Must guarantee work for at least 2 months

d. Will retreat for free if even one flea is found

e. The TAMU dermatology service strongly recommends professional extermination for flea allergic patients.

ii. Patient-- treat all contact dogs and cats

1. Flea shampoos

a. Not recommended for flea allergic patients due to limited residual effect.

b. Helpful to remove flea dirt, reduce some of the flea burden, and to provide relief of pruritus (oatmeal based shampoos).

2. Flea dips (not used as much anymore, better products available)

a. Provide fast and complete adult control for a short time

b. Excessive usage may be toxic with some products

c. Some products are drying and irritating with continuous usage.

d. Organophosphate dips are NOT appropriate for cats

3. Flea collars

a. Ineffective in reducing a flea burden

b. New products containing insect growth regulators function to prevent eggs from becoming viable and may be helpful (ie Knock out collar by Virbac, this collar has pyriproxifen).

c. Ineffective for controlling flea allergic patients

4. Flea Powders (not used as much anymore)

a. Relatively safe and effective, but messy to use

b. Must be used frequently to be effective

c. Few side effects due to lack of percutaneous absorption. Also, it is poorly absorbed by the gut if ingested.

5. Flea Sprays

a. Pyrethrin or pyrethroid based, with an insect growth regulator (ie methoprene, pyriproxyfen) are very effective. Pyrethroid based sprays should NOT be used in CATS since they are toxic to cats. Examples of pyrethroid sprays would include: permethrin, allerthrin, fenvalearte, resmethrin, sumethrin. Side effects seen in cats are: vomiting, hypersalivation, muscle tremors, depression, seizures, anorexia, ataxia, and diarrhea.

b. Follow bottle instructions for application rates

c. Read precautions about age limits and species limits as some products are not suitable for cats.

d. Water based products may be helpful for pets that seem irritated by the application of flea sprays

e. Frequent application may be needed it the pet swims or is bathed frequently. An exception to this is the Frontline® spray which is an alcohol based spray with fiprinol. This drug gets into the sebaceous gland and gets re-released after swimming or bathing.

6. Systemic Chitin Inhibitors (Program® , Sentinnel® )

a. The active ingredient, lufenuron, prevents the development of eggs and larvae by inhibiting chitin formation.

b. Flea must feed to be effective and therefore not effective by itself for flea allergic patients.

c. Since mammals do not have chitin, this product is safe and effective for keeping infestation of the environment under control. Rare reports have linked lufenuron to the development of vasculitis.

d. One product combines the flea prevention with the heartworm preventative (Sentinnel® , lufenuron and milbemycin)

7. Systemic Adulticide Treatment (Capstar® )

(1) The active ingredient in this product is

Nitenpyram which is a neonicotinoid.

(2) This medication is an oral tablet that is given as a 1 time treatment to kill adult fleas on an animal (as quickly as 30 minutes after administration).

(3) The disadvantage of this product is that it lasts only 24 hours.

(4) This medication can be administered concurrently with other flea products but the dosage should not exceed more than 1 tablet of the appropriate dosage size more than every 24 hours.

h. Topical adulticides (Advantage® , Frontline® and Frontline Plus® , Revolution® )

Ease of application make these favorite with clients

a. Expensive, and may be washed off. In the case of Advantage® , the studies were not conducted with medicated shampoo. Instead they were conducted with a mild shampoo. The Frontline® should not be washed off if the bath does not occur within 48 hours of application.

b. Function as adulticides only and should be used in conjunction with a product that affects pre-adults. Frontline Plus® has methoprene whereas Frontline and Advantage do not. For better coverage of the flea cycle either Program® (lufenuron) or a Knock-out collar® (pyriproxifen, an insect growth regulator) should be used concurrently. Revolution® , selemectin, is an avermectin and it differs from Frontline® /Frontline Plus® and Advantage® in that is has been shown to be effective against adult and immature stages of the flea cycle (prevents eggs from hatching) and some endoparasites (heartworms in dogs and cats, ear mites in dogs and cats, scabies in dogs, ticks in dogs, hookworms and roundworms in cats). Selamectin is absorbed into the bloodstream after being applied to the skin. This differs from other two topical treatments in that they are supposed to diffuse across the skin to provide protection.

c. Side effects have been associated with both Advantage® and Frontline® products. In the case of Advantage® , irritation with or without hair loss and caustic burns with skin sloughing have been seen. These side effects appear to be more common in purebred cats. Oiliness at the site of application and hair loss has been associated with Frontline® product usage in both dogs and cats. Side effects have been reported with the selemectin but appear to be rare (less than 1% of the cases). Side effects for selamectin include: stiffening and clustering of hair at the site of application, GI signs, lethargy, salivation, tachypena, and muscle tremors. However, there is one report of a debilitated cat from a shelter dying after the application of selamectin. So, animals that are in debilitated state should not have selamectin applied to them topically.

i. Adulticide Residual Sprays (Frontline® spray)

d. Claimed to have 3 month effect but very few dogs have the product last this long. Monthly or bimonthly application is more reasonable.

e. This product gets into the sebaceous glands and is found on the skin and hair coat within 48 hours of application. Do not bathe the dog within 48 hours of application. This product moves across the skin through the sebaceous glands.

(3) Functions only as an adulticide

j. What doesn't work

f. Ivermectin

g. Brewer's yeast (this is actually used to help grow fleas in the laboratory)

h. Ultrasonic collars

i. Oral organophosphates

j. Hyposensitization without flea control

iii. Secondary complications

1. Canine pruritus

a. Oral prednisolone 0.25mg/lb given BID x 7, SID x 7, EOD x 14 days. Decrease dosage as symptoms subside.

b. Long acting injectable steroids (Depo Medrol® ) are not appropriate for FAD dogs due to unpredictable efficacy and uncontrollable side effects.

c. Even though most antihistamines do not typically work for flea allergy cases, I have had some owners that have reported that hydroxyzine (Atarax® ) is useful in controlling the pruritus in their flea allergic dogs.

2. Feline pruritus

a. Oral prednisolone 0.5mg/lb in decreasing dosage

b. Depo Medrol® 15-20mg/ cat subcutaneously can be very effective in severe cases.

3. Pyoderma

a. Appropriate antibiotic therapy for one week beyond achieving clinical remission.

b. Shampoo therapy twice weekly for the same duration as oral medications are given.

c. Atopy (inhalant allergic dermatitis, atopic dermatitis, allergic dermatitis)

a. Etiology and Pathogenesis

i. Ability of an individual to produce excessive amounts of IgE

ii. Sensitization occurs when a given allergen is inhaled, ingested or percutaneously absorbed, and a specific IgE is formed to that allergen and subsequently fixes to mast cells.

iii. Upon future challenge with that specific allergen, IgE molecules are bridged on the mast cell surface. This sends a signal for the mast cell to degranulate and release inflammatory mediators. This is a type I hypersensitivity reaction. Histamine is the most important mediator but proteolytic enzymes, kinins, ECF, etc. are also involved.

iv. May also involve a specific subclass of IgG (IgGd).

v. Atopic individuals have mast cells that degranulate more readily and the patient tends to have a greater sensitivity to histamine.

vi. Concurrent abnormalities in cell mediated immunity (CMI) can lead to decreased T-lymphocytes and neutrophils and macrophages.

vii. Recently, specific IgE receptors have been found on Langerhans cells to support the role of percutaneous absorption.

b. Historical Findings

i. Onset of clinical findings is usually between one and three years of age but may be as young as 6 months old or as old as 5 years old.

ii. Breed predisposition: all terriers, Dalmatians, Maltese, Lhasa Apso, English Bulldogs, Shar Pei, Golden Retriever. Any dog may develop atopy. Poodles have a decreased incidence.

iii. Sex predisposition: 2.5:1, females: males

iv. Usually presents as a seasonal problem but may develop into a non-seasonal problem. Clinical signs can also present as a non-seasonal problem from the onset.

c. Clinical Findings

i. Dog symptoms

1. The chief complaint is pruritus with erythema, often times without overt skin changes. It is an itch that rashes.

2. The distribution pattern of pruritus is: face (muzzle, periorbital region), feet, ears, axillae, proximal forelegs and occasionally the inguinal region. Any one region or combination of the above can occur for an individual.

3. Secondary complications include: alopecia, excoriations, superficial moist dermatitis, or salivary staining. With chronicity, lichenification and hyperpigmentation can occur.

4. Secondary pyoderma formation is common due to decreased lymphocyte function, self trauma, and increased bacteria adherence to atopic corneocytes.

5. Secondary otitis externa is common and recurrent otitis may be an important reason to look for underlying atopy.

6. Hyperhidrosis in 10% of cases (pseudo-sweating).

7. Intact females may exhibit irregular heat cycles.

8. Other findings can include: urticaria, conjunctivitis, rhinitis, asthma, diarrhea, and personality changes such as irritability.

ii. Feline symptoms

1. Pruritus of the face and neck predominantly, but may include the forelegs and abdomen.

2. Miliary dermatitis or eosinophilic granuloma can occur.

3. Cats may pluck hairs and resemble an endocrine form of alopecia clinically.

4. Although secondary pyoderma is uncommon in cats, bacterial overgrowth of excoriated regions may occur.

d. Differential Diagnoses

i. Food allergy

ii. Flea allergy

iii. Scabies

iv. Malassezia dermatitis

v. Allergic contact or irritant dermatitis

vi. Pelodera or hookworm dermatitis

e. Diagnosis

i. Historical findings including age, breed, sex, seasonality and a primary complaint of pruritus.

ii. Physical findings and distribution pattern of pruritus consistent with atopy.

iii. Allergy testing should be considered when:

1. The pruritic season is longer than 3 months of the year.

2. Poor response to symptomatic therapy other than steroids.

3. Secondary problems such as pyoderma and otitis are recurrent.

4. The owner elects a safer long term therapy.

iv. Intradermal allergy testing (IDAT)

1. Considered to be the gold standard of diagnostics.

2. Requires chemical restraint and clipping of the hair.

3. Requires consistent technique and fresh allergens selected specifically for a given area of the country.

4. Patients must be off of medications before testing can be performed

a. Oral prednisolone: minimum 30 days

b. Topical steroids of any type: minimum 30 days

c. Injectable steroids (Depo Medrol® , Vetalog® ): minimum 90 days

d. Antihistamines and fatty acids: minimum 7 days.

v. Serum allergy testing

1. Similar drug withdrawal times are recommended

2. Advantages include ease of testing, no chemical restraint or clipping of the haircoat, and readily availability of testing.

3. False positives are common and lack of standardization make this test less favorable.

4. Cost to the client is usually higher than comparable skin testing

5. My response to hyposensitization is better based on skin testing.

vi. Histopathology- superficial perivascular dermatitis with or without secondary changes. This will tell you there is an allergy present but not which allergy or allergies are present.

f. Treatment

i. Treat secondary complications such as seborrhea or pyoderma

ii. Avoidance of the offending allergen if possible.

iii. Antihistamines are sometimes helpful

1. Diphenhydramine (Benadryl® ) 1 mg/lb BID to TID

2. Hydroxyzine (Atarax® ) 1 mg/lb BID to TID

3. Chlorpheniramine (Chlortimetron® ) 0.25 mg/lb BID or 2 to 4 mg BID for cats, 4 mg BID for a dog less than 20 pounds, 8 mg BID for a dog 21 to 50 pounds and 12 mg BID for a dog greater than 50 pounds.

4. Clemastine (Tavist® ) 0.05 mg/lb BID

5. Trimeprazine with prednisolone (Temaril-P® ) use according to label directions.

iv. Corticosteroids if the condition is only short seasonal (<3months)

1. Prednisolone or prednisone 0.25 mg/lb given BID for 7 days, every 24 hours for 7 days, and then every other day for 7 days. Decrease the alternating day dosage to the lowest amount to control the pruritus.

2. Injectable corticosteroids (Vetalog® , Depo-Medrol® ) are rarely if ever indicated in treating atopic dogs because:

a. Uncertainty of the onset or duration of effect

b. Inability to control side effects if they occur

c. Excessive adrenal-pituitary suppression

v. Fatty Acid supplements

1. Supplements containing eicosapentanoic acid (EPA) found in cold water fish oils. May be synergistic if used with antihistamines.

2. The net effect is anti-inflammatory.

3. Effective in about 20% of cases

4. Many product brands are available and the concentrations of EPA are variable. I have had good results with Derm Caps® , EFA caps® , and 3V caps® .

5. Loose or soft stools are an uncommon but possible side effect.

vi. Hyposensitization (Immunotherapy or Allergy shots)

1. Many different theories of how it works including modification of the T-suppressor response.

2. Need compliant owners and cooperative patients because therapy is usually for life.

3. Effective in about 75% of cases in reducing pruritus and secondary complications. Improvement may take 6-12 months of therapy before seeing a positive response. Owners should commit for a minimum of one year. Some patients do not respond.

4. Significant allergens are selected from skin test results by comparing them to the seasonality.

5. Allergens are selected based on the patient's dermatologic history and strength of reaction. A maximum of 15 allergens can be put into one set of allergy vaccines.

6. Allergens are given in increasing concentrations with a maximum of 1 cc at 20,000 PNU's (Protein Nitrogen Units). Depending on the response, injections can be given every 21 days but no longer than 30 days. The shortest interval that the vaccine can be given every 7 days. Allergens are given subcutaneously year round regardless of seasonality.

7. Many protocols exist for allergen administration.

8. If the patient is extremely pruritic, adjunct therapy should be given concurrently with the allergens. Anti-inflammatory prednisolone will not affect antibody production.

vii. Topical therapy

1. Shampoos and conditioners

a. Moisturizing, hypoallergenic, pH balanced products can give marked temporary relief.

b. Cool water itself is antipruritic

c. Washing the feet after the patient is outdoors can help reduce the percutaneous absorption. Baby wipes can also be helpful.

2. Oatmeal based products

Shampoos, conditioners, rinses and sprays are very soothing and very safe to use daily.

Corticosteroids topical anesthetics (Pramoxine), antihistamines can be added for prolonged effects

3. Topical sprays containing any combination of the above active ingredients can be helpful for spot treatment.

d. Food Allergy

a. Etiology is a type I hypersensitivity predominantly but a type III and type IV reaction may also occur. Animals are predisposed to develop food allergy through undefined genetic factors.

b. Historical findings

i. No sex predisposition exists

ii. Breed predisposition may include Labrador retrievers, Shar Pei, English Springer Spaniels, Miniature Schnauzers, Cocker Spaniels, Collies, and Golden retrievers, but any dog may develop food allergy.

iii. Primary complaint is pruritus that is non-seasonal.

iv. Age of onset is usually less than 3 years but may occur later in life or at any age.

v. Problem persists regardless of the commercial brand of food fed because of the similarity of ingredients. Onset of symptoms is usually not associated with a recent dietary change. Many dogs with food allergies have been on the diet that they are allergic to for 2 or more years before showing clinical signs.

c. Clinical findings

i. Chief complaint is pruritus

1. Dog distribution includes the face, feet, forelegs, axilla, ears, and sometimes inguinal or perianal regions (or any combination)

2. Cat distribution includes the face and neck, especially the pre-aural region between the lateral canthus of the eye and the base of the pinna. Any type of eosinophillic granuloma or miliary dermatitis may also be present.

ii. Urticaria may be present (dogs)

iii. Concurrent GI symptoms are uncommon but can occur.

iv. Seizures are occasionally associated with food allergy

v. Secondary pyoderma or otitis is common in dogs.

d. Differential diagnoses

i. Non-seasonal atopy

ii. Scabies

iii. Flea allergy (non seasonal)

iv. Allergic contact dermatitis

v. Malassezia dermatitis or pruritic pyoderma

e. Diagnosis is only made on the response to a food trial elimination diet

i. A selected diet (preferably home cooked) that consists of a protein and carbohydrate source that the animal has not eaten for an appreciable length of time is fed. Nothing else passes the lips of our patient other than water. This includes flavored heartworm tablets or vitamins, toothpaste, chew toys, raw hides, etc.

ii. Rabbit, duck , venison, white fish, salmon, kangaroo are possible protein source options. These are usually combined with either potato or rice. Reports exist of cross reactivity between beef and venison exists. Therefore, in severely beef allergic animals this may not be the best protein to chose. Either commercial diets or home-cooked diets are used.

iii. Hydrolyzed diets have recently become available and are considered the Cadillac of the food trial diets. These diets use technology similar to that used in humans. Most common food allergens are proteins with a molecular weight of 18,000 to 36, 000 Daltons. The proteins in these diets are broken down into such a low molecular weight (less than 18,000 Daltons) so that the body no longer sees them as being foreign. Two of the more popular diets are: Purina HA (hydrolyzed soy) and Hill's ZD ultra (hydrolyzed chicken).

iv. The diet is fed for a minimum of 8 weeks or until clinical symptoms of pruritus have decreased significantly. Reports of successful food trials lasting 16 weeks have been documented.

v. In order for a diagnosis of food allergy to be confirmed, a food rechallenges needs to be performed. These involve feeding the old diet (including treats) to the dog or cat. Clinical symptoms return quickly (hours to less than one week) to confirm the cause and effect. Although not as common, some reports exist that some food allergic animals may take as long as 2 weeks for their clinical signs to recur after rechallenge.

vi. The elimination diet is then given until symptoms subside (usually 1 to 2 weeks). The hypoallergenic diet can be given for life or the dog or cat may be individually rechallenged to determine which food ingredient or ingredients are causing the allergies. A commercial diet can then be selected for long term maintenance based on these rechallenge results. Most animals are allergic to 1 or 2 food ingredients but they can be allergic to as many as 5 different food ingredients.

vii. It is very uncommon that a patient will develop new sensitivities to a selected diet once the diagnosis is made.

viii. Intradermal skin testing with food allergens have been shown to be very inaccurate, and are not recommended.

ix. Serum allergy testing for food allergens is also not recommended due to accuracy problems (many false positives).

f. Treatment involves not feeding the offending allergen

i. Secondary pyoderma and otitis must be treated

ii. Anti-inflammatory dosages of oral corticosteroids may provide temporary relief of pruritus, but not all respond.

iii. Many new commercial diets have improved the treatment options for food allergic patients. However, many dogs have been exposed to lamb and others and we are running out of novel protein sources for food elimination testing.

e. Contact allergy

a. Etiology

1. Contact allergies are a type IV hypersensitivity reaction which involves an allergic reaction with a molecule called a hapten. A hapten is a small chemically active, lipid soluble molecule that binds to a protein to become a complete antigen. The hapten protein complex binds to an immune presenting cell (Langerhan cell).

2. An afferent and efferent phase is involved. The afferent phase involves the initial exposure of the animal to the offending hapten and sensitization. The efferent phase occurs when the sensitized animal is re-exposed to the offending hapten and develops an allergic reaction as a result of this re-exposure.

3. About 20% of the atopic dogs will also have contact allergies.

B. Historical findings

1. No sex, age or breed predisposition exists. The development of the allergic reaction requires previous exposure in order for the reaction to occur (see etiology section).

2. The owner's may know of previous exposure to the sensitizing hapten.

3. Pruritus in the area that is affected is the primary complaint.

4. Substances reported to cause naturally occurring allergic contact dermatitis in in dogs and cats are: plants, medications, highly chlorinated water and home furnishings. The table below gives examples of each of these categories.

Table I: Contact allergens for dogs and cats

C. Clinical findings

1. The skin lesions that are most commonly present include: erythema and pruritus in the contact area. Excoriations from the pruritus and secondary yeast and/or bacterial infections may occur.

2. Lesions occur in areas that come in contact with the offending hapten. If the hapten is found on the ground then lesional areas would include the bottoms of all four feet, the entire ventrum, and ventral neck (possible but not always present). In the case of collars, the lesions make a circle around the neck. If the hapten is a medication then the skin lesions occur in the areas of the body where the medication was applied to the skin.

D. Differential diagnoses

1. Atopy

2. Food allergy

3. Flea allergy

4. Fungal skin infection

5. Bacterial skin infection

6. Pelodera infestation (lower legs and entire ventrum)

E. Diagnosis

1. The diagnosis may be straight forward depending on the history and areas of the body affected (ie ring of alopecia and erythema around the neck and the dog is wearing a flea collar or other type of collar). Pruritus is always a consistent finding.

2. Some dermatologist will bathe the dog in a hypoallergenic shampoo and board them in a stainless steel cage with newspapers for several weeks. If the lesions resolve then recur when brought back home then this is suggestive of an underlying contact allergy.

3. The only diagnostic test which definitively diagnoses contact allergy is the patch test. This involves shaving the hair on the lateral thorax, grinding up the offending allergen and placing it in a small area in the shaved area, applying a bandage in the shaved area and monitoring for the development of skin lesions underneath the ground up material within 24 to 48 hours. This is labor intensive and there is not set group of allergens to test. You have to try to deduce which allergen is causing the problem from the history and physical examination findings.

F. Treatment

1. Contact allergies are very steroid responsive. The only problem is that if the animal comes in contact with the offending hapten again then the lesions will redevelop.

2. Identify and remove the offending hapten from the environment or prevent the animal from coming into contact with it.

3. Bathes with a mild hypoallergenic shampoo may be useful for removing the offending haptens on the skin.

Recommended Readings

Carlotti DN, Jacobs DE. Therapy, control and prevention of flea allergy dermatitis in dogs

And prevention of flea allergy dermatitis in dogs and cats. Vet Dermatol. 2000;11:83-98.

Chesney CJ. Food hypersensitivity in the dog: a quantitative study. J Small Anim Pract.


Genchi C, Traldi G, Bianciardi P. Control of flea allergy dermatitis. Compend Cont Edu

Pract Vet. 2000;22:12-14.

Leistra MHG, Markwell PJ, Willemse T. Evaluation of selected-protein-source diets for management of

dogs with adverse food reactions to foods. J Am Vet Med Assoc. 2001;219:1411-1414.

Loeffler A, Lloyd DH, Bond R, Kim JY. Pfeiffer DU. Dietary trials with a commercial chicken hydrolysate

diet in 63 pruritic dogs. Vet Rec. 2004;154:519-522.

Olivry AT, Steffan J, Fisch RD, et al. European Veterinary Dermatology Cyclosporine Group.

Randomized controlled trial of the efficacy of cyclosporine in the treatment of atopic dermatitis in dogs. J

Am Vet Med Assoc. 2002;221:370-377.

Zur G, Ihrke PJ, White SD, Kass PH. Canine atopic dermatitis: a retrospective study of 266 cases

examined at the University of California, Davis, 1992-1998. Part I. Clinical features and allergy testing

results. Vet Dermatol. 2002;13:89-102.

Zur G, White SD, Ihrke PJ, Kass PH, Toebe N. Canine atopic dermatitis: a retrospective study of 169

cases examined at the University of California, Davis, 1992-1998. Part II. Response to hyposensitization.

Vet Dermatol. 2002:13:103-111.

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