- Genetically predisposed inflammatory and pruritic skin disease associated with allergies.
- Common in dogs ( 6 months to 6 years ) and uncommon in cats.
- Second most common allergic skin disease in dogs.
- Hypersensitivity reaction to inhaled or cutaneously absorbed environmental antigens in genetically predisposed individuals.
- It is frequently associated with elevated serum IgE levels.
- Early onset is often associated with a family history of skin allergies
- This may lead the dog to become susceptible to allergens such as
Airborne pollens (grasses ,weeds, trees )
Mold spores(indoor and outdoor)
Why does a dog develop atopic dermatitis
- A combination of factors predisposes dogs to atopic dermatitis
- Both their genetic make-up and environment may interact to allow atopic dermatitis to develop
- Caused by an inappropriate immune reaction rather than by the allergens themselves
How are dogs exposed to allergens
- Many allergens are airborne and are found nearly everywhere
- Pollens are found at high levels only at some times during the year
- Skin is an important barrier to allergens
- When the barrier function of the skin is impaired due to genetics or self trauma , allergens can penetrate the skin and trigger allergies
Examples of breeds predisposed to atopic dermatitis (breed predisposition may vary from region to region)
Boxer, Belgian Tervuren, Boston Terrier, Cairn Terrier, Scottish Terrier, West Highland, White Terrier, Wire haired Fox Terrier, American Cocker Spaniel, Chinese Shar Pei, Dalmatian, English Bulldog, English Setter, Irish Setter, Golden Retriever, Labrador Retriever, Newfoundland, German Shepherd, Lhasa Apso, Shih Tzu, Miniature Schnauzer, Pug, Miniature Poodle, Shiba Inu.
The definition of classical canine AD implies a pivotal role for IgE in the pathogenesis which may well be the case. However in fact the pathogenesis of AD is exceedingly complex, and can be categorized under three headings
Defects in innate immunity
Defects in barrier function
Defects in acquired immunity.
The likely sequence of events
Impaired barrier function facilitates the percutaneous absorption of allergen. Allergen is captured by Langerhans’ cells armed with IgE antibody. In the resultant immune response to the allergen, the genetic features of the atopic trait favour the development of an IgE response which is largely elaborated in the local lymph node. Exposure of mast cells armed with IgE antibody initiates release of preformed and newly generated mediators, which aids the influx of inflammatory cells. In turn, these release other pro-inflammatory mediators. Particularly in the chronic phase, a concomitant Th1 response occurs with γIFN prominent Secondary infection compounds the problem, leading to further Th1 responses. A failure of immune regulation allows the continuation of the immune responses and resultant inflammation.
- Skin erythema
- Pruritus (licking, chewing, scratching, rubbing)
- The distribution of the pruritus usually involves the feet, flanks, groin, axillae, face, and ears.
- Erythema of pinnae
- Self-trauma often results in secondary skin lesions, including salivary staining, alopecia, excoriations, scales, crusts, hyper pigmentation, and lichenification.
Prélaud et al proposed a list of five major criteria
The presence of 3/5 criteria resulted in the diagnosis of CAD with a specificity and a sensitivity of 80%.
The five “Prelaud’s criteria” are:
– Corticosteroid-sensitive pruritus
– Erythema of pinnae
– Bilateral cranial erythematous podo dermatitis
– First clinical signs reported between the age of 6 months and 3 years
More recently, Favrot et al have reviewed the symptoms and propose the following criteria:
– Age at onset < 3 years
– Mostly indoor dog
– Corticosteroid-sensitive pruritus
– Chronic or recurrent yeasts infections
– Affected front feet
– Affected ear pinnae
– NON-affected ear margins
– NON-affected dorso-lumbar area
Five criteria provide a 85% sensitivity and a 79% specificity for a diagnosis of CAD.
The clinical manifestations of canine AD reflect a multi factorial disorder, which can be complicated by self-trauma or secondary infection. It cannot be over-emphasised that allergy tests are never a substitute for meticulous history, thorough physical examination and careful elimination of other diagnoses.Seasonal foot licking is the most unique and typical symptom of atopy. If year-round allergens (house dust mites) are causing the allergy, the foot licking may be non seasonal.
- Small amount of test allergens(60 allergens) are injected in the skin on one side of trunk after hair has been clipped and wheal (a red bump) response is measured , may also be used to identify the cause of pet’s allergic reaction…
- Positive reactions to grass, weed, tree, mould, insect, dander, or indoor environmental allergens are seen. False-negative and false-positive reactions may occur.
- This test requires sedation
- This test is often referred as ‘golden standard’ for this condition
- 100% reliable
- The term is poorly chosen because:
- These tests do not allow to distinct allergic dogs from normal dogs
- Clinically normal dogs can have a positive « allergy test »
- Atopic dogs can have negative « allergy test »
- These tests are only interesting in order to elaborate the composition of a possible specific “immunotherapy” Correlation between IDST and “blood test” is difficult to analyze.
- Actually, it is impossible to determine which of IDST or “blood test” is the most appropriate.
- May be the best solution would be to perform both tests
Allergen-specific IgE serological tests
- These tests significantly varies from one laboratory to an other and only little standardization and quality control data is available.
- The “human technique” can never be used in the dog (specificity of canine IgE, determination of the Cut-off values).
- Because of the cross reactivity of IgE antibodies against IgE and subclasses of Ig G,
- it is important to use one or more IgE specific monoclocal antibodies in blood tests in dogs (or a more specific reagent, using the IgE receptor alpha-subunit: FceRIa ).
- Only few vet labs can offer guarantee for a good quality technique.
- In the same way as the IDST, a blood test for the diagnosis of adverse reactions to food is not recommended (very poor sensitivity and specificity).
Role of the inflammatory mediators in the skin
- Histamine: it is obvious that histamine plays a role in CAD but further studies are needed to define the precise role of this mediator.
- Serotonine: this mediator, released by mast cell degranulation , also seems to play a significant role in allergic reactions in humans.
- The role of serotonine in CAD remains unknown. The use of serotonine antagonists in the management of CAD has a low efficacy (even if all these drugs also have an antihistaminic effect: cyproheptadine, amitriptyline, hydroxyzine, doxepin, fluoxepin).
- Leukotrienes: LTB4 are elevated in lesional skin of humans with AD. The importance of this mediator in CAD is suggested by the beneficial effect observed after essential fatty acids complementation in dogs (reduction of the LTB4 production, a pro inflammatory product). The efficacy of this complementation remains quite low (not so far than a placebo effect).
- Cytokines: in the dog, IL-4 and IL-5 are more commonly detected in atopic skin biopsies. IL-2 is more often found in normal skin.
- Food allergy
- Malassezia dermatitis
- Bacterial pyoderma
- Hypersensitivities (flea bite, contact)
- Parasites (cheyletiellosis, pediculosis), and folliculitis (dermatophyte, Demodex).
How to manage CAD
Treatment of CAD includes a combination of management techniques focusing on different elements constituting the severity of the symptoms: allergen avoidance, antiinflammatory treatments, anti-microbial treatments , allergen-specific immunotherapy.
It seems essential to control, as soon as possible, the gravity of the disease in order to avoid a self-inducing mechanism that could lead to a chronic stage where no more treatments could be effective.
- Antimicrobial therapy
- any secondary pyoderma, otitis externa and Malassezia dermatitis should be treated with appropriate therapies. Controlling and preventing secondary infection is an essential component of managing atopic dogs.
- Bathing every 3 to 7 days and treating the ears after every bath help to wash off pollens and disinfect the skin and ear canals, preventing secondary infections from recurring.
- Symptomatic therapy (itch control)
- Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms.
- Systemic antihistamine therapy reduces clinical symptoms in many cases Antihistamines can be used alone or in combination with glucocorticoids or essential fatty acids for a synergistic effect.
- One- to 2-week-long therapeutic trials with different antihistamines may be required to determine which is most effective.
- Chlorpheniramine 0.2–3 mg/kg PO q 8–12 hours
- Diphenhydramine 1–4 mg/kg PO q 8 hours
- Dextromethorphan, an opioid antagonist, may be a useful adjunct in managing the licking, chewing, and biting behaviors associated with allergic dermatitis in dogs. Dextromethorphan 2 mg/kg PO should be administered every 12 hours. A beneficial effect should be seen within 2 weeks.
- Injectable short-acting steroids (dexamethasone sodium phosphate 0.5–1 mg/kg or prednisolone acetate 0.1–1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if no concurrent secondary infection occurs.
- Temaril-P (trimeprazine and prednisolone combination) is a unique drug that provides significant antipruritic effects at a relatively lower dose of the prednisolone. One tablet per 10 to 20 kg should be administered every 24 to 48 hours. The dosage should be tapered to the lowest possible dose and frequency.
- Allergy treatment (immune modulation)
- Cyclosporine (Atopica) helps control pruritus in 75% of atopic dogs. A dose of 5 mg/kg PO should be administered every 24 hours until beneficial effects are seen (approximately 4–6 weeks). Then, dosage frequency should be tapered down to every 48 to 72 hours.
- The prognosis is good
- although lifelong therapy for control is needed in most dogs
- Relapses (pruritic flare-ups with/without secondary infections) are common, so individualized treatment adjustments to meet patient needs may be required periodically.
- In dogs that become poorly controlled, one should rule out secondary infection (e.g., that caused by bacteria or Malassezia); sarcoptic mange; demodicosis; and concurrent food, flea bite, and recently acquired hypersensitivity to additional environmental allergens.
- Because a strong genetic component is present, the breeding of any male or female dog with clinical signs of atopic dermatitis should be discouraged.