Canine Atopic Dermatitis & its Therapeutic Management
PUNEET GOYAL
B.V.Sc & A.H. Scholar, Apollo College of Veterinary Medicine, Agra Road, Jaipur, Rajasthan- 302031.
Abstract
Canine atopic dermatitis (CAD) is a genetically predisposed inflammatory and pruritic skin disease with and IgE-mediated type 1 hypersensitivity reaction to sensitization to environmental up to 50% of dermatological cases involve atopic dogs. Clinical signs complicated by concomitant flea allergy dermatitis (FAD), adverse food reactions (AFRs) and/or associated secondary infections (especially staphylococcus folliculitis). Clinical diagnosis is facilitated by eliminating the possibility of other diseases, and controlling any concomitant diseases. Females were more affected than males, as well as dogs of defined breeds in comparison to mixed breed dogs, with Shih Tzu being the most prevalent pure breeds, followed by mixed breed dogs. Canine atopic dermatitis is preferred by the International Task Force on Canine Atopic Dermatitis.
Key Words: – Canine atopic dermatitis, Flea allergic dermatitis, Adverse food reactions, Concomitant, Hypersensitivity, Dermatopathy.
Introduction
Canine Atopic Dermatitis is one of the most common chronic inflammatory dermatopathy in dogs, affecting 3-15% of the canine populations. It is defined as a genetically predisposed inflammatory and pruritic skin disease with characteristic clinical feature associated with IgE antibodies most commonly to environmental allergens. Its etiology is multi-factorial and main causative agent is inhalant allergens, the current preferred name is aeroallergens as they gain access to the body via the percutaneous route. The majority of CAD cases result from hypersensitivity to house dust mites and especially Dermatophagoides faninae and to a lesser extent Dermatophagoides pteronyssinus, leading to a non-seasonal dermatitis. Less commonly, pollen allergies are involved, typically lead to seasonal dermatitis.
(1) Electron micrograph of (2) Dermatophagoides farina (3) Electron micrograph of Dermatophagoides farina pollens
Pathogenesis The symptoms that affect atopic dogs are directly linked to an inherited dysfunction of the immune system and also to defects in cutaneous barrier function that facilitate access of allergens and predispose them to bacterial and yeast proliferation and infections.
- Access of allergen is via the percutaneous route. Alteration of epidermal function barrier in atopic dogs facilitates this penetration. Allergen capture is aided by epidermal Langerhan’s cells which are armed with allergens-specific IgE.
- The pathogenesis also involves interaction of allergen with IgE antibody attached to mast cells.
- A variety of mediators are involved including histamine, leukotrienes and proteases from mast cells, and probably also interleukins from keratinocytes.
- Staphylococci attach more readily to the skin of atopic dogs, and this lead to the development of a bacterial overgrowth and/or secondary pyoderma which is usually a folliculitis. Dogs have impaired cell-mediated immunity which favors the persistence of the infection, and they may develop IgE anti-staphylococcal antibodies which add to the allergenic load.
- Furthermore, proliferation of the yeast Malassezia pachydermatis with the development of IgE antibodies against soluble antigens further compounding the disease process.
- Chronically affected atopic dogs frequently develop severe seborrhoeic changes.
Epidemiology
With the exception of flea allergy dermatitis in flea-endemic areas, CAD is the most frequent allergic and pruritic skin disease, and one of the most common inflammatory dermatoses. The peak age of onset is between 1-3 years of age. It is uncommon for it to commence at less than 6 months of age and very rare at more than 7 years of age. Most cases suffer from perennial pruritus that may be subject to seasonal exacerbation in severity. However, a minority are affected for a limited every year if their sensitivities are arrested to seasonal pollen allergens.
Clinical Signs
The degree of pruritis ranges from mild to intense. The distribution of lesions is predominantly facial and ventral, with scratching of the trunk, rubbing of the face and chewing of the feet. In the early cases, there may be little primary eruption but by the time of presentation there are usually erythematous macules and papules.
Some 60% of cases suffer from a secondary pyoderma which is usually a folliculitis. Evidence of self trauma, a variety of skin changes results, commonly includes excoriations and occasionally acral lick granuloma and episode of acute moist dermatitis. An otitis externa accompanies some 80% of cases and occasionally it may be the sole presenting sign. Characteristically, the otitis commences by affecting the inner surface of the pinna and the vertical ear canal, but in long standing cases the horizontal ear canal also becomes involved with a secondary infection involving bacteria and/or the yeast Malassezia.
Seborrhoeic skin changes are commonly seen in chronic cases with greasiness of the skin and hair coat and marked scaling accompanied by varying degree of alopecia. As the disease progresses, tissue remodeling lesions, in response to chronic inflammation appear such as lichenification of the flexural surface of the tarsus, hyper-pigmentation, and hyperkeratosis. Discoloration of the hair on the extremities and bilateral front feet pododermatitis may be a very significant sign.
(4) Atopic dog, ventral generalized (5) Atopic dog, interdigital erythema
erythema
Diagnosis
Historical and clinical diagnostic criteria
Those criteria provide consistency in the diagnosis of atopic dermatitis. They should be documented after ruling out or controlling other primary dermatoses and secondary cutaneous infections.
Diagnostic tests
The gold standard test remains the intra-dermal test with a positive immediate (10-20 minutes) reaction to environmental allergens. Positive (histamine) and negative (diluents) controls are always included the possible role of concomitant FAD can be assessed by including the flea antigen.
In vitro assay tests for allergen-specific IgE are also available. They can be performed either using monoclonal or polyclonal antiserum specific for canine IgE, or alternatively using the cloned-chain of the FcA receptor (the mast cell receptor that binds IgE).
Cellular techniques (basophile degranulation tests or heterologous passive transfer) are useful laboratory tests in the diagnosis of allergies mediated by immediate hypersensitivity.
These. tests have two purposes; one is to support the clinical diagnosis and the other is to permit the selection of allergens for immunotherapy.
Treatment
Treatment is multi-factorial and mainly focused on four factors: time (acute or chronic lesions), presence of pruritis, inflammation, and secondary infections. Therapeutic approaches have been described by the International Committee on Allergic Diseases of Animals.
General remark: –Atopic dermatitis cannot usually be cured but only controlled. It is one of the most difficult skin disorders to control as, most of time; dogs cannot be protected from allergen exposure. However, quality of life can be considerably improved and atopic dermatitis such as bacterial and/or Malassezia infection or overgrowths are effectively treated. Vigorous treatment of any concomitant otitis externa and any associated FAD must be undertaken.
Allergen avoidance: –Theoretically, it is the best treatment. But usually, avoidance of allergens is not possible or practical. An accurate identification of the offending allergen is first necessary. In most cases, the aim will be to achieve a decrease in exposure. As in case of hypersensitive to dust mites, the exposure may be decreased if pets stay longer. The use of a miticide in the environment may also help. Pyriproxyfen has also been shown to be useful in reducing mite proliferation and the combination with an adulticide such as permethrin, can be very effective.
Topical treatment: –Topical products which are effective against the major pathogenic factors will be useful, if they are able to eliminate the allergens from skin surface to help restore the epidermal barrier and to help control the inflammatory process and any secondary cutaneous infections.
- Shampoos
Shampoos are helpful as an aid to the control of atopic dermatitis. A shampoo with good cleansing power limits allergen penetration. A shampoo containing immune-modulating factors such as mono-oligosaccharides provides soothing effect. A shampoo containing EFA (such as linoleic acid) may help to restore the epidermal barrier. Antipruritic shampoos, such as those containing colloidal oatmeal will provide soothing effects.
- Other topical
Spot-on preparations containing ceramides have been shown to be effective in restoring skin barrier function and should form the part of the therapeutic approach. Topical corticosteroids preparations (hydrocortisone aceponate) may be preferable to systemic administrations. An antiseptic ear cleanser may be useful for the ear cleaning and anti-inflammatory otic preparations of any concomitant otitis externa.
Systemic treatments
A number of systemic drugs are used in the control of atopic dermatitis. These include
- Corticosteroids
Corticosteroids are generally highly effective in relieving the pruritis. Oral, short acting products should be employed. The effect of corticosteroid is only transient.
- Cyclosporine
When dosed at 5mg/kg this is as effective as corticosteroid, although with a slower onset of action.
- Antihistamines
These may sometimes give partial or very occasionally complete relief. Although hydroxyzine (2mg/kg TID) is often favored, some cases respond better to one antihistamine than another.
- Essential fatty acids (EFAs)
These may have significant anti-inflammatory action and assist in restoring the barrier function of the skin if used in a formulation providing sufficient quantities of both n-6 and n-3 EFAs with a ratio close to 5:1.
- Antibiotic
Antibiotic therapy for renewable course of 2 weeks plus 1 to 2 additional weeks after clinical recovery should be used. It is helpful where there is bacterial overgrowth, with or without a hypersensitivity to the organism involved.
Immunotherapy
Immunotherapy or hyposensitisation with allergen solution is the cornerstone of the therapy in the atopic dermatitis. Response to immunotherapy may be quite brisk (within 3 months) or delayed for up to 9 months. Concomitant medical therapy can be used during the course of immunotherapy and dose required can be reduced with time as the immunotherapy treatment starts to become effective.
Conclusion
Atopic dermatitis is a genetically predisposed inflammatory and pruritic skin disease. The main challenge is to follow the clinical evolution of the plethora of clinical signs resulting from atopic dermatitis itself, and from the associated secondary complications. Following the proposed dermatological approach allows the diagnosis of CAD if clinical signs remain after having ruled out (or controlled), parasitic dermatoses, secondary cutaneous infections and other allergies (FAD and AFR). Successful management is dependent on a thorough understanding of the pathogenesis and of the potential complications, and on a willingness to modify the therapy in the light of a changing situation.
References
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