CANINE ATOPIC DERMATITIS IN DOGS
Dr. Swatantra Singh1 , Dr. Priya Singh, Dr. Neelam tandia, Dr. Dharmendra kumar, Dr. PDS Raghuvansi, Dr. Baleshwari dixit, Dr. Deepak Ningwal, Dr. Bhawana Ku shwaha, Dr. Shilpa Gajbhiye
1 Assistant Professor Department of Pharmacology
College of Veterinary Science and Animal Husbandry, NDVSU, Rewa (MP)-486001.
Canine atopic dermatitis (CAD) is a prevalent pruritic skin disease with a complex etiology and pathogenesis. Canine atopic dermatitis (CAD) appears to be caused by a confluence of genetic and environmental variables that lead to impaired skin barrier function, immunological dysregulation, and skin microbial dysbiosis. Although, immunoglobulin E (Ig E) is an important component in atopic dermatitis (AD), recent studies have shown that AD is not always Ig E-mediated. As in humans, a small subset of dogs with AD do not have detectable by either serology or intradermal testing allergen-specific Ig E. This form of AD has been recently referred to as atopic-like dermatitis. According to Scott and Miller, almost 15% to 30% of dogs are thought to be affected with canine atopic dermatitis (CAD), which is typically a chronic condition. Immune dysregulation in the skin of atopic dogs leads to overproduction of pro-inflammatory and pruritogenic mediators, such as T-helper type-2 cytokines, including interleukins IL-4, IL-5, IL-10, and IL-13. More recently, IL-31 was shown to play a significant role in CAD, inducing inflammation and pruritus in atopic dogs via activation of Janus kinase (JK) signal transduction. This led to the development of the JK inhibitor, oclacitinib maleate. Although the precise etiology of CAD is not yet fully understood, it is believed to be caused by immediate and late-phase hypersensitivity reactions to environmental allergens that are mediated by immunoglobulin Ig E. A deficiency in their skin’s natural protective barrier causes itching in atopic dermatitis-affected canines. The secondary source of infections that worsen the severity of CAD is this itching, which supports the skin microbiota. Staphylococcus pseud intermedius is the most prevalent bacteria on lesional skin of dogs with AD, while Malassezia pachydermatis is the primary fungus representative, according to canine microbial culture-based investigations. There is increasing evidence that dogs with AD have epidermal barrier abnormalities, including abnormal lipid and ceramide composition. Clinical symptoms typically start to show between the ages of 6 months and 3 years. The first sign is typically chronic itching, which is followed by “primary skin lesions” such as erythema, papules, and pustules. Alopecia, cutaneous lichenification, and frequently bacterial infections are examples of “secondary skin lesions” in chronic CAD.
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 Ig E.
- The pathogenesis also involves interaction of allergen with Ig E 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 Ig E anti-staphylococcal antibodies which add to the allergenic load.
- Furthermore, proliferation of the yeast Malassezia pachydermatis with the development of Ig E antibodies against soluble antigens further compounding the disease process.
- Chronically affected atopic dogs frequently develop severe seborrhoeic changes.
Dermatological examination-
The animal periodically rubbed her ears while attempting to reach the paws. Both auricles of ear exhibited no lesions upon otoscopic evaluation. The external auditory canals showed signs of light erythema. No indications of purulent otitis were present. Clinical examination of the lateral aspect of the thighs and neck revealed pyodermatitis over the skin with diffuse purulent lesions, lichenification, alopecia, and patchy hyperpigmentation. Ectoparasites were not observed. On the rest of the body, there were no additional primary or secondary skin lesions.
Diagnosis –
A diagnostic issue is identifying canine atopic dermatitis (CAD). There are no known pathognomonic symptoms or specific biomarkers. In general, the diagnosis is made to rule out other infections with comparable symptoms, such as ectoparasitic infestations. The two most common allergy tests are the Allergen-Specific IgE Serology (ASIS) test and Intra Dermal Testing (IDT), which was not done in this case.
Management- Topical or systemic glucocorticoids, antifungals, the implementation of a flea control program, nutritional supplementation with essential fatty acids, antibiotic treatment, and frequent shampooing comprise the symptomatic treatment for CAD.
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.
Spot-on preparations-
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-
Halliwell, R. (2006). Revised nomenclature for veterinary allergy. Veterinary Immunology and Immunopathology, 114(3-4), 207-208.
Larsson, C. E. & Lucas, R (2020). Tratado de medicina externa: dermatologia veterionaria (2a ed.), Interbook.
Olivry, T., DeBoer, D. J., Griffin, C. E., Halliwell, R. E., Hill, P. B., Hillier, A., Marsella, R., & Sousa, C. A. (2001). The ACVD task force on Canine atopic dermatitis. Veterinary Immunology and Immunopathology, 81, 143-383.
Olivry, T., DeBoer, D. J., Favrot, C., Jackson, H. A., Mueller, R. S., Nuttall, T., & Prelaud, P. (2015). Treatment of canine atopic dermatitis: 2015 updated guidelines from the International Committee on Allergic Diseases of Animals (ICADA). BMC Veterinary Research, 11(1), 1-15.
