PHOTOS 1-7: Scaling dermatosis is due to an increase in production, increase in desquamation or a decrease in cohesion of keratinocytes which causes abnormal shedding of epidermal cells as fine or coarse scale. Clinical signs of scaling dermatoses include accumulations of scale, malodour, comedones, follicular casts, alopecia, pruritis, secondary pyoderma and Malassezia overgrowth. Diagnostic procedures include skin scrapings to diagnose ectoparasites, skin biopsy, intradermal skin testing to identify atopy, food elimination trials to identify food allergies and epidermal exudate preparations to determine the microflora composition on the skin. Treatment of scaling dermatoses is mainly via frequent and appropriate topical treatment. Primary and secondary disease conditions must be identified and controlled. Controlling scaling dermatoses is often a lifelong requirement. Special shampoos and moisturisers to restore skin hydration are useful. Corticosteroids may be used to control the inflammation but will mask pyoderma and prevent accurate diagnosis of primary disease. Scaling dermatosis can be due to primary idiopathic seborrhoea, atopy, vitamin A responsive dermatosis, Zinc responsive dermatosis, ectodermal defects, sebaceous adenitis, ectoparasites, pyoderma, dermatophytosis, endocrinopathy, neoplasia or autoimmune skin diseases. Primary idiopathic seborrhoea is a primary cellular defect causing accelerated epidermopoiesis and hyperproliferation of the epidermis, follicular infundibulum and sebaceous glands. Dog breeds at high risk of developing this condition include west highland white terriers and cocker spaniels. Atopy is a hypersensitivity reaction in which animals are predisposed to become allergic to normally non allergenic substances and environmental allergens. Atopy causes animals to become sensitised to environmental allergens by production of allergen specific IgE. Clinical features of atopy include pruritis, crusts, scaling, alopecia and hyperpigmentation. Vitamin A responsive dermatosis is seen mostly in cocker spaniels, the clinical signs are similar to severe idiopathic seborrhoea but the patient responds to dietary vitamin A supplementation. Zinc responsive dermatosis results in alopecia, scaling, crusting and erythema and responds to zinc supplementation. Ectodermal defects due to follicular dysplasias or keratinisation defects cause excessive scaliness, comedone formation and secondary pyoderma. Sebaceous adenitis is an inflammatory disease which causes diffuse hair loss and excessive scaling. Ectoparasites cause scabies and demodicosis which leads to inflammation and exfoliation. Pyoderma is a bacterial skin infection which causes increased exfoliation of keratinocytes. Dermatophytosis causes increased shedding of affected keratinocytes and is commonly exfoliative. Endocrinopathies like hypothyroidism and hyperadrenocorticism commonly cause excessive scaling. Hyperthyroidism and diabetes mellitus may also cause excessive scaling. Neoplasias such as epidermotropic lymphoma damage epidermal structures and may cause scaling. Autoimmune skin diseases such as pemphigus complex may also be exfoliative causing scaling and secondary pyoderma. Pemphigus foliaceus is an autoimmune skin disease in which antibodies are produced against a component of the adhesion molecules of keratinocytes. Clinical signs of pemphigus foliaceus include superficial pustules, erosions, crusts, scales, epidermal collarettes and alopecia. Diagnosis of pemphigus foliaceus is via cytology and antinuclear antibodies. Urticaria is a cutaneous hypersensitivity reaction due to stimuli such as drugs. It begins with the appearance of acute pruritic wheals with the affected skin being erythematous without hair loss. PHOTO 8: Nasal dermatoses can be caused by nasal pyoderma, demodicosis, dermatophytosis, fungal infections, pemphigus foliaceus, pemphigus erythematosus, zinc responsive dermatosis, vitiligo, hypersensitivity, tumours and idiopathic nasal hyperkeratosis. Clinical signs of nasal dermatoses include depigmentation, hyperpigmentation, crusts, alopecia, ulceration, scarring and nodule formation. Generalised demodicosis is caused by demodectic mites. Demodicosis is defined as generalised if there are more than five focal lesions or if two or more body regions are affected. Clinical signs include crusting, lichenification, hyperpigmented and ulcerated skin. Alopecia, pruritis and erythema are common. Pemphigus foliaceus is an autoimmune skin disease in which antibodies are produced against a component of the adhesion molecules of keratinocytes. Clinical signs of pemphigus foliaceus include superficial pustules, erosions, crusts, scales, epidermal collarettes and alopecia. Diagnosis of pemphigus foliaceus is via cytology and antinuclear antibodies. Pemphigus foliaceus often begins on the bridge of the nose, around the eyes and on the ear pinnae before becoming generalised.
REFERENCES: PHOTOS 1-8: 1. Helton Rhodes, K 2002, ‘The 5-minute veterinary consult clinical companion: small animal dermatology’, Lippincott Williams & Wilkins, Philadelphia, pp. 248-252. 2. Medleau, L & Hnilica, KA 2006, ‘Small animal dermatology: a color atlas and therapeutic guide’, 2nd ed., Saunders Elsevier, St. Louis, pp.162-166, 190-191, 376-388. 3. Tilley, LP & Smith, FWK 2004, ‘The 5-minute veterinary consult: canine and feline’, 3rd ed., Lippincott Williams & Wilkins, Baltimore, pp. 336-337.
Metadata assigned by Dr. M. van Schoor, Senior Lecturer, Dept. of Companion Animal Clinical Studies