Nutritional Deficiency

Nutritional keratinization disorders that can cause ceruminous otitis are fatty acid deficiency, vitamin A-responsive dermatosis, and zinc-responsive dermatosis.

Fatty Acid Deficiency

Fatty acid binds water into the stratum corneum of normal skin, helping to main­tain the permeability properties of the skin barrier.

Prolonged storage of dry dog and cat food causes degradation of fatty acids, fatty acid deficiency, and reduced levels of antioxidants. Animals fed home-cooked diets or reduced-fat diets may develop fatty acid deficiency. Gastrointestinal diseases that cause poor absorption will result in fatty acid deficiency in spite of an adequate diet. In dogs, the essential fatty acids linolenic and arachidonic acid, can be synthesized from linoleic acid. Cats lack the enzyme omega-6-desaturase, so they cannot convert linoleic acid to arachidonic acid. Therefore, cats require linolenic and arachidonic acid in their diets. Fatty acid deficiency in cats does not become clinically apparent until many months of feeding a fatty acid-deficient diet.

Deficiency of fatty acids, especially arachidonic acid, in the diet may result in abnormalities in keratinization with microscopic epidermal changes (hypergranulosis, epidermal hyperplasia with orthokeratotic or parakeratotic hyperkeratosis).

Clinically, animals with acute fatty acid deficiency produce a dry, dull hair coat with generalized fine scaling of the skin. This also affects the ear, with involvement of the pinna and horizontal ear canal. In chronic conditions, there is epidermal thick­ening with concurrent greasiness of the ear pinna and canal and of the intertriginous and interdigital areas. The ceruminous otitis that accompanies this condition is made worse by secondary bacterial and Malassezia infection. Without appropriate treatment, pruritus and seborrhea become progressively worse.

Diagnosis and Tireatment. Diagnosis of fatty acid deficiency is based on response to therapeutic levels of fatty acid supplementation. It is mandatory to make sure that an animal’s diet contains the recommended amount of fat for proper health and that an animal on a reducing diet is given follow-up and routine veterinary care. Commercially prepared and balanced veterinary omega-6 and omega-3 fatty acid supplementations are available. They contain linoleic acid and eicosapentaenoic and docosahexaenoic acid. The latter two are marine lipids that modulate arachidonic acid metabolism, thus reducing inflammatory responses in the skin through prostaglandin and leukotrienes. They also mediate epidermal proliferation. The role of linoleic acid in controlling seborrheic dermatitis in dogs is well established. The proper storage of food at room temperature and in airtight containers away from direct light is important to ensure that an adequate level of linoleic acid is present in the diet. Diets should not be stored for prolonged periods.

Supplementation with sunflower, safflower, or vegetable oil at a dose of 5 ml per cup of dry or can of dog food should elicit a response in 3 to 8 weeks. Similar results should be seen with commercially prepared veterinary supplements. Any secondary bacterial or Malassezia infection should be treated.

Vitamin A-Responsive Dermatosis

Epithelial cells require vitamin A to maintain their integrity. Vitamin A is necessary for the proliferation and differentiation of keratinocytes. The Cocker Spaniel has a predisposition to this condition. However, it has also been reported in the Labrador Retriever and Miniature Schnauzer. Cats lack the metabolic capability to convert carotene to vitamin A.

Clinical Signs. The effects of vitamin A deficiency on the skin include marked hyperkeratosis of the epidermis, hair follicles, and sebaceous glands. The hyper­keratosis of the sebaceous glands results in the blockage of the sebaceous secretion, giving rise to a papular-type skin eruption.

Diagnosis and Tireatment. The follicular changes present in dogs with vitamin A-responsive dermatosis and the histologic findings of markedly disproportionate follicular orthokeratotic hyperkeratosis are enough to warrant treatment of this condition. The final diagnosis, however, depends on response to therapy. The condi­tion responds to 400 to 800 IU∕kg of vitamin A orally once daily with a high-fat meal. Animals on such a high level of supplementation should be monitored for signs of toxicity.

Zinc-Responsive Dermatosis

Zinc-responsive dermatosis is a chronic keratinization disorder of dogs. Predilection for the disease is observed among the Alaskan Malamutes and Siberian Huskies, with a few reports in Doberman Pinschers and Great Danes. There are two forms of this disorder: syndrome I and syndrome II.

Syndrome I. This syndrome affects mainly Siberian Huskies and Alaskan Malamutes, with reported cases in Bull Terriers. A genetic defect in the Alaskan Malamute causes a decreased ability to absorb zinc from the gastrointestinal tract.

Clinical Signs. Despite a balanced diet, clinical signs usually appear in animals between 1 and 3 years of age. Clinical signs include alopecia with crusts and scales around the eyes and on the pinnae and horizontal canals of the ears. There is erythema with some form of erosion in these areas. Excessive sebum production and secondary bacterial and Malassezia infections are common; this is noticeable on the pinna of the ear and in the horizontal ear canal. Secondary bacterial and Malassezia infections of the ear canal cause the foul odor of the otitis present in this condition.

Syndrome II.

Diagnosis. A thorough history, diet analysis, physical examination, and skin biopsy are important in the diagnosis of zinc-responsive dermatosis. A histologic finding of hyperplastic superficial perivascular dermatitis with severe epidermal and follicular parakeratosis suggests this condition.

Treatment. For dogs suffering from syndrome I, zinc supplementation is recom­mended (oral zinc sulfate or zinc methionine). For dogs with syndrome II, the correction of the diet usually produces a favorable response in 2 to 6 weeks. If dietary adjustment resolves the condition, there is no need for supplementation.