Candace A. Sousa, DVM
COCKER SPANIEL (American)
WEST HIGHLAND WHITE TERRIER
Canine uveodermatologic syndrome (Vogt-Koyanagi-Harada-like syndrome) is a syndrome of concurrent granulomatous uveitis and depigmenting dermatitis reported most commonly in the Akita, Samoyed, and Siberian husky. The cause of the disease unknown but in man a cell-mediated hypersensitivity to melanin and melanocytes in conjunction with the production of antibodies against melanin, gangliosides, and photoreceptors has been shown. Melanocytes in the uveal tract, inner ear, leptomeninges and skin are all affected.
The syndrome is characterized by an acute onset of uveitis. Subsequent symmetrical depigmentation of the nose, lips, eyelids, and other pigmented areas begins within 10 days to several months. Leukoderma and leukotrichia may result.
Histopathologic changes consist of a histiocytic interface dermatitis. Pigmentary incontinence is pronounced. Aggressive management of the uveitis is necessary to prevent posterior synechia, secondary glaucoma, cataracts, and loss of vision. Systemic glucocorticoids plus another immunosuppressive drug such as azathioprine are needed to treat both the ocular and cutaneous disease.
Pattern alopecia (or pattern baldness) is most commonly seen in small, shorthaired breeds of dogs such as dachshunds, Manchester terriers, miniature pinschers, and Chihuahuas. Three syndromes are recognized. The first is pinnal alopecia of the dachshund. Affected dogs begin to lose hair from the pinnae about 6 to 9 months of age and the hair loss progresses slowly to complete pinnal alopecia. The exposed skin hyperpigments.
In the second syndrome, dogs gradually begin to lose hair in the postauricular regions, on the ventral neck, over the entire ventrum, and on the caudomedial thighs. The condition begins at about 6 months of age and is more commonly recognized in females.
A third syndrome occurs in American water spaniels and Portuguese water dogs. Hair loss begins at about 6 months of age and is restricted to the ventral neck, the caudomedial thighs, and the tail.
In all cases, histopathology reveals a decrease in size (miniaturization) of the hair follicles with normal adnexal structure. The follicles produce fine hair shafts.
There is some evidence that treatment with oral melatonin, 3 to 5 mg q 12 hours for 30 days, may stimulate hair growth in about 60 days. Minoxidil should not be used in dogs to stimulate hair growth, as it is cardiotoxic.
Naso-digital hyperkeratosis is characterized by an increased amount of horny tissue originating from and tightly adherent to the epidermis of the footpads and/ or nasal planum. It is an idiopathic disorder, most commonly occurring in older dogs. There is no sex predilection but the American cocker spaniel may be at higher risk.The nasal planum, which is moist, soft, and shiny in normal dogs, becomes hard, dry, rough, and hyperkeratotic, especially on the dorsum of the nose. Fissures, erosions, and occasionally ulcers can develop.
The digital hyperkeratosis involves the entire surface of all the pads but is most pronounced at the edges of the weight bearing pads and on the accessory carpal pads. The hard, cracked pads contain excess keratin, which makes walking painful. Fissures and erosions add significantly to the discomfort.
The diagnosis is made based on the clinical findings. If the naso-digital hyperkeratosis is present along with other skin lesions then a skin biopsy should be taken to confirm the diagnosis and to rule out other disorders that can also produce excess keratin in these areas.
Treatment can involve the mechanical removal of the excess keratin with a scissors or blade. Caution needs to be used since aggressive treatment can remove the normal protective layer and predispose the nose and pads to lacerations. Topical treatment includes hydration and the application of a keratolytic agent such as salicylic acid.
A vitamin A-responsive dermatosis in the dog has been recognized. Vitamin A (retinol) is a fat-soluble vitamin that is essential for differentiation and maintenance of epithelial tissue. Dogs can convert plant carotenes in their diet to retinol. The skin disease in dogs is not caused by an absolute dietary deficiency of vitamin A.
Clinical signs include generalized scaling and multifocal severely crusted dermatitic lesions. The lesions are usually worse on the ventral thorax and abdomen. Histopathologic changes consist of severe follicular and mild surface hyperkeratosis with minimal acanthosis.
Therapy consists of the use of vitamin A, 10,000 IU SID up to 50,000 IU BID (300 to 2500 IU/kg/day). Clinical improvement can take from 4 to 8 weeks. Toxicities can be seen when more than 100 times the nutritional requirements are fed for several months.
Bullous pemphigoid (BP) is a rare autoimmune, vesicobullous, ulcerative dermatosis. It has been diagnosed most frequently in the collie and Doberman pinscher. The disease has not been reported in the cat. Lesions commonly affect the oral cavity as well as mucocutaneous junctions and the skin of the groin and axillae.
Blister formation occurs in 3 steps: complement-fixing pemphigoid antibody binds to the bullous pemphigoid antigen (180 kD antigen, a homologue to desmoplakin I) associated with the epidermal basal cell hemidesmosomes; complement is fixed and activated; and there is chemoattraction of neutrophils and eosinophils with subsequent release of proteolytic enzymes that results in disruption of the dermo-epidermal junction resulting in dermo-epidermal separation and vesicle formation.
BP is diagnosed by characteristic histologic findings. There is subepidermal clefting and vesicle formation without acantholysis. Direct immunofluorescence demonstrates deposition of immunoglobulin and complement at the dermo-epidermal junction. Indirect immunofluorescence may show circulating autoantibodies against basement membrane using buccal mucosa as the substrate.
As with other autoimmune dermatoses, the mainstay of treatment is glucocorticoids. Induction can be achieved with 2 to 6 mg/kg of prednisone q 24 hours. To reduce the side effects of steroid therapy, an adjunct drug such as azathioprine or chlorambucil is used.
Discoid lupus erythematosus (DLE) is the second most common autoimmune disease of the dog. In the past DLE was referred to as “nasal solar dermatitis” or “collie nose.” It is most commonly seen in collies, Shetland sheepdogs, German shepherds, and Siberian huskies.
DLE may represent a benign form of SLE in which disease is confined to the skin and other organs are unaffected. The pathomechanism of this disease is similar to that of SLE. Photoaggravation may be a significant factor in the progression of the disease.
Lesions consist of depigmentation, erythema, scaling, and erosions of the nasal planum. Loss or smoothing of the normal cobblestone-like texture of the nose is often an early change along with a dropout of pigment. In more severe cases, erosion and ulceration leading to tissue loss and hemorrhage occurs. Crusting and depigmentation of the dorsal muzzle, periocular region, lip margins, and pinnae may also develop.
The histopathology reveals an interface dermatitis with focal hydropic degeneration of basal epidermal cells, pigmentary incontinence, focal thickening of the basement membrane, apoptotic keratinocytes, and marked accumulation of mononuclear and plasma cells in the dermis. Immunofluorescence is identical to SLE.
In early mild cases, treatment with oral vitamin E, 400 to 800 IU q 12 hours, may quiet the inflammation. In addition, solar avoidance or the use of a water-resistant sunscreen can prevent further damage to depigmented skin. In more highly inflammatory cases, application of a topical potent corticosteroid such as 0.05% betamethasone may be sufficient to halt the process. In more severe or generalized cases, systemic immunosuppressive therapy may be needed. A combination of oral tetracycline and niacinamide q 8 hours (250 mg of each in dogs that weigh less than 10 kg, 500 mg of each in dogs that weigh more than 10 kg) has also been reported to be beneficial in some dogs.
Hyperadrenocorticism is an endocrinologic disorder associated with either excessive production of endogenous glucocorticoids or excessive administration of exogenous glucocorticoids. The disease can occur in any breed but is most commonly seen in dachshunds, Boston terriers, poodles, and boxers. There is no sex predilection. This is generally a disease of middle age dogs (range 1 to 18 years; average 8 to 9 years). It is a rare disease in the cat.
Naturally occurring hyperadrenocorticism is caused by idiopathic bilateral adrenocortical hyperplasia in 70 to 80% of the cases. A functional (ACTH producing) pituitary tumor can cause the disease in about 10 to 15% of the cases. A functional (cortisol-producing) adrenocortical neoplasm is present in about 5% of the cases. Ectopic ACTH syndrome is rare and is associated with non-pituitary and non-adrenocortical neoplasia.
Iatrogenic hyperadrenocorticism has been reported to be the cause in as many as 50% of the cases. There is tremendous individual variation in susceptibility to the adverse effects of glucocorticoid therapy and the clinical signs that are manifest. Caution should be used in withdrawing medications as iatrogenic secondary adrenocortical insufficiency due to the lack of endogenous CRF and/or ACTH can be seen and death may result from circulatory collapse.
Clinical signs in the dog include polyuria and polydipsia in about 85% of the cases. Polyphagia, lethargy (63 to 76%), depression, and decreased exercise tolerance (82%) are other signs often reported by owners. Most dogs have a pendulous, flaccid abdomen and hepatomegaly (61 to 91%). Skeletal muscle atrophy (most pronounced over the head, shoulders, thighs, and pelvis), weakness (43 to 70% of the cases), and lameness and pathologic fractures (33% of the cases) can occur.
Cutaneous signs include a bilaterally symmetrical “endocrine” alopecia. Calcinosis cutis, most commonly seen over the dorsum and in the inguinal and axillary regions, occurs in about 40% of the cases. The skin, especially on the ventrum, can be thin and hypotonic. Animals will frequently develop secondarily infections and pruritus. Follicular plugging (comedones) are often noted.
Clinical signs in the cat are similar to those seen in the dog. They are generally more resistant to the development of alopecia but can develop a fragile, easily torn skin secondary to cutaneous atrophy (see feline skin fragility syndrome). Pruritus may have preceded the treatment with corticosteroids in the case of iatrogenic hyperadrenocorticism.
In making the diagnosis, laboratory abnormalities are often erratic. In a complete blood count, eosinopenia (76 to 95% of the cases), lymphopenia, neutrophilia, hypersegmentation of neutrophils, and polycythemia can be noted. In the urinalysis there is usually a low specific gravity (1.009 to 1.014), proteinuria, bacteriuria, and/or hypercalciuria. Increased serum alkaline phosphatase is found in 80 to 95% of the cases. There are variable increases in SGPT, SGOT, cholesterol (77% of cats), and glucose (93% of cats). Abdominal radiographs often demonstrate hepatomegaly, dystrophic calcification (skin, lung, kidney, heart), osteoporosis, and osteomalacia. Large adrenal carcinomas may be visualized. Measurement of the urine cortisol/creatinine ratio is a useful screen for hyperadrenocorticism and can also be used to monitor Lysodren® therapy.
There are several tests used to make the diagnosis of hyperadrenocorticism. The ACTH-stimulation test involves measurement of the pre-ACTH plasma or serum cortisol, administration of 2 U/kg ACTH gel IM, and a 2 hour post-ACTH cortisol measurement. Synthetic ACTH (Cortrosyn®) can be given, 0.25 mg IV, with the post-ACTH cortisol being sampled at 1 hour. Baseline (resting) plasma cortisols are within the normal range in 50% of the cases. These tests do not reliably distinguish between dogs with adrenocortical hyperplasia and adrenocortical neoplasia. Results in dogs with iatrogenic hyperadrenocorticism show low or normal resting plasma cortisol with little or no response to ACTH. The results are similar in cats.
The dexamethasone suppression test (DST) is useful in diagnosing 95% of the cases of hyperadrenocorticism. The low dose DST involves giving dexamethasone 0.01 mg/kg IV. A pre- and 8 hour post- dexamethasone cortisol is measured. If you don’t see greater then 50% suppression of plasma cortisol, this is diagnostic of hyperadrenocorticism (normal dogs suppress cortisol to less than 1 µg/dl at 8 hours). In the high dose DST, 0.1 mg/kg of dexamethasone is given IV. Cortisol levels are measured pre-, 4, and 8 hour post dexamethasone. If there is at least 50% suppression of the plasma cortisol then most likely the disease is due to adrenal hyperplasia. If there is little or no suppression, an adrenal neoplasm should be suspected.
Measurement of endogenous plasma ACTH is useful in differentiating pituitary-dependent hyperadrenocorticism from an adrenal tumor. Normal to high levels are present in dogs with pituitary-dependent disease but low levels are measured in dogs with adrenal tumors.
Histopathology of the skin shows some features common to all endocrinopathies. There is an arrest of the follicular cycle and the majority of hair follicles arrest in the telogen or late catagen phase. Anagen hair follicles are absent. There is adnexal and epidermal atrophy, atrophy of the dermis, and formation of comedones. Calcinosis cutis with transfollicular and transepithelial elimination of mineralized material can be seen and in some cases there is osseous metaplasia of collagen.
There are several different ways of treating hyperadrenocorticism. o,p’-DDD (Lysodren®, Bristol-Meyers Oncology Division) is effective in the treatment of bilateral adrenocortical hyperplasia associated with a functional pituitary neoplasia or idiopathic in nature. Incomplete or poor response is seen in dogs with adrenocortical neoplasia. The standard way to treat this disease is with 20 to 50 mg/kg PO q 24 hours or divided q 12 hours to effect (5 to 30 days) then as a weekly maintenance for life, possibly divided into 2 to 3 doses. Absorption of o,p’-DDD is enhanced when it is given with a fatty meal. The end point of induction of therapy is a normal post ACTH serum cortisol. Side effects of the drug can be minimized by giving prednisone or prednisolone 0.2 mg/kg q 24 hours for the first 5 to 7 days. The drug is rarely used in the cat. The patient should be monitored with ACTH-stimulation tests at 1, 3, and 6 months of therapy and every 6 months thereafter. l-deprenyl (Anipryl®, Pfizer Animal Health) is a selective inhibitor of monoamine oxidase type B (MAO-B). It is given at a dose of 1 to 2 mg/kg PO q 24 hours for the life of the animal. No adverse side effects have been reported.
Ketoconazole (Nizoral®, Janssen Pharmaceuticals) is an antifungal imidazole that inhibits adrenocortical steroidogenesis. The recommended dose is 10 to 30 mg/kg PO q 24 hours.
Unilateral adrenalectomy the therapy of choice for treatment of adrenocortical neoplasm. Because the opposite adrenal gland is usually severely atrophied, the dog needs to be supported with maintenance doses of glucocorticoids for 3 to 12 months after surgery.
For iatrogenic hyperadrenocorticism, administration of excessive exogenous glucocorticoids should be stopped while maintaining maintenance and stress doses for treatment of the secondary adrenocortical (glucocorticoid) deficiency. The dog can be very gradually weaned off of all exogenous glucocorticoids.
Atopic dermatitis (AD) is a common pruritic dermatosis of dogs that is believed to be related to the development of allergen-specific IgE antibodies. According to various investigators, the incidence has been reported to vary from 2 to 15% of the canine population. Most dogs will first show evidence of the disease from 6 months to 7 years of age with 70% manifesting clinical signs between 1 and 3 years. Clinical signs may be seasonal or non-seasonal (in many animals the history is that the signs began seasonally and progressed to have no seasonality.) AD can occur in any breed of dog but there is an increased risk reported in Irish setters, Dalmatians, west highland white terriers, Scottish terriers, wire hair fox terriers, Boston terriers, cairn terriers, Lhasa apsos, and miniature schnauzers. Some authors report a slightly increased incidence in females. Several breeding studies have failed to document the exact mode of inheritance, if any, and no differences have been found in DL-A typing between normal dogs and dogs with AD.
Atopy is defined as the inherited predisposition to form allergen-specific IgE antibodies. This type I hypersensitivity reaction is the currently accepted pathogenesis of AD in dogs. Allergen-specific IgE antibodies bind to tissue mast cells, especially those in the skin. When mast cell-fixed IgE reacts with its specific allergen, mast cells degranulate and release many pharmacologically active compounds (histamine, serotonin, bradykinin, SRS-A, ECF-A, etc.) It has been shown that there is no difference in total or allergen-specific levels of IgE between clinically normal dogs and dogs with AD. In another study, the average serum histamine level in dogs with AD was actually lower than in normal dogs, although upon challenge with aerosol antigen these dogs experienced an approximately threefold increase in histamine levels and cutaneous histamine levels in dogs with AD are higher than in normal dogs. Allergen-specific IgGd or IgG4 may be the more significant antibody involved in the pathogenesis of the disease.
In dogs with AD, pruritus is the overwhelming owner complaint. Primary skin lesions (e.g. papules, wheals) are not commonly seen. Pruritus and the resultant lesions usually involve the face, particularly the periocular and perioral areas, and ear canals; the feet, especially the caudal carpii and tarsii; the axillae; and the ventrum, or some combination thereof. There are generalized cutaneous signs in about 40% of the cases. Otitis externa is present in about 50% of the cases. Pyoderma (i.e. folliculitis, furunculosis, acute moist dermatitis) caused by Staphylococcus intermedius accompanies approximately 33% of the cases. Atopy is one of the many possible causes of recurrent pyoderma. Many dogs will experience secondary colonization of their skin with Malassezia pachydermatis. Secondary seborrheic skin disease is present in about 12% of the atopic dogs. Hyperhidrosis has been reported in about 10% of the cases. Dogs often have concurrent allergic conjunctivitis (50%) but rarely allergic rhinitis, asthma, or gastrointestinal signs.
The diagnosis of AD in dogs is made by the history, physical examination, and ruling out other causes of pruritic dermatoses. Questions to be addressed in the history include the signalment; age of onset of the pruritus; seasonality, especially in the beginning; distribution of the pruritus; and known responsiveness of the disease to corticosteroid therapy. A useful tool is to apply the criteria proposed by Willemse for making a definitive diagnosis of canine AD. These include:
The differential diagnoses for AD includes flea allergy dermatitis, food allergy, contact dermatitis (irritant or allergic), scabies, intestinal parasitic hypersensitivity, folliculitis (pruritic pyoderma), pelodera dermatitis, hookworm dermatitis, subcorneal pustular dermatosis, and hormonal hypersensitivity. Results of a hemogram, urinalysis, and chemistry profile in most dogs with AD are unremarkable.
Once a clinical diagnosis of atopic dermatitis is made, the dog can be tested for the presence of allergen-specific IgE antibodies in an attempt to select allergens to include in the allergy vaccine. The currently available tests include the intradermal test (IDT) and allergen-specific IgE serology (ASIgES) for measurement of allergen-specific IgE using the radioallergosorbent test (RAST), an enzyme-linked immunosorbent assay (ELISA), or the western blot (VARL). None of these tests will diagnose atopic dermatitis. This diagnosis should be made prior to testing. These tests are only to be used for selection of allergens for hyposensitization therapy.
There are many advantages to in vitro testing for atopy compared with the IDT. Testing requires only that a fasting serum sample be taken. There is no need for sedation or mechanical restraint of the dog. Sampling of the dog is quick, safe, and relatively painless. Results are reported in a semi-quantitative manner. To perform an IDT requires maintenance of test allergens, which can be both time-consuming and costly for the average practitioner. Interpretation of skin test results is a very subjective art and differs between veterinarians reading the test as well as interpretation of the same test by an individual practitioner. To feel very comfortable reading the results of an intradermal skin test takes a lot of practice. There are currently 8 different commercial companies or universities offering ASIgES to practitioners in the United States. The question comes down to how to determine which company to use. Several investigators have shown that identical serum samples submitted to different companies would often yield different results, not only in absolute terms, but also as to which allergens are recommended for inclusion in the allergy vaccine. Each company has set a different point for positivity. It is also known that a clinically normal dog can have an elevated level of serum IgE directed against a particular allergen without manifesting pruritus.
The ideal method for comparing test results from different companies would be to evaluate the success rate of therapy in the patients who have undergone hyposensitization with allergens chosen based on the results provided by that company. There are currently no good comparative studies available. What we therefore can evaluate are comparative factors such as cost to the client, ease in submitting and obtaining results, source and numbers of allergens tested, the use of single versus grouped allergens, source of anti-canine IgE, type of anti-canine IgE (e.g. monoclonal), and specificity of anti-canine IgE (i.e. has it been tested and shown not to cross-react with IgG, etc.) Unfortunately none of the ASIgES has been shown to be accurate in the diagnosis of food allergy.
When success rates of hyposensitization are determined, investigators evaluate many different things. In some studies, patients are evaluated in a double blind method. In others, client satisfaction is the only parameter evaluated. The length of time that the patients are treated before evaluations are made also differs between studies. In some hyposensitization protocols recommended by the companies supplying the allergens, the maintenance concentration of allergens is not given until almost 9 months after the beginning of therapy where other protocols have patients receiving maintenance concentrations of allergens after only 1 month of therapy. The concentration of maintenance allergens also varies from 20,000 PNU/ml to 1/60 wt/vol.
In one well-controlled blinded study by Willemse it was determined that if a dog showed no response to hyposensitization after 9 months of therapy with a maintenance concentration of allergens, the chances were that the dog would not respond. In that study, dogs were treated with alum-precipitated allergens achieving a final pollen concentration of 10,000 Noon units/ml. One milliliter of allergy vaccine at the final concentration was given by the ninth week of therapy.
Based on these findings, I therefore treat all of my canine patients with whatever source or concentration of aqueous allergens that have been prescribed by the referral practitioner but use the intense low-dose schedule established by Reedy and Miller. In this way, after a 29-day build-up to the highest concentration of vaccine, dogs are injected subcutaneously weekly until the owners notice a clinical improvement. Once that has been achieved, the frequency of the injection is decreased until eventually, if possible, the vaccine is given no less than once a month. If the symptoms worsen, the frequency of injections is increased to weekly until improvement is once again seen. If an owner has treated a dog with aqueous allergens for 1 year at weekly intervals with the highest concentration of vaccine provided and the dog shows no improvement, I let the owner decide if they want to continue.
It seems that no matter which test is performed to select allergens, what the source of allergens, the concentration of the allergens, or the frequency of the injections, all published reports show that about 60% of the dogs show some improvement of their AD when treated with hyposensitization. This raises the question of the exact role of allergen-specific IgE in the pathogenesis of canine AD.
In addition to hyposensitization, many animals can benefit from symptomatic treatment of pruritus. Glucocorticoids are the mainstay of effective therapy. Their use is very effective but in many cases the side effects outweigh the benefits. I advise that you only use oral prednisone or prednisolone. If medication is needed for more than 4 months of the year, dose at 0.5 mg/kg or less every other day to minimize side effects. Injectable corticosteroids have no place in the long-term management of pruritic diseases of the dog.
Antihistamines are beneficial in only about 10% of the cases. Chlorpheneramine maleate (Chlortrimeton®), 0.5 to 2 mg/kg q 8 to 12 hours, diphenhydramine HCl (Benadryl®), 2 to 4 mg/kg q 8 to 12 hours, or hydroxyzine HCl (Atarax®), 2 to 6mg/kg q 8 to 12 hours, are available as generic medications and are relatively inexpensive. Astemizole (Hismanal®), 0.25 mg/kg up to q 12 hours, cetirizine (Zyrtec®) 5 to 10 mg q 24 hours in dogs < 7 kg or 10 mg q 12 to 24 hours in dogs > 7 kg, clemastine 0.05 to 0.1 mg/kg up to q12 hours, clomipramine (Anafranil®), 1.0 mg/kg q 24 hours, doxepin HCl (Sinequan®,) 0.5 to 1.0 mg/kg up to q 8 hours, loratidine (Claritin®) 0.5 to 1.0 mg/kg/ q 24 hours, or cyproheptadine HCl (Periactin®) 0.5 to 5 mg/kg given q 8 to 12 hours can be tried. Chlorpheneramine, 2 mg/ cat given q 12 hours, has some degree of success.
Miscellaneous non-steroidal anti-inflammatory drugs may also be tried. Aspirin and phenylbutazone are not particularly effective. Fatty acid nutritional supplements containing eicosapentaenoic acid (EFA-Z®, Virbac; Derm Caps® or 3V Capsules®, DVM Pharmaceuticals; and PetDerm OM®, Pfizer Animal Health) are some of the veterinary products available. It may take from 6 to 12 weeks before they are effective. These supplements are reported to reduce pruritus in 15% to 20% of atopic dogs.
Topical therapy is a valuable addition to the management of pruritic diseases. Shampoos and rinses should be used to help treat the secondary bacterial and/or yeast infections. Products containing benzoyl peroxide (DermaPet Benzoyl Peroxide, Micropearls High Suds Benzoyl Peroxide, Oxydex, Pyoben, Sulf/Oxydex) used weekly are very helpful in controlling recurrent Staphylococcal infections. Other antibacterial active ingredients include products containing povidone iodine (Welladol), and products containing chlorhexidine (Chlorhexiderm, Hexadene, Nolvasan, Resichlor). Other shampoos and rinses contain antifungal agents (Dermazole, Malaseb, Nizoral, Resizole). Some shampoos and rinses contain ingredients that can help to alleviate pruritus. The simple act of bathing itself may relieve pruritus by changing the surface temperature of the skin. Some products are non-irritating and "hypo-allergenic" (Allergroom, DermaPet, HyLyte, dishwashing liquid) while other products contain specific "anti-itch" properties or ingredients (Cortisoothe, Epi-soothe, Histacalm, Relief, Resicort, Resisoothe). Shampoos containing tar and sulfur or salicylic acid are not needed since the majority of scaling and crusting is secondary to infections, inflammation and pruritus.
A recent study showed that the symptoms of canine AD could be controlled with the use of cyclosporine (Neoral®), 5 mg/kg q 24 hours. Minimal side effects were reported. The major disadvantage to the use of this drug is the cost.
Solar dermatoses are caused by chronic exposure to direct or reflected sunlight especially in the UVA (320 to 400 nm) and UVB (290 to 320 nm) range. White skin, light skin, or damaged skin that is not sufficiently covered by hair is the most susceptible to solar damage.
There are several characteristic histopathologic changes seen in the skin of man and animals with chronic solar damage. Solar elastosis is a degeneration of the subepidermal elastin fibers forming a dense subepidermal blue meshwork of altered fibers. Solar changes to collagen involve homogenization of the subepidermal collagen until the normal fibrillar structure is no longer recognizable. Solar induced dermal fibrosis is the dense subepidermal band of fibrosis that forms as a result of a chronic, solar-induced, superficial perivascular dermatitis.
Actinic keratosis are single or multiple, plaque-like or papillated lesions with a prominent, adherent scale. These lesions are found most commonly on the pinnae, nose, and eyelids of white-faced cats and the ventral abdomen or medial thighs of short-coated, white-haired dogs. As in man, these lesions can progress to become frank squamous cell carcinomas. Histopathologically they are characterized by hyperplasia and dysplasia of the epidermis and superficial hair follicle epithelium and hyperkeratosis over areas of solar elastosis. Therapeutic options include surgical excision, cryotherapy, laser therapy, or observation without treatment.
Squamous cell carcinoma (SCC) is the most common malignant neoplasm of the skin of cats and the second most common in dogs. Cats are usually 5 years of age and older with an average age of onset of 9 years. Dogs can develop lesions as young as 3 years of age but the average age of onset is also 9 years.
The clinical signs of SCC are variable. Animals can develop plaque-like, crateriform, papillary, or nodular lesions. Most are usually alopecic, erythematous, ulcerated, and/or crusted. Lesions are found most commonly on the pinnae, nose, and eyelids of white-faced cats and the ventral abdomen or medial thighs of short-coated, white-haired dogs. In cats, the tumors may be highly destructive with a gradual loss of the pinnae or nose. Squamous cell carcinomas are generally locally invasive and slow to metastasize.
The histopathology of SCC shows lesions comprising islands and trabeculae of squamous cells originating from the epidermis and extending into the dermis. Accumulations of compact laminated keratin, or keratin pearls, are present in variable numbers.
Clinical management of SCC involves combinations of surgical excision, cryosurgery, electrosurgery, hyperthermia, and radiotherapy. Further solar avoidance may slow down the progression of the lesions but the previously existing solar damage cannot be repaired. The use of water-resistant high sun protection factor (SPF) sunscreens can aid in providing solar protection against UVB radiation.
Solar folliculitis and furunculosis has been described in some older shorthaired, light skinned dogs. Chronic solar exposure can lead to development of a deep pyoderma. Histopathologic examination of diseased skin demonstrates changes consistent both with solar damage, folliculitis, and furunculosis. Actinic comedones are seen in the upper parts of hair follicles. They are filled with dense keratin. There is also moderate to marked fibrosis around these actinic comedones. Secondary bacterial infections are due to increased keratin in the hair follicles (follicular plugging) and secondary follicular rupture leads to the development of furunculosis. Treatment of these cases involves future solar avoidance and the use of long-term anti-Staphylococcal antibiotics.
Cutaneous solar-induced hemangiomas and hemangiosarcomas have also been described. They most commonly are found in dogs about 10 years of age. There is a slightly increased incidence in females. Whippets, Dalmatians, beagles, greyhounds, American staffordshire terriers, and English pointers are at increased risk.
Lesions have been reported in the skin of the ventral abdomen and inguinal region in light-skinned breeds of dogs as the result of chronic solar irradiation. They are ill defined, red to dark blue plaques or nodules that usually measure less than 2 cm in diameter. Histopathologic examination of the lesions shows an increase in the number and size of the superficial subepidermal small blood vessels. Some post-capillary venules become tortuous. Cavernous hemangiomas and hemangiosarcomas may arise from the telangiectatic vessels and all three lesions may be seen concurrently.
Treatment consists of radical surgical excision. The development of these lesions carries a poor prognosis since metastasis and local recurrence are common. The average survival time after diagnosis is 4 months.
Color dilution alopecia/black hair follicular dysplasia (color mutant alopecia) occurs in dogs with a blue (dilution of black) or fawn (dilution of red) haircoat. The dilute hairs have larger pigment granules (macromelanosomes) than their nondilute counterparts. The condition is most widely recognized in blue and fawn Doberman pinschers but has also been reported in dachshunds, great Danes, whippets, Italian greyhounds, chow chows, and others.
The syndrome is first seen as a dorsally oriented recurrent bacterial folliculitis or hypotrichosis. The onset of the signs is tardive and may occur as early as 6 months or as late as 3 years of age.
The diagnosis can be made by microscopic examination of plucked hairs. Macromelanosomes of irregular size and shape will be found unevenly distributed along the hair shaft. The cuticle may be absent or fractured over the bulging pigment clumps. Histopathology shows melanin clumping in the epidermal and follicular basal cells and hair matrix cells. Numerous peribulbar melanophages are recognized. In time, the follicles become dilated and cystic and follicular activity ceases.
Early hair loss is due to fracture of the hair shaft so the animal should be bathed and groomed gently. Many of these animals are treated very frequently or with low doses of maintenance antibiotics. There are anecdotal reports of improvement with the use of oral retinoic acids but details are unavailable and the drugs are very expensive when used in large dogs for long periods of time.
Black hair follicular dysplasia is the same syndrome but occurs only in the black areas of dogs with bicolor or tricolor coats. Basset hounds, Boston terriers, and pointers as well as mongrel dogs have been diagnosed with this condition. The diagnosis can be made by examination of hairs from the affected areas or by skin biopsy.
Hypothyroidism is the most common endocrinopathy of the dog; it is very rare in other species. Hypothyroidism as a clinical entity has not been well documented in the cat. The disease can occur at any age but is most commonly seen in dogs between 6 and 10 years. The onset tends to occur at an earlier age (2 to 3 years) in large and giant breeds. There is no sex predilection. Hypothyroidism may affect any breed (including mixed breeds) but there is a predisposition in the Doberman pinscher, golden retriever, chow chow, Afghan hound, great Dane, English bulldog, dachshund, boxer and malamute.
The clinical disease is caused by diminished circulating levels of thyroxine (T4) and triiodothyronine (T3). Affected dogs may present with a variety of clinical signs including lethargy or depression, increased sleeping, personality changes, weight gain, hypothermia, and a "tragic" expression (due to an accumulation of hyaluronic acid (mucin) in the interstitial ground substance). Cutaneous changes include alopecia, symmetrical or asymmetrical, that is usually worse in frictional areas such as the tail, under the collar, and ventral abdomen. The remaining hairs are usually dull, dry, brittle and easily epilated. The skin may be thick, cool and puffy due to edema and pigmentary changes (hyperpigmentation is more common) can be seen. Many dogs will present with a pyoderma or follicular plugging with comedone formation and folliculitis. Hypothyroid dogs are usually not pruritic but may be pruritic if there is pyoderma or Malassezia colonization of the skin. Many dogs will also have otitis externa.
In diagnosing hypothyroidism, non-specific changes can be noted in routine blood work. Approximately 25% of the cases will have a normocytic, normochromic, nonregenerative anemia (PCV=25 to 36%). Approximately 30 to 60% of the cases will have hypercholesterolemia (260 to 1000 ug/dl), lipidemia, an increased CPK, LDH, SGOT, SGPT and/or SAP.
No single test is completely reliable for diagnosing hypothyroidism. Radioimmunoassay of T3 and T4 is the most sensitive, specific, and reproducible test. Measuring baseline thyroid hormone levels (T4 and/or T3) will miss approximately one third of the hypothyroid cases. The methodology of the TSH response test varies from one report to another. There is no data to suggest that one method is superior to another and TSH is currently unavailable. A thyroid biopsy is always diagnostic and can distinguish between primary and secondary hypothyroidism. It is the only reliable method to diagnose lymphocytic thyroiditis. Other tests involve the measurement of free T4, the measurement of TSH, or determination of "k" values.
Once a diagnosis is made, therapy needs to be continued for the life of the animal. Sodium levothyroxine (T4) 0.02 mg/kg body weight PO q 12 hours is the recommended drug of choice. It is difficult to overdose a patient with this medication and complications are rare. Attitudinal changes are seen within 2 to 4 weeks and skin and hair coat response are seen from 6 weeks to 5 months after the initiation of therapy.
Once therapy has been initiated, post-pill testing should be performed 6 to 12 weeks after beginning therapy. Serum T4 is measured either 6 hours (4 to 8 hours) after medicating, looking for a level in the mid to high normal range, or 12 hours after medicating, looking for a value in the mid to low normal range. Blood values should correlate with clinical signs. Therapeutic failures are seen if the diagnosis is wrong, the dose of medication is incorrect, or the animal produces autoantibodies against T3 and/or T4.
Pemphigus foliaceus (PF) is the most common disease in the pemphigus complex. The major p. foliaceus antigen is a 150-kD glycoprotein (desmoglein I) from the cadherin group of adhesion molecules. Canine breeds at highest risk for developing PF are the Akita, chow chow, and Doberman pinscher. The average age of onset is 4 to 5 years.
Lesions consist of a transient subcorneal pustule that leads to extensive areas of erythema, crusting, and hair loss. The disease usually begins on the face around the nose, lips, eyes, and pinnae. The footpads and groin are also commonly involved. In cats, paronychia and lesions around the nipples are common. Mucosal lesions are rare. Severely affected animals are often pyrexic and have secondary bacterial infections of the skin.
A direct impression smear from a pustule or erosion may demonstrate neutrophils and acantholytic keratinocytes. Histologically PF is characterized by intragranular or subcorneal acantholysis with cleft, vesicle, or pustule formation. Within the resultant epidermal pustules, individual or rafts of keratinocytes may be seen. These cells can be attached to the overlying stratum corneum or floating freely. Direct immunofluorescence demonstrates intercellular deposition of IgG or complement
Vitiligo is believed to be a hereditary disease that also has an autoimmune basis. The onset of the condition is usually in young adulthood. It has been described in the Belgian Tervueren, German shepherd, rottweiler, Doberman pinscher, giant schnauzer, and Siamese cat. Antimelanocyte antibodies have been identified in some cases.
Affected animals develop a symmetric macular to generalized depigmentation of the nose, lip margins, buccal mucosa, footpads, and skin. Eventually the claws and haircoat may become involved.
A diagnosis is based in the signalment, history, physical examination, and histopathologic changes. Late lesions of vitiligo are characterized by a relatively normal epidermis and dermis except that no melanocytes are seen.
Successful treatment has not been reported, although a small number of cases may spontaneously improve.
Nodular dermatofibrosis is an inherited syndrome in the dog with a tardive onset. It is characterized by multiple cutaneous collagenous nodules, primary bilateral multifocal renal cystadenomas, cystadenocarcinomas, and/or uterine leiomyomas. The disease affects primarily German Shepherd dogs but has been reported in a rare few other breeds. The age of onset of the dermatosis is average of 8.5 years and there is an equal distribution seen between males and females.
In theory, the pathogenesis consists of genetic factors plus some other unknown trigger that leads to the production of cytokines (growth factors). These cytokines in turn lead to renal tubular epithelial cell proliferation, uterine smooth muscle cell proliferation, and dermal fibroblast proliferation.
Clinical signs consist of cutaneous nodules, from a few to many. These are firm, well-circumscribed dermal and subcutaneous nodules that vary from several millimeters to up to 4 cm in diameter. The surface can be haired or alopecic and the nodules are often hyperpigmented. Nodules are most commonly located on the distal extremities, head, and ears. Systemic signs may consist of hematuria, weakness, anorexia or weight loss. In some dogs there are clinical signs associated with renal failure or metastatic disease.
The differential diagnosis for the cutaneous nodules consists of granulomas or pyogranulomas (bacterial, fungal, mycetomas), cutaneous histiocytosis, or neoplasia.
Results of a complete blood count and serum chemistry analysis are usually within normal limits unless the animal is in renal failure. The urinalysis may demonstrate white blood cells, red blood cells, or crystals. A urine culture is usually negative. Abdominal radiographs may detect an enlarged cystic kidney. Thoracic radiographs may detect pulmonary metastasis. An abdominal ultrasound can detect small renal cysts and renal scintigraphy may detect a reduced glomerular filtration rate.
Histopathology of skin biopsies reveals increased collagen which can be sclerotic (pathologists often report normal skin). The renal gross pathology shows renal enlargement and multiple cortical cysts (1 mm to 10 cm) which often contain yellow, gray, brown, or red fluid or soft gelatinous debris. Renal histopathology of early lesions demonstrates a hyperplastic papillomatous tubular epithelium and cystic dilation of renal tubules. In late stages there are large cystic tubules lined by neoplastic cubiodal tubular epithelium or solid neoplastic nodules. At necropsy you may find osseous metaplasia in the lungs, collagenous proliferation, a hemoperitoneum and peritonitis, and possibly metastasis of renal adenocarcinoma.
If the cutaneous nodules are small, no treatment is necessary. If they are large and ulcerated, they can be surgically removed or the dog can be treated with antibiotics. It has been suggested that colchicine or glucocorticoids may be useful. The renal adenocarcinomas can be surgically removed and the dog treated with chemotherapy. If there is a uterine leiomyoma, ovariohysterectomy is recommended.
Nodular dermatofibrosis is a slowly progressive disease with a poor long-term prognosis. Death usually results from renal failure, metastatic disease, or euthanasia.
In many cases of canine claw disease the dog is presented with onychorrhexis, onycholysis, onychomadesis and/or onychodystrophy of all the claws. If a biopsy is obtained either with the use of an 8 mm punch biopsy or by amputation of the third phalanx of an affected digit, the changes seen are diagnostic of a condition called symmetric lupoid onychodystrophy. Histopathologically the disorder is characterized by hydropic and lichenoid interface dermatitis with pigmentary incontinence. The exact etiology of this condition is unknown. In several studies the German Shepherd dog was noted to be predisposed.
Several different therapeutic protocols have been tried with success. If the claws are loose, they should be avulsed under general anesthesia. There is usually minimal hemorrhage so bandaging is usually not necessary. Antibiotics can be prescribed to be used for 4 to 8 weeks if bacteria are either identified with a cytologic examination or by culture. If the underlying bone is normal then the claw will regrow normally. If the third phalanx has undergone deterioration then when the claw regrows it will be hollow. If the claws are still tightly adhered then treatment with fatty acid supplements such as Derm Caps® has been reported to be of benefit. Others have reported success with treatment using doxycycline (5 mg/kg/day) and niacinamide (250 mg if the dog weighs less than 10 kg or 500 mg for dogs weighing more than 10 kg q 8 hours).
Systemic lupus erythematosus (SLE) is an uncommon disease in veterinary medicine. Collies, Shetland sheepdogs, and German shepherds are the most common canine breeds affected and Siamese, Persian, and Himalayan cats may be predisposed.
SLE frequently affects the kidneys (proteinuria), joints (polyarthritis), hematopoetic system (anemia, thrombocytopenia), and muscles. Dermatologic lesions are usually not the most significant symptom. When present, cutaneous lesions are diverse and include scaling, alopecia, ulceration, and loss of pigment. Skin lesions may be multifocal or generalized and commonly involve the face, ears and distal extremities.
Cutaneous lesions of SLE occur by three proposed steps. First, ultraviolet light induces expression of ICAM-1 and autoantigens previously found only in the nucleus or cytoplasm (e.g. native and denatured DNA) on the keratinocyte surface. The autoantibodies specific to these antigens attach to the keratinocytes and induce antibody-dependent cytotoxicity. The injured keratinocytes then release IL-2 and other lymphocyte attractants as well as inflammatory mediators associated with elevation of antinuclear antibody (ANA).
Histologic findings in SLE are variable. The most characteristic findings include interface and/or lichenoid dermatitis, subepidermal vacuolar alteration, thickening of the basement membrane zone, and dermal mucinosis. Direct immunofluorescence reveals the deposition of immunoglobulin (IgA and IgM most commonly) and/or complement (C3) at the basement membrane zone.
Acral lick dermatitis, also known as lick granulomas, results from licking, usually on the lower cranial portion of a leg, producing a thickened, firm, oval, ulcerated lesion. Boredom or a psychological insult is often the initiating cause of this habit.
Lesions can occur in any age dog but the majority appear in dogs over 5 years of age. Males are predisposed over females two to one. Predisposed breeds include the Doberman pinscher, great Dane, Labrador retriever, Irish setter, golden retriever, and German shepherd dog.
In most cases the dog develops a single lesion. The most common site is the cranial carpal or metacarpal area. Alopecia is the first sign but chronic lesions become hard, thickened plaques or nodules that have an ulcerated surface and are surrounded by an area of hyperpigmentation.
A tentative diagnosis can be made from the history and clinical examination. A biopsy and histopathologic examination will rule out other diseases such as neoplasia, mycotic granuloma, or pressure point pyoderma.
There are many potential therapies that have been shown to be helpful in the management of this disease. The first step is to try and identify the cause of the dog's anxiety and eliminate it. Many ulcerated lesions are secondarily infected so the use of oral antibiotics for 30 to 60 days will help heal may of them. Topical, oral, or intralesional corticosteroids may be helpful. Topical capsaicin or foul-tasting substances such as Bitter Apple may break the cycle of licking in some cases. Other drugs that have been reported useful are phenobarbital, diazepam, hydroxyzine, fluoxetine (Prozac®), amitriptyline (Elavil®), clomipramine (Anafranil®), naltrexone (Trexan®), and megestrol acetate (in male dogs). Other treatments have involved the use of surgery, radiation therapy, cryosurgery, or acupuncture.
Icthyosis is a rare congenital disease that has been reported in dogs and 1 litter of cats. Too few dogs have been reported in veterinary medicine to characterize the disorder. Because the parents of affected dogs have been normal and the disease has been recognized in both sexes, an autosomal recessive mode of inheritance is most likely. Most cases resemble lamellar icthyosis in man due to epidermal hyperproliferation.
The disease is most common the west highland white terriers but has also been recognized in the Doberman pinscher, Golden retriever, Irish setter, Collie, Bull terrier, Cavalier King Charles spaniel, Norfolk terrier, Rottweilers, and others.
Much of the body is covered with tightly adherent, verrucous, tannish-gray scales and feathered keratinous projections which give the skin a rough texture. Large quantities of odorous debris accumulate on the skin surface. Scaly, erythematous dry patches are particularly prominent in the flexural creases and intertriginous areas. Masses of hard keratin accumulate at the margins of the pads. Some dogs have erythroderma and hair loss.
The diagnosis is made as the dog is presented in early puppyhood and no other diagnoses are appropriate. Confirmation is made with a skin biopsy that reveals changes of a prominent granular cell layer and an excessive number of keratinocytes in mitosis. Orthokeratotic hyperkeratosis is marked on the surface and within the follicular epithelium.
Management of the disease involves the frequent use of baths and emollient rinses. Ointments or solutions of 3 to 12% lactic acid, 60% propylene glycol, or both are beneficial in humans.
Hyposomatotropism (pseudo-Cushing’s syndrome or growth hormone-responsive dermatosis) is a rare condition. The disease has been reported predominantly in male dogs. Chow chows, keeshonds, Pomeranians, and miniature poodles are at higher risk for developing this disease. The age of onset is between 9 months and 11 years with about 50% of the affected dogs being younger than 2 years of age.
The cause and pathogenesis are unknown. There is a gradual loss of primary hairs with retention of secondary hairs giving the coat a puppy-like appearance. With time, all of the hairs are lost around the neck, pinnae, tail, and caudomedial thighs. In many cases the exposed skin may be thin and hypotonic and hyperpigmented. In some cases dogs are presented after having been shaved and failing to regrow a normal haircoat.
The diagnosis is based on the history, physical examination, laboratory tests that rule out other endocrinopathies, and a response to therapy. Histopathology of the skin reveals changes consistent with an endocrinopathy. Measurement of plasma GH levels before and after an IV injection or clonidine or xylazine can document GH deficiency in some cases. The University of Tennessee Clinical Endocrinology Service (865 974 5638) can measure 6 different adrenal steroidal hormones pre and post ACTH stimulation which can also aid in the diagnosis of this condition.
Until the pathogenic mechanism of this disorder is completely defined, treatment recommendations are difficult. Some dogs will regrow hair after neutering or treatment with o,p’-DDD. Response has been seen with the use of bovine, porcine, and human growth hormone but GH is not available to veterinarians on a regular basis. A few dogs have been reported to regrow their hair 60 days after treatment with oral melatonin, 3 to 5 mg BID PO for 30 days.
Sebaceous adenitis is a clinical disease that results from destruction of the sebaceous glands. Studies in the standard poodle suggest that the disease may have an autosomal recessive mode of inheritance. There is no sex predilection but there may be a breed predilection for the Vizsla, Akita, Samoyed, and standard poodle. A few rare cases have been reported in the cat.
The dermatologic abnormalities are usually bilaterally symmetrical. Lesions are usually worse on the head, pinnae, and trunk. In the Vizsla, lesions are generally annular areas of scaling and alopecia. The scales are fine, white, and nonadherent. The lesions are usually asymptomatic unless a secondary staphylococcal infection occurs. The standard poodle manifests marked hyperkeratosis followed by alopecia. The hairs are dull and brittle with tightly adherent silver-white scale that incorporates small tufts of matted hair. Akitas tend to have a fairly generalized skin disease with erythematous and greasy skin changes. Papules, pustules, scales, matting of the hair, and accumulations of greasy keratosebaceous debris are prominent. Severe hair loss, especially of the undercoat, is prominent. Samoyeds develop moderate to severe, predominantly trunkal alopecia and scaling. Hairs are dull, brittle, and broken. Follicular casts are prominent.
The diagnosis is made by noting the signalment of the dog and the finding of follicular casts attached to the hairs when they are epilated. Histopathology will confirm the diagnosis. In early cases there is sebaceous adenitis which is granulomatous to pyogranulomatous. Later, the glands are no longer visible and the diagnosis is based on the finding of discrete perifollicular granulomas in areas where sebaceous glands are normally found. In long-standing cases there is prominent hyperkeratosis of the surface and follicular epithelium.
The disease process cannot be reversed but the patient can be managed with several therapies. Keratolytic shampoos and emollient rinses are useful in the early and mild cases. Topical application of 50 to 75 percent propylene glycol in water as a spray or final rinse can be used in more severe cases. Some dogs respond to the addition of fatty acids to the diet. Vitamin A or synthetic retinoids have been reported to help some animals. Dogs that are pruritic or have an odor usually respond to antibiotic therapy and some need to be treated with maintenance doses.
Schnauzer comedo syndrome is a seborrheic or acneiform disorder that occurs only in predisposed individuals of this breed. Comedones form over the dorsal trunk. These can be palpated as sharp, crusted, papular projections. There is no pain or discomfort. In some cases, the comedo changes into a soft, small, acne-like pustule and causes slight irritation. In some dogs the plugged follicles become secondarily infected and pain or pruritus can develop secondary to the staphylococcal infection.
The diagnosis is made by visualization of the comedones and papules on the dorsum of a miniature schnauzer with no other signs of disease. The diagnosis can be confirmed with a skin biopsy.
Mild cases require no treatment. If the owner finds the lesions objectionable then topical therapy with either a benzoyl peroxide-containing gel or shampoo or a shampoo containing sulfur and benzoyl peroxide can be used.
Follicular dysplasia is actually a group of diseases characterized by coat changes including alopecia. The condition is non-color-linked and has been recognized in a variety of breeds. The alopecia can begin during puppyhood or early adult life and is slowly progressive. The features of the disorder vary somewhat with the breed involved.
In Siberian huskies and malamutes multiple dogs in a litter can be affected. Around 3 to 4 months of age the guard hairs on the trunk are lost in a slowly progressive fashion. The coat will change to a reddish color. The head and distal extremities are usually spared. If the hair is clipped it usually does not regrow.
The Irish water spaniels, Portuguese water dogs, and curly-coated retrievers lose hair secondary to the fracture of the hair. Alopecia is usually not recognized until 2 to 4 years of age. Hair loss is first evident over the causal dorsum and spreads slowly to involve most of the trunk. The distribution of the alopecia can mimic pattern alopecia. Regrowth of hair can occur but the new hairs are not of normal quality.
The diagnosis is confirmed by histopathology. Surface and follicular hyperkeratosis, a variation in follicular activity with a high frequency of catagen arrest, melanin clumping within the hairs and hair bulbs, fractured hair shafts with clumps of free melanin in the hair follicle lumen, and peribulbar melanophages are characteristic findings.
Several different zinc responsive dermatoses have been recognized. Zinc deficiency in bull terriers is inherited as an autosomal recessive trait called lethal acrodermatitis. The clinical condition is postulated to be due to abnormal zinc absorption and/or metabolism. Clinical signs include growth retardation, gastrointestinal disorders, and increased susceptibility to infections. Cutaneous signs are first seen around 6 weeks and include fissured footpads, pododermatitis, and facial and pressure point pyoderma. Affected dogs have a cell-mediated immunodeficiency and usually die of bronchopneumonia. The mean survival time is 7 months. There is usually minimal to no response to treatment with oral or parenteral zinc supplementation.
Three additional subgroups of zinc responsive dermatosis have been described. The first is seen in Arctic breeds of dogs such as Siberian huskies and Alaskan malamutes. The second occurs in large, rapidly growing puppies, especially those fed diets that have been over supplemented with calcium. The third has been described in dogs (especially puppies) that have been fed a poor quality food that fails to meet NRC standards and contains low amounts or poorly bioavailable amounts of zinc.
Histopathology of any zinc-deficiency or zinc-responsive condition shows large amounts of both surface and follicular parakeratosis with dyskeratosis.
Therapy involves improving the diet and supplementation with zinc. Zinc sulfate can be used at 10 mg/kg SID. Zinc gluconate given so that the dog receives 1.5 mg of elemental zinc/kg SID is also effective. Side effects include anorexia, nausea, and vomiting. These may be avoided by dividing the daily dose or administering it with food.
Epidermal dysplasia of the west highland white terrier is an uncommon condition, which tends to occur in families. It is probably transmitted as an autosomal recessive trait. Dogs with this condition have a dysplastic epidermis and inflammatory perivascular dermatitis associated with Malassezia colonization.
Dogs of either sex can be affected and clinical signs usually begin between 6 and 12 months of age. Typically, affected dogs have a greasy coat before developing pruritus, the primary clinical sign of this disorder. The pruritus is initially focused at the face, ears, feet, and ventrum. The involved skin is inflamed, greasy, and collects large amounts of keratosebaceous debris. With advanced disease there is almost total alopecia, lichenification, and hyperpigmentation of the skin and the pruritus is intense. The pruritus does not respond to the use of antibiotics, antihistamines, or antiseborrheic shampoos and minimally to corticosteroids.
The diagnosis is one of exclusion. Diseases such as food allergy, scabies, and Malassezia dermatitis need to be ruled out. Histopathologic changes seen on a skin biopsy are not diagnostic for this condition.
The condition is frustrating to manage and many dogs are euthanized at a young age. Treatment of the Malassezia dermatitis improves many of the animals but the infections frequently recur. Attempts to prevent recolonization with the use of shampoos has been unrewarding.