Small and Large Animal Dermatology

Disorders of Keratinization Skin Diseases

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Disorders of KeratinizationGeneral Considerations – Canine

A. General Considerations:

1. Keratinization disorder is a term used to describe clinical findings associated with abnormalities in the process of epidermopoiesis, keratinization, apocrine or sebaceous gland function, intercellular lipid formation, cell cohesion, or cell desquamation.

2. Scaling is a clinical sign always present .

3. Alterations in glandular secretions will result in either excessive sebum production (seborrhea oleosa) or deficient sebum secretion (seborrhea sicca).

4. Alterations in hair follicles will result in follicular casts (keratin surrounding the follicular portion of the hair shaft) and comedones (black heads – the infundibulum (portion of the follicle close to the skin surface) of the hair follicle is dilated and filled with keratin).

5. Malassezia and bacterial infections are frequently observed in many keratinization disorders due to alterations in the surface microenvironment and alterations in the stratum corneum.

6. The diagnostic challenge when managing a scaling disorder is to determine if the clinical signs are secondary to an underlying dermatosis or are the result of a primary keratinization defect.

7. Therapeutic and prognostic factors for keratinization disorders are variable.

8. In general, if the keratinization disorder is secondary to an underlying disease and the underlying dermatosis is identified and treated, the keratinization disorder has an excellent prognosis for complete cure and control.

9. If there is a primary keratinization defect, some continued therapy is usually required for the life of the animal.

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Important Facts

Scaling is always present with any disorder of keratinization.

Alterations in glandular function can also occur resulting in seborrhea oleosa, if excessive sebum secretion accompanies the scaling or seborrhea sicca, if decreased sebum secretion is associated with scaling.

Comedones (black heads) and follicular casts (keratin surrounding the follicular portion of the hair shafts) are also signs of disorder of keratinization.

Secondary pyoderma and malassezia infections are common!

In general, if the keratinization disorder is secondary to an underlying disease and the underlying dermatosis is identified and treated, the keratinization disorder has an excellent prognosis for complete cure and control.

If there is a primary keratinization defect, some continued therapy is usually required for the life of the animal.

B. Classification:

1. Keratinization disorders can be classified by 2 methods:

a. Clinical signs.

b. Etiology: primary or secondary.

2. Clinical Signs:

a. Seborrhea sicca:

1. White, loose scales. Dry form. Hair coat is dull, dry.

2. Odor is usually not present.

b. Seborrhea oleosa:

1. Greasy yellow brown scales. Hair coat is oily. Keratin deposits adhere to hairs.

2. “Rancid fat” (seborrheic) odor.

3. Secondary Malassezia and bacterial infections are common.

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4. In some cases, you need to touch the animal to differentiate a seborrhea oleosa from a seborrhea sicca. If the seborrhea is oleosa, your fingers become coated with a thin layer of oil.

c. Seborrheic dermatitis:

1. It is the inflammatory form.

2. Scaling with or without greasiness and gross evidence of inflammation characterize this form.

3. Multifocal hyperkeratotic plaques.

4. Rule out Malassezia and bacterial infections.

d. Seborrheic (ceruminous) otitis externa:

1. Excessive waxy debris in the ear canal.

2. Seborrheic odor and erythema.

3. Secondary Malassezia and bacterial infections are common.

4. The external ear canal is a modified extension of the skin, therefore seborrheic otitis externa is common in generalized seborrheic dermatosis.

e. REMEMBER! Secondary Malassezia and bacterial infections are common.

Important Facts

Based on clinical signs, the keratinization disorders can be classified in: seborrhea sicca, seborrhea oleosa, seborrheic dermatitis and seborrheic otitis externa.

Seborrhea sicca is characterized by white, loose scales. The coat is dry and dull.

Seborrhea oleosa is characterized by greasy yellow-brown scales which can adhere to the hair, oily coat, and “rancid fat” odor.

Seborrheic dermatitis is characterized by scaling and inflammation.

Secondary Malassezia and bacterial infections are commonly present in disorders of keratinization.

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3. Etiology:

a. Secondary Keratinization Disorders:

1. External or internal cause with effect on keratinization or sebum production.

2. Inflammation associated with the primary condition and/or self-trauma result in the keratinization disorder. Therefore, scaling with or without excessive sebum secretion is observed in areas affected by the dermatosis.

3. Secondary keratinization disorders may occur with most types of diseases, including:

a. Parasitic: Cheyletiella, Demodex, Sarcoptes.

b. Allergic: atopic dermatitis, food, flea, contact.

c. Endocrine: hypothyroidism, Cushing’s, sex hormone dermatoses.

d. Pyoderma: epidermal collarettes associated with superficial pyodermas.

e. Autoimmune: pemphigus foliaceous.

f. Dermatophytosis.

g. Neoplastic: mycosis fungoides.

Important Facts

Secondary keratinization disorders may occur with most types of diseases and, as a result, it is seen much more often than primary keratinization disorders.

Scaling, with or without excessive sebum secretion, is observed in areas affected by the underlying dermatosis.

b. Primary Keratinization Disorders:

1. The diseases classified as primary keratinization defects are either hereditary, idiopathic, or nutritional.

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2. Hereditary Keratinization Disorders:

a. Color dilution (mutant) alopecia.

b. Follicular dysplasia/dystrophy.

c. Ichthyosis.

d. Lichenoid-psoriasiform dermatosis.

e. Sebaceous adenitis.

f. Schnauzer comedo syndrome.

g. Epidermal dysplasia.

h. Primary idiopathic seborrhea.

3. Idiopathic Keratinization Disorders:

a. Acne.

b. Ear margin seborrhea.

c. Nasodigital hyperkeratosis.

4. Nutritional Keratinization Disorders:

a. Zinc responsive dermatosis.

b. Vitamin-A responsive dermatosis.

c. Fatty acid deficiency.

Important Facts

Primary keratinization disorders can be hereditary, idiopathic or nutritional.

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I. Primary Keratinization Disorders - Hereditary Disorders

A. Color Dilution Alopecia:

1. General Considerations:

a. Color dilution alopecia is a hereditary disease characterized by a tardive alopecia (born with normal coats).

b. The disease is found in several breeds of dogs that have blue- or fawn-colored mutations.

c.The highest incidence is in the blue Doberman (93%) and fawn Irish setter (73%).

d. Other breeds in which color dilution alopecia has been observed include miniature schnauzer, dachshund, chow chow, poodle, Great Dane, whippet, Yorkshire terrier, Chihuahua, Italian greyhound, saluki and Newfoundland.

e.This disease is discussed under “keratinization disorders” because the keratinizing epithelium of the follicle and the hair cuticle are affected (ectodermal defects) as part of the disease process.

f. Defective melanization may also play a role in the pathogenesis of this condition.

g. Affected dogs have many large, irregularly shaped melanin granules in the basal keratinocytes, hair matrix cells, and the hair shafts.

h. It has been suggested that hair matrix cells are affected by the cytotoxic effects of melanin precursors which results in cessation of hair growth and eventually follicular dysplasia.

i. The extensive melanin clumping in the hair shaft and associated distortion of the cuticular-cortical structure of the hair are thought to lead to fragility and breaking of hair shafts at the sites.

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Important Facts

Color dilution alopecia is a hereditary disease characterized by a tardive alopecia.

The disease is found in several breeds of dogs that have blue- or fawn-colored mutations.

The highest incidence is in the blue Doberman (93%) and fawn Irish setter (73%).

The keratinizing epithelium of the follicle and the hair cuticle are affected as part of the disease process.

Defective melanization may also play a role in the pathogenesis of this condition.

2. History and Clinical Signs:

a. The main history is a slowly progressive alopecia in a blue or fawn colored dog.

b. Clinical signs are first noticed between 6 months and 3 years of age.

c. Recurrent superficial pyoderma is common .

d. Pruritus occurs if secondary pyoderma is present.

e. Clinical signs are characterized by the development of hypotrichosis that slowly progresses to complete alopecia. The alopecia is irreversible.

f. Dry scaling is common and usually severe.

g. Papules and pustules (cystic hair follicles with secondary bacterial infection) are also commonly seen.

h. The trunk is most severely affected, and the head and extremities least affected.

i. Tan points remain normal.

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Important Facts

Clinical signs are first noticed between 6 months and 3 years of age.

Recurrent superficial pyoderma is common .

Pruritus occurs if secondary pyoderma is present.

Clinical signs are characterized by the development of hypotrichosis that slowly progresses to complete and irreversible alopecia.

Dry scaling is common and usually severe.

Papules and pustules are also commonly seen.

The trunk is most severely affected, and the head and extremities least affected.

Tan points remain normal.

3. Diagnosis:

a. The early age of onset of progressive alopecia in one of the predisposed breeds is compatible with a clinical diagnosis of color dilution alopecia.

b. A tentative diagnosis is made from direct examination of the hair shafts (trichogram).

c. Large clumps of free melanin (macromelanosomes) are found within the hair cortex and medulla of the hair shaft. Distortion and breakage of the hair cortex or absence of cuticle may be seen.

d. Histopathological examination of biopsy samples will confirm the diagnosis.

e. Biopsies show characteristic epidermal, follicular, and pigmentary changes.

f. Differential diagnosis includes: demodicosis, bacterial folliculitis, dermatophytosis, idiopathic seborrhea and hypothyroidism in the older dog.

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Important Facts

The early age of onset of progressive alopecia in one of the predisposed breeds is compatible with a clinical diagnosis of color dilution alopecia.

A tentative diagnosis is made from direct examination of the hair shafts which shows large clumps of free melanin within the cortex and medulla. Distortion and breakage of the hair cortex or absence of cuticle may be seen.

Histopathological examination of biopsy samples will confirm the diagnosis.

Differential diagnosis includes: demodicosis, bacterial folliculitis, dermatophytosis, idiopathic seborrhea and hypothyroidism in the older dog.

4. Treatment:

a. Treatment is symptomatic.

b. This disease is chronic and poorly responsive to treatment.

c. Hair will not regrow.

d. The goal is to keep the follicles open and free of keratinous debris, and therefore less likely to become secondarily infected.

e. Benzoyl peroxide shampoo (oxyDex, SulfOxyDex, Pyoben) is especially effective because of its follicular flushing and antibacterial activity.

f. To prevent worsening of the dry scale, baths with benzoyl peroxide should be followed by a moisturizing rinse. For dogs with very dry skin the rinses can be diluted and sprayed on daily.

g. Systemic antibiotics are indicated when secondary pyoderma develops.

h. Coexisting diseases, such as hypothyroidism should also be treated since this may improve the dry skin and decrease the incidence of recurrent pyoderma.

i. These dogs should not be used for breeding.

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Important Facts

Color dilution alopecia is a chronic disease, and poorly responsive to treatment.

The alopecia is irreversible.

The goal is to keep the follicles open and free of keratinous debris, and therefore less likely to become secondarily infected.

Benzoyl peroxide shampoo (oxyDex, SulfOxyDex, Pyoben) followed by a moisturizer to prevent worsening of the dry scale, is especially effective because of its follicular flushing and antibacterial activity.

Systemic antibiotics are indicated when secondary pyoderma develops.

Coexisting diseases, such as hypothyroidism should also be treated since this may improve the dry skin and decrease the incidence of recurrent pyoderma.

These dogs should not be used for breeding.

B. Ichthyosis:

1. General Considerations:

a. Ichthyosis is an extremely rare congenital keratinization defect of dogs characterized by very severe scaling of the skin and footpads.

b. Ultrastructural studies suggest that the lesions are the result of hyperproliferation of the epidermis.

c. Ichthyosis is reported most commonly in terriers and terrier crosses.

Important Facts

Ichthyosis is an extremely rare congenital keratinization defect of dogs characterized by very severe scaling of the skin and footpads.

Ichthyosis is reported most commonly in terriers and terrier crosses.

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2. Clinical Signs:

a. Onset of clinical signs is usually observed by the owners within 1 to 2 months.

b. In most cases, the entire body is covered with tightly adherent fine white scales.

c. Some of these may appear as feathered keratinous projections.

d. The ventrum may be more severely affected.

e. There also may be extensive alopecia, hyperpigmentation, and lichenification.

f. Severe footpad hyperkeratosis is present, with the margins of the pads more severely affected.

Important Facts

Onset of clinical signs is usually observed by the owners within 1 to 2 months.

In most cases, the entire body is covered with tightly adherent fine white scales, which in some sites may appear as feathered keratinous projections.

Severe footpad hyperkeratosis is present, with the margins of the pads more severely affected.

3. Diagnosis:

a. The diagnosis of ichthyosis is strongly suggestive based on the presence of severe generalized scaling and footpad hyperkeratosis at a very young age.

b. Biopsies are the definitive diagnostic test.

Important Facts

The diagnosis of ichthyosis is strongly suggestive based on the presence of severe generalized scaling and footpad hyperkeratosis at a very young age.

Biopsies are the definitive diagnostic test.

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4. Treatment:

a. The long-term prognosis for ichthyosis is poor, not because scale formation can not be controlled but because continual therapy will be needed for the entire life of the patient.

b. Treatment is directed at controlling the scaling.

c. Topical therapy includes warm water soaks to help remove scales, antiseborrheic shampoos (sulfur, salicylic acid), antiseborrheic gels for locally severe lesions (tretinoin-Retin-A), (urea and salicylic acid-KeraSolv), and moisturizers.

d. Systemic therapy of choice is isotretinoin (1 to 2 mg/kg every 12 hours) and acitretin (1 to 2 mg/kg every 24 hours.

e. Once remission is achieved, usually in 8 to 12 weeks, alternate-day therapy with systemic retinoids may keep the scaling under control.

Important Facts

Treatment will be needed for the entire life of the patient and it is directed at controlling the scaling.

Topical therapy includes antiseborrheic shampoos and gels to help remove the scales, and moisturizers.

Systemic therapy includes the retinoids, isotretinoin or acitretin which will help control the keratinization disorder.

C. Lichenoid-Psoriasiform Dermatosis:

1. General Considerations:

a. Lichenoid-psoriasiform dermatosis is a rare, suspected hereditary condition of English Springer spaniels.

b. The pathogenesis of lesions is unknown.

c. It has been suggested that an exaggerated reaction to a superficial staphylococcal infection predisposes to the lichenoid lesions.

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d. Lesions are present in young dogs of both sexes under 2 years of age, with the most common age of onset being 4 to 18 months.

e. The lesions may wax and wane.

Important Facts

Lichenoid-psoriasiform dermatosis is a rare, suspected hereditary condition of English springer spaniels.

Lesions are present in young dogs of both sexes under 2 years of age, with the most common age of onset being 4 to 18 months.

The lesions may wax and wane.

2. Clinical Signs:

a. The clinical lesions are refractory, nonpruritic, erythematous, lichenoid papules and plaques.

b. Initial distribution includes the pinnae, external ear canal, preauricular, periorbital, and inguinal skin.

c. Papillomatous-like lesions are seen in chronic cases, which can involve the face, ventral trunk and perineal regions.

d. Generalized, greasy seborrheic scales and crusts are visible.

Important Facts

The clinical lesions are refractory, nonpruritic, erythematous, lichenoid papules and plaques.

Initial distribution includes the pinnae, external ear canal, preauricular, periorbital, and inguinal skin.

Papillomatous-like lesions are seen in chronic cases, which can involve the face, ventral trunk and perineal regions.

Generalized, greasy seborrheic scales and crusts are visible.

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3. Diagnosis:

a. A tentative diagnosis of lichenoid-psoriasiform dermatosis is made on the basis of breed, age of onset, and clinical findings.

b. Biopsies yield a definitive diagnosis.

c. Differential diagnosis includes demodicosis and dermatophytosis.

d. Skin scrapings and fungal cultures are indicated.

Important Facts

A tentative diagnosis of lichenoid-psoriasiform dermatosis is made on the basis of breed, age of onset, and clinical findings.

Biopsies yield a definitive diagnosis.

Skin scrapings and fungal cultures are indicated to rule out demodicosis and dermatophytosis.

4. Treatment:

a. Response to therapy is generally unsatisfactory.

b. Antiseborrheic shampoos are indicated if generalized seborrhea is present.

c. A few dogs have been reported to respond satisfactorily to oral cephalexin (20 mg/kg every 12 hours).

d. Prednisone (2.2 mg/kg orally every 24 hours) has resulted in partial improvement in some cases.

Important Facts

Antiseborrheic shampoos are indicated if generalized seborrhea is present.

A few dogs have been reported to respond satisfactorily to oral cephalexin.

Prednisone has resulted in partial improvement in some cases.

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D. Sebaceous Adenitis:

1. General Considerations:

a. Sebaceous adenitis is an inflammatory disease directed against the sebaceous glands of the skin.

b. There is a breed predilection for standard Poodles.

c. Other breeds with a higher incidence include the Akita, Samoyed, and Vizsla.

d. The pathophysiology of sebaceous adenitis is unknown, but speculations include the following: (1) Sebaceous gland destruction is a developmental and genetically inherited defect; (2) Sebaceous gland destruction is an immune mediated or autoimmune disease directed against a component of the sebaceous glands; (3) The initial defect is a keratinization abnormality with subsequent obstruction of the sebaceous ducts resulting in sebaceous adenitis; (4) The sebaceous adenitis and keratinization defects are the result of an abnormality in lipid metabolism affecting keratinization and the production of sebum.

Important Facts

Sebaceous adenitis is an inflammatory disease directed against the sebaceous glands of the skin.

Breed predilection includes standard Poodle, Akita, Samoyed, and Vizsla.

The pathophysiology of sebaceous adenitis is unknown.

2. History and Clinical Signs:

a. Clinical signs usually appear in young adult to middle-aged dogs (1 to 5 years). Two different clinical and histopathologic presentations are associated with different breeds including:

1. Long-coated breeds:

Standard Poodle:

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1. Symmetrical, partial alopecia of dorsal trunk, neck, and head, nasal planum, and pinnae.

2. Mild scaling with dull, brittle hair to severe hyperkeratosis with a tightly adhered, white scale.

3. Follicular casts around hair shafts may be observed.

4. Secondary bacterial folliculitis is common.

5. Pruritus and malodor may be observed with pyoderma.

6. 25% of affected dogs may have subclinical disease.

Akita:

1. This condition is most severe in Akitas.

2. Generalized, erythematous, papules, pustules, and scales.

3. Greasy keratosebaceous debris is common.

4. Follicular casts are present.

5. Generalized partial alopecia.

6. Systemic signs of fever and weight loss may be observed.

Samoyed:

1. Moderate to severe truncal alopecia and scaling.

2. Dull, brittle, and broken hairs.

3. Follicular casts are commonly present.

2. Short-coated breeds:

a. Vizsla:

1. Multifocal (moth-eaten), circular to serpiginous or diffuse alopecia.

2. Mild scaling (fine, white, nonadherent).

3. Follicular cats are present.

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4. Intermittent swelling of muzzle, lips, and eyelids occasionally reported.

5. Usually nonpruritic.

6. Bacterial folliculitis is rare.

Important Facts

Clinical signs usually appear in young adult to middle-aged dogs.

The clinical presentation and histopathologic findings vary with different breeds.

Akitas present with the most severe disease.

The condition in Akitas is often associated with chronic or recurrent secondary bacterial folliculitis with signs of systemic illness.

Vizslas and other short-coated breeds will present with circular to serpiginous or diffuse alopecia with mild scaling that affects the trunk, head, and ears.

Follicular casts around hair shafts is a sign observed in all breeds.

3. Diagnosis:

a. A tentative diagnosis is based on breed and physical findings.

b. Skin biopsies showing inflammation of the sebaceous glands or a granulomatous dermal reaction with destruction of sebaceous glands is supportive of sebaceous adenitis.

c. Multiple biopsies of different stages of the lesion as well as normal skin should be obtained.

d. Skin scrapings, fungal cultures, and thyroid profiles are indicated to rule out other differential diagnosis.

e. Differential diagnosis includes: bacterial folliculitis, demodicosis, dermatophytosis, primary idiopathic seborrhea, follicular dysplasia, hypothyroidism.

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Important Facts

A tentative diagnosis is based on breed and physical findings.

Skin biopsies showing inflammation of the sebaceous glands or a granulomatous dermal reaction with destruction of sebaceous glands is supportive of sebaceous adenitis.

Multiple biopsies of different stages of the lesion as well as normal skin should be obtained.

Differential diagnosis includes: bacterial folliculitis, demodicosis, dermatophytosis, primary idiopathic seborrhea, follicular dysplasia, hypothyroidism.

4. Treatment:

a. Milder forms of sebaceous adenitis may be controlled with topical keratolytic agents directed at removing the scale.

b. Antiseborrheic shampoos (sulfur, salicylic acid, tar) and emollient rinses are used as needed.

c. A topical spray or rinse containing 50% to 75% propylene glycol in water may be applied every 1 to 3 days as needed.

d. If a bacterial folliculitis is present, shampoos containing an antibacterial agent (benzoyl peroxide, chlorhexidine, ethyl lactate) should be prescribed in addition to appropriate systemic antibiotic therapy (refer to Bacterial Skin Diseases-Canine Pyoderma).

e. Some dogs with milder clinical signs respond to high doses of essential fatty acids (omega-3 and omega-6), found in many commercial fatty acid supplements and evening primrose oil.

f. The dogs with severe dermal fibrosis and destruction of sebaceous glands have the poorest prognosis for therapeutic response.

g. Isotretinoin (1 mg/kg orally every 12 to 24 hours) is administered for 4 weeks.

h. The response to isotretinoin is variable. If there is a good response, the lowest effective dosage should be used as maintenance therapy.

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i. Cyclosporine (5 mg/kg every 12 hours) has been used to treat dogs that did not respond to isotretinoin.

j. Potential adverse effects include vomiting, diarrhea, gingival hyperplasia, increased incidence of infections, nephrotoxicity, hepatotoxicity, hirsutism, B-lymphocyte hyperplasia, and papillomatous skin lesions.

k. In general, the response to therapy is quite variable from one patient to the next, with the Akita being the most refractory.

Important Facts

Milder forms of sebaceous adenitis may be controlled with topical keratolytic agents directed at removing the scale such as, antiseborrheic shampoos (sulfur, salicylic acid, tar) and emollient rinses.

If a bacterial folliculitis is present, shampoos containing an antibacterial agent (benzoyl peroxide, chlorhexidine, ethyl lactate) should be prescribed in addition to appropriate systemic antibiotic therapy.

High doses of essential fatty acids can be tried in mild cases.

Isotretinoin or cyclosporine (for cases resistant to isotretinoin) are the treatment options for more severe cases

In general, the response to therapy is quite variable from one patient to the next, with the Akita being the most refractory.

The dogs with severe dermal fibrosis and destruction of sebaceous glands have the poorest prognosis for therapeutic response.

E. Schnauzer Comedo Syndrome:

1. General Considerations:

a. It is suspected to be a hereditary follicular keratinization defect of miniature schnauzers characterized by multiple comedones on the dorsal midline.

b. Lesions are first noticed during grooming in the young adult as small crusts on the dorsum.

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c. Lesions are asymptomatic unless a secondary infection is present. Then pruritus may be observed.

Important Facts

Schnauzer comedo syndrome is suspected to be a hereditary follicular keratinization defect of miniature schnauzers characterized by multiple comedones on the dorsal midline.

Lesions are asymptomatic unless a secondary infection is present. Then pruritus may be observed.

2. Clinical Signs:

a. Crusted, papular comedones (blackheads) are present along the dorsal midline of the back from the neck to the tail.

b. Secondary superficial bacterial folliculitis is common in chronic cases.

c. Occasionally, there is a furunculosis (deep pyoderma).

d. The infection leads to alopecia with a moth-eaten appearance of the coat.

e. The condition is chronic for the life of the dog.

Important Facts

Crusted, papular comedones (blackheads) are present along the dorsal midline of the back from the neck to the tail.

Secondary superficial bacterial folliculitis and occasionally deep pyoderma (furunculosis) are common in chronic cases.

The infection leads to alopecia with a moth-eaten appearance of the coat.

The condition is chronic for the life of the dog.

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3. Diagnosis:

a. The presence of comedones in a miniature Schnauzer is strongly suggestive of this condition.

b. The definitive diagnosis is confirmed from skin biopsy showing dilated hair follicles filled with keratinous debris.

c. Differential diagnosis includes demodicosis, dermatophytosis, and superficial bacterial folliculitis. Therefore, all suspected cases should be scraped and fungal-cultured.

Important Facts

The presence of comedones in a miniature Schnauzer is strongly suggestive of this condition.

The definitive diagnosis is confirmed from skin biopsy showing dilated hair follicles filled with keratinous debris.

All suspected cases should be scraped and fungal-cultured to rule out demodicosis or dermatophytosis.

4. Treatment:

a. Topical therapy involves the periodic use of antiseborrheic shampoos (benzoyl peroxide, salicylic acid, sulfur, tar).

b. Benzoyl peroxide gels (Pyoben Gel, OxyDex Gel) are helpful to remove tightly adherent comedones.

c. Systemic antibiotics for a minimum of 4 weeks (rule of thumb: 1 week past resolution of clinical signs) are indicated if there is a secondary bacterial folliculitis.

d. In the few cases that do not respond to topical antiseborrheic agents and systemic antibiotics, isotretinoin (1 to 2 mg/kg orally every 24 hours) is reported to be effective.

e. A maintenance alternate-day dose may be needed.

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Important Facts

Topical therapy involves the periodic use of antiseborrheic shampoos (benzoyl peroxide, salicylic acid, sulfur, tar).

Systemic antibiotics for a minimum of 4 weeks (rule of thumb: 1 week past resolution of clinical signs) are indicated if there is a secondary bacterial folliculitis.

In the few cases that do not respond to topical antiseborrheic agents and systemic antibiotics, isotretinoin is reported to be effective.

F. Epidermal Dysplasia:

1. General Considerations:

a. It is a hereditary, very severe keratinization disorder reported only in West Highland White Terriers.

b. It is often associated with secondary Malassezia infection.

Important Facts

It is a hereditary, very severe keratinization disorder reported only in West Highland White Terriers.

It is often associated with secondary Malassezia infection.

2. Clinical Signs:

a. Onset of signs usually occurs between 6 and 12 months of age.

b. Pruritus and erythema are the primary complaints.

c. The initial distribution of lesions is on the ventrum, extremities, and face.

d. The lesions become more generalized with variable alopecia, lichenification, hyperpigmentation, greasy skin, and malodor.

e. Ceruminous otitis, secondary bacterial pyoderma, and lymphadenopathy are common.

f. Malassezia is frequently identified although it is not found in all dogs with epidermal dysplasia.

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Important Facts

Onset of signs usually occurs between 6 and 12 months of age.

Pruritus and erythema are the primary complaints

The initial distribution of lesions is on the ventrum, extremities, and face.

The lesions become more generalized with variable alopecia, lichenification, hyperpigmentation, greasy skin, and malodor.

Ceruminous otitis, secondary bacterial pyoderma, and lymphadenopathy are common.

Malassezia is frequently identified although it is not found in all dogs with epidermal dysplasia.

3. Diagnosis:

a. The early age of onset of severe ventral erythema and pruritus rapidly progressing to chronic lesions in a West Highland White Terrier is compatible with a clinical diagnosis of epidermal dysplasia.

b. A tentative diagnosis is made from skin biopsy findings.

c. The real diagnostic challenge in these cases is to determine whether the condition is due to epidermal dysplasia, some other pruritic skin disease, or a combination.

d. Differentials include atopic dermatitis, food allergy, scabies, and primary idiopathic seborrhea.

e. These should all be evaluated by appropriate testing or response to therapy in the diagnostic workup.

f. A definitive diagnosis of epidermal dysplasia can be made only with characteristic clinical and histologic findings and after the differentials have been eliminated.

g. Another challenge is to determine how much the secondary bacterial infection or Malassezia colonization is contributing to the severity of the clinical condition.

h. This can be assessed only by evaluating response after appropriate topical and systemic antimicrobial therapy.

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Important Facts

The early age of onset of severe ventral erythema and pruritus rapidly progressing to chronic lesions in a West Highland White Terrier is compatible with a clinical diagnosis of epidermal dysplasia.

A tentative diagnosis is made from skin biopsy findings.

The real diagnostic challenge in these cases is to determine whether the condition is due to epidermal dysplasia, some other pruritic skin disease, or a combination.

Differentials include atopic dermatitis, food allergy, scabies, and primary idiopathic seborrhea.

A definitive diagnosis of epidermal dysplasia can be made only with characteristic clinical and histologic findings and after the differentials have been eliminated.

4. Treatment:

a. Epidermal dysplasia is usually nonresponsive to medical therapy with drugs including antibiotics, antiinflammatory doses of glucocorticoids, antiseborrheic shampoos, vitamin A alcohol, systemic retinoids, vitamin E, and essential fatty acids.

b. The prognosis is poor, especially if the condition is chronic and severe secondary changes have occurred.

c. In patients with secondary Malassezia colonization, there may be significant improvement in pruritus and skin condition with ketoconazole (Nizoral) at 10 mg/kg q24h PO and twice-weekly application of topical ketoconazole (Nizoral shampoo) for 3 to 4 weeks.

d. Recurrence of the Malassezia infection is common. Periodic ketoconazole shampoos help to prevent relapses.

e. A sulfur and benzoyl peroxide shampoo has also been helpful in long-term management of some cases.

f. For cases in which the chronic cutaneous changes have not occurred, there may be a dramatic response to immunosuppressive doses of oral prednisone or prednisolone at 1.1 to 2.2 mg/kg q12h PO until the condition is controlled followed by a gradual decrease in the dose to alternate-day for long-term maintenance.

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g. Before such therapy is used, allergies should be ruled out and the side effects associated with chronic steroid therapy should be discussed with the owner.

Important Facts

Epidermal dysplasia is usually nonresponsive to medical therapy.

The prognosis is poor, especially if the condition is chronic and severe secondary changes have occurred.

In patients with secondary Malassezia colonization, there may be significant improvement in pruritus and skin condition with ketoconazole (Nizoral) at 10 mg/kg q24h PO and twice-weekly application of topical ketoconazole (Nizoral shampoo) for 3 to 4 weeks.

For cases in which the chronic cutaneous changes have not occurred, there may be a dramatic response to immunosuppressive doses of oral prednisone or prednisolone at 1.1 to 2.2 mg/kg q12h PO until the condition is controlled followed by a gradual decrease in the dose to alternate-day for long-term maintenance.

G. Primary Idiopathic Seborrhea:

1. General Considerations:

a. It is a hereditary disorder of keratinization characterized by variable clinical signs.

b. Primary idiopathic seborrhea is the most common chronic keratinization of dogs.

c. Many breeds have primary idiopathic seborrhea including the following: Basset hound, Cocker spaniel, Dachshund, Doberman pincher, English springer spaniel, German shepherd, Irish setter, Shar-Pei, and West Highland white terrier.

Important Facts

Primary idiopathic seborrhea is the most common chronic keratinization of dogs.

Clinical signs are variable.

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2. Pathogenesis:

a. The pathogenesis of primary idiopathic seborrhea is not completely understood.

b. Most studies demonstrate proliferative changes in the epidermis, hair follicle, infundibulum, and sebaceous glands.

c. The epidermal cell renewal time is approximately 62% faster (8 days versus 21 days) in seborrheic dogs.

d. A primary cellular defect is suspected because the hyperproliferative changes of seborrheic skin persist when grafted onto the skin of normal dogs.

Important Facts

The pathogenesis of primary idiopathic seborrhea is not completely understood.

The epidermal cell renewal time is approximately 62% faster (8 days versus 21 days) in seborrheic dogs.

A primary cellular defect is suspected because the hyperproliferative changes of seborrheic skin persist when grafted onto the skin of normal dogs.

3. Clinical Signs:

a. The onset of signs is usually before 2 years of age.

b. Depending on the breed, clinical signs may range anywhere from dry scaling (seborrhea sicca), to greasy scaling (seborrhea oleosa), to scaling and greasiness with inflammation and pruritus (seborrheic dermatitis), to any combination of these clinical abnormalities.

c. Seborrhea sicca :

1. It is characterized by focal to diffuse accumulations of a dry, nonadhered white to gray scale.

2. The haircoat is usually dull and dry.

3. Breeds predisposed to seborrhea sicca include: Doberman pinchers, Irish setters, German shepherd dogs, and Dachshunds.

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d. Seborrhea oleosa :

1. It is characterized by a generalized, malodorous, greasy skin and hair coat.

2. There are accumulations of brownish-yellow, greasy material that adhere to the hair and skin.

3. Follicular casts are common.

4. Intertriginous areas, neck, and feet (ventral aspect and interdigital) are the most severely affected regions.

5. Frequently, there is a concurrent ceruminous otitis and hyperplastic otitis.

6. Breeds predisposed to seborrhea oleosa include: Basset hound, Cocker spaniel, English springer spaniel, Labrador retriever, Shar-Pei, and West Highland white terrier.

e. Seborrheic dermatitis :

1. It is characterized by generalized, malodorous, greasy skin and hair coat (seborrhea oleosa), along with moderate to severe generalized inflammation, bacterial folliculitis, Malassezia dermatitis, pruritus, and inflamed hyperkeratotic plaques.

2. The most commonly involved areas are the external ear canals, pinnae, ventral neck, chest, intertriginous regions, and perineum.

3. This presentation of primary idiopathic seborrhea appears to be a more severe variant of seborrhea oleosa since it is generally seen in the same breeds.

Important Facts

The onset of signs is usually before 2 years of age.

Depending on the breed, clinical signs may range anywhere from dry scaling (seborrhea sicca), to greasy scaling (seborrhea oleosa), to scaling and greasiness with inflammation and pruritus (seborrheic dermatitis), to any combination of these clinical abnormalities.

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4. Diagnosis:

a. A definitive diagnosis of primary idiopathic seborrhea requires a number of supporting factors including: age, breed, history, elimination of secondary causes of scaling, and findings on histopathologic examination of skin biopsies.

b. The most important aspect of the diagnostic plan is a full investigation for secondary causes of scaling.

c. The primary differentials are allergic dermatitis, scabies, dermatophytosis, demodicosis, bacterial folliculitis, hypothyroidism, and vitamin A responsive dermatosis. An additional differential in Doberman pinchers is color mutant alopecia and adult-onset follicular dysplasia.

Important Facts

A definitive diagnosis of primary idiopathic seborrhea requires a number of supporting factors including: age, breed, history, elimination of secondary causes of scaling, and findings on histopathologic examination of skin biopsies.

The primary differentials are allergic dermatitis, scabies, dermatophytosis, demodicosis, bacterial folliculitis, hypothyroidism, and vitamin A responsive dermatosis. An additional differential in Doberman pinchers is color mutant alopecia and adult-onset follicular dysplasia.

5. Treatment:

a. As with most primary keratinization disorders, the goal in primary idiopathic seborrhea is not to cure the disease but to control the scale formation.

b. Topical therapy is always indicated in primary idiopathic seborrhea.

c. The specific type and frequency will vary with the severity of clinical signs.

d. Mild seborrhea sicca cases will respond to frequent applications of moisturizers shampoos and rinses (HyLytefa, Allergroom, Humilac).

e. Mild to moderate keratolytic shampoos (sulfur, salicytic acid) may be needed to remove heavier, dry scales.

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f. Stronger keratolytic, keratoplastic, and degreasing agents (benzoyl peroxide, tar, sulfur, selenium sulfide) are needed to control the greasy scale, crust, and odor associated with seborrhea oleosa.

g. Moisturizing rinses are often recommended to be used after shampooing.

h. Initially, shampoos and rinses may be used 2 to 3 times a week until the excessive scaling is controlled. Then, a maintenance-bathing program is continued as needed, often at least weekly.

i. Seborrhea sicca may respond partially to systemic essential fatty acids.

j. Acitretin (1 mg/kg orally every 24 hours) has been an effective therapy for some idiopathic seborrhea problems of Cocker spaniels, English springer spaniels, Irish setters, and Golden retrievers.

k. Response to acitretin is usually seen within 2 months. Maintenance alternate-day may be required for the life of the animal.

l. Systemic antibiotic are indicated if there is a secondary bacterial infection.

m. Prednisone (1.1 mg/kg orally every 24 hours) for 1 to 2 weeks may be needed to reduce severe inflammation and pruritus associated with seborrheic dermatitis.

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Important Facts

As with most primary keratinization disorders, the goal in primary idiopathic seborrhea is not to cure the disease but to control the scale formation.

Topical therapy is always indicated in primary idiopathic seborrhea.

Mild seborrhea sicca cases will respond to frequent applications of moisturizers shampoos and rinses (HyLytefa, Allergroom, Humilac).

Mild to moderate keratolytic shampoos (sulfur, salicytic acid) may be needed to remove heavier, dry scales.

Stronger keratolytic, keratoplastic, and degreasing agents (benzoyl peroxide, tar, sulfur, selenium sulfide) are needed to control the greasy scale, crust, and odor associated with seborrhea oleosa.

Seborrhea sicca may respond partially to systemic essential fatty acids.

Acitretin (1 mg/kg orally every 24 hours) has been an effective therapy for some idiopathic seborrhea problems of Cocker spaniels, English springer spaniels, Irish setters, and Golden retrievers.

Systemic antibiotic are indicated if there is a secondary bacterial infection.

Prednisone (1.1 mg/kg orally every 24 hours) for 1 to 2 weeks may be needed to reduce severe inflammation and pruritus associated with seborrheic dermatitis.

II. Primary Keratinization Disorders - Idiopathic Disorders

A. Canine Acne:

1. General Considerations:

a. It is a fairly common disorder of follicular keratinization resulting in comedones and secondary bacterial folliculitis and furunculosis.

b. It may be similar to acne in humans – beginning during the period of sexual maturity, being self-limited or persisting into adulthood, and arising from abnormalities in sebaceous secretions that alter follicular keratinization, causes comedones to form, and induce secondary bacterial folliculitis.

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c.The organisms isolated are usually Staphylococcus intermedius and, in rare cases, Staphylococcus aureus.

d. There is a probable hereditary predisposition based on the increased incidence in some short-coated dogs: English bulldogs, Boxers, Doberman pinchers, and Great Danes.

Important Facts

Canine acne is a fairly common disorder of follicular keratinization resulting in comedones and secondary bacterial folliculitis and furunculosis.

The organisms isolated are usually Staphylococcus intermedius and rarely Staphylococcus aureus.

There is a probable hereditary predisposition based on the increased incidence in some short-coated dogs: English bulldogs, Boxers, Doberman pinchers, and Great Danes.

2. History and Clinical Signs:

a. The history usually includes chin lesions starting around the time of sexual maturity in short-coated breeds.

b. In the majority of dogs, spontaneous remission occurs after sexual maturity.

c. Especially in the predisposed breeds, the chin lesions may be a recurrent problem for the life of the animal.

d. Clinical signs are variable.

e. Lesions may be limited to the anterior ventral chin or may be more generalized on the lips and muzzle.

f. Lesions include comedones, papules, pustules, and furuncles (characterized by draining tracts) of the chin, lips, and muzzle.

g. In some cases, lesions may be so mild as to be inapparent to the owner.

h. In others, there may be severe furunculosis and cellulitis with multiple draining tracts and pain.

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Important Facts

The history usually includes chin lesions starting about the time of sexual maturity in short-coated breeds.

Especially in the predisposed breeds, the chin lesions may be a recurrent problem for the life of the animal.

Lesions may be limited to the anterior ventral chin or may be more generalized on the lips and muzzle.

Lesions include comedones, papules, pustules, and furuncles (characterized by draining tracts) of the chin, lips, and muzzle.

In some cases, lesions may be so mild as to be inapparent to the owner.

In others, there may be severe furunculosis and cellulitis with multiple draining tracts and pain.

3. Diagnosis:

a. A tentative clinical diagnosis is made by history, age, breed, and clinical appearance of the lesions.

b. Differentials include demodicosis, dermatophytosis, and bacterial folliculitis.

c. Therefore, skin scrapings, fungal culture and cutaneous cytology (direct smears) should be routinely performed.

d. Culture and susceptibility testing should be considered in cases with deep infection when a systemic antibiotic is to be selected.

e. Skin biopsy findings provide a definitive diagnosis but are rarely needed.

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Important Facts

A tentative clinical diagnosis is made by history, age, breed, and clinical appearance of the lesions.

Differentials include demodicosis, dermatophytosis, and bacterial folliculitis.

Therefore, skin scrapings, fungal culture and cutaneous cytology (direct smears) should be routinely performed.

Culture and susceptibility testing should be considered in cases with deep infection when a systemic antibiotic is to be selected.

4. Treatment:

a. Mild cases of chin acne need no treatment and will spontaneously resolve with sexual maturity.

b. In more severe cases, treatment includes benzoyl peroxide shampoos (Pyoben, OxyDex, SufOxyDex) and gels(OxyDex gel, Pyoben gel).

c. These are used twice daily until controlled and then as needed for maintenance.

d. Benzoyl peroxide is effective because of its follicular flushing and antimicrobial activity. It may cause cutaneous irritation.

e. Mupirocin (Bactoderm) has excellent activity against gram-positive cocci, is bactericidal, works well in acid pH, and is not systemically absorbed.

f. Apply Mupirocin initially every 12 hours and then as needed.

g. Systemic antibiotics (cephalexin, cefadroxil) should be prescribed for 7 to 14 days past clinical resolution of signs.

h. If marked edema and deep inflammation are present, prednisone (1.1 mg/kg orally per day) may be given for not longer than 7 to 10 days concurrently with the initiation of antibiotic therapy.

i. In the few cases that are refractory to routine topical and systemic therapy, use tretinoin (Retin-A) topically q12h or systemic isotretinoin (Accutane) at 1 to 2 mg/kg q24h PO.

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Important Facts

Mild cases of chin acne need no treatment and will spontaneously resolve with sexual maturity.

If there are active papules and pustules, topical treatment with antibacterial shampoos and gels (benzoyl peroxide, sulfur) are used every 12 to 24 hours.

Mupirocin ointment may be applied every 12 to 24 hours.

Systemic antibiotics (cephalexin, cefadroxil) should be prescribed for 7 to 14 days past clinical resolution of signs.

If marked edema and deep inflammation are present, prednisone (1.1 mg/kg orally per day) may be given for not longer than 7 to 10 days concurrently with the initiation of antibiotic therapy.

In the few cases that are refractory to routine topical and systemic therapy, use tretinoin (Retin-A) topically q12h or systemic isotretinoin (Accutane) at 1 to 2 mg/kg q24h PO.

B. Ear Margin Dermatosis:

1. General Considerations:

a. Ear margin dermatosis is an uncommon idiopathic keratinization defect of the pinnal margins.

b. Lesions are usually bilateral.

c. Dachshunds are predisposed. However, other breeds with pendulous ears can also develop this disease.

Important Facts

Ear margin dermatosis is an uncommon idiopathic keratinization defect of the pinnal margins.

Lesions are usually bilateral.

Dachshunds are predisposed.

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2. Clinical Signs:

a. Greasy plugs (follicular casts) are tightly adhered to the skin surface and hair shafts of the lateral and medial margins of the pinnae.

b. Hairs epilate very easily on affected areas and alopecia may develop with time.

c. In severe untreated cases, a progression to ulceration and necrosis may be seen due to thrombosis of the capillaries supplying blood to the pinnal margins, and may result in severe scarring and fissures.

d. Pruritus is usually absent.

Important Facts

Greasy plugs (follicular casts) are tightly adhered to the skin surface and hair shafts of the lateral and medial margins of the pinnae.

In severe untreated cases, a progression to ulceration and necrosis may be seen due to thrombosis of the capillaries supplying blood to the pinnal margins, and may result in severe scarring and fissures.

Pruritus is usually absent.

3. Diagnosis:

a. The diagnosis of early ear margin dermatosis is based on the history, breed, and presence of the characteristic ear margin lesions.

b. Skin scrapings should be performed to rule out scabies (if severe pruritus is present), and demodicosis.

c. If crusts, ulcerations and fissures are present on the ear margins, vasculitis must be considered.

d. Causes of vasculitis affecting the ear margins include lupus erythematosus, cutaneous vasculitis, cold agglutinin disease, and frostbite.

e. Diagnostic procedures to differentiate these diseases may require an extensive work up including CBC, chemistry profile, ANA testing, Coomb’s testing, and biopsies.

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Important Facts

The diagnosis of early ear margin dermatosis is based on the history, breed, and presence of the characteristic ear margin lesions.

If crusts, ulcerations and fissures are present on the ear margins, vasculitis must be considered.

Causes of vasculitis affecting the ear margins include lupus erythematosus, cutaneous vasculitis, cold agglutinin disease, and frostbite.

Diagnostic procedures to differentiate these diseases may require an extensive work up including CBC, chemistry profile, ANA testing, Coomb’s testing, and biopsies.

4. Treatment:

a. The mild scaling form of ear margin dermatosis is usually controllable with topical therapy but rarely is curable.

b. In the early marginal lesions, topical treatment with antiseborrheic agents (benzoyl peroxide, tar, sulfur, salicylic acid) will remove the greasy scales, with the frequency of application varying from daily to weekly.

c. Topical glucocorticoid creams and/or systemic prednisone (1.1 mg/kg per day) may be indicated to reduce inflammation in severe cases.

d. The advanced ulcerative and necrotic stage is resistant to medical therapy. However, it can be usually cured by surgical removal of the affected ear margin.

e. Tissue should be removed well into the normal portion of the pinnae.

f. However, the full list of differentials should be considered before such aggressive surgery.

g. The procedure will not be effective if ulceration is due to autoimmune disease or vasculitis.

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Important Facts

Treatment is symptomatic.

In the early marginal lesions, topical treatment with antiseborrheic agents (benzoyl peroxide, tar, sulfur, salicylic acid), applied daily to weekly, will remove the greasy scales.

Topical glucocorticoid creams and/or systemic prednisone (1.1 mg/kg per day) may be indicated to reduce inflammation in severe cases.

The advanced ulcerative and necrotic stage is resistant to medical therapy. However, it can be usually cured by surgical removal of the affected ear margin.

The full list of differentials should be considered before such aggressive surgery.

The procedure will not be effective if ulceration is due to autoimmune disease or vasculitis.

C. Idiopathic Nasodigital Hyperkeratosis:

1. General Considerations:

a. It is an idiopathic keratinization disorder characterized by an accumulation of tightly adhered keratin on the planum nasal, footpads, or both.

b. Nasodigital hyperkeratosis is seen commonly in the older dog, probably as a senile change.

c. There is a reported breed predilection for Cocker spaniels and English springer spaniels although any breed may be affected.

d. A hereditary footpad hyperkeratosis has been reported for Irish terriers and Dogues de Bordeaux.

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Important Facts

Nasodigital hyperkeratosis is an idiopathic keratinization disorder characterized by an accumulation of tightly adhered keratin on the planum nasal, footpads, or both.

Nasodigital hyperkeratosis is seen commonly in the older dog, probably as a senile change.

There is a reported breed predilection for Cocker spaniels and English springer spaniels although any breed may be affected.

2. Clinical Signs:

a. Idiopathic nasodigital hyperkeratosis usually occurs in the older dog with no other systemic or dermatologic lesions.

b. Lesions may be focal or diffuse and characterized by tightly adherent thick accumulations of keratin on the planum nasal, footpads, or both.

c. This material is usually extremely dry and may be accompanied by cracks, fissures, erosions, and ulcers.

d. Severe footpad involvement causes lameness.

Important Facts

Idiopathic nasodigital hyperkeratosis usually occurs in the older dog with no other systemic or dermatologic lesions.

Lesions may be focal or diffuse and characterized by tightly adherent thick accumulations of keratin on the planum nasal, footpads, or both.

This material is usually extremely dry and may be accompanied by cracks, fissures, erosions, and ulcers.

Severe footpad involvement causes lameness.

3. Diagnosis:

a. Nasal or digital hyperkeratosis without evidence of other concurrent diseases establishes the diagnosis of idiopathic nasodigital hyperkeratosis.

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b. If other clinical signs, either systemic or dermatologic, are present, a thorough workup to identify an underlying etiology is necessary.

c. All diseases that can cause the lesions must be considered and include: canine distemper, pemphigus foliaceous, pemphigus erythematosus, lupus erythematosus, nasal solar dermatitis, hypothyroidism, zinc responsive dermatosis, generic dog food dermatosis, and superficial necrolytic dermatosis.

d. Biopsies are usually the most definitive diagnostic test, either to confirm an idiopathic nasodigital hyperkeratosis or to identify an underlying disease.

Important Facts

Nasal or digital hyperkeratosis without evidence of other concurrent diseases establishes the diagnosis of idiopathic nasodigital hyperkeratosis.

If other clinical signs, either systemic or dermatologic, are present, a thorough workup to identify an underlying etiology is necessary.

Biopsies are usually the most definitive diagnostic test, either to confirm an idiopathic nasodigital hyperkeratosis or to identify an underlying disease.

4. Treatment:

a. Treatment of nasal and digital keperkeratotic lesions is symptomatic.

b. The excess keratin needs to be softened and removed.

c. Since there is continuous keratin production, there is a constant need for controlling the accumulation of keratin.

d. Initially, hydrating the lesions with water soaks or wet dressings may be sufficient to allow the physical removal of excessive keratin.

e. In many cases, a topical keratolytic agent in a gel formulation is applied every 12 hours initially and then as needed to keep the condition under control. Examples: KeraSolv Gel (salicylic acid, lactic acid, urea) or topical 0.025 or 0.01% tretinoin gel (Retin-A).

f. If fissures are present, topical corticosteroids and antibiotics may be needed to control secondary inflammation and infection.

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g. Continued application of hydrating agents, such as propylene glycol, petroleum jelly and salicylic acid, are usually required at varying frequencies.

h. Any underlying disease must be controlled along with the symptomatic treatment of the nasal and digital hyperkeratotic lesions.

Important Facts

Treatment of nasal and digital keperkeratotic lesions is symptomatic.

Initially, hydrating the lesions with water soaks or wet dressings may be sufficient to allow the physical removal of excessive keratin.

In many cases, a topical keratolytic agent in a gel formulation is applied every 12 hours initially and then as needed to keep the condition under control.

If fissures are present, topical corticosteroids and antibiotics may be needed to control secondary inflammation and infection.

Continued application of hydrating agents, such as propylene glycol, petroleum jelly and salicylic acid, are usually required at varying frequencies.

Any underlying disease must be controlled along with the symptomatic treatment of the nasal and digital hyperkeratotic lesions.

III.Primary Keratinization Disorders - Nutritional Keratinization Disorders

A. Zinc-responsive Dermatosis:

1. General Considerations:

a. Zinc-responsive dermatosis is a rare chronic keratinization disorder that responds to zinc supplementation.

b. Two clinical syndromes are seen.

c. Syndrome I occurs in dogs that are on balanced diets. Siberian husky and Alaskan malamutes are the breeds most frequently representing syndrome I. However, syndrome I has also been reported in Doberman pinchers and Great danes.

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d. In the malamute, a genetic defect affecting the absorption of zinc from the intestinal tract has been identified. Thus, the condition may occur even while the dog is on a well-balanced commercial diet.

e. It may be precipitated by stress, estrus, and gastrointestinal disorders affecting absorption.

f. Diets high in calcium and phytate (primary protein source of plant origin) may also precipitate the disorder by binding zinc in the gastrointestinal tract.

g. Syndrome II affects mainly puppies on zinc-deficient diets or regimens that involve high levels of vitamin and mineral (especially calcium) supplementation. This syndrome is also seen in dogs being fed diets high in phytate.

h. Breeds representing syndrome II are: Great danes, Doberman pinchers, Beagles, German shorthaired pointers, Labrador retrievers, and Rhodesian ridgebacks.

Important Facts

Zinc-responsive dermatosis is a rare chronic keratinization disorder that responds to zinc supplementation.

Syndrome I occurs in dogs that are on balanced diets. Siberian husky and Alaskan malamutes are the breeds most frequently representing syndrome I.

In the malamute, a genetic defect affecting the absorption of zinc from the intestinal tract has been identified.

It may be precipitated by stress, estrus, and gastrointestinal disorders affecting absorption.

Diets high in calcium and phytate (primary protein source of plant origin) may also precipitate the disorder by binding zinc in the gastrointestinal tract.

Syndrome II affects mainly puppies on zinc-deficient diets or regimens that involve high levels of vitamin, mineral (especially calcium) supplementation and diets high in phytate.

Breeds representing syndrome II are: Great danes, Doberman pinchers, Beagles, German shorthaired pointers, Labrador retrievers, and Rhodesian ridgebacks.

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2. Clinical Signs:

a. Signs usually develop in young adults, 1 to 3 years of age.

b. Erythema, alopecia, tightly adhered scales, and crusts are the predominant lesions.

c. Distribution primarily involves the face, periorbital region, mouth, chin, ears, and prepuce.

d. Heavy crusts or tightly adhered scales are observed on pressure points, especially elbows and hocks.

e. The footpads are often hyperkeratotic.

f. Hyperpigmentation may be seen in chronic lesions.

g. The hair coat may be dry and dull.

h. Secondary bacterial and Malassezia infections are common.

Important Facts

Signs usually develop in young adults, 1 to 3 years of age.

Erythema, alopecia, tightly adhered scales, and crusts localized to the face, periorbital region, mouth, chin, ears, and prepuce are the predominant lesions.

Heavy crusts or tightly adhered scales are observed on pressure points, especially elbows and hocks.

The footpads are often hyperkeratotic.

Secondary bacterial and Malassezia infections are common.

3. Diagnosis:

a. A tentative diagnosis may be made based on the breed, age of onset, distribution, and appearance of gross lesions.

b. Measurements of zinc levels in hair or serum are variable and unreliable.

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c. A biopsy showing a severe, diffuse surface and follicular parakeratotic hyperkeratosis along with a hyperplastic superficial dermatitis is supportive of zinc responsive dermatosis.

d. A therapeutic trial with zinc is the definitive diagnostic test.

e. Differential diagnosis include demodicosis, dermatophytosis, Malassezia dermatitis, pemphigus foliaceous, generic dog food dermatitis and superficial necrolytic dermatitis.

f. Skin scrapings and cutaneous cytology should be performed on all suspect cases in addition to the skin biopsies.

Important Facts

A tentative diagnosis may be made based on the breed, age of onset, distribution, and appearance of gross lesions.

Measurements of zinc levels in hair or serum are variable and unreliable.

A biopsy showing a severe, diffuse surface and follicular parakeratotic hyperkeratosis along with a hyperplastic superficial dermatitis is supportive of zinc responsive dermatosis.

A therapeutic trial with zinc is the definitive diagnostic test.

4. Treatment:

a. Zinc supplementation usually results in satisfactory control of clinical signs within 4 to 8 weeks.

b. Several forms of zinc have been used.

c. Zinc sulfate (10 mg/kg orally every 24 hours), zinc methionine (2 mg/kg orally every 24 hours), or elemental zinc (1.1 mg/kg orally every 12 hours) have been recommended.

d. The zinc supplementation is required for the life of the dog.

e. If vomiting occurs, the zinc supplement should be given with food or divided into smaller doses more frequently.

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f. All potential dietary imbalances should be corrected by feeding good quality balanced diets.

g. An alternative intravenous zinc therapy has been used in cases refractory to oral supplementation.

h. Sterile zinc sulfate solutions (10 to 115 mg/kg) are administered intravenously weekly for 4 weeks.

i. Maintenance injections may be needed at intervals of 1 to 6 months to prevent relapses.

j. Symptomatic topical therapy with water soaks and antiseborrheic shampoos are indicated to loosen and remove the excessive well-adhered scaling and crusting.

Important Facts

Zinc supplementation usually results in satisfactory control of clinical signs within 4 to 8 weeks.

Zinc sulfate (10 mg/kg orally every 24 hours), zinc methionine (2 mg/kg orally every 24 hours), or elemental zinc (1.1 mg/kg orally every 12 hours) have been recommended for the life of the animal.

All potential dietary imbalances should be corrected by feeding good quality balanced diets.

Symptomatic topical therapy with water soaks and antiseborrheic shampoos are indicated to loosen and remove the excessive well-adhered scaling and crusting.

B. Vitamin A-Responsive Dermatosis:

1. General Considerations:

a. Vitamin A-responsive dermatosis is a rare, chronic scaling disorder that responds to Vitamin A supplementation.

b. Cocker spaniels have the highest incidence although a similar condition has been reported in Labrador retrievers, Miniature schnauzers, and Shar-peis.

c. Vitamin A-responsive dermatosis is not a systemic vitamin A deficiency but probably represents a local deficiency in the epidermis,

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a problem with epidermal uptake, a disorder of cutaneous utilization, or a positive pharmacological effect of high doses on the skin.

Important Facts

Vitamin A-responsive dermatosis is a rare, chronic scaling disorder that responds to Vitamin A supplementation.

Cocker spaniels have the highest incidence although a similar condition has been reported in Labrador retrievers, Miniature schnauzers, and Shar-peis.

Vitamin A-responsive dermatosis is not a systemic vitamin A deficiency but probably represents a local deficiency in the epidermis, a problem with epidermal uptake, a disorder of cutaneous utilization, or a positive pharmacological effect of high doses on the skin.

2. History and Clinical Signs:

a. Clinical signs are usually present by 2 to 3 years of age and are very similar to those seen in primary idiopathic seborrhea.

b. Some dermatologists believe that these two conditions are the same.

c. The symptomatic therapeutic response is frequently less for vitamin A-responsive dermatosis than primary idiopathic seborrhea.

d. Clinical signs include refractory generalized scaling, a dry hair coat with easy epilation, prominent comedones.

e. Hyperkeratotic plaques with large surface “fronds” of keratinous material protruding from the follicular ostia are most prominent on the ventral and lateral thorax and abdomen.

f. Focal papules and crusts and variable alopecia are observed.

g. Ceruminous otitis is common.

h. Varying degrees of pruritus are noted.

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Important Facts

Clinical signs are usually present by 2 to 3 years of age and are very similar to those seen in primary idiopathic seborrhea.

Clinical signs include refractory generalized scaling, a dry hair coat with easy epilation, prominent comedones.

Hyperkeratotic plaques with large surface “fronds” of keratinous material protruding from the follicular ostia are most prominent on the ventral and lateral thorax and abdomen.

Ceruminous otitis is common and pruritus is variable.

3. Diagnosis:

a. The early age of onset of refractory generalized scaling with hyperkeratotic plaques in a Cocker spaniel is compatible with a clinical diagnosis of Vitamin A-responsive dermatosis.

b. A tentative diagnosis is made from skin biopsy findings, consisting of marked follicular hyperkeratosis with distended follicular ostia, mild orthokeratotic hyperkeratosis of the epidermis, and mild irregular epidermal hyperplasia.

c. Even with the classic clinical and histologic findings, a definitive diagnosis can be confirmed only by the response to supplementation with vitamin A alcohol.

d. Primary idiopathic seborrhea is the most common differential diagnosis for Cocker spaniels.

e. Other differentials include zinc-responsive dermatosis, generic dog food dermatosis, sebaceous adenitis, and superficial necrolytis dermatitis.

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Important Facts

The early age of onset of refractory generalized scaling with hyperkeratotic plaques in a Cocker spaniel is compatible with a clinical diagnosis of Vitamin A-responsive dermatosis.

A tentative diagnosis is made from skin biopsy findings.

Even with the classic clinical and histologic findings, a definitive diagnosis can be confirmed only by the response to supplementation with vitamin A alcohol.

Primary idiopathic seborrhea is the most common differential diagnosis for Cocker spaniels.

4. Treatment:

a. Vitamin A alcohol at the dose of 625 to 800 IU/kg q24h PO is recommended for the life of the patient.

b. Improvement is seen within 4 to 6 weeks.

c. Complete remission is obtained by 10 weeks of treatment.

d. This dosage is well-tolerated in dogs with no significant side effects.

e. Keratinolytic shampoos containing benzoyl peroxide (oxyDex, Sulf OxyDex, Pyoben) have excellent follicular flushing activity.

f. Twice to three times weekly usage helps remove keratinous debris from follicles and hastens recovery.

Important Facts

Vitamin A alcohol at the dose of 625 to 800 IU/kg q24h PO is recommended for the life of the patient.

Improvement is seen within 4 to 6 weeks and complete remission is obtained by 10 weeks of treatment.

Keratinolytic shampoos containing benzoyl peroxide (oxyDex, Sulf OxyDex, Pyoben) have excellent follicular flushing activity when used 2 to 3 times weekly.

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C. Fatty Acid Deffciency:

1. General Considerations:

a. Fatty acid deficiencies are very uncommon, occurring occasionally with dry rations that have been stored for long periods of time (more than 6 months), especially at high temperatures.

b. The fat may become rancid with a lack of adequate levels of antioxidants.

c. Oxidation may be observed in canned food stored for long periods of time, usually in excess of 1 year.

d. Occasionally, reducing diets with lower fat content may lead to a fatty acid deficiency.

e. Chronic intestinal absorption disorders may lead to decreased fatty acid absorption.

Important Facts

Fatty acid deficiencies are very uncommon, occurring occasionally with dry rations that have been stored for long periods of time (more than 6 months), especially at high temperatures.

Oxidation may be observed in canned food stored for long periods of time, usually in excess of 1 year.

Occasionally, reducing diets with lower fat content may lead to a fatty acid deficiency.

Chronic intestinal absorption disorders may lead to decreased fatty acid absorption.

2. History and Clinical Signs:

a. Animals must be fed a fatty acid deficiency diet for many months before mild clinical signs are observed.

b. A dry, lusterless coat and mild diffuse scaling are observed initially.

c. In long-term deficiencies, signs of seborrhea oleosa with greasiness of the ears and interdigital and intertriginous regions may be observed.

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d. Variable alopecia, pruritus, and secondary bacterial and Malassezia infections are usually present.

Important Facts

Animals must be fed a fatty acid deficiency diet for many months before mild clinical signs are observed.

A dry, lusterless coat and mild diffuse scaling are observed initially.

In long-term deficiencies, signs of seborrhea oleosa with greasiness of the ears and interdigital and intertriginous regions may be observed.

Variable alopecia, pruritus, and secondary bacterial and Malassezia infections are usually present.

3. Diagnosis:

a. A tentative diagnosis of fatty acid deficiency is based on the dietary history, clinical signs and, most importantly, elimination of all other primary and secondary causes of the seborrheic signs.

b. The most definitive test is a therapeutic response to fatty acid supplementation.

Important Facts

A tentative diagnosis of fatty acid deficiency is based on the dietary history, clinical signs and, most importantly, elimination of all other primary and secondary causes of the seborrheic signs.

The most definitive test is a therapeutic response to fatty acid supplementation.

4. Treatment:

a. Therapeutic recommendations are variable depending on the underlying cause of the fatty acid deficiency.

b. In most cases, changing to a well-balanced diet of higher quality and fat content as well as observing storage and usage recommendations will result in clinical improvement within several weeks.

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c. Commercial essential fatty acid supplements may be administered.

d. The addition of equal parts of animal fats and vegetable oils also may be used as a dietary supplement.

e. One teaspoon of the animal fat and vegetable oil mixture is recommended for each cup or can of dog food.

f. Fatty acid supplementation may aggravate or predispose to pancreatitis and hyperlipidemia disorders.

g. Topical application of rinses containing essential fatty acids are often helpful in the mild seborrheic conditions.

h. Mild antiseborrheic shampoos that are not degreasing (sulfur, salicylic acid) are indicated to remove excessive scale.

i. Any secondary bacterial or Malassezia infections or systemic diseases must be treated concurrently.

Important Facts

In most cases, changing to a well-balanced diet of higher quality and fat content as well as observing storage and usage recommendations will result in clinical improvement within several weeks.

Commercial essential fatty acid supplements may be administered.

The addition of one teaspoon for each cup or can of dog food, of a mixture containing equal parts of animal fats and vegetable oils also may be used as a dietary supplement.

Topical application of rinses containing essential fatty acids are often helpful in the mild seborrheic conditions.

Mild antiseborrheic shampoos that are not degreasing (sulfur, salicylic acid) are indicated to remove excessive scale.

Any secondary bacterial or Malassezia infections or systemic diseases must be treated concurrently.

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References

1. Kwochka KW: Primary Keratinization Disorders of Dogs. In: Griffin CE, Kwochka KW, MacDonald JM (eds). Current Veterinary Dermatology. St Louis, Mosby Year Book, 1993, pp 176-190.

2. Kwochka KW: Overview of normal keratinization and cutaneous scaling disorders of dogs. In: Griffin CE, Kwochka KW, MacDonald JM (eds). Current Veterinary Dermatology. St Louis, Mosby Year Book, 1993, pp 167-175.

3. Power HT, Ihrke PJ. Synthetic retinoids in veterinary dermatology. Vet Clin North Am Small Anim Pract, Philadelphia, WB Saunders, 1990, p 1525.

Learning Objectives

1. Remember! Keratinization disorders is a term used to describe clinical findings associated not only with abnormalities in the process of formation of the epidermis (epidermogenesis) and, particularly stratum corneum (keratinization) but also with abnormalities in apocrine or sebaceous gland function, intercellular lipid formation, cell cohesion, or cell desquamation.

2. Scaling is a clinical sign always present.

3. Important! Malassezia and bacterial infections are frequently observed in many keratinization disorders due to alterations in the surface microenvironment and alterations in the stratum corneum.

4. The diagnostic challenge when managing a scaling disorder is to determine if the clinical signs are secondary to an underlying dermatosis or are the result of a primary keratinization defect. Most cases that you will be dealing with in practice will be secondary to an underlying disorder.

5. Know! Keratinization disorders can be classified by 2 methods: clinical signs or etiology (primary or secondary).

6. Based on clinical signs, the keratinization disorders can be classified in: seborrhea sicca, seborrhea oleosa, seborrheic dermatitis and seborrheic otitis externa.

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7. How do you differentiate clinically each type of seborrhea? Remember! Secondary Malassezia and bacterial infections are common in seborrhea oleosa.

8. Based on etiology the disorder of keratinization can be classified in primary and secondary.

9. Know! Secondary keratinization disorders may occur with most types of diseases and, as a result, it is seen much more often than primary keratinization disorders. Scaling, with or without excessive sebum secretion, is observed in areas affected by the underlying dermatosis.

10. Know! Primary keratinization disorders can be hereditary, idiopathic or nutritional.

11. Know! Hereditary keratinization disorders include: color mutant alopecia, follicular dysplasia/dystrophy, epidermal dysplasia, ichthyosis, lichenoid-psoriasiform dermatosis, primary idiopathic seborrhea, sebaceous adenitis, Schnauzer comedo syndrome.

12. Know! Idiopathic keratinization disorders include: acne, ear margin dermatosis, nasodigital hyperkeratosis.

13. Know! Nutritional keratinization disorders include: zinc-responsive dermatosis, vitamin A-responsive dermatosis, fatty acid deficiency.

14. Know well the clinical presentation, diagnosis and treatment of the following: color mutant alopecia, primary idiopathic seborrhea, sebaceous adenitis, Schnauzer comedo syndrome, acne, ear margin dermatosis, and zinc responsive dermatosis. You will be seeing these conditions!

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Disorders of KeratinizationGeneral Considerations – Feline

A. Primary Keratinization Disorders:

1. General Considerations:

a. Keratinization disorder is a term used to describe clinical findings associated with abnormalities in the process of epidermopoiesis, keratinization, apocrine or sebaceous gland function, intercellular lipid formation, cell cohesion, or cell desquamation.

b. There are relatively few primary feline keratinization disorders.

c. The diseases classified as primary keratinization defects have hereditary, idiopathic, or nutritional predispositions.

d. Two feline primary keratinization disorders will be discussed in this section: primary seborrhea and feline acne.

B. Primary Seborrhea:

1. General Considerations:

a. A primary seborrhea has been reported in Persian cats.

b. An autosomal recessive mode of inheritance was verified.

c. No sex predisposition was reported.

Important Facts

A primary seborrhea has been reported in Persian cats.

An autosomal recessive mode of inheritance was verified, without sex predilection.

2. Clinical Signs:

a. Clinical signs were variable.

b. Kittens as young as 2 to 3 days of age had hairs pasted together.

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c. There was a gradual progression to involve the entire body with a scaly and greasy seborrhea.

d. Wax accumulated in the facial folds and ears.

e. In milder cases, the early signs were not apparent until 6 weeks of age.

Important Facts

Kittens as young as 2 to 3 days of age had hairs pasted together.

There was a gradual progression to involve the entire body with a scaly and greasy seborrhea.

Wax accumulated in the facial folds and ears.

In milder cases, the early signs were not apparent until 6 weeks of age.

3. Diagnosis:

a. Breed, age of onset and clinical findings suggest the diagnosis of primary idiopathic seborrhea.

b. A biopsy showing orthokeratotic hyperkeratosis and papillomatosis is highly supportive of keratinization disorder.

Important Facts

Breed, age of onset and clinical findings suggest the diagnosis of primary idiopathic seborrhea.

A biopsy showing orthokeratotic hyperkeratosis and papillomatosis is highly supportive of keratinization disorder.

4. Treatment:

a. Treatment is symptomatic.

b. The haircoat should be kept short and frequently groomed and bathed with mild antiseborrheic shampoos.

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Important Facts

Treatment is symptomatic.

The haircoat should be kept short and frequently groomed and bathed with mild antiseborrheic shampoos.

C. Feline Acne:

1. General Considerations:

a. Feline acne is an idiopathic, facial dermatosis that can affect cats of all ages.

b. There is no sex predilection.

Important Facts

Feline acne is an idiopathic, facial dermatosis that can affect cats of all ages.

There is no sex predilection.

2. Pathogenesis:

a. The pathogenesis and specific etiology of feline acne is unknown.

b. Feline acne is not associated with puberty; therefore, circulatory androgenic effects on the sebaceous glands and hair follicles are not a primary cause.

c. Several factors have been suggested as predisposing causes including:

1. Poor grooming habits.

2. Abnormal sebum production.

3. Hair cycle influences.

4. Stress.

5. Direct viral influences.

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6. Immunosuppression.

7. Possible inability of the telogen hair to extrude the developing keratosebaceous plug.

8. A localized keratinization defect that is exacerbated by increased sebum secretion.

9. Although each of these would be an aggravating factor, none has been proven causal.

Important Facts

The pathogenesis and specific etiology of feline acne is unknown.

Feline acne is not associated with puberty; therefore, circulatory androgenic effects on the sebaceous glands and hair follicles are not a primary cause.

Several factors have been suggested as predisposing causes including: poor grooming habits, an underlying seborrheic predisposition, the production of abnormal sebum, hair cycle influences, stress, direct viral influences, and immunosuppression.

Although each of these would be an aggravating factor, none has been proven causal.

3. History and Clinical Signs:

a. Feline acne lesions usually start at a young age (1-year) and are cyclic for the life of the cat.

b. The severity of lesions is variable, but typically mild and asymptomatic.

c. Pruritus and pain are uncommon unless there is a secondary deep bacterial folliculitis and furunculosis.

d. Acne lesions are characterized by dark brown comedones on the chin and lower lip.

e. Crusted, mildly erythematous papules may be observed.

f. Swelling of the chin and occasionally around the lips may be observed.

g. In some cases, a bacterial folliculitis characterized by pustules may develop.

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h. If there is continued inflammation, furunculosis and deep pyoderma may follow.

i. Some lesions will ulcerate and discharge exudate.

j. At this stage, firm nodules, marked erythema, alopecia, and pain may be noticed.

k. Scarring is often a sequela to chronic, deep inflammation.

l. Bacteria isolated from the secondary folliculitis lesions include Pasteurella multocita, B-hemolytic streptococci, and Staphylococcus.

m. Occasionally, Malassezia will be identified in the comedone.

Important Facts

Feline acne lesions usually start at a young age (1-year) and are cyclic for the life of the cat.

The severity of lesions is variable, but typically mild and asymptomatic.

Pruritus and pain are uncommon unless there is a secondary deep bacterial folliculitis and furunculosis.

Acne lesions are characterized by dark brown comedones on the chin and lower lip.

Crusted, mildly erythematous papules may be observed.

Swelling of the chin and occasionally around the lips may be observed.

If there is continued inflammation, furunculosis and deep pyoderma may follow.

At this stage, firm nodules, marked erythema, alopecia, and pain may be noticed.

Scarring is often a sequela to chronic, deep inflammation.

Bacteria isolated from the secondary folliculitis lesions include Pasteurella multocita, B-hemolytic streptococci, and Staphylococcus.

Occasionally, Malassezia will be identified in the comedone.

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4. Diagnosis:

a. The history and clinical signs are usually diagnostic.

b. Cytology is indicated to identify secondary Malassezia and bacterial organisms.

c. Skin scrapings should be performed to rule out demodicosis.

d. In cases of marked chin edema, biopsies may be needed to differentiate eosinophilic granuloma.

Important Facts

The history and clinical signs are usually diagnostic.

Cytology is indicated to identify secondary Malassezia and bacterial organisms.

Skin scrapings should be performed to rule out demodicosis.

In cases of marked chin edema, biopsies may be needed to differentiate eosinophilic granuloma.

5. Treatment:

a. Overtreatment of mild cases of feline acne is believed to be an important predisposing cause of more severe lesions.

b. In mild, asymptomatic cases of feline acne, treatment usually is not necessary.

c. Topical therapy is indicated to help remove the comedones.

d. Careful clipping of the lesional area will facilitate cleaning and application of topical medications.

e. Mild comedolytic agents, such as alcohol or Listerine antiseptic, may be used.

f. Antiseborrheic shampoos containing sulfur and salicylic acid or ethyl lactate are often helpful.

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g. Benzoyl peroxide shampoo can be very helpful for its follicular flushing and keratolytic effects. It is very important to recommended rinsing the shampoo off very well after application to prevent irritation.

h. If there is drainage, edema, or other signs of secondary bacterial infection, hot compresses and topical and systemic antibiotics are recommended.

i. Mupirocin (Bactoderm – Pfizer) has been reported to be very effective in the management of feline acne. Topical clindamycin or metronidazole ointments can also be tried.

j. Systemic antibiotics that are usually effective include clavulanated amoxicillin, enrofloxacin, and cephalosporins.

k. In a limited number of refractory cases, isotretinoin (2 mg/kg every 24 hours) may be tried.

l. Fatty acid supplements have been used to help prevent or to minimize severity of recurrence of lesions.

m. If Malassezia is identified and there is a poor response to topical therapy, oral ketoconazole or itraconazole therapy may be needed.

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Important Facts

In mild, asymptomatic cases of feline acne, treatment usually is not necessary.

Careful clipping of the lesional area will facilitate cleaning and application of topical medications.

Antiseborrheic shampoos containing sulfur and salicylic acid or ethyl lactate are often helpful.

Benzoyl peroxide shampoo can be very helpful for its follicular flushing and keratolytic effects. It is very important to recommended rinsing the shampoo off very well after application to prevent irritation.

If there is drainage, edema, or other signs of secondary bacterial infection, hot compresses and topical and systemic antibiotics are recommended.

Mupirocin (Bactoderm – Pfizer) has been reported to be very effective in the management of feline acne. Topical clindamycin or metronidazole ointments can also be tried.

In a limited number of refractory cases, isotretinoin (2 mg/kg every 24 hours) may be tried.

Fatty acid supplements have been used to help prevent or to minimize severity of recurrence of lesions.

If Malassezia is identified and there is a poor response to topical therapy, oral ketoconazole or itraconazole therapy may be needed.

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References

1. Scott, Miller, Griffin. Small Animal Dermatology, 5th ed., Philadelphia, WB Saunders, 1995.

2. Nesbitt & Ackerman. Canine & Feline Dermatology, 1st ed., New Jersey, Veterinary Learning Systems, 1998, p 446-447.

Learning Objectives

1. Know! Keratinization disorder is a term used to describe clinical findings associated with abnormalities in the process of epidermopoiesis, keratinization, apocrine or sebaceous gland function, intercellular lipid formation, cell cohesion, or cell desquamation.

2. Know! There are relatively few primary feline keratinization disorders. Only primary seborrhea and feline acne are included in the category of feline keratinization disorders.

3. Know the clinical presentation, diagnosis and management of the reported primary seborrhea of Persian cats.

4. You will see feline acne a lot! Therefore, know very well the various clinical presentation, diagnosis and management of this condition.

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