Small Animal Dermatology, A Color Atlas and Therapeutic Guide, 4th Edition PDF

C H A P T E R | 11 Pigmentary Abnormalities Lentigo Vitiligo Postinflammatory Hyperpigmentation Canine Uveodermatologic Syndrome Nasal Depigmentation (Dudley Nose, Snow Nose)...

C H A P T E R | 11 Pigmentary Abnormalities Lentigo Vitiligo Postinflammatory Hyperpigmentation Canine Uveodermatologic Syndrome Nasal Depigmentation (Dudley Nose, Snow Nose) (Vogt-Koyanagi-Harada–like Syndrome) Lentigo Features Top Differentials Lentigo is an asymptomatic condition characterized by one Melanoma is the differential. (lentigo) or more (lentigines) flat macule(s) or patch(es) of black skin. It is common in dogs, with highest incidences Diagnosis reported in middle-aged to older dogs. It is uncommon in cats, 1. History and clinical findings with the highest incidence in young orange cats. 2. Dermatohistopathology: epidermal hyperplasia, hyperpig- mentation, and increased numbers of melanocytes Dogs In dogs, lentigo appears as one or more macular to patchy Treatment and Prognosis areas of hyperpigmented skin. Lesions are most commonly found on the ventral abdomen and chest. 1. No medical treatment is known. 2. The prognosis is good as lentigines are benign skin changes Cats and a cosmetic problem only. In cats, multiple 1- to 10-mm-diameter black macules may coalesce on the lips, gingiva, pinnae, or eyelids. 371 372 CHAPTER 11 Pigmentary Abnormalities Lentigo—cont’d FIGURE 11-1 Lentigo. Multiple pigmented macules on the lips of a FIGURE 11-2 Lentigo. Multiple pigmented macules on the ear pinna young adult cat. of a young adult cat.  Postinflammatory Hyperpigmentation 373 Postinflammatory Hyperpigmentation Features Diagnosis In postinflammatory hyperpigmentation, skin (melanoderma) History, clinical findings, and identification of underlying or hairs (melanotrichia) become hyperpigmented as a sequela diseases to an underlying skin disease such as pyoderma, demodicosis, dermatophytosis, or hypersensitivity. This hyperpigmentation Treatment and Prognosis may be focal and circumscribed, patchy, or diffuse. It is 1. The underlying cause should be identified and treated. common in dogs and uncommon in cats. 2. The prognosis is good. Melanoderma usually resolves slowly after the underlying cause has been treated. Mela- Top Differentials notrichia usually resolves at the next shedding cycle. Differentials include lentigo and melanoma. FIGURE 11-3 Postinflammatory Hyperpigmentation. Generalized FIGURE 11-4 Postinflammatory Hyperpigmentation. Multiple hyperpigmentation associated with resolving erythema multiforme. pigmented macules on the lateral flank of a dog. The initial papular dermatitis was caused by contact dermatitis associated with a medicated shampoo. 374 CHAPTER 11 Pigmentary Abnormalities Nasal Depigmentation (Dudley Nose, Snow Nose) Features Nasal depigmentation is an idiopathic disorder in which affected dogs are born with a pigmented nose, which later in life lightens to a light brown or whitish color. Nasal depig- mentation may wax and wane, may be seasonal, may resolve spontaneously, or may be a permanent change. Only the nose is affected, and the normal cobble texture of the nose is pre- served (autoimmune skin diseases destroy the normal archi- tecture). It is common in dogs, with the highest incidence in golden retrievers, yellow Labrador retrievers, Siberian huskies, and Alaskan malamutes. Whereas Dudley nose usually describes a permanent pig- mentary defect (undesirable show fault), snow nose describes transient, seasonal depigmentation changes. Top Differentials Differentials include uveodermatologic syndrome, vitiligo, nasal solar dermatitis, autoimmune skin diseases, and cutane- ous lymphoma. Diagnosis FIGURE 11-5 Nasal Depigmentation. Nasal depigmentation in a golden retriever that occurred during the winter. 1. History and clinical findings 2. Dermatohistopathology: marked reduction of epidermal melanocytes and melanin Treatment and Prognosis 1. No treatment is known. 2. The prognosis is good because this is a cosmetic problem only. However, it is considered a defect in show dogs. FIGURE 11-6 Nasal Depigmentation. Close-up of the dog in Figure 11-5. Seasonal depigmentation on the nose of a golden retriever. The nose repigmented completely during the spring and summer.  Vitiligo 375 Vitiligo Features Vitiligo is an asymptomatic condition that is characterized by one or more macular areas of depigmented skin (leukoderma) or depigmented hair (leukotrichia). Lesions are usually first noted in young adulthood and often affect the nose, lips, face, buccal mucosa, and footpads. It is uncommon in dogs, with the highest incidence in Belgian Tervurens, German shep- herds, Rottweilers, and Doberman pinschers. It is rare in cats, with the highest incidence in Siamese cats. Top Differentials Differentials include uveodermatologic syndrome, nasal depigmentation, autoimmune skin diseases, and cutaneous FIGURE 11-8 Vitiligo. Multifocal areas of depigmentation on the nasal planum and face of an adult Doberman pinscher. lymphoma. Diagnosis Dermatohistopathology: essentially normal skin, except no melanocytes are seen. A transient inflammatory phase may be observed. Treatment and Prognosis 1. No treatment has been consistently documented in veteri- nary species; however, treatments used for autoimmune skin diseases (pemphigus and lupus) may be beneficial. 2. Treatment with L-phenylalanine 50 mg/kg orally (PO) q 24 hours may be effective. 3. The prognosis is good. This is a cosmetic disease that does not affect the animal’s quality of life. The depigmentation is usually permanent, but in some animals, spontaneous repigmentation eventually may occur. FIGURE 11-9 Vitiligo. Close-up of the dog in Figure 11-8. The spotty depigmentation of the nasal planum and hair is apparent. FIGURE 11-7 Vitiligo. Depigmentation on the nose of an adult Rottweiler typical of this syndrome. Note the spotty pattern, which differentiates this disease from seasonal nasal depigmentation and most FIGURE 11-10 Vitiligo. Well-demarcated depigmentation on the ear autoimmune skin disorders. pinna of a cat. Note the unusual asymmetrical pattern. 376 CHAPTER 11 Pigmentary Abnormalities Vitiligo—cont’d FIGURE 11-12 Vitiligo. Depigmentation on the eyelids of an affected dog. Note the normal tissue architecture has not been altered, and there is a dearth of inflammation, which is more typical of autoimmune skin diseases. FIGURE 11-11 Vitiligo. Depigmentation on the nasal planum of an affected dog. Note the normal tissue architecture has not been altered, and there is a dearth of inflammation, which is more typical of autoimmune skin diseases. FIGURE 11-13 Vitiligo. Depigmentation affecting the nasal planum, muzzle, and lips of a dog.  Canine Uveodermatologic Syndrome 377 Canine Uveodermatologic Syndrome (Vogt-Koyanagi-Harada–like Syndrome) Features Treatment and Prognosis The cause of this disorder is not completely understood, but 1. To prevent blindness, early and aggressive treatment is immune-mediated and hereditary factors appear to be essential. involved. The production of autoantibodies against melano- 2. The eyes should be treated with topical or subconjunctival cytes results in granulomatous panuveitis, leukoderma (skin glucocorticoids until uveitis has resolved. Effective thera- depigmentation), and leukotrichia (hair depigmentation). It pies include the following: is rare in dogs, with the highest incidence in young adult and 0.1% dexamethasone ophthalmic solution OU q 4 middle-aged dogs, especially Akitas. Other affected breeds hours include Siberian husky, Samoyed, chow chow, Irish setter, 1% prednisone ophthalmic solution OU q 4 hours Dachshund, fox terrier, Shetland Sheep dog, St. Bernard, Old Dexamethasone 1 to 2 mg subconjunctivally OU English sheepdog, and Brazilian Fila dog. Triamcinolone 10 to 20 mg subconjunctivally OU once An acute onset of ophthalmic signs may include dimin- Depot betamethasone 6 mg subconjunctivally OU once ished or absent pupillary light reflexes, blepharospasm, pho- 3. Also, a topical cycloplegic (1% atropine ophthalmic solu- tophobia, anterior uveitis, keratic precipitates, hyphema, tion) should be instilled OU every 6 to 24 hours or to chorioretinitis, conjunctivitis, serous ocular discharge, and effect. sometimes retinal detachment; cataracts, iris bombe, second- 4. Immunosuppressive doses of oral prednisone or methyl- ary glaucoma, and blindness may ensue. Ocular signs develop prednisolone should be given (see Table 8-1). After ocular shortly before, concurrently with, or subsequent to well- lesions have resolved (≈4–8 weeks), the dosage should be demarcated symmetrical depigmentation of the nose, lips, and gradually tapered over a period of several (8–10) weeks eyelids. Occasionally, the scrotum or vulva, anus, footpads, until the lowest possible alternate-day dose that maintains and hard palate also are depigmented. Rarely, skin lesions remission is being given. If no significant improvement become eroded, ulcerated, and crusted. In some dogs, general- is seen within 2 weeks of initiation of therapy, one ized skin and hair coat depigmentation may develop. should consider alternate or additional immunosuppres- sive medications. Top Differentials 5. Alternative glucocorticoids for refractory cases include tri- amcinolone and dexamethasone (see Table 8-1). Bilateral Uveitis 6. If systemic glucocorticoid therapy alone is ineffective, or if For bilateral uveitis, differentials include toxins, infection, undesirable adverse effects develop, treatment with cyclo- trauma, neoplasia, and immune-mediated disease. sporine, oral azathioprine, combination tetracycline and niacinamide, or cyclophosphamide may have a steroid- Skin Depigmentation sparing effect (see Table 8-2). A beneficial response should For skin depigmentation, differentials include vitiligo, other be noted within 8 to 12 weeks of initiation of treatment. autoimmune skin diseases, and cutaneous lymphoma. Once remission has been achieved, attempt to taper or discontinue steroid administration, then taper azathio- Diagnosis prine, tetracycline–niacinamide, or cyclophosphamide dose and frequency of administration for long-term main- 1. History, clinical findings, and rule out other differentials. tenance therapy (see Table 8-2). 2. Ophthalmic findings: sterile uveitis and chorioretinitis. 7. The prognosis is guarded to fair. Lifelong therapy is usually 3. Dermatohistopathology: pigmentary incontinence and needed, and control may be difficult to maintain. If uveitis lichenoid interface dermatitis composed of large histio- is not treated early and aggressively, or if it is poorly con- cytes, small mononuclear cells, and multinucleated giant trolled, glaucoma, cataracts, and blindness are likely cells. Occasionally, plasma cells and lymphocytes may sequelae. Cutaneous depigmentation is usually a cosmetic predominate. problem only, and it may become permanent or may be incompletely improved in some cases. 378 CHAPTER 11 Pigmentary Abnormalities Canine Uveodermatologic Syndrome—cont’d FIGURE 11-14 Canine Uveodermatologic Syndrome. This young FIGURE 11-15 Canine Uveodermatologic Syndrome. The same dog sheltie was diagnosed early. As the disease progresses, the cutaneous as in Figure 11-11. The depigmentation has progressed over several pigmentation is lost. (Courtesy Campbell K, McLaughlin S: Generalized years. (Courtesy Campbell K, McLaughlin S: Generalized leukoderma and leukoderma and poliosis following uveitis in a dog, J Am Anim Hosp Assoc poliosis following uveitis in a dog, J Am Anim Hosp Assoc 22:121, 1986.) 22:121, 1986.) FIGURE 11-16 Canine Uveodermatologic Syndrome. Close-up of the FIGURE 11-17 Canine Uveodermatologic Syndrome. Depigmentation dog in Figure 11-12. The nasal depigmentation has progressed and is of the hair and skin around the eye of an affected dog. Note the alopecia almost complete. (Courtesy Campbell K, McLaughlin S: Generalized may or may not be associated with this disease. leukoderma and poliosis following uveitis in a dog, J Am Anim Hosp Assoc 22:121, 1986.) FIGURE 11-18 Canine Uveodermatologic Syndrome. Focal depigmented FIGURE 11-19 Canine Uveodermatologic Syndrome. Depigmentation alopecic lesion. Note the mild seborrhea associated with this lesion. of the nails and hair on the foot of an affected dog.  C H A P T E R | 12 Keratinization and Seborrheic Disorders Callus Canine Ear Margin Dermatosis Feline Acne Zinc-Responsive Dermatosis Idiopathic Nasodigital Hyperkeratosis Tail Gland Hyperplasia (Stud Tail) Hereditary Nasal Parakeratosis of Labrador Sebaceous Adenitis Retrievers Hepatocutaneous Syndrome (Superficial Necrolytic Parasympathetic Nasal Hyperkeratosis Dermatitis, Superficial Necrolytic Migratory (Xeromycteria: Dry Nose) Erythema, Metabolic Epidermal Necrosis, Diabetic Canine Primary Seborrhea Dermatopathy) Vitamin A–Responsive Dermatosis Familial Footpad Hyperkeratosis Schnauzer Comedo Syndrome (Schnauzer Bumps) Facial Dermatitis of Persian Cats Callus Features 2. If lesion is secondarily infected, long-term systemic antibiotics (minimum, 4–6 weeks) should be adminis- Callus occurs as a localized, hyperplastic skin reaction to tered. Alternatively, topical dimethyl sulfoxide (DMSO) trauma caused by pressure or friction. It is common in dogs, combined with enrofloxacin (to make a 10-mg/mL with highest incidences noted in large and giant-breed dogs. solution) could be applied every 12 to 72 hours until A round to oval, alopecic, hyperpigmented, hyperkeratotic, lesions resolve. hyperplastic plaque forms over a bony pressure point. The 3. Special efforts should be taken to remove the “ingrown elbow, hock, or sternum (deep-chested dogs) is most com- hairs” from the callus because these will eventually lead monly affected. Lesions may become ulcerated, fistulated, and to furunculosis and infection. Scrub the hairs out fre- exudative from secondary bacterial infection. Impacted follicles quently (every 2–7 days) using a cloth, brush, or sponge (“ingrown hairs”) can become dilated and cystic over time. in the direction of hair growth. Tape-strip the hairs using a very sticky tape product; typically, only the Top Differentials ingrown hairs are removable, leaving the healthy and Differentials include dermatophytosis, demodicosis, pyo- active hairs intact. derma, and neoplasia. 4. Bedding and other sleeping and resting areas should be padded, and padded bandages should be used to prevent Diagnosis trauma to the affected area. 5. Moisturizers, antibiotic ointments (mupirocin), 2.5% 1. Usually based on history and clinical findings. benzoyl peroxide gel, or salicylic acid–sodium lactate– 2. Cytology (exudate): keratin debris, purulent or pyogranu- urea gel should be applied to the affected area every lomatous inflammation, free hair shafts, and bacteria may 12 to 24 hours to soften the skin. However, secondary be seen. infections are likely to occur if moisturizers are used 3. Dermatohistopathology: marked epidermal hyperplasia, without the implementation of protective padding orthokeratotic to parakeratotic hyperkeratosis, follicular measures. keratosis, and dilated follicular cysts. 6. Surgical excision usually is not recommended because wound dehiscence is a possible postoperative complication. Treatment and Prognosis 7. The prognosis is good for noninfected lesions. This is a 1. Observation without treatment is appropriate for nonin- cosmetic disease that does not affect the dog’s quality fected lesions. of life. 379 380 CHAPTER 12 Keratinization and Seborrheic Disorders Callus—cont’d FIGURE 12-1 Callus. Thickening of the skin over the elbow of a dog. FIGURE 12-2 Callus. Close-up of the lesion in Figure 12-1. The large The hair is clumped, and skin appears partially alopecic, which is typical alopecic area of thickened skin over the elbow is typical of this syndrome. of a callus. Often in short-coated dogs, the hairs become impacted within the follicles and callus. FIGURE 12-3 Callus. Close-up of the lesion in Figure 12-1. The clinician FIGURE 12-4 Callus. Close-up of the lesion in Figure 12-1. The exuded is gently squeezing the callus to express the impacted hairs, which are hairs are apparent. This technique is not recommended because forcing now exuding from the surface of the skin. These hairs serve as a nidus the hairs to rupture internally could result in cellulitis and scarring. for recurrent infection. FIGURE 12-5 Callus. A focal area of alopecia and thickened skin over FIGURE 12-6 Callus. Severe alopecia and thickening of the skin with the elbow. The large cystic structures are hair follicles that became ulceration over the hock of a dog. The chronic pressure that causes callus obstructed and filled with keratin debris. formation can also lead to decubital ulcers.  Callus 381 FIGURE 12-7 Callus. A sternal plaque demonstrating the focal area of FIGURE 12-8 Callus. Keratin material has been expressed from the alopecia and comedo formation caused by chronic pressure and friction comedones of the sternal plaque of a Dachshund. Note the large keratin in deep-chested dogs. This is most often seen in Dachshunds. plugs that were formed by persistent pressure produced when the dog rests in a sternal position. FIGURE 12-9 Callus. The ingrown, dead hairs have been removed. FIGURE 12-10 Callus. Ingrown hairs that have been removed from a Note the unexpected length of the hair shaft, which was embedded in callus. the callus. FIGURE 12-11 Callus. A focal callus with ulceration resulting from FIGURE 12-12 Callus. Numerous embedded hairs that were removed extreme focal pressure and secondary infection. Embedded hairs have from a chronic callus. been removed. 382 CHAPTER 12 Keratinization and Seborrheic Disorders Callus—cont’d FIGURE 12-13 Callus. Embedded hairs are being removed from a FIGURE 12-14 Callus. A chronic callus demonstrating the dilated cystic chronic callus. Note how little of the hair shaft is exposed above the follicles that develop from chronic pressure and subsequent obstruction surface of the callus. of the follicular opening. Note the lack of active infection despite the large cystic follicles. FIGURE 12-15 Callus. A chronic callus demonstrating the dilated cystic FIGURE 12-16 Callus. The comedones create dilated follicles that often follicles that develop from chronic pressure and subsequent obstruction become secondarily infected and may rupture, resulting in furunculosis. of the follicular opening. Note the lack of active infection despite the The follicles are plugged (comedones) as a result of the constant pressure large cystic follicles. applied when the deep-chested dog rests in a sternal position.  Feline Acne 383 Feline Acne Features Mupirocin ointment or cream 2.5% benzoyl peroxide gel (Note: may be irritating in Feline acne is a disorder of follicular keratinization and glan- some cats) dular hyperplasia. It is common in cats. 0.01% to 0.025% tretinoin cream or lotion Asymptomatic comedones (blackheads) form on the chin, 0.75% metronidazole gel the lower lip, and occasionally, the upper lip. Papules and Clindamycin-, erythromycin-, or tetracycline-containing pustules and, rarely, furunculosis and cellulitis may develop if topicals lesions become secondarily infected. In severe cases, affected 4. For severe refractory cases, systemic vitamin A therapy may skin may become edematous, thickened, cystic, or scarred. be effective. 5. The prognosis is good, but lifelong symptomatic treatment Top Differentials is often necessary for control. Unless secondary infection Differentials include demodicosis, dermatophytosis, Malasse- occurs, this is a cosmetic disease that does not affect the zia dermatitis, and eosinophilic granuloma (if edematous). animal’s quality of life. Diagnosis 1. History, clinical findings, and rule out other differentials. 2. Dermatohistopathology: follicular keratosis, plugging, and dilation. Glandular hyperplasia, perifolliculitis, folliculitis, furunculosis, or cellulitis may be seen if secondary bacte- rial infection is present. Treatment and Prognosis 1. Any secondary bacterial infection should be treated with appropriate systemic antibiotics for at least 2 to 3 weeks. Malassezia infections should be treated with fluconazole 10 mg/kg PO daily for 30 days. 2. Hairs around lesions should be clipped, warm water com- presses applied, and affected areas cleansed with human alcohol-free acne pads, or with benzoyl peroxide–, sulfur- FIGURE 12-18 Feline Acne. The hair has been clipped to provide salicylic acid–, or ethyl lactate–containing shampoo every better visualization of the erythema, hyperpigmentation, and comedones. 1 to 2 days until lesions resolve, and then as needed for maintenance control. Often frequent chin cleaning (every 2–3 days) is needed to prevent relapses. 3. Alternative topical products that may be effective when used every 1 to 3 days, or on an as-needed basis, include the following: FIGURE 12-17 Feline Acne. Moist, draining papular lesions on the chin of an adult cat. furunculosis and cellulitis caused the tissue swelling and FIGURE 12-19 Feline Acne. Alopecia and scarring remained as exudate. sequelae after treatment with topical mupirocin ointment. 384 CHAPTER 12 Keratinization and Seborrheic Disorders Feline Acne—cont’d FIGURE 12-21 Feline Acne. The brown discoloration is typical of comedo formation associated with feline acne. FIGURE 12-20 Feline Acne. The hair has been clipped, allowing better visualization of the comedones, papules, and draining lesions in this severe case of feline acne, which usually is limited to the chin. FIGURE 12-23 Feline Acne. Cellulitis and deep pyoderma caused by chronic feline acne. FIGURE 12-22 Feline Acne. Close-up of the cat in Figure 12-21. The lesions extended along the lateral lip surface. This is unusual for feline acne. FIGURE 12-24 Feline Acne. Cellulitis and tissue bruising caused by the severe and chronic nature of this disease.  Idiopathic Nasodigital Hyperkeratosis 385 Idiopathic Nasodigital Hyperkeratosis Features Treatment and Prognosis Idiopathic nasodigital hyperkeratosis is an idiopathic condi- 1. The intensity of therapy depends on the severity of the tion that is characterized by the excessive formation of nasal lesions. or footpad keratin. It is common in older dogs, especially 2. The nasolacrimal ducts should be flushed. cocker spaniels. 3. For mild, asymptomatic cases, benign neglect and observa- Thickened, hard, dry keratin accumulates on the nasal tion without treatment may be appropriate. planum, footpads, or both. Accumulated keratin usually is 4. For moderate to severe cases, affected areas should be most prominent on the dorsum of the nose and at the hydrated with a warm water soak or compressed for 5 to edges of the footpads. Secondary erosions, ulcers, and 10 minutes. Then a softening agent should be applied fissures may suggest an autoimmune skin disease. Excessive every 24 hours until excessive keratin has been removed digital hyperkeratosis may result in horny growths, which (≈7–10 days). Treatment should be continued on an can cause pain from pressure against adjacent footpads. as-needed basis for control. Effective softening agents Nasolacrimal duct blockage may present a contributing include the following: factor. Petroleum jelly A&D diaper rash ointment Top Differentials Ichthammol ointment Salicylic acid–sodium lactate–urea gel Differentials include distemper, zinc-responsive dermatosis, Tretinoin gel superficial necrolytic dermatitis, hereditary nasal parakerato- 5. For horny growths, excessive keratin should be trimmed sis, familial footpad hyperkeratosis, pemphigus foliaceus, sys- away before hydration and softening therapy are begun. temic or discoid lupus erythematosus, and leishmaniasis. 6. For fissured lesions, combination antibiotic–glucocorticoid ointment may be applied to lesions every 8 to 12 hours Diagnosis until healed. 1. History, clinical findings, and rule out other differentials 7. The prognosis is good. Although it is incurable, this 2. Dermatohistopathology: epidermal hyperplasia with marked is a cosmetic disease that usually can be managed orthokeratotic or parakeratotic hyperkeratosis symptomatically. FIGURE 12-25 Idiopathic Nasodigital Hyperkeratosis. Severe FIGURE 12-26 Idiopathic Nasodigital Hyperkeratosis. Severe frondlike hyperkeratotic projections with crust formation on the nose of crusting and frondlike projections on the nose. an old boxer. 386 CHAPTER 12 Keratinization and Seborrheic Disorders Idiopathic Nasodigital Hyperkeratosis—cont’d FIGURE 12-27 Idiopathic Nasodigital Hyperkeratosis. Thick, adher- FIGURE 12-28 Idiopathic Nasodigital Hyperkeratosis. Mild hyper­ ent crusts cover most of the nasal planum in this dog. keratosis of the footpads without other lesions (which would be more typical of autoimmune skin disease or hepatocutaneous syndrome). FIGURE 12-29 Idiopathic Nasodigital Hyperkeratosis. Hyperkeratosis FIGURE 12-30 Idiopathic Nasodigital Hyperkeratosis. A focal area of and crusting of the metacarpal pad. hyperkeratosis on the central pad of a greyhound (greyhound corns).  Idiopathic Nasodigital Hyperkeratosis 387 FIGURE 12-31 Idiopathic Nasodigital Hyperkeratosis. Hyperkeratosis FIGURE 12-32 Idiopathic Nasodigital Hyperkeratosis. Hyperkeratosis and crusting on the footpads. and crusting with frondlike projections on the footpads. FIGURE 12-33 Idiopathic Nasodigital Hyperkeratosis. Keratinic fronds on the nasal planum of an affected dog. FIGURE 12-34 Idiopathic Nasodigital Hyperkeratosis. Thickening and crusting of the footpads. 388 CHAPTER 12 Keratinization and Seborrheic Disorders Hereditary Nasal Parakeratosis of Labrador Retrievers Features corneum and superficial stratum spinosum, mild to mod- erate superficial interstitial to interfacial lymphoplasma- Hereditary nasal parakeratosis of Labrador retrievers is a clini- cytic dermatitis, lymphocytic and neutrophilic exocytosis, cally manageable but incurable familial dermatosis that and mild to moderate pigmentary incontinence. becomes apparent between 6 and 12 months of age. An auto- somal recessive mode of inheritance is suspected. It is uncom- Treatment and Prognosis mon in Labrador retrievers and their crosses. Grayish or brownish adherent keratinaceous debris accu- 1. No specific treatment is known, but treatments as for idio- mulates on the dorsal aspect of the nasal planum. Crusting, pathic nasodigital hyperkeratosis may be effective. (See erosions, ulcerations, fissures, or depigmentation may develop, previous section.) but the nose is not pruritic or painful. The dermatosis may 2. Alternatively, improvement is usually obtained with remain stable, may wax and wane, or may progressively topical propylene glycol (diluted 50 : 50 in water), topical worsen. Lesions are usually limited to the nasal planum, but petroleum jelly, or topical vitamin E. Initially, treatment mild scaly and crusty lesions on the hairy part of the bridge should be applied to lesions every 12 hours until a satisfac- of the nose and hyperkeratotic footpads may also be seen. tory response is seen and then used as needed for lifelong Affected dogs are otherwise healthy. control. 3. Immunosuppressive doses of oral prednisone (2 mg/kg q Top Differentials 24 hours) may be effective, but long-term daily dosing is required to maintain control. Therefore, the likelihood of Differentials include distemper, ichthyosis, zinc-responsive der- unacceptable steroid adverse effects makes this an inap- matosis, pemphigus erythematosus, pemphigus foliaceus, sys- propriate treatment option in most cases. temic or discoid lupus erythematosus, leishmaniasis, idiopathic 4. The prognosis for cure is poor, but dogs enjoy a good nasal hyperkeratosis, and primary seborrheic dermatitis. quality of life with routine symptomatic therapy. Affected dogs should not be bred. Diagnosis 1. Rule out other differentials. 2. Dermatohistopathology (nasal planum): moderate to marked parakeratosis, multifocal accumulations of pro- teinaceous fluid between keratinocytes within the stratum FIGURE 12-36 Hereditary Nasal Parakeratosis of Labrador Retrievers. Severe crusting and hyperkeratosis covering almost the entire nasal planum. (Courtesy of M. Paradis.) FIGURE 12-35 Hereditary Nasal Parakeratosis of Labrador Retrievers. Hyperkeratosis and crusting on the nose of a young adult Labrador retriever. (Courtesy of M. Paradis.)  Parasympathetic Nasal Hyperkeratosis 389 Parasympathetic Nasal Hyperkeratosis (Xeromycteria: Dry Nose) Features 2. Dermatohistopathology: epidermal hyperplasia with marked orthokeratotic or parakeratotic hyperkeratosis. Parasympathetic dysfunction may result in loss of function of the normal nasal gland, which is located in the lateral mucosa Treatment and Prognosis of the nose. The gland has parasympathetic innervation via the facial nerve. If concurrent keratoconjunctivitis sicca (KCS) 1. The intensity of therapy depends on the severity of the is present, damage to the preganglionic parasympathetic fibers lesions. proximal to the pterygopalatine ganglion may have occurred 2. Pilocarpine may be helpful. in association with possible concurrent otitis, damaging the 3. Treatment as for idiopathic nasal hyperkeratosis should be nerve fibers as they course through the temporal bone. used: Lesions may be unilateral or bilateral. Grayish or brownish The nasolacrimal ducts should be flushed. adherent keratinaceous debris accumulates on the dorsal For mild, asymptomatic cases, benign neglect and aspect of the nasal planum. The dermatosis may remain stable, observation without treatment may be appropriate. may wax and wane, or may progressively worsen. Lesions are For moderate to severe cases, affected areas should be usually limited to the nasal planum, but mild scaly and crusty hydrated with a warm water soak or compressed for lesions may appear on the hairy part of the bridge of the nose. 5 to 10 minutes. Then a softening agent should be Affected dogs should be evaluated for KCS and otitis. applied every 24 hours until excessive keratin has been removed (≈7–10 days). Treatment should be continued Top Differentials on an as-needed basis for control. Effective softening agents include the following: Differentials include idiopathic nasal parakeratosis, autoim- – Petroleum jelly mune skin disease (pemphigus foliaceus, systemic or discoid – A&D diaper rash ointment lupus erythematosus), distemper, zinc-responsive dermatosis, – Salicylic acid–sodium lactate–urea gel superficial necrolytic dermatitis, and leishmaniasis. 4. The prognosis is good. Diagnosis 1. History, clinical findings, and rule out other differentials; concurrent KCS and otitis may provide supporting evidence. FIGURE 12-37 Parasympathetic Nasal Hyperkeratosis. Hyperker­ FIGURE 12-38 Parasympathetic Nasal Hyperkeratosis. Close-up of atosis and crusting asymmetrically affecting the nasal planum. the dog in Figure 12-37. The asymmetrical (only half ) pattern of crusting is apparent. 390 CHAPTER 12 Keratinization and Seborrheic Disorders Parasympathetic Nasal Hyperkeratosis—cont’d FIGURE 12-39 Parasympathetic Nasal Hyperkeratosis. A symmetrical FIGURE 12-40 Parasympathetic Nasal Hyperkeratosis. The nasal hyperkeratosis of the nasal planum. planum is dry and crusted from the lack of normal nasal gland secretions. The normal cobblestone surface remains intact, making a diagnosis of autoimmune skin disease less likely.  Canine Primary Seborrhea 391 Canine Primary Seborrhea Features BOX 12-1 Causes of Secondary Seborrhea Canine primary seborrhea is a hereditary disorder of keratini- in Dogs zation. It is common in dogs, with the highest incidence in American cocker spaniels, English springer spaniels, West Infectious Highland white terriers, and basset hounds. Clinical symp- toms initially appear during puppyhood and may be mild at Pyoderma first but worsen with age. Symptoms may become apparent or Dermatophytosis worsen as an adult if underlying concurrent diseases develop. Malassezia dermatitis Clinical signs may include a dull, dry, lusterless hair coat; Leishmaniasis excessive scaling (dandruff); follicular casts; scaly and crusty Allergic seborrheic patches and plaques; and greasy, malodorous skin. Flea allergy dermatitis Most of the body is involved to some degree, with interdigital Atopy areas, perineum, face, axillae, ventral neck, abdomen, and skin Food hypersensitivity folds usually most severely affected. Pruritus is mild to intense, Contact dermatitis and ceruminous otitis externa is common. Secondary skin and ear infections with bacteria and Malassezia are often present. Endocrine Hypothyroidism Hyperadrenocorticism Top Differentials Sex hormone imbalance Differentials include vitamin A–responsive dermatosis and Diabetes mellitus other causes of secondary seborrhea (Box 12-1). Parasitic Demodicosis Diagnosis Scabies 1. Based on early age of onset and rule out other causes of Cheyletiellosis seborrhea. Pediculosis 2. Dermatohistopathology (nonspecific): hyperplastic, super- Otodectes spp. ficial, perivascular dermatitis with orthokeratotic or para- Nutritional keratotic hyperkeratosis, follicular keratosis, and variable Vitamin A–responsive dermatosis dyskeratosis. Bacteria and yeast may be seen within surface Zinc-responsive dermatosis and follicular keratin. Secondary bacterial folliculitis and Dietary imbalance yeast dermatitis are common. Immune Mediated Treatment and Prognosis Pemphigus foliaceus Pemphigus erythematosus 1. Ensure good nutrition. A commercially balanced dog food Discoid lupus erythematosus that meets Association of American Feed Control Officials Systemic lupus erythematosus (AAFCO) requirements should be fed. Cutaneous drug reaction 2. Any secondary bacterial and Malassezia skin and ear infec- Sebaceous adenitis tion should be treated with appropriate topical and systemic therapies. Periodic retreatments or long-term, Metabolic low-dose maintenance therapy may be needed because Malabsorption or maldigestion these dogs are susceptible to recurring infection. Superficial necrolytic dermatitis 3. For symptomatic control of ceruminous otitis, long-term Neoplastic maintenance ear care is necessary. Ear treatments with a multimodal therapy or ear cleaner should be administered Cutaneous epitheliotropic lymphoma AU every 1 to 7 days to control cerumen accumulation. 4. For symptomatic control of seborrhea, antiseborrheic 6. Vitamin A 8000 to 10,000 IU per 20 lb orally (PO) admin- shampoos and emollients may be used every 2 to 7 days istered with a fatty meal every 24 hours. Improvement until the skin condition is improved (≈2–3 weeks); then should be seen within 4 to 6 weeks. bathing frequency should be decreased to every 1 to 2 7. Historical therapies varied; they were often ineffective weeks or as needed for maintenance. and caused numerous adverse effects but included the 5. Daily oral fatty acid supplementation may be helpful following: as an adjunct therapy (180 mg eicosapentaenoic acid For dogs with severe, greasy, malodorous, pruritic seb- [EPA]/10 lb). orrhea, treatment with systemic corticosteroids may 392 CHAPTER 12 Keratinization and Seborrheic Disorders Canine Primary Seborrhea—cont’d be helpful. Prednisone 1 to 2 mg/kg PO adminis- Calcitriol (vitamin D) 10 ng/kg/day PO may be helpful tered every 24 hours until symptoms are controlled in some cases. Serum calcium levels should be closely (≈2 weeks) and then tapered to the lowest possible monitored. alternate-day dosage if maintenance therapy is needed. 8. The prognosis is variable, depending on the severity of the However, unacceptable steroid adverse effects and seborrhea. This is an incurable condition that requires recurrent skin and ear infections are potential sequelae lifelong therapy for control. Affected dogs should not be if long-term steroid therapy is used. bred. Acitretin (a retinoid) 0.5 to 1 mg/kg PO administered every 24 hours may be helpful in some dogs. FIGURE 12-41 Canine Primary Seborrhea. Greasy, poor-quality fur FIGURE 12-42 Canine Primary Seborrhea. Close-up of the dog in coat in a 4-year-old female spayed cocker spaniel. (Courtesy of A. Yu.) Figure 12-41. Partial alopecia and seborrheic dermatitis on the ventral abdomen. (Courtesy of A. Yu.) FIGURE 12-43 Canine Primary Seborrhea. Close-up of the dog in FIGURE 12-44 Canine Primary Seborrhea. Crusting around the nose Figure 12-41. The fur coat has been clipped, revealing generalized is characteristic of this disease. (Courtesy of A. Yu.) seborrhea, scales, crusts, and erythema. (Courtesy of A. Yu.)  Canine Primary Seborrhea 393 FIGURE 12-45 Canine Primary Seborrhea. Hyperkeratosis of the FIGURE 12-46 Canine Primary Seborrhea. Waxy seborrheic dermatitis footpads. (Courtesy of A. Yu.) causing discoloration and clumping of the hairs. FIGURE 12-47 Canine Primary Seborrhea. Follicular casts are FIGURE 12-48 Canine Primary Seborrhea. Generalized alopecia and apparent after the hair was epilated. Follicular casts are a characteristic lichenification affecting the entire cutaneous surface area. finding in several primary keratinization disorders (primary seborrhea, vitamin A–responsive dermatosis, sebaceous adenitis). FIGURE 12-49 Canine Primary Seborrhea. Same dog as in Figure FIGURE 12-50 Canine Primary Seborrhea. Close-up of the dog in 12-48. Alopecia and lichenification affect the entire cutaneous surface, Figure 12-48. Alopecic, lichenified skin is typical of a secondary Malassezia including the eyelid margins. dermatitis associated with primary seborrhea. 394 CHAPTER 12 Keratinization and Seborrheic Disorders Canine Primary Seborrhea—cont’d FIGURE 12-51 Canine Primary Seborrhea. Cutaneous horn forming FIGURE 12-52 Canine Primary Seborrhea. Alopecia and lichenification on the margin of a footpad associated with primary seborrhea. affecting the entire cutaneous surface are apparent. FIGURE 12-53 Canine Primary Seborrhea. Alopecia, erythema, scale, and crusts are typical of this disease. Lesions may be focal or generalized. (Courtesy of A. Yu.)  Vitamin A–Responsive Dermatosis 395 Vitamin A–Responsive Dermatosis Features Treatment and Prognosis Vitamin A–responsive dermatosis is an incompletely under- 1. Ensure good nutrition. A commercially balanced dog food stood disorder of keratinization that that is most likely a mild that meets AAFCO requirements should be fed. variant of canine primary seborrhea. This disorder responds 2. Any secondary bacterial and Malassezia skin and ear completely to treatment with high doses of vitamin A. It is infection should be treated with appropriate topical and rare in dogs, with highest incidences reported in young (2- to systemic therapies. Periodic retreatments or long-term, 3-year-old) American cocker spaniels. low-dose maintenance therapy may be needed because Marked follicular plugging, focal areas of crusting, and these dogs are susceptible to recurring infection. hyperkeratotic plaques have keratinaceous frondlike plugs. 3. For symptomatic control of ceruminous otitis, long-term Lesions are most commonly found on the ventral and lateral maintenance ear care is necessary. Ear treatments with a aspects of the chest and abdomen. Mild to moderate pruritus, multimodal therapy or ear cleaner should be administered a dull dry hair coat that epilates easily, a rancid body odor, AU every 1 to 7 days to control cerumen accumulation. and generalized scaling may be present. Concurrent cerumi- 4. For symptomatic control of seborrhea, antiseborrheic nous otitis externa is common. shampoos and emollients may be used every 2 to 7 days until the skin condition is improved (≈2–3 weeks); then Top Differentials bathing frequency should be decreased to every 1 to 2 weeks or as needed for maintenance. Differentials include primary seborrhea, sebaceous adenitis, 5. Daily oral fatty acid supplementation may be helpful as zinc-responsive dermatosis, and other causes of secondary an adjunct therapy (180 mg EPA/10 lb). seborrhea (see Box 12-1). 6. Vitamin A 8000 to 10,000 IU per 20 lb PO administered with a fatty meal every 24 hours. Improvement should be Diagnosis seen within 4 to 6 weeks and complete clinical remission 1. Rule out other differentials. within 8 to 10 weeks. 2. Dermatohistopathology: marked, disproportionate follic- 7. The prognosis is good, but lifelong vitamin A therapy is ular orthokeratotic hyperkeratosis with minimal epider- usually necessary to maintain remission. mal hyperkeratosis. 3. Response to vitamin A. FIGURE 12-54 Vitamin A–Responsive Dermatosis. Greasy, poor- FIGURE 12-55 Vitamin A–Responsive Dermatosis. Close-up of the quality fur coat in an adult Cocker spaniel. Note the similarity to canine dog in Figure 12-54. Scale and follicular casts can be seen. The skin primary seborrhea. (Courtesy of A. Yu.) lesions are generalized. (Courtesy of A. Yu.) 396 CHAPTER 12 Keratinization and Seborrheic Disorders Schnauzer Comedo Syndrome (Schnauzer Bumps) Features Treatment and Prognosis Schnauzer comedo syndrome is a common acne-like dis­ 1. For any secondary pyoderma, appropriate systemic antibi- order of follicular keratinization that occurs in miniature otics should be administered for 3 to 4 weeks. schnauzers. 2. For mild to moderate lesions, affected areas should be Few to many nonpainful, nonpruritic comedones (black- cleansed with human acne pads, chlorhexidine/miconazole heads) and crusted papules are found on the dorsal midline pledgets, or 2% benzoyl peroxide gel every 1 to 2 days until of the back between the shoulders and the sacrum. If lesions comedones have resolved (≈1–3 weeks). Then these areas become secondarily infected, a widespread papular eruption should be cleansed every 2 to 7 days or as needed for and pruritus may develop. maintenance control. 3. For moderate to severe lesions, affected areas should be Top Differentials cleansed with a sulfur and salicylic acid, ethyl lactate, tar and sulfur, or benzoyl peroxide– and sulfur-containing Differentials include demodicosis, superficial pyoderma, and shampoo every 2 to 3 days until comedones have resolved dermatophytosis. (≈1–3 weeks). Then these areas should be cleansed as needed for long-term control. Diagnosis 4. Vitamin A 8000 to 10,000 IU/20 lb PO q 24 hours may be 1. Signalment, history, clinical findings, and rule out other beneficial. differentials. 5. The prognosis is good. Unless lesions are secondarily 2. Dermatohistopathology: superficial portion of the hair fol- infected, this is a cosmetic disease that does not affect the licle is distended with keratin. The keratin-dilated infun- dog’s quality of life and is usually readily controlled with dibulum may have a cystic appearance. Secondary bacterial routine symptomatic therapy. folliculitis and furunculosis with comedone rupture may be present. FIGURE 12-56 Schnauzer Comedo Syndrome. Comedones are visible FIGURE 12-57 Schnauzer Comedo Syndrome. This moth-eaten through the partial alopecia. (Courtesy of W. Miller.) alopecia was caused by numerous comedones on the lumbar area of this Schnauzer. (Courtesy of L. Frank.)  Canine Ear Margin Dermatosis 397 Canine Ear Margin Dermatosis Features 3. To remove accumulated debris, gently cleanse ear margins with a sulfur and salicylic acid– or benzoyl peroxide– Canine ear margin dermatosis is a common idiopathic sebor- containing shampoo every 1 to 2 days until all debris is rheic condition of ear margins in dogs with pendulous ears, eliminated (≈5–14 days, depending on severity). Con- especially Dachshunds. Many dogs progress over time to dem- tinue cleansing ear margins on an as-needed basis for onstrate symptoms typical of vascular disease (vasculitis). maintenance control. Initially, an asymptomatic accumulation of soft, greasy, 4. If accumulated crusts are tightly adherent and hardened, keratinaceous debris occurs along the edges of the ears. With the first few shampoo applications should be preceded chronicity, the ear margins may become alopecic, crusted, by a 5- to 10-minute warm water soak. cracked, ulcerated, and fissured. Fissured lesions may be 5. A moisturizer may be applied to ear margins after each painful and may induce head shaking, which further exacer- shampoo therapy. bates the fissuring and pain. Except for the ear margins, the 6. If ear margins are mildly to moderately inflamed, topical skin is otherwise normal. If the lesions progress and notch therapy with a steroid-containing ointment should be defects develop or if other body regions are affected (e.g., nose, provided every 24 hours for the first 5 to 10 days. nails, oral cavity), autoimmune skin disease or vasculitis 7. Daily supplementation with oral essential fatty acids should be considered. (180 mg EPA/10 lb), vitamin A (8000–10,000 IU), or zinc (zinc methionine or zinc sulfate 2–3 mg/kg/day of elemen- Top Differentials tal zinc) may be beneficial for the skin lesions. Improve- ment should be seen after 1 to 2 months of therapy. Differentials include scabies, vasculitis, neoplasia, autoimmune 8. Treatment with vitamin E, tetracycline, doxycycline, or skin disease, and causes of secondary seborrhea (see Box 12-1). niacinamide may be beneficial (see Table 8-2). 9. Treatment with pentoxifylline 25 mg/kg PO every 12 Diagnosis hours with food may be beneficial in some dogs. Improve- 1. Signalment, history, clinical findings, and rule out other ment should be seen within 1 to 3 months of therapy. differentials. 10. If ear margins are severely inflamed and if evidence of 2. Dermatohistopathology: marked orthokeratotic or para- vasculitis is present, the patient should be evaluated and keratotic hyperkeratosis and follicular keratosis. treated for vasculitis and autoimmune skin disease. 11. If ear margins are extensively fissured and respond poorly to topical therapy, a cosmetic ear crop to remove the fis- Treatment and Prognosis sured tissue may be considered. Lesions may recur at the 1. No specific treatment is known. surgical site. 2. The dog should be kept away from dry heat sources (e.g., 12. The prognosis is variable, depending on severity. This wood stoves, fireplaces, forced air ducts) because dry heat condition is incurable, but most cases can be controlled aggravates the dermatosis. symptomatically. FIGURE 12-58 Canine Ear Margin Dermatosis. Alopecia with a FIGURE 12-59 Canine Ear Margin Dermatosis. Alopecia and crusting crusting dermatitis on the ear margin of an adult Dachshund. on the distal ear margin of a young adult Dachshund. 398 CHAPTER 12 Keratinization and Seborrheic Disorders Canine Ear Margin Dermatosis—cont’d FIGURE 12-60 Canine Ear Margin Dermatosis. More severe alopecia FIGURE 12-61 Canine Ear Margin Dermatosis. Diffuse alopecia extending onto the lateral ear pinna. covering almost the entire ear pinna. FIGURE 12-62 Canine Ear Margin Dermatosis. Alopecia and crusting FIGURE 12-63 Canine Ear Margin Dermatosis. Alopecia and scaling on the ear margin with a notch defect. The notch is typical of a vasculitis affected only the distal margin of this adult Dachshund’s ear pinna. The lesion. lesions are not pruritic. FIGURE 12-64 Canine Ear Margin Dermatosis. Alopecic crusting dermatitis on the ear margin.  Zinc-Responsive Dermatosis 399 Zinc-Responsive Dermatosis Features 2. For dogs with diet-induced zinc deficiency, the dietary imbalance should be identified and corrected. Only Zinc-responsive dermatosis is a zinc deficiency–induced dis- AAFCO-approved dog foods should be fed. Skin lesions order of keratinization. An inherent diminished ability to should resolve within 2 to 6 weeks of the dietary change. absorb zinc from the intestinal tract, a diet low in absolute 3. Zinc supplementation may be needed in some dogs, either zinc concentration, or mineral antagonisms that prevent zinc initially for the first few weeks of the dietary change or absorption from the food (e.g., diets high in phytate [plant lifelong if there is a diminished ability to absorb zinc. Zinc protein], a cereal- or soy-based diet, excessive calcium supple- methionine or zinc sulfate (2–3 mg/kg/day of elemental mentation) can cause zinc deficiency. It is rare in dogs, with zinc) PO should be administered with food. Improvement the highest incidence in young adult Northern breed dogs should occur within 6 weeks. If no response is seen, the (Siberian huskies, Boston terriers, Samoyeds, and Alaskan zinc dosage can be doubled or a different zinc product malamutes) and in young, rapidly growing puppies of any tried. Signs of zinc toxicosis include depression, anorexia, breed. vomiting, and diarrhea. Cutaneous lesions of zinc toxico- Crusting, scaling, erythema, and alopecia typically develop sis can mimic zinc deficiency; therefore, blood levels around the eyes and mouth; the muzzle, nasal planum, ear should be monitored. pinnae, and genitalia may also be involved. Hyperkeratotic or 4. Initiating oral essential fatty acid therapy may allow for a thick, crusty plaques may be present on the elbows, stifles, and reduction in zinc dosage or may eliminate the need for other pressure points and at sites of trauma. The footpads may zinc supplementation altogether in some dogs. be hyperkeratotic and fissured. Lesions may be asymmetrical 5. Concurrent symptomatic therapy with warm water soaks, and mildly to moderately pruritic in some dogs. Secondary antiseborrheic shampoos, and topical applications of oint- bacterial and Malassezia skin infections are common. Concur- ments on the lesions may be helpful. rent depression, anorexia, lymphadenomegaly, and pitting 6. Intact females that are not well controlled with zinc sup- edema of the distal extremities may be seen. Severely affected plementation should be neutered because estrus may exac- puppies may have stunted growth. erbate the disease. 7. The prognosis is good for most dogs, although lifelong Top Differentials zinc supplementation sometimes is needed. Differentials include primary seborrhea, autoimmune skin disease, and other causes of secondary seborrhea (see Box 12-1). Diagnosis 1. Rule out other differentials. 2. Dermatohistopathology: marked, diffuse epidermal and follicular parakeratosis and superficial perivascular derma- titis. Papillomatosis, spongiosis, and evidence of second- ary infection (intraepidermal pustules, folliculitis) are common. 3. Response to zinc therapy. Treatment and Prognosis 1. Any secondary bacterial or Malassezia skin infection should be treated with appropriate medical therapy for at least 3 FIGURE 12-65 Zinc-Responsive Dermatosis. Alopecia and hyperker­ to 4 weeks. atotic plaques on the face of a young adult Siberian husky. 400 CHAPTER 12 Keratinization and Seborrheic Disorders Zinc-Responsive Dermatosis—cont’d FIGURE 12-67 Zinc-Responsive Dermatosis. An alopecic, seborrheic plaque on the abdomen. FIGURE 12-66 Zinc-Responsive Dermatosis. Same dog as in Figure 12-65. Alopecia and crusting around the nose and eyes resolved with zinc supplementation.  Tail Gland Hyperplasia 401 Tail Gland Hyperplasia (Stud Tail) Features Diagnosis Tail gland hyperplasia is a seborrheic condition that is associated 1. History, clinical findings, and rule out other differentials with hyperplastic sebaceous glands in the tail gland area (dogs, 2. Dermatohistopathology: sebaceous gland hyperplasia cats) or the perianal region (dogs). In cats, it occurs as a localized idiopathic condition. In dogs, it may be localized or may be associated with a generalized primary or secondary seborrheic Treatment and Prognosis disorder. It is common in dogs, with intact males possibly pre- 1. In dogs, if generalized skin disease is present, the underly- disposed. The condition is uncommon in cats, with the highest ing cause of the seborrhea should be identified and incidence in cage-confined cattery cats or in cats with poor controlled. grooming habits. Intact male cats may be predisposed. 2. Appropriate systemic antibiotics should be administered for 3 to 4 weeks if lesions in dogs are secondarily infected. Dogs 3. Clinical improvement in dogs and cats may be seen with In dogs, the lesion is a slowly enlarging, asymptomatic, oval, localized topical antiseborrheic therapy applied on an raised area of hair loss on the dorsum of the tail approximately as-needed basis. 2.5 to 5.0 cm distal to the tail head. Affected skin may be scaly, 4. In cats, self-grooming should be encouraged by minimiz- greasy, and hyperpigmented. Pustules from secondary bacte- ing cage confinement. Regular grooming and combing rial infection may be seen. In dogs with primary or secondary by the owner may be necessary in cats that are poor seborrhea, other skin lesions are present. groomers. 5. In intact male dogs, castration may induce partial to com- Cats plete lesion regression or may prevent further lesion enlargement. Improvement should be seen within 2 A bandlike strip of matted hair or an accumulation of waxy, months of castration. In intact male cats, castration may seborrheic debris occurs along the dorsum of the tail. Affected not induce lesion resolution but may help prevent further skin may become hyperpigmented or partially alopecic. progression. Lesions are asymptomatic, and no other skin involvement is 6. For cosmetically unacceptable lesions in dogs, excess glan- noted. dular tissue can be surgically resected. Without concurrent castration, however, lesion recurrence within 1 to 3 years Top Differentials is likely. Wound closure may be extremely difficult. Differentials include demodicosis, dermatophytosis, superfi- 7. The prognosis is good. This is a cosmetic disease that does cial pyoderma, and neoplasia. not affect the animal’s quality of life. FIGURE 12-68 Tail Gland Hyperplasia. A focal area of alopecia with a FIGURE 12-69 Tail Gland Hyperplasia. Alopecic dermatitis with crusting dermatitis developed over the area of the tail gland. cystlike structures over the tail gland in an adult Brittany spaniel. 402 CHAPTER 12 Keratinization and Seborrheic Disorders Tail Gland Hyperplasia—cont’d FIGURE 12-71 Tail Gland Hyperplasia. Partial alopecia with a focal, greasy, poor-quality fur coat on the dorsal tail region is characteristic of this disorder. (Courtesy of D. Angarano.) FIGURE 12-70 Tail Gland Hyperplasia. Alopecic dermatitis over the tail gland. FIGURE 12-73 Tail Gland Hyperplasia. Alopecia and comedone formation caused by hypertrophy of the tail gland. FIGURE 12-72 Tail Gland Hyperplasia. Close-up of the cat in Figure 12-69. Discoloration of the skin and hair is caused by abnormal glandular secretion. (Courtesy of D. Angarano.) FIGURE 12-74 Tail Gland Hyperplasia. Alopecia and crusting of the skin over the tail gland caused by hypertrophy of the gland and resulting dermatitis.  Sebaceous Adenitis 403 Sebaceous Adenitis Features 3. For more severe cases, daily treatments with high doses of oral fatty acids and topical spray applications of 50% to Sebaceous adenitis is a destructive inflammatory disease of 75% propylene glycol in water or water-based moisturiz- sebaceous glands. It is uncommon in dogs, with the highest ing spray may be helpful. incidence reported in young adult to middle-aged standard 4. Systemic therapy may be effective in preventing further poodles, Hungarian vizslas, Akitas, and Samoyeds. An autoso- sebaceous gland destruction and even in restoring more mal recessive mode of inheritance is suspected in standard normal glandular function in some dogs. Dogs should be poodles and Akitas. treated using the following: Mild to severe scaling most often involves the dorsum of Vitamin A 8000 to 10,000 IU/20 lb PO q 24 hours. the back and neck, top of the head, face (dorsal planum of Cyclosporine (Atopica) 5 to 10 mg/kg PO q 24 hours nose), ears (pinnae or external canals), and tail. The skin for 6 to 8 weeks or until improvement occurs; then the disease may remain localized, become multifocal, or be gen- cyclosporine should be tapered to the lowest possible eralized over the trunk. In short-coated dogs, the scales are dose to prevent recurrence of the disease (usually every usually fine and nonadherent. In longer-coated dogs, the other day). scales tightly adhere to the hairs, and the hair coat may be 5. Historically, many drugs have been used with variable dull, dry, or matted; follicular casts are common. Annular to results; these include the following, as well as drugs typi- patchy (short-haired dogs) or diffuse (long-haired dogs) alo- cally used for autoimmune skin disorders: pecia occurs frequently. In long-haired dogs, the undercoat Tetracycline and niacinamide (as described in Table tends to be lost while the primary hairs are usually spared. 8-2) Akitas may also have a greasy skin and hair coat, with papules Prednisone 2 mg/kg PO q 24 hours until lesions are and pustules; they may be concurrently febrile and depressed, controlled; then tapered to the lowest possible and may lose weight. Pruritus is not usually seen unless there alternate-day dosage that controls signs is a secondary bacterial or Malassezia infection, which is Isotretinoin 1 mg/kg PO q 12–24 hours until lesions common. Subclinical disease (histologic lesions without clini- improve (≈6 weeks), then 1 mg/kg PO q 24–48 hours cal symptoms) has also been documented in standard poodles. for 6 weeks; then 1 mg/kg PO q 48 hours or 0.5 mg/ kg PO q 24 hours for maintenance; liver adverse effects Top Differentials are common Differentials include primary seborrhea and causes of second- Acitretin 1 mg/kg PO q 12–24 hours until lesions ary seborrhea (see Box 12-1). improve (≈6 weeks); then 1 mg/kg PO q 24–48 hours for 6 weeks; then 1 mg/kg PO q 48 hours or 0.5 mg/ Diagnosis kg PO q 24 hours for maintenance Asparaginase 10,000 IU IM q 7 days for two or three 1. Rule out other differentials. treatments; then as needed 2. Dermatohistopathology (from dorsum of neck in sus- 6. The prognosis is variable, depending on disease severity. pected subclinical cases): in early lesions, there are discrete This is an incurable disease, but early diagnosis and treat- granulomas in areas of the sebaceous glands, with no ment improve the prognosis for long-term control. Short- involvement of other adnexa. In chronic lesions, the seba- coated dogs, which tend to have milder symptoms, may ceous glands are absent and are replaced by fibrosis. Fol- have a more favorable prognosis than longer-coated dogs. licular plugging and hyperkeratosis may be seen. Standard poodles and Akitas have the greatest tendency to develop progressive, refractory disease, and if hair regrowth Treatment and Prognosis does occur in standard poodles, the hair may be straight 1. Any secondary bacterial or Malassezia skin infections rather than curled. Affected dogs should not be bred. should be treated with appropriate systemic medications. 2. For mild cases, daily oral essential fatty acid supplementa- AUTHOR’S NOTE tion and topical therapy with antiseborrheic shampoos, When needed, use flea and tick prevention prod- emollient rinses, and humectants applied every 2 to 4 days ucts that do not rely on sebaceous gland function or as needed may effectively control symptoms. Essential to be effective. fatty acid supplementation may be effective. 404 CHAPTER 12 Keratinization and Seborrheic Disorders Sebaceous Adenitis—cont’d FIGURE 12-75 Sebaceous Adenitis. Generalized alopecia and FIGURE 12-76 Sebaceous Adenitis. Same dog as in Figure 12-75. After erythema caused by sebaceous adenitis. therapy with vitamin A and topical therapies, the alopecia and dermatitis are much improved. FIGURE 12-77 Sebaceous Adenitis. Generalized alopecia, erythema, FIGURE 12-78 Sebaceous Adenitis. Alopecia and crusting dermatitis and scaling typical of sebaceous adenitis. are caused by the lack of sebum production, which results in abnormal moisture and barrier function. This often leads to secondary infection. FIGURE 12-79 Sebaceous Adenitis. Clumping of hairs at the face, FIGURE 12-80 Sebaceous Adenitis. The poor-quality hair coat with typical of primary keratinization defects. adherent scales and crusts on the ear pinna is typical of this disease.  Sebaceous Adenitis 405 FIGURE 12-81 Sebaceous Adenitis. When the hairs are epilated, FIGURE 12-82 Sebaceous Adenitis. Alopecia and crusting on the follicular casts adhere to the hair shaft, which is classic for primary distal tail of a dog with generalized lesions. keratinization defects such as sebaceous adenitis, primary seborrhea, and vitamin A–responsive dermatosis. FIGURE 12-84 Sebaceous Adenitis. The poor-quality hair coat and FIGURE 12-83 Sebaceous Adenitis. Crusts on the bridge of the nose clumping of hairs are apparent on the ear pinna of this dog. These and clumping of the fur on the face are apparent. lesions are most often found in a generalized pattern. 406 CHAPTER 12 Keratinization and Seborrheic Disorders Sebaceous Adenitis—cont’d FIGURE 12-86 Sebaceous Adenitis. Generalized, multifocal alopecia on the trunk of a dog. FIGURE 12-85 Sebaceous Adenitis. Multifocal alopecia with well demarcated margins on the ear pinnae and neck of an affected dog. FIGURE 12-87 Sebaceous Adenitis. Hair pluck demonstrating the follicular casts that are typical primary keratinization disorders.  Hepatocutaneous Syndrome 407 Hepatocutaneous Syndrome (Superficial Necrolytic Dermatitis, Superficial Necrolytic Migratory Erythema, Metabolic Epidermal Necrosis, Diabetic Dermatopathy) Features with parenchymal collapse or by extensive liver fibrosis (cirrhosis). Hepatocutaneous syndrome/superficial necrolytic dermatitis 7. Dermatohistopathology: early lesions show the diagnostic is a unique skin disease in animals that have chronic liver findings of marked, diffuse parakeratotic hyperkeratosis disease or glucagon-secreting pancreatic tumors. The exact with striking intercellular and intracellular edema, kerati- pathogenesis is unknown, but increased gluconeogenesis trig- nocyte degeneration in the upper epidermis, and hyper- gered by hyperglucagonemia (pancreatic tumor) or increased plastic basal cells, which give the characteristic “red, white, hepatic catabolism of amino acids (chronic liver disease) is and blue” histologic appearance of a striatonigral degen- thought to result in low plasma amino acid concentrations eration (SND) lesion. Mild, superficial, perivascular der- and epidermal protein depletion, which causes the skin matitis with evidence of secondary bacterial, dermatophyte, lesions of superficial necrolytic dermatitis. It is uncommon in or yeast infection may be present. Chronic lesions usually dogs and rare in cats, with the highest incidence in older reveal nonspecific changes that are rarely diagnostic. animals. Among dogs, Shetland sheep dogs, West Highland White terriers, cocker spaniels, and Scottish terriers may be predisposed. Treatment and Prognosis Skin lesions are characterized by minimally to intensely 1. Any secondary bacterial or yeast skin infection should be pruritic, bilaterally symmetrical erythema; scaling; crusting; treated with appropriate antimicrobial therapies. erosions; and ulcers on the distal limbs and around the mouth 2. If the underlying cause is a resectable glucagonoma, surgi- and eyes. Lesions also may involve the ear pinnae, elbows, cal excision of the tumor is curative. hocks, external genitalia, ventrum, and oral cavity. The foot- 3. If the underlying problem is liver disease, its cause should pads are usually mildly to markedly hyperkeratotic, fissured, be identified and corrected (e.g., anticonvulsant drug hep- and ulcerated. Lameness secondary to footpad lesions may be atotoxicity). To symptomatically improve liver function, evident. Polydipsia and polyuria may be present if there is therapy with one of the following antioxidants may be concurrent diabetes mellitus. Otherwise, systemic signs of helpful: underlying metabolic disease are rarely evident at initial pre- S-adenosylmethionine (sAME) denosyl 18–22 mg/kg sentation but usually become apparent a few to several months PO daily (90 mg small animals, 225 mg larger animals) later. Ursodiol (Actigall) 10 mg/kg PO daily Vitamin E 400 IU PO q 12 hours Top Differentials 4. In dogs with liver fibrosis, colchicine 0.03 mg/kg PO administered every 24 hours may help slow the progres- Differentials include cutaneous epitheliotropic lymphoma, sion of fibrosis. Potential adverse effects of long-term pemphigus foliaceus or vulgaris, systemic lupus erythemato- colchicine use include vomiting, hyperperistalsis, and sus, drug eruption, severe furunculosis (demodicosis, derma- diarrhea. tophytosis, pyoderma), and zinc-responsive dermatosis. 5. Parenteral amino acid supplementation is the symptomatic treatment of choice for improving skin lesions in animals Diagnosis with chronic liver disease and may prolong survival time 1. Hemogram: neutrophilia or normocytic, normochromic, by several months. A 10% crystalline amino acid solution nonregenerative anemia may be present. (Aminosyn; Abbott Laboratories, Abbott Park, IL) 25 mL/ 2. Serum biochemistry panel (liver failure): findings usually kg intravenously (IV) can be administered via jugular cath- include mild to moderate increases in serum alkaline eterization over 6 to 8 hours, or a 3% amino acid and phosphatase (ALP) and alanine aminotransferase (ALT) electrolyte solution (ProcalAmine; Braun Medical, Bethle- activities, total bilirubin, and bile acids. Hypoalbumin- hem, PA) 25 mL/kg IV can be administered via peripheral emia and decreased blood urea nitrogen (BUN) are also catheterization over 8 hours. Treatments may be repeated common. Hyperglycemia may be present. every 7 to 10 days or as needed. Marked improvement in 3. Plasma amino acid concentrations: markedly decreased skin lesions should be seen within 1 to 3 weeks. (hypoaminoacidemia). 6. Oral administration of amino acid solutions works well. 4. Serum glucagon concentrations: elevated with gluca- Alternatively, oral supplementation with three to six raw gonoma, may or may not be elevated with hepatopathy. egg yolks per day, zinc, and essential fatty acids may help 5. Abdominal ultrasonography: evidence of chronic liver improve skin lesions in some animals, but these treat- disease (small liver with hyperechoic, reticular pattern sur- ments are usually not as effective as intravenous amino rounding hypoechoic areas in a “honeycombed” pattern), acid therapy. pancreatic tumor, or metastasis to liver (hyperechoic or 7. Treatment with anti-inflammatory doses of prednisone hypoechoic foci in liver parenchyma). may temporarily improve skin lesions, but some dogs are 6. Histopathology (liver biopsy): chronic liver disease is susceptible to diabetes or additional liver disease after glu- usually characterized by a distinctive vacuolar hepatopathy cocorticoid use. 408 CHAPTER 12 Keratinization and Seborrheic Disorders Hepatocutaneous Syndrome—cont’d 8. Symptomatic topical therapies (keratolytic or moisturizing AUTHOR’S NOTE shampoos) may help improve skin lesions. 9. The prognosis for animals with chronic hepatic disease Severe bacterial and yeast pododermatitis often or metastatic pancreatic neoplasia is poor, and survival complicates the clinical presentation of this time after the onset of skin lesions may be only a syndrome. few months. Distribution Pattern of Hepatocutaneous Syndrome  Hepatocutaneous Syndrome 409 FIGURE 12-88 Hepatocutaneous Syndrome. Alopecic, crusting der- FIGURE 12-89 Hepatocutaneous Syndrome. Close-up of the dog in matitis on the nasal planum and muzzle. Figure 12-88. Alopecic crusting dermatitis on the lips and nasal planum is similar to lesions found in autoimmune skin disease. FIGURE 12-90 Hepatocutaneous Syndrome. Severe hyperkeratosis FIGURE 12-91 Hepatocutaneous Syndrome. Lesions around the and crusting of the footpads are common findings in hepatocutaneous mucous membrane are common in hepatocutaneous syndrome. Perianal syndrome. Note the similarity to autoimmune skin disease. dermatitis is apparent. FIGURE 12-92 Hepatocutaneous Syndrome. Severe crusting of the FIGURE 12-93 Hepatocutaneous Syndrome. Footpad hyperkeratosis footpads of a dog with hepatocutaneous syndrome. and crusting. Note the similarities to autoimmune skin disease. 410 CHAPTER 12 Keratinization and Seborrheic Disorders Hepatocutaneous Syndrome—cont’d FIGURE 12-96 Hepatocutaneous Syndrome. Severe hyperkeratosis of the foot pads is a classic lesion caused by this disease. FIGURE 12-94 Hepatocutaneous Syndrome. Severe crusting and hyperkeratosis of the footpads developed over several months in this older mixed-breed dog. (Courtesy of A. Yu.) FIGURE 12-97 Hepatocutaneous Syndrome. Footpad hyperkeratosis with tissue erosions on the footpads is typical of this disease. FIGURE 12-95 Hepatocutaneous Syndrome. Severe crusting on the muzzle and periocular skin of a dog. Note the erosions and depigmentation is very similar with lesions caused by autoimmune skin diseases.  Familial Footpad Hyperkeratosis 411 Familial Footpad Hyperkeratosis Features Diagnosis Familial footpad hyperkeratosis is a familial disorder that 1. Rule out other differentials. results in severe digital hyperkeratosis by 5 to 6 months of 2. Dermatohistopathology: marked orthokeratotic hyperker- age. It is rare in dogs, with the highest incidence in Irish atosis with mild to severe epidermal hyperplasia. terriers, Dogues de Bordeaux, and Kerry blue terriers. An autosomal recessive mode of inheritance is suspected in Treatment and Prognosis Irish terriers. 1. No specific treatment is known, but treatments as for idio- At birth, the footpads appear to be normal, but by 4 to 6 pathic nasodigital hyperkeratosis may be effective. months of age, affected dogs begin to develop marked hyper- 2. Symptomatically treat with daily foot soaks in 50% pro- keratotic, thickened, hard, and cracked footpads. The entire pylene glycol combined with frequent filing of the foot- surfaces of all footpads are involved, and subsequent forma- pads to remove surplus keratin. Significant improvement tion of horny growths, expanding fissures, and secondary bac- should be seen within 5 days, but lifelong maintenance terial infection usually result in severe, intermittent lameness. therapy is required for control. No other skin involvement occurs, but concurrent abnormal 3. Topical salicylic acid and urea products may be beneficial. nail development, characterized by slightly faster growth and 4. For fissured lesions, a combination antibiotic–glucocorticoid round profiles instead of the normal U-shaped ones, may be ointment may be applied every 8 to 12 hours until lesions seen in Irish terriers. are healed; appropriate systemic antibiotics should be admin- istered for 3 to 4 weeks if footpads are secondarily infected. 5. Fast-growing nails should be trimmed frequently. Top Differentials 6. The prognosis for cure is poor, but most dogs enjoy a good Differentials include distemper, zinc-responsive dermatosis, quality of life with routine symptomatic therapy. Affected autoimmune skin disease, and superficial necrolytic dermatitis. dogs should not be bred. FIGURE 12-98 Familial Footpad Hyperkeratosis. Severe hyperkera­ FIGURE 12-99 Familial Footpad Hyperkeratosis. Severe hyperkera­ tosis and crusting of the pads are characteristic of this disorder. (Courtesy tosis resulted in footpad disfigurement. (Courtesy of Paradis M: Footpad of Paradis M: Footpad hyperkeratosis in a family of Dogues de Bordeaux, Vet hyperkeratosis in a family of Dogues de Bordeaux, Vet Dermatol 3:75, 1992, Dermatol 3:75, 1992, Blackwell Science Ltd.) Blackwell Science Ltd.) 412 CHAPTER 12 Keratinization and Seborrheic Disorders Facial Dermatitis of Persian Cats Features Facial dermatitis of Persian cats is a facial skin disease of unclear cause. It is uncommon to rare in Persian and Himala- yan cats, with the highest incidence in older kittens and young adult cats. Black, waxy debris that mats the hair accumulates sym- metrically around the eyes or mouth or on the chin. Initially, lesions are not pruritic, but as they progress and become inflamed, moderate to severe pruritus develops. Exudative and erythematous facial folds, a m