Numerous skin diseases, other than seborrhea, result in excessive scale and crust formation.
Numerous skin diseases, other than seborrhea, result in excessive scale and crust formation. Many veterinary clinicians inappropriately use the term seborrhea as a clinical description of excessive scaling instead of a disease diagnosis. Scale and crust formation may also result from abnormalities in keratinization, epithelialization or cornification and this may have a genetic basis in some breeds. The diseases we will consider as scaling disorders include primary idiopathic seborrhea, epidermal dysplasia, cornification disorders, ichthyosis, zinc responsive dermatosis. Other localized breed-specific keratinization disorders will be covered in a separate session and will include schnauzer comedo syndrome, nasodigital hyperkeratosis, idiopathic facial dermatitis, stud tail, acne, linear keratosis and ear margin dermatosis. It is important to realize that even though these diseases tend to be breed oriented that these breeds also develop scaling for other reasons. In addition sometimes it is possible that other breeds can develop these disorders. In general the disorders are often genetic alterations in normal skin production and therefore they often occur at young age though early skin lesions may be subtle and go unrecognized or attributed to other problems. Topical and systemic antiseborrheic therapy will be covered in other sessions.
Certain breeds have been described as developing primary idiopathic seborrhea and it is considered to be more common in the American cocker spaniel, English Springer spaniel, West Highland White terrier and Basset hound. Other breeds described as having it also include the Irish Setter, Doberman pinscher, Chinese Shar pei, Dachshund, Labrador retriever, German Shepherd Dog and Newfoundland.
American cocker spaniels are undoubtedly the most common breed presenting with primary idiopathic seborrhea and the most studied. Much of this work was reviewed by Kwochka.(Kwochka 1993) The defect in these dogs is a genetic programmed abnormality in epidermal proliferation. Affected cockers have shortened epidermal transit times and increased DNA synthesis in the basal cells. By doing epidermal-grafting studies Kwochka has shown the defect is epidermal and not related to serum or dermal factors. Clinical lesions most commonly seen are keratinous plaques that may occur on an erythematous base. The surface is a thick golden brown scale/crust. It is not uncommon to find subcorneal pustules in some areas along the margin of the plaques. In those instances the plaques will be crusty. The pustules indicate the presence of secondary pyoderma. Scaly lesions, comedones and follicular casts are usually prominent around the nipples, on the ventral surface of the tail, medial thighs, the perineal region, and the ventral cervical area. Often different areas of the body will have different lesions. Comedones are often present in the perineal and perirectal area; scaling and flaking on dorsal thorax; follicular casts interdigital and lower extremities; waxy comedones with plugs or fronds in the peri-nipple location. Generally these dogs are not very pruritic unless concurrent pyoderma or Malassezia are present. The association with pruritus is an important distinction to make. An interdigital yellow, waxy accumulation is usually found and may be associated with follicular casts. Ceruminous waxy ears are almost always present. The waxy ears frequently progress to otitis externa, which is what prompts many people to see their veterinarian. Many cases progress into proliferative otitis externa with many developing chronic bacterial and yeast infections and some progress to calcifying otitis externa and media. Food allergy and atopic dermatitis may mimic the ceruminous otitis and when presented for ceruminous otitis without other seborrheic lesions then allergies are more likely than the diagnosis of primary idiopathic seborrheic otitis. Secondary infections either bacterial or Malassezia are common and contribute significantly to the clinical lesions. Long-term antimicrobial therapy will often resolve much of the keratinous crusting but skin biopsies will still show microscopic abnormalities.
Some cases especially the milder forms of seborrhea may respond to sulfur and salicylic acid or phytosphingosine shampoos. The advantage of these shampoos over tar based products is the better cosmetic qualities that may improve client compliance. The more severe cases may require the most potent combination tar, sulfur and salicylic acid shampoos, although these are rarely used by the author due to the success of utilizing other products. The follicular involvement also makes the use of benzoyl peroxide shampoos useful. These cases frequently do best by doing combination shampooing. For cases that cannot be bathed routinely or are not responsive to topical therapy, calcitriol (1,25 dihydroxy vitamin D3 analog) at 10 ng/kg q24h can be helpful in 60% of cases. Retinoids can also be tried and the author's favorite is acitretin used at 0.5 to 1mg/kg q24 h then taper to least effective dose; however the option is very expensive.
Two keratinization disorders have been described. One is somewhat similar to cocker spaniels in lesion development however these dogs are more pruritic. This pruritus and inflammation does not resolve with antibiotics and antiyeast therapy. The disease tends to have a facial and ventral distribution and often mimics a scabies case. However yellow casts and fronds will also be found. The pathogenesis is unknown and work similar to what has been performed in the cocker spaniel is lacking. Although the cases are not as antibiotic responsive as American cocker spaniels, secondary pyoderma and Malassezia are common and need to be addressed.
It is important to rule out atopic dermatitis with appropriate history, physical findings and ruling out other differentials. Intradermal testing and serum invitro allergy tests can be of some value. Proper elimination diet trials are indicated. I have seen a couple cases where food reactions to appear to play a role in this syndrome. Unfortunately diet modification only helps decrease the severity and frequency of more severe outbreaks. These dogs are very difficult to treat. Often combination regiments are required even when retinoids are used. Long term pulse antibiotics, ketoconazole, cyclosporine or glucocorticoids with shampoo therapy have been used in some cases.
Psoriasiform-Lichenoid dermatosis has also been described in Springer spaniels and some also believe this may be a primary keratinization disorder. It is seen in young dogs and is usually asymptomatic, symmetric erythematous, lichenoid papules and plaques usually starting on the pinnae and inguinal region. Chronic cases may resemble a sever seborrhea. It is typically diagnosis with physical and histopathology showing psoriasiform hyperplasia and lichenoid to interface dermatitis. It can wax and wane and response to anti-inflammatory and antimicrobial therapy have been limited.
Basset Hounds develop a condition referred to as seborrhea oleosa because of the generalized greasy oily coat and skin appearance. Intertriginous areas may have erythematous macules and plaques. Some scale as well as follicular casts may be present and may be associated with Malassezia. The macules and plaques are usually pronounced on the anterior forelegs, ventral cervical, flexor surface of the elbows, hocks and interdigitally. Some lesions are usually found around the base of the tail, inguinal folds, groin and axilla. The concave aspects of the pinnae are erythematous and a yellow ceruminous otitis externa may also be present. Some cases develop a yellow, greasy to waxy exudate in the more severely affected areas and follicular casts may be present. These cases often develop secondary Malassezia of the ears and body. Most are often moderately pruritic and should be allergy tested and have elimination diets performed. . In general these cases have responded best to a combination of oral ketoconazole, antibiotics and utilizing shampoos containing phytosphingosine, sulfur, salicylic acid and benzoyl peroxide. Fatty acid supplements may be beneficial. Limited trials with systemic retinoids have not show much value in this breed. Cyclosporine may be helpful in cases where allergies are more of a contributing factor.
A keratinization disorder characterized by white scales and a poor, dry coat has been described. One study looked at epidermal kinetics and similar to the cocker spaniel the seborrheic Irish setters had rapid turnover. The lesions tend to be more prominent over the dorsal trunk but the ventrum and extremities may be affected. Ventrally, comedones over the point of the sternum or at other sites of pressure may be seen. Otitis externa has been seen but is not as prominent as with the cocker spaniel. Thin poor dry hair coat is common, leading many to be diagnosed as hypothyroidism when thyroid test results are marginal and are often more likely "euthyroid sick syndrome". However, most cases do not respond to thyroid supplementation. Allergic dermatitis and hypothyroidism are the main differentials in these cases. Treatment with phytosphingosine and sulfur salicylic acid shampoos and moisturizing rinses is initially the treatment of choice. Fatty acids should also be given orally.
A truncal scaling condition is occasionally seen in Doberman pinschers. The scaling is usually severe over the dorsal and lateral thorax and lumbar regions. These cases tend to do well with sulfur salicylic acid shampoos and frequent use of moisturizing rinses and sprays as well as systemic fatty acid therapy. Follicular dystrophy or color mutant alopecia are major differential diagnosis and are other types of keratinization disorders that primarily affect the follicular epithelium. Follicular dystrophy or color mutant alopecia is most commonly seen in the blue and fawn Dobermans. However milder forms of follicular dystrophy may be seen in black and red Dobermans. Lesions tend to occur more on the dorsal and lateral trunk. Scaling, alopecia, broken, fractured, twisted or kinked hairs and papules are typically found. Hypothyroidism is the other non-pruritic differential, but can be found concurrently. In some cases, atopic disease may also cause a scaling disorder that appears similar but is often associated with pruritus. The other major differential is folliculitis, which also may result in scaling and can occur secondary to many underlying diseases. Histopathology can be helpful in distinguishing these cases. Depending on the etiology, fatty acid supplements, antibiotics, thyroid supplementation and emollient shampoos and rinses can be helpful. On occasion the author will use vitamin A or other retinoids.
The Chinese Shar pei has been described as having a very oily seborrhea oleosa type of syndrome. The accumulation of this lipid material in folds predisposes to fold pyoderma and Malassezia. Concurrent hypothyroidism, mucinosis, atopic disease, food allergy, pyoderma and demodex must also be considered as a differential or coexistent disease. No studies or documentation of this as a true entity is yet available. Many Chinese Shar pei's have dry scaly skin and this is often in association with other inflammatory skin diseases. Most commonly folliculitis and allergies create the dryer form of seborrhea seen in this breed.
Dachshunds may present with a scaly, greasy seborrhea. They often have concurrent ear margin dermatoses and may also have lesions in the intertriginous skin fold areas and when the axilla and groin are affected this condition can appear very hyperpigmented and lichenified has been described as a "acanthosis nigricans" like appearance. Scaling over the dorsal trunk is often seen but the more severe lesions will be found ventrally and in areas of friction or body folds. Comedones may be seen particular on the ventral chest location. Secondary pyoderma and Malassezia should be ruled out or treated. Hypothyroidism and allergy are the major differentials unless lesions are lichenified and predominantly limited to the axilla. Although "acanthosis nigricans" has been described by other researchers as a specific syndrome the author feels that most cases are in fact related to keratinization defects, hypothyroidism or allergies with secondary pyoderma and Malassezia.
Labrador retrievers have a highly pruritic disease that has been referred to as "waterline disease". This seems to be a primarily inflammatory pruritic disease. Greasy hair coat and scaling are present and have led to this being referred to as seborrhea oleosa. The extremities, ventral thorax, chest and face are most often affected. Partial alopecia is present. Lichenification and hyperpigmentation may occur in chronic cases. Whether this is a primary epidermal inflammatory disease or a symptom of another problem is not known, the author believes that most of these cases are not primary keratinization defect cases but allergic dogs with secondary pyoderma and Malassezia dermatitis. Often working these cases up for allergic skin disease can be frustrating, many have poor IDT reactions due to the chronicity of their skin lesions and some do not respond well to elimination diets. However pursuing allergic diseases in the form of in vitro allergy testing and ASIT can occasionally produce favorable results. The author has also seen good responses to cyclosporine therapy. Eliminating secondary infections may improve many cases but many will often require glucocorticoids or cyclosporine. Treatment of the secondary pyoderma and Malassezia is often required. Topical therapy has not been very rewarding though moisturizing and antiseborrheic shampoos can be beneficial.
This breed has been described as having a primary seborrhea sicca, although it can occur as a combination seborrhea with both sicca/oleosa seen in the same case. This greasy form is often associated with allergic diseases with moderate to marked lichenification and hyperpigmentation to the intertriginous areas over the cervical, axilla, groin and flanks. This form is generally complicated by secondary pyoderma and Malassezia dermatitis. The seborrhea sicca form also is seen with allergies, in particular with flea allergy and food allergies. Hypothyroidism is also seen in this breed and should always be ruled out. Appropriate topical antiseborrheic and moisturizing shampoos should be used. Systemic antimicrobial therapy is almost always required especially with the seborrhea oleosa form.
These two breeds have not been described as having a primary seborrhea but I see then often with a scaly crusty seborrhea oleosa and often-secondary pyoderma and Malassezia. Similar to cocker spaniels they often have a ceruminous otitis and ventral cervical and groin lesions consisting of greasy plaques. Many cases have been associated with underlying allergies, but some have not had any response to therapy for allergies. Although glucocorticoids and cyclosporine can be helpful assuming infections are well managed. Specific case studies utilizing the Douxo ® Seborrhea Micro-emulsion Spray can be combined with Douxo Seborrhea Shampoo have produced impressive results.
Recently the author has recognized a large number of Newfoundland's with a generalized form of a keratinization defect that clinical presents as "seborrhea oleosa". A large number of these cases have common genetics but no specific form of inheritance has been established. Affected dogs have poor dull try hair coats with marked greasy oil, malodorous intertriginous fold areas. Marked secondary Malassezia and pyoderma are seen. Concurrent otitis is usually present. Variable degrees of pruritus can be present. Limited responses have been seen to elimination diets and ASIT. Some response has been seen with combination systemic antimicrobial therapy and cyclosporine. Topical antiseborrheic and antimicrobial shampoos are indicated in all cases.
West Highland White terriers (WHWT) have been described as having a keratinization disorder and it was eventually referred to as epidermal dysplasia.(Scott and Miller 1989; Power, Ihrke et al. 1992; Scott, Miller et al. 2001) It is an autosomal recessive polygenetic familial disease with histopathologic evidence of epidermal hyperproliferation. As with most primary seborrhea syndromes onset is relatively young but in WHWT it often is severe enough in young dogs to draw the owner's attention even by one year of age. In the early stages these dogs develop hyperpigmentation of the pinnae and axilla. The disorder tends to be most severe on the ventral trunk and extremities. Lesions include hyperpigmentation, erythema, lichenification, scaling and partial alopecia. Pruritus is often intense. Thyroid studies and intradermal skin testing have been normal in most cases. However, some cases can have atopic disease and/or dietary allergies as well as the keratinization disorder and will be extremely difficult to manage. These dogs may have a bile acid defect and will become more erythematous and pruritic following eating, although this is considered quite controversial. All agree that this disease is very difficult to manage. Secondary pyoderma and particularly Malassezia are common and antibiotic and antiyeast therapy is frequently required. One report suggests that some cases that clinical are compatible with this syndrome may not have a congenital keratinization disorder but be related to atopic dermatitis and possibly a hypersensitivity to Malassezia, as the two cases reported responded well to Malassezia therapy and ASIT.(Nett, Reichler et al. 2001) It is the author's opinion that most cases will not completely respond to Malassezia therapy and ASIT, although many WHWT with this condition do have secondary pyoderma and Malassezia and concurrent allergies. Aggressive bathing programs with sulfur, salicylic acid, benzoyl peroxide, and phytosphingosine and antiyeast shampoos will help some. Long term systemic ketoconazole or occasional pulse ketoconazole and antibiotic may be required. Once the Malassezia is controlled some cases will also respond to cyclosporine and/or retinoids (etretinate and acitretin).
A study in Norfolk terriers has shown they have a heritable defect in cornification.(Barnhart, Credille et al. 2004) This is likely an autosomal recessive trait that results in a decreased keratin ten production.(Barnhart, Credille et al. 2004) Lesions were present at birth and pedigree analysis suggested an autosomal recessive mode of inheritance. The affected dogs had hyperpigmented skin with scaling following mild trauma. The lesions were generalized but most prominent in the glabrous skin of the axillary and inguinal regions-areas where the epidermis is not protected by hair and is subject to frequent trauma. The most striking histological change was vacuolation in the upper epidermis, which often resulted in epidermolysis and blister formation. All of the affected dogs showed similar gross and histological changes. Ultrastructural changes included abnormal keratin filament clumping, prominent clear spaces in the cytoplasm of suprabasal keratinocytes, and abnormal keratohyaline granules. Immunohistochemical labeling for keratin 10 demonstrated a lack of expression in the superficial epidermis of affected dogs. All of the morphological changes noted in the Norfolk terriers were consistent with a mild form of a heritable defect in superficial keratin synthesis. Treatment has been suggested to be symptomatic with antiseborrheic shampoos and fatty acid supplementation. No cases have been treated with retinoids to date.
A report of 5 female rottweilers described a cornification disorder that likely is an x linked autosomal dominant mode of inheritance.(Lewis, Messinger et al. 1998) The lesions consisted of generalized scaling to hyperkeratotic, variably pigmented plaques that could form fronds. Lesions developed early in life and tended to cover much of the body except in the dam of the 4 most severely affected. One case the lesions followed lines of Blaschko. Blaschko's lines follow a V-shape over the spine, an S-shape on the abdomen, and an axial distribution on the limbs. The dam's lesions were milder and confined to the head and left lateral thigh. Four of the five cases were euthanized or died. Histologically they were different from ichthyosis as they had intracellular edema, epidermal vacuoles and parakeratosis especially of the hair follicles. The changes have led to this disease being referred to as congenital follicular parakeratosis, CFP. Another report described another Rottweiler as well as an affected Siberian Husky.(Scott and Miller 2000) One study evaluating this disease with parakeratosis and intracorneal vacuoles has shown they these features are not specific for this disease though large vacuoles over 5 microns may be.(Senter, Scott et al. 2002) In later stages follicles were parakeratotic dilated and markedly acanthotic with folliculitis and furunculosis. There was no response to a variety of treatments including calcitriol, zinc, vitamin A, and antibiotics.
Ichthyosis has also been referred to as fish scale disease and is a rare condition in dogs and cats. In cats and West Highland White Terriers documented cases have not been published and they are just mentioned to occur in a textbook. There are many forms in humans with differing defects but generally they have been associated with cornification and keratin disorders. In humans they usually occur at birth or young ages though some forms have occurred later in life. Only a few reports are found in dogs and cats and most have not determined the exact abnormality to be able to show it exactly represents the human disease. Histopathology varies with some human forms of the disease having characteristic features while others do not have typical histopathologic abnormalities.
It seems to occur sporadically in dogs and though purebreds may be affected it has also been reported in mongrel or mix breed dogs.(August, Chickering et al. 1988; Mecklenburg, Hetzel et al. 2000) In general these dogs have varying degrees of adherent scale that may be large or fine. The whole body or just regions may be affected. Pads may be affected in some cases. Two littermate Cavalier King Charles spaniels were reported with irregular keratin 14 labeling and keratinocytes that had 3 distinct compartments in the cytoplasm similar to a form of ichthyosis described in a human family.(Alhaidari and Ortonne 1994) The dam and another littermate were unaffected and even the two affected dogs varied in severity. The more severely affected dog also has poor dry thinned haircoat. These dogs did not respond to etretinate. A Soft-Coated Wheaten Terrier with an ichthyosiform dermatosis has been described.(Gayman-Helman, Rames et al. 1997) Patches of thick, scaly skin were apparent from birth and progressed in extent as the dog aged. At 3 months of age, the scaling was generalized and was accompanied by a greasy exudation, which matted the hair coat. The skin was greasy and there was generalized scaling, but the skin on the head and pinnae of the ears were most affected. There was minimal involvement of the footpads. Microscopically, the skin had patchy areas of ortho-and parakeratotic hyperkeratosis, follicular keratosis, superficial perivascular dermatitis, and variable hypergranulosis with irregular thickening of the stratum granulosum. Electron microscopic findings showed a paucity of keratin filaments though the cytoskeleton appeared normal. The dog did not respond to treatment with benzoyl peroxide shampoos, humectant sprays, and isotretinoin and was euthanized. In a report in a Jack Russell terrier there was a favorable clinical response to etretinate therapy though histology and epidermal kinetics remained abnormal.(Lewis, Ford et al. 1998) Though most reports describe the appearance compatible with a hyperproliferative state in this case epidermal cell renewal time was markedly decreased.
Golden retrievers are recognized as a breed prone to a cornification disorder often referred to as ichthyosis. A retrospective review of 45 cases submitted for pathology only took 23 months to acquire those cases, suggesting this may be one of the more common forms of the disease.(Mauldin, Credille et al. 2007) There was no sex predilection and 57% of the cases started scaling under one year of age. This appears to be a complex mode of inheritance when 14 cases had there pedigree studied. The histopathology appears characteristic with moderate to severe laminar orthokeratotic hyperkeratosis, absence of epidermal hyperplasia and dermal inflammation. There are scattered keratinocytes with clear cytoplasmic vacuoles in the upper stratum spinosum/ granulosum. Electron microscopy showed retained and convoluted membranes with crystalline structures in stratum corneum and scattered keratinocytes with clear large membrane bound vacuoles in the stratum granulosum. In a more recent study of 17 young golden retrievers with predominantly a ventro-lateral scaling and hyperpigmentation of the trunk, histopathological and ultrastructural changes of the stratum corneum were noted and consistent with ichthyosis. The histopathology showed compact keratin, mostly in the absence of acanthosis, that was matched by the ultrastructural evidence within the stratum corneum of more cohesive corneocytes and more numerous desmosomes, suggesting abnormal desquamation due to delayed degradation of corneodesmosomes. Based on clinical and histopathological features this cornification disorder in Golden retrievers falls into the non-epidermolytic category A genetic aetiology is proposed, and a single-trait autosomal recessive mode of inheritance is most likely (Cadiergues, Patel et al. 2008).
The author has seen several cases of ichthyosis in California in mixed terrier type breeds as well as several golden retrievers and America bull dogs with the same clinical and histopathology as reported by other investigators. Affected dogs have a dry fish scale appearance with large flakes most noticeable over the ventral abdomen. Treatment is symptomatic with oral fatty acids, topical antiseborrheic and emollient shampoos as well as topical phytosphingosine and propylene glycol sprays. A few cases have also shown response to glucocorticoids and oral cyclosporine.
Zinc is an important element in the maturation and maintenance of a healthy skin and hair coat. Zinc plays a role as an antioxidant in the skin and helps to protect against photo damage.(Pinnell 2003) It also plays a role in controlling transepidermal water loss and when it and linoleic acid are supplemented in diets there is a significant improvement in coat gloss and scale.(Marsh, Ruedisueli et al. 2000) Zinc responsive dermatosis is a disease characterized by tightly adherent scaly crusty plaques that has not been definitely shown to be a deficiency of zinc.
This is often a disease of young dogs with the largest study having a range from 2 months to 11 years with a median of three years age onset.(White, Bourdeau et al. 2001) Northern breeds, particularly Siberian husky, are predisposed though non northern breeds are occasionally affected. There is no recognized sex predilection. In 12 of 17 dogs, lesions were unilateral initially, and then became symmetrical as the disease progressed. Pyoderma was evident in 5 of 17 dogs, whereas 10 were pruritic.(Colombini and Dunstan 1997) Another study reviewed 41 cases and found more symmetry and only 16 were reported pruritic.(White, Bourdeau et al. 2001) The main lesion is a crust followed by alopecia. In my experience these lesions tend to be light brown to yellow crusts that are tightly adherent to the skin surface. Lesions predominate in a facial periocular pattern, pinnae, pads and lower legs and perigenital region. A similar syndrome may be seen in dogs on diets that have inadequate levels of zinc.(Sousa, Stannard et al. 1988) These dogs are somewhat different from the typical zinc responsive dermatitis of northern breeds in that all were lethargic and most were pyrexic and had peripheral lymphadenopathy. Lesions are also more likely to occur on the trunk. Although the original reports described parakeratosis one report failed to identify this as a characteristic feature.(Thoday 1989)
Therapy is with oral zinc supplements. Zinc sulfate, zinc gluconate and zinc methionine are most commonly used. The amount of zinc in each form of supplement is different but it has been recommended that the initial therapy should be 2-3 mg kg/day elemental zinc per day.(White, Bourdeau et al. 2001) A review of therapy in 17 dogs showed effective maintenance dosages ranged from 0.5 mg/kg (0.23 mg/lb.), twice weekly, to 8.0 mg/kg/d (3.6 mg/lb./d).(Colombini and Dunstan 1997) Fifteen of 17 dogs had complete resolution of lesions after zinc supplementation. Lesions recurred in 9 of 16 dogs. Approximately half of the recurrent lesions were a result of a missed dose or a decrease in dosage or frequency of zinc supplementation. The author has also seen several cases requiring oral glucocorticoid therapy at low dosages .5mg/kg q 24h before complete responses are seen. It is not know if the glucocorticoids aid in zinc absorption or has additional anti-inflammatory effect.
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