Primary idiopathic seborrhea is a skin disease seen in dogs and rarely in cats. It is characterized by a defect in keratinization or cornification that results in increased scale formation, occasionally excessive greasiness of the skin and hair coat, and often secondary inflammation and infection. Secondary seborrhea, in which a primary underlying disease causes similar clinical signs, is more common than primary seborrhea.
Etiology, Clinical Findings, and Diagnosis
Primary seborrhea is an inherited skin disorder characterized by faulty keratinization or cornification of the epidermis, hair follicle epithelium, or claws. It is seen more frequently in American Cocker Spaniels, English Springer Spaniels, Basset Hounds, West Highland White Terriers, Dachshunds, Labrador and Golden Retrievers, and German Shepherd dogs. There is usually a familial history of seborrhea, suggesting genetic factors are involved. The disease begins at a young age (usually <18–24 mo) and usually progresses throughout the animal's life. A diagnosis of generalized primary idiopathic seborrhea should be reserved for cases in which all possible underlying causes of seborrhea have been ruled out.
Most seborrheic animals have secondary seborrhea, in which a primary underlying disease predisposes to excessive scale, crusting, or oiliness, often accompanied by superficial pyoderma, Malassezia (yeast) infection, and alopecia. The most common underlying causes are endocrinopathies and allergies. The goal is to identify and treat any underlying cause of the seborrhea. Palliative therapies that do not compromise the diagnostic evaluation should be instituted concurrently to provide as much immediate relief as possible.
Underlying diseases may present with seborrhea as the primary clinical problem. The signalment (age, breed, sex) and history may provide clues in diagnosing the underlying cause. Allergies are more likely to be the underlying cause if the age of onset is <5 yr, whereas an endocrinopathy or neoplasia (especially cutaneous lymphoma) is more likely if the seborrhea begins in middle-aged or older animals.
The degree of pruritus should also be noted. If pruritus is minimal, endocrinopathies, other internal diseases, or certain diseases limited to the skin (eg, demodicosis or sebaceous adenitis) should be ruled out. If pruritus is significant, allergies and pruritic ectoparasitic diseases (eg, scabies, fleas) should be considered. The presence of pruritus does not rule out nonpruritic disease as the underlying cause, because the presence of a pyoderma, Malassezia infection, or the inflammation from the excess scale can cause significant pruritus. However, a lack of pruritus helps to rule out allergies, scabies, and other pruritic diseases as the underlying etiology.
Other important considerations include the presence of polyuria, polydipsia, or polyphagia; heat-seeking behavior; abnormal estrous cycles; occurrence of pyoderma; the influence of seasonality; diet; response to previous medications (including corticosteroids, antibiotics, antifungals, antihistamines, or topical treatments); zoonosis or contagion; and the environment. The duration and severity of disease as well as level of owner frustration are important factors in determining the aggressiveness of the diagnostic plan.
A thorough physical examination, including internal organ systems and a comprehensive dermatologic examination, is the first step in identifying the underlying cause. The dermatologic examination should document the type and distribution of the lesions; the presence of alopecia; and the degree of odor, scale, oiliness, and texture of the skin and hair coat. The presence of follicular papules, pustules, crusts, and epidermal collarettes usually indicates the existence of a superficial pyoderma. Hyperpigmentation indicates a chronic skin irritation (such as pruritus, infection, or inflammation), and lichenification indicates chronic pruritus. Yeast (Malassezia spp) infection should always be considered when evaluating a seborrheic animal.
Secondary infection plays a significant role in most cases of seborrhea. The sebum and keratinization abnormalities that are common in seborrhea frequently provide ideal conditions for bacterial and yeast infections. The self-trauma that occurs in pruritic animals increases the likelihood of a secondary infection. Often, coagulase-positive Staphylococcus spp or Malassezia spp are present. The infections add to the pruritus and are usually responsible for a significant amount of the inflammation, papules, crusts, alopecia, and scales.
One of the first diagnostic steps is to obtain superficial cytology of the affected areas to identify the quantity and type of bacteria or yeast present. If numerous cocci and neutrophils are present, pyoderma is likely. In addition to systemic therapy, topical shampoos will aid in the treatment of secondary infections. In a seborrheic dog with pruritus, the infection may cause all or most of the pruritus. Instead of considering allergies as the underlying disease in these dogs, nonpruritic diseases (eg, endocrinopathies) may be uncovered by addressing the infections.
After the infections have been addressed, other diagnostic tests that should be considered include multiple deep skin scrapings, dermatophyte culture, impression smears, trichograms, and flea combing. If these are negative or normal, a skin biopsy, CBC, serum biochemical profile, and complete urinalysis will complete the minimum database. Examples of diagnostic clues include increased serum alkaline phosphatase (which may suggest hyperadrenocorticism or previous steroid therapy), cholesterol (which may suggest hypothyroidism), blood glucose (which suggests diabetes mellitus), and BUN or creatinine (which may suggest renal disease).
Palliative therapy is needed to keep the animal comfortable while the underlying cause is identified and secondary skin diseases are corrected. For treatment of pyoderma, an antibiotic with known sensitivity against Staphylococcus pseudintermedius should be appropriate. Malassezia may be treated systemically with an azole such as ketoconazole or fluconazole. In addition to addressing any secondary infections, antipruritic therapy and shampoo therapy are usually needed to help control the seborrhea and speed the return of the skin to a normal state. Shampoo therapy can decrease the number of bacteria and yeast on the skin surface, the amount of scale and sebum present, and the level of pruritus; it also helps normalize the epidermal turnover rate.
In the past, seborrhea has been classified as seborrhea sicca (dry seborrhea), seborrhea oleosa (oily seborrhea), or seborrheic dermatitis (inflammatory seborrhea). This scheme can still be used in determining the type of shampoo needed; however, most seborrheic animals have varying degrees of all 3 of these classifications of seborrhea.
Most products contained in shampoos can be classified based on their effects as keratolytic, keratoplastic, emollient, antipruritic, or antimicrobial. Keratolytic products include sulfur, salicylic acid, tar, selenium sulfide, propylene glycol, fatty acids, and benzoyl peroxide. They remove stratum corneum cells by causing cellular damage that results in ballooning and sloughing of the surface keratinocytes. This reduces the scale and makes the skin feel softer. Shampoos containing keratolytic products frequently exacerbate scaling during the first 14 days of treatment, due to the sloughed scales getting caught in the hair coat. The scales will be removed by continued bathing, but owners should be warned that the scaling often worsens initially. Keratoplastic products help normalize keratinization and reduce scale formation by slowing down epidermal basal cell mitosis. Tar, sulfur, salicylic acid, and selenium sulfide are examples of keratoplastic agents. Emollients (eg, lactic acid, sodium lactate, lanolin, and numerous oils, such as corn, coconut, peanut, and cottonseed) are indicated for any scaling dermatosis because they reduce transepidermal water loss. They work best after the skin has been rehydrated and are excellent adjunct products after shampooing. Antibacterial agents include benzoyl peroxide, chlorhexidine, ethyl lactate, and triclosan. Antifungal ingredients include chlorhexidine, sulfur, ketoconazole, and miconazole. Boric and acetic acids are also used as topical antimicrobials.
It is important to know how individual shampoo ingredients act, as well as any additive or synergistic effects they have, because most shampoos are a combination of products. The selection of appropriate antiseborrheic shampoo therapy is based on hair coat and skin scaling and oiliness, of which there are 4 general presentations: 1) mild scaling and no oiliness, 2) moderate to marked scaling and mild oiliness (the most common), 3) moderate to marked scaling and moderate oiliness, 4) mild scaling and marked oiliness. These categories are intended to guide the type of shampoo therapy necessary; however, all factors for each individual patient should be considered.
Animals with mild scaling and no oiliness need mild shampoos that are gentle, cleansing, hypoallergenic, or moisturizing. These shampoos are indicated for animals that have mild seborrheic changes, are irritated by medicated shampoos, or bathed too often. These products often contain emollient oils, lanolin, lactic acid, urea, glycerin, or fatty acids. Emollient sprays or rinses are often used in conjunction with these shampoos.
Animals with moderate to marked scaling and mild oiliness should be bathed with shampoos that contain sulfur and salicylic acid. Both agents are keratolytic, keratoplastic, antibacterial, and antipruritic. In addition, sulfur is antiparasitic and antifungal. Some of these shampoos also contain ingredients that are antibacterial, antifungal, and moisturizing, which can help control secondary pyoderma, Malassezia spp, and excessive scaling. Shampoos that contain ethyl lactate lower the cutaneous pH (which has a bacteriostatic or bactericidal action by inhibiting bacterial lipases), normalize keratinization, solubilize fats, and decrease sebaceous secretions. These actions also result in potent antibacterial activity.
Animals with moderate to severe scaling and moderate oiliness often benefit most from tar-containing shampoos. Tar exerts potent keratoplastic effects by slowing basal epidermal cell DNA synthesis. It is often combined with sulfur and salicylic acid. Wood and coal are distilled to produce a tremendous variety of products called crude coal tars. Because of the variation in agents and techniques used, exact comparisons of shampoos are difficult. More refined tars are usually less irritating and more stable but are more expensive to produce. More tar is not necessarily better. Only those tar products from reputable companies should be used. Tar shampoos usually have a distinct and unpleasant odor that lessens as the hair coat dries. Owner compliance is often diminished for products that have a prominent odor.
In animals with severe oiliness and minimal scaling, profound odor, erythema, inflammation, and a secondary generalized pyoderma or Malassezia dermatitis are often present. This group requires the most aggressive topical therapy. Shampoos that contain benzoyl peroxide provide strong degreasing actions along with potent antibacterial and follicular flushing activities. Because benzoyl peroxide shampoos are such strong degreasing agents, they can be irritating and drying. Other antibacterial shampoos are better suited in animals that have superficial pyoderma without significant oiliness. As with tar, benzoyl peroxide has critical production requirements, and only refined products from reputable companies should be used. Most human products contain 5–10% benzoyl peroxide and should not be used because irritation can occur. The follicular flushing action of benzoyl peroxide makes it ideal for animals with numerous comedones or with demodicosis. Benzoyl peroxide gels (5%) are good choices when antibacterial, degreasing, or follicular flushing actions are desired for focal areas, such as in localized demodicosis, canine acne, or Schnauzer comedone syndrome. However, these gels also may be irritating.
Last full review/revision July 2011 by Stephen D. White, DVM, DACVD