Dermatological Problems in Animals

There are many causes of alopecia; any disease that can affect hair follicles can cause hair loss. Alopecia falls into two broad etiological categories: 1) congenital or hereditary, and 2) acquired. Acquired alopecia is further divided into two categories: inflammatory and noninflammatory.

Congenital or hereditary alopecia has been described in cows, horses, dogs, cats, and pigs. Hairless breeds of mice, rats, cats, and dogs have been bred and developed for personal and research interests. Congenital alopecia may or may not be hereditary. It is caused by a lack of hair follicle development and is apparent at birth or shortly after.

Animals with tardive alopecias are born with normal coats, and focal or generalized hair loss occurs when the animal sheds its juvenile coat or when it becomes a young adult. Examples include pattern baldness in Dachshunds, color dilution alopecia (most common in Doberman Pinschers), and certain types of follicular dysplasias.

Acquired alopecia encompasses all nonhereditary causes of hair loss. In acquired alopecia, the animal is born with normal hair, has normal hair follicles or had them at one time, and is or was capable of producing structurally normal hairs. Acquired alopecia can be noninflammatory (eg, endocrine alopecia, pattern baldness, alopecia X, or some types of immune-mediated alopecia, such as alopecia areata), or inflammatory.

Inflammatory acquired alopecia is the most common type of alopecia. Acquired alopecia develops because a disease destroys the hair follicle or shaft, interferes with the growth of hair or wool, or causes the animal discomfort (eg, pain, pruritus), leading to self-trauma and loss of hair.

Diseases that can directly cause destruction or damage to the hair shaft or follicle include bacterial skin diseases, dermatophytosis, demodicosis, severe inflammatory diseases of the dermis (eg, juvenile cellulitis, deep pyoderma), traumatic episodes (eg, burns, radiation), chemotherapy (eg, doxorubicin-associated alopecia), and, rarely, toxicoses caused by mercury, thallium, and iodine. These diseases tend to be inflammatory.

Diseases that can directly inhibit or slow hair follicle growth include nutritional deficiencies (particularly protein deficiencies), hypothyroidism, hyperadrenocorticism, and excessive estrogen production or administration (hyperestrogenism, Sertoli cell tumors, estrogen injections for mismating).

Temporary alopecia in horses, sheep, and dogs can occur during pregnancy or lactation, or several weeks after a severe illness or fever. Marked hair loss (effluvium) is common in cats after respiratory infection. These types of alopecia tend to be noninflammatory unless a secondary skin infection develops.

Pruritus or pain is a common cause of acquired inflammatory alopecia in animals. Diseases that commonly cause pruritus or pain include infectious skin diseases (eg, bacterial pyoderma and dermatophytosis), diseases caused by ectoparasites, allergic skin diseases (eg, atopic dermatitis, food allergy, contact, insect bite hypersensitivity), and, less commonly, neoplastic skin diseases.

Friction (eg, from poorly fitted halters or collars) can cause local hair loss. Rarely, excessive grooming can cause hair loss in some animals, particularly cats.

Feline endocrine alopecia is no longer recognized as a bona fide disease; the current name is "feline symmetrical alopecia." To date, there is no documented evidence of an endocrine disease in cats with this disorder, and the symmetrical alopecia is due to an underlying disease, most commonly a pruritic disease.

The most common cause of feline symmetrical alopecia is flea allergy dermatitis. In cats that do not have an obvious flea infestation, a CBC with differential is recommended for diagnosis; many cats that have flea allergy dermatitis have eosinophilia. A finding of flea allergy dermatitis might help convince owners to pursue flea control as a first step toward diagnosing feline symmetrical alopecia.

Clinical signs of hair loss can be obvious or subtle, depending on the cause. Congenital or hereditary hair loss is commonly symmetrical and not accompanied by many inflammatory changes; in some cases, areas of hair loss are localized to one region (eg, ear flaps) or to well-demarcated areas.

Clinical signs of acquired hair loss vary and are often influenced by underlying causes; the pattern of hair loss can be focal, multifocal, symmetrical, or generalized. Inflammatory changes such as hyperpigmentation, lichenification (increased thickening and hyperpigmentation of the skin), erythema, scaling, excessive shedding, and pruritus are common.

Some causes of acquired alopecia can predispose the animal to developing secondary skin diseases, such as bacterial pyoderma or seborrhea. The presence of pruritus depends on the primary cause.

In endocrine alopecias, hair loss usually develops in a symmetrical pattern, often in wear areas first; pruritus is uncommon unless there is a secondary infection. Now that the early, nondermatological clinical signs of endocrine alopecia are more widely recognized, hair loss is not generally considered an early clinical sign of endocrine alopecia.

Many animal owners seek veterinary assistance because of perceived excessive shedding. Shedding might be abnormal (excessive) if it results in obvious loss of hair and areas of alopecia. A common cause of abnormal shedding is bacterial pyoderma. However, if shedding is not accompanied by the development of patchy or symmetrical hair loss, it is probably just a stage in natural replacement of the hair.

• Clinical examination

• Presence of pruritus

• In-house diagnostic testing

• Reference laboratory testing

Accurate diagnosis of the cause of alopecia requires a careful history and physical examination. Key points in the history include recognition of breed predispositions for congenital or hereditary alopecias; the duration and progression of lesions; and the presence or absence of pruritus, evidence of contagion, or nondermatological problems (eg, polyuria/polydipsia).

On physical examination, the distribution of lesions should be noted (focal, multifocal, symmetrical, generalized), and the hairs should be examined to determine whether they are being shed from the hair follicle or broken off—the latter suggesting pruritus. Signs of secondary skin infections or ectoparasites should be noted, and a careful nondermatological examination should be performed.

Initial in-house diagnostic tests for alopecia include skin scraping for ectoparasites (particularly Demodex mites); combing of the hair for fleas, mites, and lice; impression smears of the skin for evidence of bacterial or yeast infections; fungal culture for identification of dermatophytosis; and examination of plucked hairs, looking at both the shaft and the ends for evidence of parasites, dermatophytosis, or self-barbering.

In many cases of bacterial pyoderma, impression smears of the skin do not show neutrophils and/or cocci, but they can show large numbers of shed keratinocytes. Neutrophils and cocci are present if pustules or recently ruptured pustules are sampled.

If these tests do not identify or suggest an underlying cause, a skin biopsy might be indicated to evaluate hair follicle structures, numbers, and anagen:telogen ratios, as well as to look for evidence of bacterial, fungal, or parasitic skin infections. In addition, skin biopsies are often needed to confirm congenital or tardive causes of hair loss and to identify inflammatory or neoplastic causes of hair loss.

Skin biopsies from normal and abnormal sites should be submitted for evaluation. CBC, serum chemistry panels, and urinalyses generally are helpful only when endocrinopathy is suspected. Specific endocrine function tests can be performed if indicated by routine laboratory work or clinical signs.

• Antimicrobial treatment for bacterial and yeast overgrowth

• Treatment for parasites

• Management of underlying allergic diseases

• Appropriate endocrine hormone replacement or treatment

In patients with alopecia, comprehensive parasite control should be started to ensure that the cause of hair loss is not pruritis associated with parasite infestation. In addition, topical antimicrobial therapy can be started to rule out concurrent bacterial or yeast infections. If pruritis continues after these steps, diagnostic tests for allergic skin disease should be performed.

Pruritus can be well or poorly localized. It can manifest as a sharp sensation or a diffuse, burning sensation. Although the skin is richly innervated, there are no known specialized pruritus receptors.

The sensation of itch is transmitted via a specialized set of afferent fibers. Myelinated fibers that conduct sensations at 10–20 meters per second carry the well-localized pricking itch sensation. In contrast, the sensation of burning itch is transmitted via nonmyelinated fibers that conduct sensations at 2 meters per second.

Both myelinated and nonmyelinated fibers enter the dorsal root of the spinal cord, ascend through the dorsal column, and cross into the lateral spinothalamic tract. From there they go to the thalamus and on to the sensory cortex.

The mediators of pruritus are controversial and can vary by species. These putative mediators include histamines (released from mast cell degranulation), proteolytic enzymes (proteases), and leukotrienes. Proteases are released by fungi, bacteria, and mast cell degranulation, and during antigen-antibody reactions. Leukotrienes, prostaglandins, and thromboxane A₂, which are broken down from arachidonic acid, are proinflammatory.

Pruritus is a clinical sign, not a diagnosis or specific disease. In general, the most common causes of pruritus are parasites, infections, allergic skin diseases, and miscellaneous causes (eg, cutaneous neoplasia). Many diseases that are nonpruritic (eg, endocrinopathies) become pruritic when the animal develops secondary bacterial or yeast infections.

• Careful dermatological history

• Clinical examination for primary or secondary lesions and clues to trigger

• Diagnostic testing for bacterial or yeast overgrowth

• Diagnostic testing for parasites

Diagnosis of pruritus requires a methodical workup performed in a logical sequence in a compact period of time. A thorough dermatological history and physical examination should be performed. Parasitic causes of pruritus, including Demodex mites, fleas and ticks, contagious mites, and lice, should be excluded, because they are the most common. Skin scraping or hair trichography can exclude (or include) infestations by various mites, including Demodex. However, some mite infestations (eg, by Sarcoptes, Cheyletiella, Psoroptes, Chorioptes) might be missed with skin scraping.

If a mite infestation is suspected, a response-to-therapy trial should be undertaken. The most commonly used drug in large animals is ivermectin, which should be administered concurrently with a topical product such as lime sulfur. In small animals, the best option is a species-approved form of isoxazoline.

After parasitic causes of pruritic disease have been excluded, infectious causes should be investigated. These include bacterial infections (primarily staphylococcal) and Malassezia overgrowth.

Concurrent bacterial and yeast infections are increasingly recognized as a common cause of pruritus in dogs, cats, and large animals. Bacterial pyoderma and yeast overgrowth is underdiagnosed in cats, and a response-to-therapy trial might be needed to exclude or include it.

Infectious causes of pruritus commonly induceclinical signs of hair loss, scaling, scales piercing hairs, odor, and/or greasy seborrhea. Marked pedal pruritus and facial rubbing are common signs in animals with concurrent yeast and bacterial infections. Before a clinician pursues allergies as a cause of pruritus or performs skin biopsies or other more expensive and/or invasive diagnostic testing, concurrent bacterial and yeast infections should be excluded.

Topical antimicrobial shampoo (2% chlorhexidine/2% miconazole) can be used every 24–48 hours. Oral antimicrobials should be administered only if an infection has been confirmed on culture and susceptibility testing. The number of yeast organisms found on cytological examination is not relevant in animals with pruritis, because it is a hypersensitivity to Malassezia that causes the pruritus.

Systemic antifungal drugs include ketoconazole (dogs only: 5 mg/kg, PO, every 24 hours) and itraconazole (cats or small dogs: 5 mg/kg, PO, every 24 hours). A treatment course of at least 2–3 weeks is recommended for both ketoconazole and itraconazole, and it should be extended as needed, depending on the clinical response. Fluconazole and terbinafine should be avoided because they are less effective than ketoconazole or itraconazole.

The initial trigger of pruritus could be long past or seasonal. However, if the animal’s pruritus remains unchanged or improves only slightly over a long period of time, the most likely underlying cause is allergic (assuming parasitic and infectious causes have been excluded). The most common causes of allergic pruritus are insect bite hypersensitivity (eg, flea allergy, mosquito bite allergy, fly bite) and atopic dermatitis. Food allergy is less common as a sole cause of pruritus. Flea allergy dermatitis and insect bite hypersensitivity are excluded on the basis of the response to insect control.

Animals that do not have insect bite hypersensitivity but are seasonally pruritic most likely have atopic dermatitis. Animals with year-round allergic pruritus have atopic dermatitis and/or food allergy. Food allergy is excluded or included on the basis of a response-to-diet trial and provocative challenge. Merely changing diet is not adequate, and hydrolyzed diets are the standard of care.

Atopic dermatitis is a clinical diagnosis; in vitro allergy testing and intradermal skin testing show only antigen exposure patterns. These tests are used to determine the contents of an immunotherapy vaccine.

• Topical therapy to cleanse the skin, alleviate pruritus, remove scales and odor

• Topical antimicrobial therapy

• Systemic antimicrobial therapy

• Parasiticidal therapy

• Systemic antipruritic therapy

• Allergen-specific therapy

Successful treatment of pruritus depends on identifying the underlying cause; it can consist of one or more than one of the treatment modalities mentioned above. Animals with idiopathic pruritus or those in which treatment of the underlying disease does not eliminate pruritus (eg, atopic animals) require medical management. Currently, evidence-based reviews of antipruritic treatment do not support the use of antihistamines to control pruritus.