CHAPTER | 8 Autoimmune and Immune-Mediated Skin Disorders

The most efficient way to confirm an autoimmune skin disease is through biopsy; however, using a dermatopathologist will greatly increase the usefulness of reported results. Unfortunately, there is a paucity of dermatohistopathologists; currently vin.com and itchnot.com provide the most current listings.

Historically, steroid therapy has been the mainstay of treatment for these diseases. We are beginning to realize the usefulness of nonsteroid alternatives (Table 8-1) in many cases, with mild cases often not requiring any steroid therapy.

TABLE 8-1 Immunosuppressive Therapies for Autoimmune and Immune-Mediated Skin Disease

Drug—Species	Induction Dosage	Maintenance Dosage
Topical Therapy
Steroids (hydrocortisone, dexamethasone, triamcinolone, fluocinolone, betamethasone, mometasone, etc.)	Applied every 12 hours	Taper to lowest effective dose
Tacrolimus	Applied every 12 hours	Taper to lowest effective dose
Conservative Oral Treatments With Very Few Adverse Effects
Essential fatty acids—dogs and cats		180 mg EPA/10 lb PO daily
Vitamin E		400 IU PO daily
Tetracycline and niacinamide—dogs	Dogs >10 kg—500 mg of each drug PO q 8 hours Dogs <10 kg—250 mg of each drug PO q 8 hours	Dogs >10 kg—500 mg of each drug PO q 12–24 hours Dogs >10 kg—250 mg of each drug PO q 12–24 hours
Doxycycline may be substituted for tetracycline	5–10 mg/kg q 12 hours	Then, taper to lowest effective dose
Cyclosporine (Atopica)—dogs and cats	5–12.5 mg/kg PO q 12–24 hours	After remission is achieved, taper slowly to lowest effective dose
Reliably Effective Treatments But Adverse Effects Are Common and May Be Severe
Prednisone—dogs	1–3 mg/kg PO q 12–24 hours	0.5–2 mg/kg PO q 48 hours
Prednisolone—cats	2–2.5 mg/kg PO q 12–24 hours	2.5–5 mg/kg PO q 2–7 days
Methylprednisolone—dogs	0.8–1.4 mg/kg PO q 12–24 hours	0.4–0.8 mg/kg PO q 48 hours
Triamcinolone—dogs	0.1–0.3 mg/kg PO q 12–24 hours	0.1–0.2 mg/kg PO q 48–72 hours
Triamcinolone—cats	0.3–1 mg/kg PO q 12–24 hours	0.6–1 mg/kg PO q 2–7 days
Dexamethasone—dogs and cats	0.1–0.2 mg/kg PO q 12–24 hours	0.05–0.1 mg/kg PO q 48–72 hours
Azathioprine—dogs	1.5–2.5 mg/kg PO q 24–48 hours	1.5–2.5 mg/kg PO q 48–72 hours
Chlorambucil—dogs and cats	0.1–0.2 mg/kg PO q 24 hours	0.1–0.2 mg/kg PO q 48 hours
Dapsone—dogs only	1 mg/kg PO q 8 hours	Taper to lowest effective dose
Aggressive Treatments With Few Studies Documenting Efficacy and Safety
Methylprednisolone sodium succinate (pulse therapy)—dogs and cats	1 mg/kg IV over a 3- to 4-hour period q 24 hours for 2–3 consecutive days	Alternate-day oral glucocorticosteroid
Dexamethasone (pulse therapy)—dogs and cats	1 mg/kg IV once or twice 24 hours apart	Alternate-day oral glucocorticosteroid
Cyclophosphamide—dogs and cats	50 mg/m² (or 1.5 mg/kg) PO q 48 hours	25–50 mg/m² (or 0.75–1.5 mg/kg) PO q 48 hours
Mycophenolate mofetil	10–20 mg/kg q 8–12 hours	Then, taper to lowest effective dose
Leflunomide	2 mg/kg q 12 hours	Then, taper to lowest effective dose

The goal of therapy is to control 90% of the symptoms 90% of the time while minimizing the adverse effects of treatments. Normally, flare-ups will occur, and it is important to differentiate infection (especially pyoderma and demodicosis) from an actual disease flare.

Pemphigus Foliaceus

Features

Pemphigus foliaceus is an autoimmune skin disease that is characterized by the production of autoantibodies against a component of the adhesion molecules on keratinocytes. The deposition of antibody in intercellular spaces causes the cells to detach from each other within the uppermost epidermal layers (acantholysis). Pemphigus foliaceus is probably the most common autoimmune skin disease in dogs and cats. Any age, sex, or breed can be affected, but among dogs, Akitas and Chow Chows may be predisposed. Pemphigus foliaceus is usually idiopathic, but some cases may be drug induced, or it may occur as a sequela to a chronic inflammatory skin disease.

The primary lesions are superficial pustules. However, intact pustules are often difficult to find because they are obscured by the hair coat, are fragile, and rupture easily. Secondary lesions include superficial erosions, crusts, scales, epidermal collarettes, and alopecia. Lesions on the nasal planum, ear pinnae, and footpads are unique and characteristic of autoimmune skin disease. The disease often begins on the bridge of the nose, around the eyes, and on the ear pinnae, before it becomes generalized. Nasal depigmentation frequently accompanies facial lesions. Skin lesions are variably pruritic and may wax and wane. Footpad hyperkeratosis is common and may be the only symptom in some dogs and cats. Oral lesions are rare. Mucocutaneous involvement is usually minimal in dogs. In cats, lesions around the nail beds and nipples are a unique and common feature of pemphigus. With generalized skin disease, concurrent lymphadenomegaly, limb edema, fever, anorexia, and depression may be present.

Top Differentials

Differentials include demodicosis, superficial pyoderma, dermatophytosis, other autoimmune skin diseases, subcorneal pustular dermatosis, eosinophilic pustulosis, drug eruption, dermatomyositis, zinc-responsive dermatosis, cutaneous epitheliotropic lymphoma, hepatocutaneous syndrome, and mosquito bite hypersensitivity (cats).

Treatment and Prognosis

1 Symptomatic shampoo therapy to remove crusts may be helpful.

2 To treat or prevent secondary pyoderma in dogs, appropriate long-term systemic antibiotics should be administered (minimum 4 weeks). Dogs treated with antibiotics during the induction phase of immunosuppressive therapy have significantly higher survival rates than do dogs treated with immunosuppressive drugs alone. Antibiotics should be continued until concurrent immunosuppressive therapy has the pemphigus under control.

3 The goal of treatment is to control the disease and its symptoms with the safest treatments used at the lowest possible doses. Typically, combinations of therapies (see Table 8-1) will have to be used to provide a multimodal treatment plan, minimizing the adverse effects of any one therapy. Depending on the severity of the disease, more or less aggressive treatments will have to be selected. To push the disease into remission, higher doses are used initially and then are tapered over 2 to 3 months to the lowest effective dose.

a Topical therapy applied every 12 hours with steroid-containing products or tacrolimus will help reduce focal inflammation and will lower the doses of systemic treatments required to control the symptoms. Once in remission, the frequency of application should be minimized to reduce local adverse effects.

b Conservative systemic treatments (see Table 8-1) include drugs that help reduce the inflammation with few to no adverse effects. These treatments help reduce the need for more aggressive therapy such as steroids or chemotherapeutics.

c Steroid therapy is one of the most reliably predictable treatments for autoimmune skin disease; however, adverse effects associated with the high doses needed to control symptoms may be severe. Although glucocorticoid therapy alone may be effective in maintaining remission, the dosages needed may result in undesirable adverse effects, especially in dogs. For this reason, the use of nonsteroidal immunosuppressive drugs, alone or in combination with glucocorticoids, is usually recommended for long-term maintenance.

Immunosuppressive doses of oral prednisone or methylprednisolone should be administered daily (see Table 8-1). After lesions resolve (after approximately 2–8 weeks), the dosage should be gradually tapered over a period of several (8–10) weeks until the lowest possible alternate-day dosage that maintains remission is being administered. If no significant improvement is seen within 2 to 4 weeks of initiation of therapy, a concurrent skin infection should be ruled out, then alternative or additional immunosuppressive medications considered.

Alternative steroids for prednisone- and methylprednisolone-refractory cases include triamcinolone and dexamethasone (see Table 8-1).

In cats, treatment with immunosuppressive doses of triamcinolone or dexamethasone is often more effective than therapy with prednisolone or methylprednisolone. Oral triamcinolone or dexamethasone should be administered daily until remission is achieved (approximately 2–8 weeks), then the dosage should be gradually tapered until the lowest possible and least frequent dosage that maintains remission is being administered (see Table 8-1).

If unacceptable adverse effects develop, or if no significant improvement is seen within 2 to 4 weeks of initiation of therapy, consider using an alternate glucocorticosteroid or a nonsteroidal immunosuppressive drug (see Table 8-1).

d Nonsteroidal immunosuppressive drugs that may be effective include cyclosporine (Atopica), azathioprine (dogs only), chlorambucil, cyclophosphamide, mycophenolate mofetil, and leflunomide (see Table 8-1). A beneficial response occurs within 8 to 12 weeks of initiation of therapy. Once remission is achieved, gradually attempt to taper the dosage and frequency of the nonsteroidal immunosuppressive drug for long-term maintenance.

4 The prognosis is fair to good. Although some animals remain in remission after immunosuppressive therapy is tapered and discontinued, most animals require lifelong therapy to maintain remission. Regular monitoring of clinical signs, hemograms, and serum biochemistry panels with treatment adjustments as needed is essential. Potential complications of immunosuppressive therapy include unacceptable drug adverse effects and immunosuppression-induced bacterial infection, dermatophytosis, or demodicosis.

FIGURE 8-1 Pemphigus Foliaceus.

An adult Doberman with pemphigus foliaceus. Note the diffuse pattern of lesions.

FIGURE 8-2 Pemphigus Foliaceus.

Same dog as in Figure 8-1. Alopecic, crusting, papular lesions on the face are apparent. Note the similarity of lesions to folliculitis; however, the pattern of distribution is unique.

FIGURE 8-3 Pemphigus Foliaceus.

Alopecic, crusting, papular dermatitis on the face. Lesions on the nasal planum and ear pinnae are characteristic of autoimmune skin disease.

FIGURE 8-4 Pemphigus Foliaceus.

Same dog as in Figure 8-3. Alopecic, crusting, papular dermatitis on the face and nasal planum is characteristic of autoimmune skin disease. Note the similarity to folliculitis lesions; however, no follicles are present on the nasal planum, making these lesions a unique feature.

FIGURE 8-5 Pemphigus Foliaceus.

Crusting erosive dermatitis on the nasal planum with depigmentation and loss of the normal cobblestone texture is a unique feature of autoimmune skin disease.

FIGURE 8-6 Pemphigus Foliaceus.

Same dog as in Figure 8-5. Lesions on the nasal planum are characteristic of autoimmune skin disease.

FIGURE 8-7 Pemphigus Foliaceus.

Crusting papular dermatitis on the ear pinna of a dog with pemphigus foliaceus. Lesions on the nasal planum, ear pinnae, and footpads are characteristic of autoimmune skin disease.

FIGURE 8-8 Pemphigus Foliaceus.

Alopecic, crusting dermatitis on the ear margin of a Doberman with pemphigus foliaceus. Note the similarity to scabies; however, this dog was not intensely pruritic.

FIGURE 8-9 Pemphigus Foliaceus.

Alopecic, crusting, papular, dermatitis that covered the entire cutaneous surface area of this Dalmatian. Note the similarity to folliculitis.

FIGURE 8-10 Pemphigus Foliaceus.

Alopecia with a crusting papular rash on the trunk.

FIGURE 8-11 Pemphigus Foliaceus.

Hyperkeratosis and crusting of the footpads are characteristic of autoimmune skin disease. Note that the lesions are on the actual pad rather than on the interdigital surface, which would be typical of allergic dermatitis or bacterial or yeast pododermatitis.

FIGURE 8-12 Pemphigus Foliaceus.

Hyperkeratosis and crusting of the footpads.

FIGURE 8-13 Pemphigus Foliaceus.

Hyperkeratosis and crusting of the scrotum of a dog with pemphigus foliaceus.

FIGURE 8-14 Pemphigus Foliaceus.

Depigmentation of the nasal planum with loss of the normal cobblestone texture is an early change associated with autoimmune skin disease.

FIGURE 8-15 Pemphigus Foliaceus.

Severe moist dermatitis is a rare feature of pemphigus foliaceus.

FIGURE 8-16 Pemphigus Foliaceus.

Facial dermatitis (alopecic, crusting, papular rash) in a cat. Note the similarity to facial dermatitis of Persian cats.

FIGURE 8-17 Pemphigus Foliaceus.

Close-up of the cat in Figure 8-16. The alopecic, crusting, papular dermatitis on the face and ear pinna is characteristic of autoimmune skin disease.

FIGURE 8-18 Pemphigus Foliaceus.

Same cat as in Figure 8-16. The crusting papular rash on the ear pinna is a unique feature of autoimmune skin disease.

FIGURE 8-19 Pemphigus Foliaceus.

Same cat as in Figure 8-16. Alopecic, crusting, erosive dermatitis around the nipples is a common and unique feature of pemphigus foliaceus in cats.

FIGURE 8-20 Pemphigus Foliaceus.

Papular crusting dermatitis. Note the similarity with dermatophytosis, ectoparasitism, and other allergic causes.

FIGURE 8-21 Pemphigus Foliaceus.

Hyperkeratosis and crusting on the footpads are common features of autoimmune skin disease.

FIGURE 8-22 Pemphigus Foliaceus.

Crusting dermatitis of the nail beds (paronychia) is a common and unique feature of pemphigus foliaceus in cats.

FIGURE 8-23 Pemphigus Foliaceus.

Paronychia and hyperkeratosis of the footpads in a cat with pemphigus foliaceus.

FIGURE 8-24 Pemphigus Foliaceus.

Microscopic image of acantholytic cells and numerous neutrophils as viewed with a 10× objective.

FIGURE 8-25 Pemphigus Foliaceus.

Microscopic image of acantholytic cells as viewed with a 100× (oil) objective.

FIGURE 8-26 Pemphigus Foliaceus.

Severe crusting on the footpads of an affected dog.

FIGURE 8-27 Pemphigus Foliaceus.

Severe crusting of the footpads developed over several weeks in a middle-aged dog.

FIGURE 8-28 Pemphigus Foliaceus.

Severe facial crusting with alopecia in a cat. The nasal planum is affected but not to the extent that a dog’s nasal planum typically is affected.

FIGURE 8-29 Pemphigus Foliaceus.

Severe paronychia, exudative dermatitis with crusting, is a common feature of pemphigus in cats.

FIGURE 8-30 Pemphigus Foliaceus.

Severe erosive dermatitis with crusting alopecia on the face of an affected dog. The lesions on the nasal planum, around the eyes, and on the lips are typical of pemphigus.

FIGURE 8-31 Pemphigus Foliaceus.

Close-up of the dog as in Figure 8-30. Alopecia with crusting around the eye is apparent.

FIGURE 8-32 Pemphigus Foliaceus.

Same dog as in Figure 8-30. Crusting of the footpads is a characteristic feature of most autoimmune skin diseases.

FIGURE 8-33 Pemphigus Foliaceus.

Close-up of the footpad demonstrating the thickened keratin and crusting of the pad, especially at the margin.

FIGURE 8-34 Pemphigus Foliaceus.

Severe erosive, crusting, alopecic dermatitis on the face of a dog with pemphigus. Depigmentation, loss of normal cobblestone texture, erosion, and crusting on the nasal planum are characteristic of autoimmune skin disease.

FIGURE 8-35 Pemphigus Foliaceus.

Severe crusting on the ear pinna of a dog with pemphigus. Crusted ear pinnae (with or without otitis externa) is a common characteristic of autoimmune skin disease.

FIGURE 8-36 Pemphigus Foliaceus.

Severe alopecic, crusting dermatitis on the ear pinna is typical of pemphigus and other autoimmune skin diseases.

FIGURE 8-37 Pemphigus Foliaceus.

Severe erosive, depigmenting, crusting dermatitis of the nasal planum is a classic characteristic of autoimmune skin disease.

FIGURE 8-38 Pemphigus Foliaceus.

Severe alopecia with punctate, crusted erosions on the ear pinna of a dog with pemphigus.

FIGURE 8-39 Pemphigus Foliaceus.

Severe crusting dermatitis on the ear pinna typical of autoimmune skin disease. Note that the ear canal appears to be normal; otitis externa may or may not be present in patients with autoimmune skin disease.

FIGURE 8-40 Pemphigus Foliaceus.

Severe crusting, erosive dermatitis on the nasal planum of a dog with pemphigus. Loss of normal cobblestone texture and depigmentation usually occur first, followed by erosive, crusting lesions as the disease progresses.

FIGURE 8-41 Pemphigus Foliaceus.

Alopecic, crusting dermatitis around the eye of a dog with pemphigus.

FIGURE 8-42 Pemphigus Foliaceus.

Pustules on the skin of a dog with pemphigus. Pustules are the primary lesions caused by pemphigus; however, they usually are destroyed very quickly by the dog’s normal activity.

FIGURE 8-43 Pemphigus Foliaceus.

Pustular dermatitis on the skin of a dog with pemphigus.

FIGURE 8-44 Pemphigus Foliaceus.

Severe crusting dermatitis caused by a drug-induced pemphigus after the dog was treated with Promeris. Pemphigus-induced Promeris drug reactions have been well documented.

(Courtesy S. Sargent.)

Pemphigus Erythematosus

Features

This disease may be a benign form of pemphigus foliaceus or a crossover between pemphigus and lupus erythematosus. It is uncommon in cats and common in dogs, with an increased incidence in German shepherds, collies, and Shetland Sheep dogs.

The disease is usually limited to the face (bridge of the nose and around the eyes) and ear pinnae. Superficial erosions, scales, and crusts are typical. Pustules may be present but are usually difficult to find. Skin lesions may be minimally to mildly pruritic. Concurrent nasal depigmentation is common. The oral cavity is not involved.

Top Differentials

Differentials include demodicosis, nasal pyoderma, dermatophytosis, discoid lupus erythematosus, pemphigus foliaceus, dermatomyositis, nasal solar dermatitis, mosquito bite hypersensitivity (cats), uveodermatologic syndrome, and zinc-responsive dermatosis.

Diagnosis

1 Rule out other differentials.

2 Cytology (pustule): neutrophils and acantholytic cells are seen. Eosinophils may also be present.

3 Antinuclear antibody (ANA) test: may be positive; however, a positive result is only supportive and is not pathognomonic for pemphigus erythematosus because positive titers can be associated with many other chronic diseases.

4 Dermatohistopathology: subcorneal pustules that contain neutrophils and acantholytic cells with or without eosinophils. Lichenoid infiltration with mononuclear cells, plasma cells, neutrophils, or eosinophils may also be present.

5 Immunofluorescence or immunohistochemistry (skin biopsy specimen): detection of intercellular antibody deposition. Antibody deposition along the dermal-epidermal junction may also be present. False-positive and false-negative results are common. Positive results should be confirmed histologically.

6 Bacterial culture (pustule): usually sterile, but occasionally bacteria are isolated if secondary infection is present.

Treatment and Prognosis

1 Sunlight exposure should be avoided and topical sunscreens used to prevent ultraviolet light from exacerbating nasal lesions. Products containing titanium dioxide are especially effective.

2 Symptomatic shampoo therapy may be helpful for removing crusts.

3 To treat or prevent secondary pyoderma in dogs, appropriate long-term systemic antibiotics should be administered (minimum 4 weeks). Dogs treated with antibiotics during the induction phase of immunosuppressive therapy have significantly higher survival rates than dogs treated with immunosuppressive drugs alone. Antibiotics should be continued until concurrent immunosuppressive therapy has the pemphigus under control.

4 The goal of treatment is to control the disease and its symptoms with the safest treatments used at the lowest possible doses. Typically, combinations of therapies (see Table 8-1) will have to be used to provide a multimodal treatment plan, minimizing the adverse effects of any one therapy. Depending on the severity of the disease, more or less aggressive treatments will have to be selected. To push the disease into remission, higher doses are used initially and then are tapered over 2 to 3 months to the lowest effective dose.

Immunosuppressive doses of oral prednisone or methylprednisolone should be administered daily (see Table 8-1). After lesions resolve (after approximately 2–8 weeks), the dosage should be gradually tapered over a period of several (8–10) weeks until the lowest possible alternate-day dosage that maintains remission is being administered. If no significant improvement is seen within 2 to 4 weeks of initiation of therapy, concurrent skin infection should be ruled out, then alternative or additional immunosuppressive medications considered.

Alternative steroids for prednisone- and methylprednisolone-refractory cases include triamcinolone and dexamethasone (see Table 8-1).

In cats, treatment with immunosuppressive doses of triamcinolone or dexamethasone often is more effective than therapy with prednisolone or methylprednisolone. Oral triamcinolone or dexamethasone should be administered daily until remission is achieved (approximately 2–8 weeks), then the dosage should be gradually tapered until the lowest possible and least frequent dosage that maintains remission is being administered (see Table 8-1).

5 The prognosis is good because even without treatment, this disease usually remains benign and localized. If systemic immunosuppressive drugs are used, regular monitoring of clinical signs, hemograms, and serum biochemistry panels, with treatment adjustments as needed, is essential. Potential complications of systemic immunosuppressive therapy include unacceptable drug adverse effects and immunosuppression-induced secondary bacterial infection, dermatophytosis, or demodicosis.

FIGURE 8-45 Pemphigus Erythematosus.

Depigmentation and erosive dermatitis on the nasal planum. Lesions on the nasal planum are a common and unique feature of autoimmune skin disease.

FIGURE 8-46 Pemphigus Erythematosus.

Same dog as in Figure 8-45. Depigmenting erosive lesions on the nasal planum.

FIGURE 8-47 Pemphigus Erythematosus.

Depigmentation and erosions on the nasal planum.

Pemphigus Vulgaris

Features

Pemphigus vulgaris is an autoimmune skin disease characterized by the production of autoantibodies against antigens in or near the epidermal-dermal junction. The deposition of antibody in intercellular spaces causes cell detachment within the deeper epidermal layers (acantholysis). It is the most severe form of pemphigus and is rare among dogs and cats.

Erosions, ulcers, and, rarely, vesicles and bullae occur on the skin (especially on the axillae and groin), mucocutaneous junctions (nail beds, lips, nares, eyelids), and mucous membranes (oral cavity, anus, vulva, prepuce, conjunctiva). Concurrent fever, depression, and anorexia are common. Marked salivation and halitosis may accompany oral lesions. Lesions on the nasal planum, ear pinnae, and footpads are unique and characteristic of autoimmune skin disease.

Top Differentials

Differentials include bullous pemphigoid, systemic lupus erythematosus, erythema multiforme/toxic epidermal necrolysis, drug reaction, infection (bacterial, fungal), vasculitis, and cutaneous epitheliotropic lymphoma.

Treatment and Prognosis

1 Symptomatic shampoo therapy may be helpful for removing crusts.

2 To treat or prevent secondary pyoderma in dogs, appropriate long-term systemic antibiotics should be administered (minimum 4 weeks). Dogs treated with antibiotics during the induction phase of immunosuppressive therapy have significantly higher survival rates than dogs treated with immunosuppressive drugs alone. Antibiotics should be continued until concurrent immunosuppressive therapy has the pemphigus under control.

Because Pemphigus vulgaris is usually severe, aggressive therapy is usually required.

Although glucocorticoid therapy alone may be effective in maintaining remission, the dosages needed may result in undesirable adverse effects, especially in dogs. For this reason, the use of nonsteroidal immunosuppressive drugs, alone or in combination with glucocorticoids, is usually recommended for long-term maintenance.

a Immunosuppressive doses of oral prednisone or methylprednisolone should be administered daily (see Table 8-1). After lesions resolve (after approximately 2–8 weeks), the dosage should be gradually tapered over a period of several (8–10) weeks until the lowest possible alternate-day dosage that maintains remission is being administered. If no significant improvement is seen within 2 to 4 weeks of initiation of therapy, concurrent skin infection should be ruled out, then alternative or additional immunosuppressive medications considered.

b Alternative steroids for prednisone- and methylprednisolone-refractory cases include triamcinolone and dexamethasone (see Table 8-1).

c In cats, treatment with immunosuppressive doses of triamcinolone or dexamethasone is often more effective than therapy with prednisolone or methylprednisolone. Oral triamcinolone or dexamethasone should be administered daily until remission is achieved (approximately 2–8 weeks), then the dosage should be gradually tapered until the lowest possible and least frequent dosage that maintains remission is being administered (see Table 8-1).

d If unacceptable adverse effects develop, or if no significant improvement is seen within 2 to 4 weeks of initiation of therapy, consider using an alternate glucocorticosteroid or a nonsteroidal immunosuppressive drug (see Table 8-1).

4 Nonsteroidal immunosuppressive drugs are usually needed in addition to steroidal therapy to control severe lesions and minimize the side effects of steroids. Treatments that may be effective include cyclosporine (Atopica), azathioprine (dogs only), chlorambucil, cyclophosphamide, mycophenolate mofetil, and leflunomide (see Table 8-1). A beneficial response occurs within 8 to 12 weeks of initiation of therapy. Once remission is achieved, gradually attempt to taper the dosage and frequency of the nonsteroidal immunosuppressive drug for long-term maintenance.

5 The prognosis is fair to poor, and lifelong therapy is usually required to maintain remission. Regular monitoring of clinical signs, hemograms, and serum biochemistry panels, with treatment adjustments as needed, is essential. Potential complications of immunosuppressive therapy include unacceptable drug adverse effects and immunosuppression-induced bacterial infection, dermatophytosis, or demodicosis.