Small Animal Dermatology PDF

CHAPTER | 7 Hypersensitivity Disorders Canine Atopy (Atopic Dermatitis, Environmental, Feline Eosinophilic Plaque Pollen Allergies) Feline Eosinophilic Granuloma (Linear Granuloma) Canine Food Hypersensitivi...

CHAPTER | 7 Hypersensitivity Disorders Canine Atopy (Atopic Dermatitis, Environmental, Feline Eosinophilic Plaque Pollen Allergies) Feline Eosinophilic Granuloma (Linear Granuloma) Canine Food Hypersensitivity Indolent Ulcer (Rodent Ulcer, Eosinophilic Ulcer) Acral Lick Dermatitis (Lick Granuloma) Feline Plasma Cell Pododermatitis Flea Allergy Dermatitis (Flea Bite Hypersensitivity) Feline Idiopathic Ulcerative Dermatosis Feline Atopy Urticaria and Angioedema (Hives) Feline Food Hypersensitivity Canine Eosinophilic Furunculosis of the Face Mosquito Bite Hypersensitivity Contact Dermatitis (Allergic Contact Dermatitis) AUTHOR’S NOTE Treating Allergic Dogs 3. Use simplified charts and handouts to organize By far the most common skin disorders that we treat the diagnosis and treatment phases of the allergy are allergies with the secondary infections and chronic education discussion. These focus the educational skin and ear changes caused by those allergies. Despite message and improve the client’s understanding (see many attempts to simplify the diagnostic and treat- Chapter 1). Additionally, draw and write on these ment process as well as the development of amazingly handouts for the client to review later. This increases beneficial new therapies, we continue to struggle to acceptance of the message and improves compliance find easy, practical, and economical strategies for the with therapy. diagnosis and treatment of the primary allergic condi- 4. Organize the diagnostic testing and treatment options tions and the secondary infections. What follows are into groups based on the severity of the patient’s signs the author’s best ideas, tips, and perspective for the and response to previous treatments (mild patients need effective management of allergic dogs. a, b, and c: moderately severe patients need d, e, and f: severe patients need g, h, and i). Optimizing Owner Understanding 5. Assess the risk to the patient and family members and Compliance for methicillin-resistant Staphylococcus (MRS) infec- Much of the problem veterinarians face when treating tions. Families at risk for MRS contagion and zoonosis the allergic patient is the pet owner’s lack of under- must be willing to accept aggressive medical manage- standing and ability to adhere to long-term prevention ment to reduce the risk. All three species of MRS can and treatment protocols. There is great information potentially be transmitted from dogs to people and available regarding cognitive psychology that can opti- from people to dogs. If family members have a history mize human factors improving successful outcomes. of methicillin-resistant Staphylococcus aureus (MRS), Here are some suggestions: consider aggressively moni­toring the patient with cul- 1. Have the pet owner complete a patient history form. tures because dogs can acquire MRS from humans. If This allows the client to focus on the details of the family members are immu­no­suppressed, monitor the skin disease and symptoms and primes him or her patient for methicillin-resistant Staphylococcus pseud- to listen better and accept the diagnosis and infor- intermedius and methicillin-resistant Staphy­lococcus mation that will be provided by the health care team. schleiferi, which can be a source of contagious infec- 2. Try to avoid a rambling, stream-of-consciousness tion to at-risk, immunosuppressed people. These approach to the discussion of allergy. Many of us patients need the most aggressive diagnostic workup have an “automatic” allergy spiel that only confuses and treatments achievable to protect the entire family the client and does not focus on the specific prob- from con­tagion and zoonosis. In these families, avoid lems of the individual patient. the indiscriminate use of steroids or fluoroquinolone 188  Hypersensitivity Disorders 189 AUTHOR’S NOTE—cont’d antibiotics, which can increase the risk of MRS pyo- tramadol will help alleviate the severe itching. Obvi- derma in favor of antiseptic topical treatments or ously, this is not a practical long-term solution. culture-based systemic antibiotics (or both). 3. A tapering course of oral steroids may be admin­ istered at anti-inflammatory doses (e.g., prednisone Treating the Infection 0.5–1.0 mg/kg) for 1 to 2 weeks, but because of the risk Although dermatologists have been teaching and of MRS, diabetes, and iatrogenic Cushing’s disease, stressing the necessity and importance of treating sec- long-term use should be avoided. ondary bacterial and yeast infections caused by the 4. Oclacitinib (Apoquel) may be administered on a short- primary allergic skin disease, the failure to identify, term basis to reduce the sensation of itch, but long- diagnose, successfully treat, and then prevent the bac- term use should be avoided because of an increased terial and yeast infections remains the most significant risk of adverse events, including tumors (18%), pyo- factor needing improvement. In recent years, the prac- derma (12%), otitis (9.9%), vomiting (9.2%), diarrhea tice of bypassing the identification and treatment of (6%), cystitis (3.5%), anorexia (3.2%), lethargy (2.8%), the primary underlying disease or inappropriately yeast skin infections (2.5%), and pododermatitis (2.5%). treating the secondary pyoderma has led to the emergence and increasing trend towards resistant Preventing Allergies infections. These infections in particular are quickly The best solution is to use simple over-the-counter becoming a major contagious-zoonotic concern lead­ (OTC) treatment options, when available, to help prevent ing to ethical and legal ramifications associated with the allergy and secondary infections. These treatment malpractice. options should be the backbone of any allergy therapy 1. The risk of MRS contagion and family immunosup- protocol. The principle of combination anesthesia is to use pression must be assessed, discussed, and proactively multi­ple drugs at reduced dosages and with different managed to limit the transfer of resistant infection, mechanisms of action to achieve a plane of desired anes- genes, or both between pet and human family thesia and analgesia. This approach reduces the members. risk of adverse events compared with using a single drug at 2. Cytology must be incorporated into every derma­ a higher dose to accomplish the same desired effect. Simi- tology examination as part of the minimum data- larly, treatment of allergic skin disease should follow the base for skin disease assessment. This simple test same logic—the use of multiple therapies that target differ- allows for the cytologic diagnosis of infection (bac- ent aspects of the pathophysiology (e.g., skin barrier teria, yeast, or both). therapy, immunomodulation, and antimicrobials). A 3. Culture the skin when the history is suggestive of a regimen of therapy that the patient will tolerate and the resistant bacterial infection (see Chapter 3). owner will administer will provide the best results. 4. Treatments targeting the primary, underlying aller- 1. Bathe the pet every 3 to 7 days with a disinfecting and gic cause of the infections must be initiated to antiseptic shampoo to wash off pollens and kill bacte- reduce the recurrence of the infection and the ria and yeast. repeated use of chronic antibiotics. 2. Place ear cleaner or medicine in the ear canal after every bath (every 3–7 days) to prevent allergic otitis Stopping the Itch from progressing to infectious otitis. Despite the all-important medical issues, the client 3. Wipe off the feet, chin, and face folds with wipes as mainly wants the itch to stop. Our obsession with the often as possible to remove pollen, bacteria, and yeast. treatment of this single symptom has led to an This is especially helpful right before bedtime because unhealthy tunnel vision focus on itch to the exclusion pruritus escalates during times of less environmental of the real problem, the secondary infections caused by stimuli. the primary underlying allergic disease. 4. The routine use of antihistamines may help reduce skin Regardless, there are only four ways to stop severe irritation and have few side effects. itch quickly: 5. Give essential fatty acids every 12 to 24 hours to 1. For suspected or known atopic dogs, Canine Atopic decrease the inflammatory properties (omega-3) of Dermatitis Immunotherapeutic (Zoetis) is an inject- the allergic process and improve the barrier of the skin able caninized monoclonal antibody that blocks (omega-6). the pruritogenic effects of IL-31. This injection is 6. For young allergic dogs, administration of nonflavored highly effective at reducing pruritic atopic symp- h probiotic once each day may help delay or prevent toms with minimal adverse effects at the time of this the full effect of allergies. writing. 7. Make sure all pets and animals are treated with a new- 2. Sedate the patient. This sounds unusual, but generation total internal and external parasite control high-dose diphenhydramine, gabapentin, and/or therapy to prevent parasitic pruritic flares. Continued 190 CHAPTER 7 Hypersensitivity Disorders AUTHOR’S NOTE—cont’d 8. Avoid common food allergens if possible. Feed a Salvage Therapy for Severe Refectory Patients diet without beef, dairy, or chicken protein. Rarely, allergic patients fail to respond to the aforemen- 9. Keep pets indoors during the dawn and dusk time tioned therapy, thus requiring chronic treatment with periods when pollens and insects are at their peak. steroids or oclacitinib (Apoquel) for humane reasons. However, using these medications may have serious and Advanced Allergy Treatment significant adverse effects when used long term. These When the relative simple and easy prevention thera- treatments should only be used over extended time pies are insufficient, the patient should be treated with periods after a complete and thorough discussion about more advanced allergy treatments. their negative consequences has been had with the pet 1. Consider a home-cooked food trial to avoid any and owner. all preservatives, dyes, and contamination in com- 1. Oral steroids may be administered at the lowest mercially prepared foods. possible dose and frequency to control the pruritus. 2. Cyclosporine (Atopica) and allergy vaccines (immu- Frequent or extended use will likely result in the devel- notherapy) are the only effective, safe treatments opment of adverse medical outcomes, including, but that have a documented rate of disease remission not limited to, MRS infection, iatrogenic Cushing’s for allergic patients over the long haul. Again, oral disease, demodicosis, calcinosis cutis, diabetes, UTIs, steroids and oclacitinib (Apoquel) are best suited for ruptured cruciate ligaments, and so on. stopping acute pruritic flares. 2. Oclacitinib (Apoquel) may be administered at the Cyclosporine (Atopica) has reported adverse lowest possible dose and frequency. Higher dosing events with use including vomiting (26%), soft and frequent administration increase the risk of stool (15%), anorexia (2%), nodules or cysts (1%), adverse events, including tumors (18%), pyoderma urinary tract infection (UTI) (1%), gingival hyper- (12%), otitis (9.9%), vomiting (9.2%), diarrhea (6%), cys- plasia (1%), lethargy (1%), reproductive issues titis (3.5%), anorexia (3.2%), lethargy (2.8%), yeast skin (1%), papillomatosis (1%), lymphadenopathy infections (2.5%), and pododermatitis (2.5%). (0.8%), neurologic (0.8%), and urticaria or angio- edema (0.3%). Overall Goals of Allergy Management 3. For known atopic dogs, Canine Atopic Dermatitis Reduce 80% to 90% of the itch about 80% to 90% of Immunotherapeutic (Zoetis) is an injectable cani- the time. nized monoclonal antibody that blocks the prurito- Reduce the frequency of skin and ear infections. genic effects of IL-31. This monthly injection is highly Limit the use of repeated courses of antimicrobials. effective at reducing pruritic atopic symptoms with Limit adverse events associated with allergy manage- minimal adverse effects at the time of this writing. ment treatments and strategies. 4. Referral to a veterinary dermatologist for veri- Improve the patient and owner’s quality of life within fication of the diagnosis and advanced medical a defined budget. management. Canine Atopy (Atopic Dermatitis, Environmental, Pollen Allergies) Features recurrent pyotraumatic dermatitis, conjunctivitis, hyperhidro- sis (sweating), and, rarely, allergic bronchitis or rhinitis may Canine atopy is a hypersensitivity reaction to inhaled (possi- be seen. bly a historical theory) or cutaneously absorbed environmen- tal antigens (allergens) in genetically predisposed individuals. It is common in dogs, with the age of onset ranging from 6 Top Differentials months to 6 years. However, in most atopic dogs, symptoms Differentials include food allergy, scabies, Malassezia dermati- first appear at between 1 and 3 years of age. tis, and bacterial pyoderma, as well as other hypersensitivities Symptoms begin as skin erythema and pruritus (licking, (flea bite, contact), parasites (cheyletiellosis, pediculosis), and chewing, scratching, rubbing), which may be seasonal or folliculitis (dermatophyte, Demodex). nonseasonal, depending on the offending allergen. The distribution of the pruritus usually involves the feet, flanks, groin, axillae, face, and ears. Self-trauma often results in sec- Diagnosis ondary skin lesions, including salivary staining, alopecia, 1. Seasonal foot licking is the most unique and typical excoriations, scales, crusts, hyperpigmentation, and licheni- symptom of atopy. If year-round allergens (house dust fication. Secondary pyoderma, Malassezia dermatitis, and mites) are causing the allergy, the foot licking may be otitis externa are common. Chronic acral lick dermatitis, nonseasonal.  Canine Atopy 191 2. Allergy testing (intradermal, serologic): allergy testing can be highly variable according to the method used. Positive TABLE 7-1 Antihistamine Therapy in Dogs* reactions to grass, weed, tree, mold, insect, dander, or Antihistamine Dose indoor environmental allergens are seen. False-negative Chlorpheniramine 0.2–0.5 mg/kg PO q 8–12 hours and false-positive reactions may occur. 3. Dermatohistopathology (nondiagnostic): superficial peri- Diphenhydramine 1–4 mg/kg PO q 8 hours vascular dermatitis that may be spongiotic or hyperplastic. Hydroxyzine 2 mg/kg PO q 8 hours Inflammatory cells are predominantly lymphocytes and Amitriptyline 1–2 mg/kg PO q 12 hours histiocytes. Eosinophils are uncommon. Neutrophils or plasma cells suggest secondary infection. Cyproheptadine 0.1–2 mg/kg PO q 8–12 hours Trimeprazine 0.5–5 mg/kg PO q 8–12 hours Treatment and Prognosis Brompheniramine 0.5–2 mg/kg PO q 12 hours 1. Infection prevention: any secondary pyoderma, otitis Terfenadine 0.25–1.5 mg/kg PO q 12–24 hours externa, and Malassezia dermatitis should be treated with Astemizole 1 mg/kg PO q 12–24 hours appropriate therapies. Controlling and preventing second- ary infection is an essential component of managing atopic Promethazine 0.2–0.4 mg/kg PO q 12 hours dogs. Bathing every 3 to 7 days and treating the ears after Loratadine 0.5 mg/kg PO q 24 hours every bath help to wash off pollens and disinfect the skin and ear canals, preventing secondary infections from Cetirizine 0.5–1 mg/kg PO q 24 hours recurring. Doxepin 0.5–1 mg/kg PO q 8–12 hours 2. Symptomatic therapy (itch control): Dimenhydrinate 8 mg/kg PO q 8 hours a. An integrated flea control program should be instituted to prevent flea bites from aggravating the pruritus. Tripelennamine 1 mg/kg PO q 12 hours b. Topical therapy with antimicrobial shampoos and Clomipramine 1–3 mg/kg PO q 24 hours anti-itch conditioners, and sprays (i.e., those contain- ing oatmeal, pramoxine, antihistamines, or glucocorti- coids) applied every 2 to 7 days or as needed may help effects ranging from increased risk for MRS infections, reduce clinical symptoms. mild (polyuria [PU]/polydipsia [PD]) to severe c. Systemic antihistamine therapy reduces clinical symp- (immune dysfunction, demodicosis, and calcinosis toms in many cases (Table 7-1). Antihistamines can be cutis). It is a therapeutic option if the allergy season is used alone or in combination with glucocorticoids or very short but may result in unacceptable adverse essential fatty acids for a synergistic effect. One- to effects, especially if used over the long term. 2-week-long therapeutic trials with different antihista- – Potent, long-acting injectable steroids are contrain- mines may be required to determine which is most dicated for the treatment of allergies because of effective. their comparatively short anti-inflammatory bene- d. Oral essential fatty acid supplements (180 mg eicosa- fits (3 weeks) relative to their prolonged metabolic pentaenoic acid [EPA]/40 mg/kg) help control pruritus and immunodepressive and immunosuppressive in 20% to 50% of cases, but 8 to 12 weeks of therapy effects (6–10 weeks). may be needed before beneficial effects are seen. Also, – Injectable short-acting steroids (dexamethasone a synergistic effect is often noted when essential fatty sodium phosphate 0.5–0.8 mg/kg or prednisolone acid supplements are administered in combination acetate 0.1–1 mg/kg) are effective at providing with glucocorticoids or antihistamines. relief and may last 2 to 3 weeks if no concurrent e. Dextromethorphan, an opioid antagonist, may be a secondary infection occurs. This treatment option useful adjunct in managing the licking, chewing, and allows the clinician to more closely control and biting behaviors associated with allergic dermatitis in monitor the patient’s use of steroids compared with dogs. Dextromethorphan 2 mg/kg orally (PO) should oral treatments administered by the owner. be administered every 12 hours. A beneficial effect – Temaril-P (trimeprazine and prednisolone combi- should be seen within 2 weeks. nation) is a unique drug that provides significant f. Oclacitinib (Apoquel) may be administered for 1 to antipruritic effects at a relatively lower dose of the 2 weeks to reduce the symptoms (itch), but long- prednisolone. One tablet per 10 to 20 kg should be term use should be avoided because of an increased administered every 24 to 48 hours. The dosage risk of adverse events, including tumors (18%), pyo- should be tapered to the lowest possible dose and derma (12%), otitis (9.9%), vomiting (9.2%), diarrhea frequency. (6%), cystitis (3.5%), anorexia (3.2%), lethargy – Prednisone 0.25 to 1 mg/kg (or methylpredniso- (2.8%), yeast skin infections (2.5%), and pododerma- lone 0.2–0.8 mg/kg) PO should be administered titis (2.5%). every 24 to 48 hours for 3 to 7 days. The dosage g. Systemic glucocorticoid therapy is often effective in should be tapered to the lowest possible dose and controlling pruritus but almost always results in adverse frequency. 192 CHAPTER 7 Hypersensitivity Disorders Canine Atopy—cont’d – All dogs treated with long-term steroids (>3 3 to 5 months of initiation of immunotherapy. Both months) should be frequently monitored for liver needle and needle-free options are available for deliv- disease and UTI. ering ASIT (allergen-specific immunotherapy). Tradi- 3. Allergy treatment (immune modulation): tionally, ASIT has been given by injection, but a. Exposure to offending allergens should be reduced, if sublingual immunotherapy (SLIT) is now a means of possible, by their removal from the environment. administering vaccine through the oral mucosa. When High-efficiency particulate air (HEPA) and charcoal prescribing SLIT, it important to instruct clients not to filters should be used to reduce pollens, molds, and squirt or spray the allergen solution directly in the back dust in the home. For house dust mite–sensitive of the patient’s mouth but rather along the inner cheek. dogs, household treatments for carpets, mattresses, and If swallowed, SLIT will be ineffective, so the client upholstery with the acaricide benzyl benzoate once a should keep the pet from eating and drinking for 20 month for approximately 3 months and then every 3 minutes after administration. These options for deliv- months thereafter may effectively eliminate house dust ery allow veterinarians to better tailor therapy to the mites from the environment. Old dog beds should be temperament of the patient and lifestyle of the client, discarded because they accumulate house dust mite thereby improving compliance, and, ultimately, success antigens. Dehumidifying the house to below 40% rela- of treatment. At the time of this writing, there is no tive humidity decreases house dust mite, mold, and strong evidence for or against the use of nonspecific flea antigen loads. To achieve this, high-efficiency immunotherapy (e.g., Regionally-specific immuno- dehumidifiers that are capable of pulling several liters therapy [RESPIT]) in human or veterinary medicine. of water from the air per day are required. d. For known atopic dogs, Canine Atopic Dermatitis b. Cyclosporine (Atopica) helps control pruritus in 75% Immunotherapeutic (Zoetis) is an injectable caninized of atopic dogs. A dose of 5 mg/kg PO should be monoclonal antibody that blocks the pruritogenic administered every 24 hours until beneficial effects are effects of IL-31. This monthly injection is highly effec- seen (≈4–6 weeks). Then dosage frequency should be tive at reducing pruritic atopic symptoms with minimal tapered down to every 48 to 72 hours. For long-term adverse effects at the time of this writing. control, approximately 25% of dogs require daily 4. The prognosis is good, although lifelong therapy for dosing, 50% can be controlled with every-other-day control is needed in most dogs. Relapses (pruritic flare- dosing, and approximately 25% can be controlled with ups with or without secondary infections) are common, twice-weekly dosing. Glucocorticoids can be used ini- so individualized treatment adjustments to meet patient tially to speed response. As of this writing, no statisti- needs may be required periodically. In dogs that become cally significant increases in tumor risk or severe poorly controlled, one should rule out secondary infec- infection resulting from the immune effects of cyclo- tion (e.g., that caused by bacteria or Malassezia); sarcop­ sporine have been noted. tic mange; demodicosis; and concurrent food, flea bite, c. Immunotherapy (allergy vaccine): 60% to 75% of and recently acquired hypersensitivity to additional envi- atopic dogs show good (some medical therapy still ronmental allergens. Because a strong genetic com­ponent needed) to excellent (no other therapy needed) is present, the breeding of any male or female dog with response. Clinical improvement is usually noted within clinical signs of atopic dermatitis should be discouraged. AUTHOR’S NOTE Our profession has excelled at reducing the use of ste- alternative, safer treatment options. To achieve best medi- roids for arthritis; however, we have failed to make cine, the frequency of steroid use should be similar for similar achievements for allergic disease, including patients with arthritis and those with allergy. atopy. Because the two diseases have many similarities, The use of long-acting, injectable steroids should be including chronicity and multimodal therapeutic stopped because of their profound impact on the meta- options, our goal should be to minimize the use of bolic and immune systems, as well as growing concern of steroids for allergic disease through the use of legal liability for the practitioner. Text continued on p. 202  Canine Atopy 193 Distribution Pattern of Canine Atopy FIGURE 7-1 Canine Atopy. Subtle symptoms, including alopecia, FIGURE 7-2 Canine Atopy. Alopecia with erythema and erythema, and excoriations on the face, extremities, and flank of an adult hyperpigmentation on the ventrum of an atopic dog, demonstrating Shar Pei. typical lesion distribution for atopy. Note the similarity in distribution with Malassezia dermatitis. 194 CHAPTER 7 Hypersensitivity Disorders Canine Atopy—cont’d FIGURE 7-3 Canine Atopy. Generalized alopecia and hyperpigmentation FIGURE 7-4 Canine Atopy. Close-up of the dog in Figure 7-3. The in a severely pruritic Labrador retriever. The lesions are especially periocular alopecia and hyperpigmentation caused by facial pruritus are noticeable on the face, axilla, and flank. typical of allergic disease. FIGURE 7-5 Canine Atopy. Periocular alopecia, erythema, hyperpig- FIGURE 7-6 Canine Atopy. Perioral dermatitis with alopecia, erythema, mentation, and lichenification caused by pruritus. and crusting caused by a secondary bacterial and yeast infection associated with underlying allergic disease. FIGURE 7-7 Canine Atopy. Pododermatitis demonstrating the salivary FIGURE 7-8 Canine Atopy. Pododermatitis with alopecia and erythema staining caused by chronic licking. affecting the interdigital tissue between the central pad and digits. Pododermatitis and foot pruritus are some of the most consistent findings of atopy.  Canine Atopy 195 FIGURE 7-9 Canine Atopy. Pododermatitis demonstrating alopecia, FIGURE 7-10 Canine Atopy. Alopecia and erythema on the caudal erythema, hyperpigmentation, and lichenification caused by a secondary aspect of the distal extremities just proximal to the central footpad is a yeast infection associated with underlying allergic disease. common finding in allergic dogs. FIGURE 7-11 Canine Atopy. Erythema and lichenification of the ear FIGURE 7-12 Canine Atopy. Sterile otitis caused by allergy often canal associated with secondary yeast otitis. Otitis (sterile or infectious) presents with erythema of the ear pinna and external canal. is a common finding in allergic dogs. FIGURE 7-13 Canine Atopy. Secondary bacterial pyoderma is one of FIGURE 7-14 Canine Atopy. Secondary bacterial pyoderma (erythem- the most common findings in allergic dogs. The erythematous papular atous papular rash) on the inguinal area of an allergic dog. rash on the abdomen of this dog was caused by a secondary pyoderma associated with underlying atopy. 196 CHAPTER 7 Hypersensitivity Disorders Canine Atopy—cont’d FIGURE 7-15 Canine Atopy. Secondary Malassezia dermatitis caused FIGURE 7-16 Canine Atopy. An intradermal allergy test result by underlying allergy. The alopecic, erythematous, lichenified lesion on demonstrating numerous positive reactions with typical wheal and flare the ventral neck of this allergic dog is typical of Malassezia dermatitis. reactions. FIGURE 7-17 Canine Atopy. Severe erythema of the feet caused by FIGURE 7-18 Canine Atopy. Same dog as in Figure 7-17 demonstrating intense pruritus and by the patient self-mutilating his feet. the severe pododermatitis typical of atopy. Note the erythema on the abdomen, which is common with allergies. FIGURE 7-19 Canine Atopy. This intradermal allergy test result FIGURE 7-20 Canine Atopy. Same patient as in Figure 7-19. This demonstrates positive reactions with classic erythematous, well- intradermal allergy test result demonstrates positive reactions with demarcated, raised reactions. classic erythematous, well-demarcated, raised reactions. Note the difference between negative and positive reactions.  Canine Atopy 197 FIGURE 7-21 Canine Atopy. Erythema on the proximal carpus or tarsus FIGURE 7-22 Canine Atopy. Erythema on the feet caused by a is a classic symptom of atopy and usually occurs with podopruritus. combination of the underlying allergic reaction and the patient licking. FIGURE 7-23 Canine Atopy. Dermatitis (erythema and lichenification) FIGURE 7-24 Canine Atopy. Severe interdigital dermatitis with of the interdigital space is an extremely common symptom of atopy. ulceration caused by secondary bacterial and yeast infections. Often a secondary bacterial or yeast infection is present. FIGURE 7-25 Canine Atopy. Uninfected interdigital dermatitis typical FIGURE 7-26 Canine Atopy. Periocular alopecia, lichenification, and of atopy alone. mild crusting in an atopic dog. Periocular inflammation with resulting dermatitis is a common feature of atopy. 198 CHAPTER 7 Hypersensitivity Disorders Canine Atopy—cont’d FIGURE 7-27 Canine Atopy. Same dog as in Figure 7-26. Periocular FIGURE 7-28 Canine Atopy. Interdigital dermatitis with salivary dermatitis caused by the allergic reaction is obvious. staining is extremely common in atopic patients. FIGURE 7-29 Canine Atopy. Sterile, allergic otitis in a dog with atopy. FIGURE 7-30 Canine Atopy. Alopecia and mild lichenification around Note the generalized erythema without obvious otic exudate. the eyelids is a typical allergic symptom. FIGURE 7-31 Canine Atopy. Alopecia, lichenification, and hyper­ FIGURE 7-32 Canine Atopy. Facial dermatitis and allergic otitis causing pigmentation in the axilla of an atopic dog. The atopy often allows a severe alopecia and lichenification. secondary yeast infection to develop, worsening the clinical symptoms.  Canine Atopy 199 FIGURE 7-33 Canine Atopy. Severe ventral dermatitis affecting the axilla and abdominal regions. The moist, erosive lesions are indicative of FIGURE 7-34 Canine Atopy. Allergy skin test demonstrating the a secondary bacterial and yeast infection. intradermal injections using a side-light shadowing technique. FIGURE 7-35 Canine Atopy. Highly reactive allergy skin test FIGURE 7-36 Canine Atopy. Intradermal allergy skin test demonstrat- demonstrating the bee sting–like positive reactions. ing more subtle positive and negative reactions to the injected allergens. FIGURE 7-37 Canine Atopy. Intradermal injection of allergen during FIGURE 7-38 Canine Atopy. Periocular alopecia and lichenification are the allergy skin testing procedure. a classic symptom of atopy. 200 CHAPTER 7 Hypersensitivity Disorders Canine Atopy—cont’d FIGURE 7-39 Canine Atopy. Allergic pododermatitis with erythema FIGURE 7-40 Canine Atopy. Highly reactive intradermal allergy skin and alopecia is a classic lesion of atopy. test result. FIGURE 7-41 Canine Atopy. Allergic otitis precedes secondary FIGURE 7-42 Canine Atopy. Erythematous interdigital pododermatitis infections and is characterized by a swollen, erythematous ear canal with in an atopic dog. mild to moderate waxy exudate.  Canine Atopy 201 FIGURE 7-43 Canine Atopy. Interdigital pododermatitis in an atopic FIGURE 7-44 Canine Atopy. Alopecia and lichenification with dog should not affect the footpads (more typical of vasculitis and hyperpigmentation in the axilla of an atopic dog with a secondary yeast autoimmune skin disease). infection. Note the positive intradermal allergy skin test result. FIGURE 7-45 Canine Atopy. Highly reactive intradermal allergy skin test result. 202 CHAPTER 7 Hypersensitivity Disorders Canine Food Hypersensitivity Features contain food ingredients previously administered in dog Canine food hypersensitivity is an adverse reaction to a food food, treats, or table scraps, nor should flavored heart- or food additive. It can occur at any age, from recently weaned worm preventive, flavored medications, nutritional sup- puppies to elderly dogs that have been eating the same dog plements, or chewable treats (i.e., pig ears, cow hooves, food for years. Approximately 30% of dogs diagnosed with rawhide, dog biscuits, table food such as cheese) be admin- food allergy are younger than 1 year of age. Food allergy is istered during the hypoallergenic diet trial. Beef and dairy common in dogs. are the most common food allergens in dogs, and avoiding Canine food hypersensitivity is characterized by nonsea- these alone may result in clinical improvement. Other sonal pruritus that may or may not respond to steroid therapy. common food allergies include chicken, eggs, soy, corn, The pruritus may be regional or generalized and usually and wheat. involves the ears, feet, inguinal or axillary areas, face, neck, 5. Provocative challenge: recurrence of symptoms within and perineum. Affected skin is often erythematous, and a hours to days of reintroduction of suspect allergen into the papular rash may be present. Self–trauma-induced lesions diet. include alopecia, excoriations, scales, crusts, hyperpigmenta- tion, and lichenification. Secondary superficial pyoderma, Treatment and Prognosis Malassezia dermatitis, and otitis externa are common. Other 1. Infection prevention: any secondary pyoderma, otitis symptoms that may be seen are acral lick dermatitis, chronic externa, and Malassezia dermatitis should be treated with seborrhea, and recurring pyotraumatic dermatitis. Some dogs appropriate therapies. Controlling and preventing second- are minimally pruritic, with the only symptom being recurrent ary infection is an essential component of managing atopic infection with pyoderma, Malassezia dermatitis, or otitis. In dogs. Bathing every 3 to 7 days and treating the ears after these cases, the pruritus is present only when secondary infec- every bath helps wash off pollens and disinfect the skin tions are left untreated. Occasionally, urticaria or angioedema and ear canals, preventing secondary infections from may occur. Concurrent gastrointestinal (GI) signs (e.g., fre- recurring. quent bowel movements, vomiting, diarrhea, flatulence) are 2. Symptomatic therapy (itch control) is variably effective for reported in 20% to 30% of cases. food allergy: a. An integrated flea control program should be instituted Top Differentials to prevent flea bites from aggravating the pruritus. Differentials include atopy, scabies, Malassezia dermatitis, and b. Topical therapy with antimicrobial shampoos and anti- bacterial pyoderma, as well as other hypersensitivities (flea itch conditioners, and sprays (i.e., those containing bite, contact), parasites (cheyletiellosis, pediculosis), and fol- oatmeal, pramoxine, antihistamines, or glucocorti- liculitis (dermatophyte, Demodex). coids) applied every 2 to 7 days or as needed may help reduce clinical symptoms. c. Systemic antihistamine therapy reduces clinical symp- Diagnosis toms in many cases (see Table 7-1). One- to 2-week- 1. Perianal dermatitis with or without recurrent otitis is the long therapeutic trials with different antihistamines most common and unique feature of food allergy. However, may be required to determine which is most effective. food allergy can manifest in many patterns and should be d. Oral essential fatty acid supplements (180 mg EPA/ suspected for atypical pruritic patients, including those 40 mg/kg) help control pruritus in 20% to 50% of with recurrent infections without pruritus. cases, but 8 to 12 weeks of therapy may be needed 2. Dermatohistopathology (nondiagnostic): varying degrees before beneficial effects are seen. Also, a synergistic of superficial perivascular dermatitis. Mononuclear cells or effect is often noted when essential fatty acid supple- neutrophils may predominate. Eosinophils may be more ments are administered in combination with glucocor- numerous than in atopy. ticoids or antihistamines. 3. Food allergy testing (intradermal, serologic) (nondiagnos- e. Dextromethorphan, an opioid antagonist, may be a tic): not recommended because test results are unreliable. useful adjunct in managing the licking, chewing, and Some dogs will have positive reactions to storage mite biting behaviors associated with allergic dermatitis antigens, which may be clinically relevant, or that may be in dogs. Dextromethorphan 2 mg/kg PO should be caused by cross-reactivity with other insects. Storage mites administered every 12 hours. A beneficial effect should are ubiquitous, and their clinical significance is currently be seen within 2 weeks. unknown. f. Oclacitinib (Apoquel) may be administered for 1 to 4. Response to elimination diet trial: symptoms improve 2 weeks to reduce the symptoms (itch), but long- within 10 to 12 weeks of initiation of a strict home-cooked term use should be avoided because of an increased (one protein and one carbohydrate source) or commer- risk of adverse events including tumors (18%), pyo- cially prepared restricted diet (novel protein, vegetable derma (12%), otitis (9.9%), vomiting (9.2%), diarrhea protein, or hydrolyzed protein). The diet should not (6%), cystitis (3.5%), anorexia (3.2%), lethargy  Canine Food Hypersensitivity 203 (2.8%), yeast skin infections (2.5%), and pododerma- c. Anecdotal reports suggest that higher doses (10 mg/kg) titis (2.5%). of cyclosporine (Atopica) may be beneficial in reducing g. Systemic glucocorticoid therapy is only variably effec- the allergic immune response and symptoms of food tive (unpredictable minimal to good response) in con- allergy. trolling pruritus caused by food allergy but almost 4. The prognosis is good. In dogs that are poorly controlled, always results in adverse effects ranging from increased owner noncompliance should be ruled out along with risk for MRS infections, mild (PU/PD) to severe development of hypersensitivity to an ingredient in the (immune dysfunction, demodicosis, and calcinosis hypoallergenic diet, secondary infection (caused by bacte- cutis) (see “Atopy” section). ria, Malassezia, dermatophyte), scabies, demodicosis, atopy, – Potent, long-acting injectable steroids are contrain- flea allergy dermatitis, and contact hypersensitivity. dicated for the treatment of allergies because of their comparatively short anti-inflammatory bene- AUTHOR’S NOTE fits (3 weeks) relative to their prolonged metabolic and immunodepressive effects (6–10 weeks). Recent food industry changes have caused an – Injectable short-acting steroids (dexamethasone explosion of products available by prescription or sodium phosphate 0.5–0.8 mg/kg or prednisolone OTC, and the listing is beyond the scope of this text. acetate 0.1–1 mg/kg) are effective at providing Many of the OTC diets are sufficiently restricted relief and may last 2 to 3 weeks if no concurrent and of high enough quality to produce clinical secondary infection occurs. This treatment option benefit when a food-allergic patient is restricted to allows the clinician to more closely control and one of the nonbeef and nondairy products. monitor the patient’s use of steroids compared with Food allergy is responsible for most of the very oral treatments administered by the owner. unusual clinical symptom patterns in dogs with – All dogs treated with long-term steroids (>3 recurrent infection (with or without pruritus). months) should be frequently monitored for liver Poor owner compliance should be expected, disease and UTI. making the long-term management of food-allergic 3. Food allergy treatment: patients difficult and frustrating; repeated lapses in a. Offending dietary allergen(s) should be avoided. A bal- diet result in flare-ups of pruritus and secondary anced home-cooked diet or a commercial hypoaller- infection. genic diet should be provided. b. To identify offending substances to be avoided (chal- lenge phase after food allergy has been confirmed with the dietary trial), one new food item should be added AUTHOR’S NOTE to the hypoallergenic diet every 2 to 4 weeks. If the item The use of long-acting, injectable steroids should is allergenic, clinical symptoms will recur within 7 to be stopped because of their profound impact on 10 days. Note: Some dogs (≈20%) should be fed home- the metabolic and immune systems, as well as cooked diets to remain symptom free. For these dogs, growing concern for the legal liability of the commercial hypoallergenic diets are ineffective, pre- practitioner. sumably because their hypersensitivity relates to a food preservative or dye. Text continued on p. 208 204 CHAPTER 7 Hypersensitivity Disorders Canine Food Hypersensitivity—cont’d Distribution Pattern of Canine Food Hypersensitivity FIGURE 7-46 Canine Food Hypersensitivity. Severe periocular FIGURE 7-47 Canine Food Hypersensitivity. Alopecia, erythema, and dermatitis (alopecia, erythema, and hyperpigmentation) is a common excoriations around the eye and ear. The crusting papular rash is caused finding in allergic dogs. by a secondary superficial pyoderma associated with the allergic disease.  Canine Food Hypersensitivity 205 FIGURE 7-48 Canine Food Hypersensitivity. Close-up of the dog in FIGURE 7-49 Canine Food Hypersensitivity. Close-up of the dog in Figure 7-47. Erythema, alopecia, and papular rash involving the ear Figure 7-47. Alopecia and erythema are seen in the axillary area. Mild pinnae. No infectious otitis is present—only external lesions associated hyperpigmentation and lichenification are caused by a secondary yeast with the underlying allergy. dermatitis. Note the similarity to lesions seen with atopy. FIGURE 7-50 Canine Food Hypersensitivity. Pododermatitis is a FIGURE 7-51 Canine Food Hypersensitivity. Alopecia and erythema common symptom of allergic dermatitis in dogs. Alopecia and with papules and early lichenification on the ventral neck and axillary hyperpigmentation on the dorsal foot are apparent. area, caused by a secondary yeast dermatitis associated with underlying allergic disease. FIGURE 7-52 Canine Food Hypersensitivity. Secondary Malassezia FIGURE 7-53 Canine Food Hypersensitivity. Otitis is an extremely dermatitis caused by underlying allergy, demonstrating the classic common finding in allergic dogs. The erythematous pinna and external alopecic, hyperpigmented, lichenified “elephant skin” dermatitis and canal without secondary infection were caused by primary allergic axillary area of an allergic dog. disease in this patient. 206 CHAPTER 7 Hypersensitivity Disorders Canine Food Hypersensitivity—cont’d FIGURE 7-54 Canine Food Hypersensitivity. Chronic otitis in a food- allergic cocker spaniel. Severe swelling and stenosis of the external ear canal and lichenification of the pinna with erythema and hyperpigmen- tation are chronic changes. FIGURE 7-55 Canine Food Hypersensitivity. Severe allergic otitis with secondary bacterial infection in a cocker spaniel. Lateral ear canal resection without dietary therapy failed to resolve the underlying cause of the chronic otitis. FIGURE 7-56 Canine Food Hypersensitivity. Perianal dermatitis is a FIGURE 7-57 Canine Food Hypersensitivity. Perianal dermatitis in a common finding in food-allergic dogs. Alopecic, hyperpigmented, food-allergic cocker spaniel. lichenified perianal skin is caused by chronic inflammation and pruritus.  Canine Food Hypersensitivity 207 FIGURE 7-58 Canine Food Hypersensitivity. Secondary bacterial FIGURE 7-59 Canine Food Hypersensitivity. Facial dermatitis pyoderma is common in allergic dogs. The moth-eaten hair coat with (alopecia, erythema, and pruritus) is a common finding in allergic dogs. underlying erythematous skin was caused by secondary bacterial infection associated with the underlying allergy. FIGURE 7-60 Canine Food Hypersensitivity. Perianal dermatitis is one of the most consistent and unique features of food allergy. FIGURE 7-61 Canine Food Hypersensitivity. Severe lichenification, hyperpigmentation, and alopecia affecting the perianal area of this food- allergic dog. FIGURE 7-62 Canine Food Hypersensitivity. Facial dermatitis with FIGURE 7-63 Canine Food Hypersensitivity. From a distance, this pruritus is not a unique feature of food allergy and is indistinguishable food-allergic dog appears to have minimal lesions; however, multiple from the facial dermatitis caused by atopy. areas of alopecia and erythema affecting the face, abdomen, and feet are apparent. Note the identical pattern to atopy. 208 CHAPTER 7 Hypersensitivity Disorders Acral Lick Dermatitis (Lick Granuloma) Features 2. One should treat for secondary bacterial infection with long-term systemic antibiotics (minimum 6–8 weeks and Acral lick dermatitis is first noted as excessive, compulsive as long as 4–6 months in some dogs). Antibiotic therapy licking at a focal area on a limb, resulting in a firm, prolifera- should be continued at least 3 to 4 weeks beyond regres- tive, ulcerative, alopecic lesion. Causes of the licking are mul- sion of the lesion. The antibiotic should be selected tifactorial, and although environmental stress (e.g., boredom, according to bacterial culture and sensitivity results. confinement, loneliness, separation anxiety) may be a con- 3. Anecdotal reports suggest good efficacy with combined tributor, other factors are usually more important (Box 7-1). antibiotic, amitriptyline (2 mg/kg q 12 hours) and hydro- This dermatitis is common in dogs, with the highest incidence codone (0.25 mg/kg q 8–12 hours), administered until in middle-aged to older, large-breed dogs, especially Dober- lesions resolve. Then one drug should be discontinued man pinschers, Great Danes, golden retrievers, Labrador every 2 weeks until it can be determined which drug (if retrievers, German shepherds, and boxers. any) may be required for maintenance therapy. The lesion usually begins as a small area of dermatitis that 4. Topical application of analgesic, steroidal, or bad-tasting slowly enlarges because of persistent licking. The affected area medications every 8 to 12 hours may help stop the becomes alopecic, firm, raised, thickened, and plaquelike to licking, but response is unpredictable and often nodular, and it may be eroded or ulcerated. With chronicity, disappointing. extensive fibrosis, hyperpigmentation, and secondary bacterial 5. When no underlying cause can be found, treatment with infection are common. Lesions are usually single but may be behavior-modifying drugs may be beneficial in some multiple, and they most often are found on the dorsal aspect dogs (Table 7-2). Trial treatment periods of up to 5 weeks of the carpus, metacarpus, tarsus, or metatarsus. should be used until the most effective drug is identified. Lifelong treatment is often necessary. Top Differentials 6. Alternative medical treatments such as cold laser therapy Differentials include demodicosis, dermatophyte kerion, or acupuncture have been beneficial in some patients. fungal or bacterial granuloma, and neoplasia. 7. Mechanical barriers such as wire muzzles and bandaging, Elizabethan collars, and side braces may be helpful. Diagnosis 8. Surgical excision is not recommended because postop- erative complications, especially wound dehiscence, are 1. Usually based on history, clinical findings, and ruling out other differentials. 2. Dermatohistopathology: ulcerative and hyperplastic epi- dermis, mild neutrophilic and mononuclear perivascular dermatitis, and varying degrees of dermal fibrosis. 3. Bacterial culture (exudates, biopsy specimen): Staphylo- coccus is often isolated. Mixed gram-positive and gram- TABLE 7-2 Drugs for Psychogenic Dermatoses negative infections are common. in Dogs Drug Dose Treatment and Prognosis Anxiolytics 1. The underlying causes should be identified and corrected Phenobarbital 2–6 mg/kg PO q 12 hours (see Box 7-1). Diazepam 0.2 mg/kg PO q 12 hours Hydroxyzine 2.2 mg/kg PO q 8 hours Tricyclic Antidepressants BOX 7-1 Underlying Causes of Acral Lick Fluoxetine 1 mg/kg PO q 24 hours Dermatitis Amitriptyline 1–3 mg/kg PO q 12 hours Imipramine 2–4 mg/kg PO q 24 hours Hypersensitivity (atopy, food) Clomipramine 1–3 mg/kg PO q 24 hours Fleas Endorphin Blocker Trauma (cut, bruise) Naltrexone 2 mg/kg PO q 24 hours Foreign body reaction Endorphin Substitute Infection (bacterial, fungal) Hydrocodone 0.25 mg/kg PO q 8 hours Demodicosis Topical Products Hypothyroidism Fluocinolone acetonide Neuropathy + flunixin meglumine Osteopathy Deep Heet + bitter apple Arthritis PO, Oral; q, every.  Acral Lick Dermatitis 209 common. Laser ablation may help sterilize the lesion 10. The prognosis is variable. Chronic lesions that are unre- and deaden nerve endings; however, response is highly sponsive or extensively fibrotic and those for which no variable. underlying cause can be found have a poor prognosis for 9. CO2 laser resurfacing for refractory, proliferative, or mul- resolution. Although this disease is rarely life threatening, tidrug resistant infections may be beneficial. its course may be intractable. FIGURE 7-64 Acral Lick Dermatitis. This focal alopecic erosive lesion FIGURE 7-65 Acral Lick Dermatitis. A focal alopecic erosive lesion on the medial aspect of the distal leg is typical of this disease. demonstrating the raised infiltrative nature typical of this disease. FIGURE 7-66 Acral Lick Dermatitis. A focal area of alopecia and FIGURE 7-67 Acral Lick Dermatitis. A focal area of alopecia with tissue thickening on the distal extremity. thickening and minimal erosion. FIGURE 7-68 Acral Lick Dermatitis. A large alopecic lesion FIGURE 7-69 Acral Lick Dermatitis. Same dog as in Figure 7-68. The demonstrating severe swelling and tissue erosion. Alopecia and erosions swollen infiltrative nature of the lesion causes it to protrude from the are the result of persistent licking. surrounding, more normal skin. 210 CHAPTER 7 Hypersensitivity Disorders Acral Lick Dermatitis—cont’d FIGURE 7-70 Acral Lick Dermatitis. Close-up of the lesion in Figure FIGURE 7-71 Acral Lick Dermatitis. A focal area of alopecia with 7-69. Alopecia and the erosive surface of the swollen lesion are apparent. hyperpigmentation and erosion on the foot. FIGURE 7-73 Acral Lick Dermatitis. Severe proliferative lesion demonstrating the thickened tissue associated with the erosive lesion. FIGURE 7-72 Acral Lick Dermatitis. Severe proliferative lesion on the carpus of a dog.  Acral Lick Dermatitis 211 FIGURE 7-74 Acral Lick Dermatitis. Laser treatment (CO2 laser) of a FIGURE 7-75 Acral Lick Dermatitis. Laser treatment (CO2 laser) of chronic lesion. a chronic lesion. Because of the large extent of the lesion, multiple treatments maybe needed. FIGURE 7-76 Acral Lick Dermatitis. Post laser treatment (CO2 laser). Note the proliferative tissue has been removed to allow healing. 212 CHAPTER 7 Hypersensitivity Disorders Flea Allergy Dermatitis (Flea Bite Hypersensitivity) Features as the result of chronic exposure and genetic drift of the flea. Flea allergy dermatitis is a common skin disease in dogs and 2. Topical or systemic insect growth regulators (lufenuron, cats sensitized to flea saliva proteins through repeated and pyriproxifen, methoprene) may be effective alone or used intermittent flea bites. Symptoms are usually seasonal (warm in combination with adulticidal therapy. weather months and in the fall) in temperate zones and are 3. Affected and all in-contact dogs and cats should be treated often nonseasonal in subtropical and tropical areas. Fall is with adulticidal (orals, sprays, spot-on solutions, or dips) often the most severe season according to when the first cold every 7 to 30 days, as instructed on the label. Products that snap occurs. contain fipronil, imidacloprid, dinotefuran, indoxacard, and selamectin are efficacious when administered every 2 to 4 Dogs weeks. Oral treatment options seem to be especially effective Distribution typically involves the caudodorsal lumbosacral and include fluralaner (Bravecto) administered every 30 to area, dorsal tail head, caudomedial thighs, abdomen, and 60 days and afoxolaner (Nexgard), sarolaner (Simparica), flanks. Lesions include pruritic, papular, crusting eruptions and spinosad (Comfortis, Trifexis) administered every 30 with secondary erythema, seborrhea, alopecia, excoriations, days. In heavily flea-infested environments, fleas may con- pyoderma, hyperpigmentation, and lichenification. tinue to be found on the animals despite topical flea control. 4. In severe cases, affected animals should be administered Cats nitenpyram, minimum dose 1 mg/kg PO, every 24 to 48 hours for 4 weeks; the environment should also be treated Cats do not have a pattern unique to flea allergy dermatitis. (see #7). Alternatively, the application of a 0.2% pyrethrin Patients commonly present with pruritic miliary dermatitis water-based spray every 1 to 2 days as a repellent may with secondary excoriations, crusting, and alopecia of the provide substantial protection for socially active dogs. neck, dorsal lumbosacral area, caudomedial thighs, and 5. Flea-allergic animals should be treated prophylactically with ventral abdomen. Other symptoms include symmetrical alo- nitenpyram (minimum dose, 1 mg/kg PO) on any day that pecia secondary to excessive grooming and eosinophilic gran- an encounter is planned with other potentially flea-infested uloma complex lesions. animals (e.g., a visit to the groomer, veterinary hospital, park, another household with animals). No more than one Top Differentials treatment with nitenpyram should be administered per day. Differentials include atopy, food hypersensitivity, other ecto- 6. In heavily flea-infested environments, areas where pets parasites (scabies, cheyletiellosis, pediculosis, demodicosis), spend the most time should be treated. Indoor premises superficial pyoderma, dermatophytosis, demodicosis, and should be treated with an insecticide and an insect growth Malassezia dermatitis. regulator (e.g., methoprene, pyriproxyfen). The outdoor environment should be treated with insecticidal or bio- Diagnosis logic products designed for such use. 7. Flea control therapy should be continued from spring until 1. Lumbar dermatitis in the dog is the most consistent and first snowfall in temperate areas and year round in warm unique feature of flea allergy dermatitis. Flea allergy should climates. Year-round flea infestations can be perpetuated be highly suspected in any cat with skin disease. indoors and on wildlife despite extreme cold outdoors. 2. Visualization of fleas or flea excreta on the body: may be 8. Symptomatic therapy (itch control): difficult with flea-allergic animals as flea-allergic animals a. Topical therapy with antimicrobial shampoos and anti- are very effective at removing fleas through grooming. itch conditioners, and sprays (i.e., those containing 3. Allergy testing (intradermal, serologic): positive skin test oatmeal, pramoxine, antihistamines, or glucocorti- reaction to flea antigen or positive serum immunoglobulin coids) applied every 2 to 7 days or as needed may help (Ig)E antiflea antibody titer is highly suggestive, but false- reduce clinical symptoms. negative results are possible. b. Systemic antihistamine therapy reduces clinical symp- 4. Dermatohistopathology (nondiagnostic): varying degrees toms in many cases (see Table 7-1). of superficial or deep perivascular to interstitial dermatitis, c. Oclacitinib (Apoquel) may be administered for 1 to 2 with eosinophils often predominating. weeks to reduce the symptoms (itch), but long-term use 5. Response to aggressive flea control (nitenpyram adminis- should be avoided because of an increased risk of adverse tered every other day for 1 month): symptoms resolve. events including tumors (18%), pyoderma (12%), otitis (9.9%), vomiting (9.2%), diarrhea (6%), cystitis (3.5%), Treatment and Prognosis anorexia (3.2%), lethargy (2.8%), yeast skin infections 1. An integrated flea management program (insect growth (2.5%), and pododermatitis (2.5%). regulator combined with an adulticide combined with d. Systemic glucocorticoid therapy is often effective environmental treatments) is essential because of the (75%) in controlling pruritus but almost always results progressive tolerance of the flea to available adulticides. in adverse effects ranging from increased risk for Over time, specific active ingredients typically lose efficacy MRS infections, mild (PU/PD) to severe (immune  Flea Allergy Dermatitis 213 dysfunction, demodicosis, and calcinosis cutis). It is a to 48 hours for 3 to 7 days. The dosage should be therapeutic option if the allergy season is very short but tapered to the lowest possible dose and frequency. may result in unacceptable adverse effects, especially if – All dogs treated with long-term steroids (>3 used over the long term. months) should be frequently monitored for liver – Potent, long-acting injectable steroids are contrain- disease and UTI. dicated for the treatment of allergies because of 9. The prognosis is good if strict flea control is practiced. Fleas their comparatively short anti-inflammatory bene- may infest other in-contact animals and humans. They may fits (3 weeks) relative to their prolonged metabolic carry bloodborne diseases in a manner similar to ticks. and immunodepressive effects (6–10 weeks). AUTHOR’S NOTE – Injectable short-acting steroids (dexamethasone sodium phosphate 0.5–0.8 mg/kg or prednisolone The use of long-acting, injectable steroids should acetate 0.1–1 mg/kg) are effective at providing be stopped because of their profound impact relief and may last 2 to 3 weeks if no concurrent on the metabolic and immune systems, as well secondary infection occurs. This treatment option as growing concern for the legal liability of the allows the clinician to more closely control and practitioner. monitor the patient’s use of steroids compared with Any dog with lumbar dermatitis or any cat oral treatments administered by the owner. with skin disease should be highly suspected of – Temaril-P (trimeprazine and prednisolone combi- having flea allergy dermatitis, even if the patient nation) is a unique drug that provides significant has been treated with seemingly good flea control antipruritic effects at a relatively lower dose of the therapies. prednisolone. One tablet per 10 to 20 kg should be A nitenpyram trial (every other day for 1 month) administered every 24 to 48 hours. The dosage is an efficient and cost-effective way to convince the should be tapered to the lowest possible dose and owner and yourself of the role of flea allergy in a frequency. pruritic patient. – Prednisone 0.25 to 1 mg/kg (or methylprednisolone 0.2–0.8 mg/kg) PO should be administered every 24 Text continued on p. 218 Distribution Pattern of Flea Allergy Dermatitis 214 CHAPTER 7 Hypersensitivity Disorders Flea Allergy Dermatitis—cont’d FIGURE 7-77 Flea Allergy Dermatitis. Moth-eaten alopecia on the FIGURE 7-78 Flea Allergy Dermatitis. Lumbar dermatitis caused by a lumbar and caudal flank area is typical of flea allergy dermatitis in dogs. flea allergy. Most lesions in flea-allergic patients are caudal to the rib cage. FIGURE 7-80 Flea Allergy Dermatitis. Hot spots (pyotraumatic dermatitis) are usually caused by exposure to fleas. Severe, erythematous, moist, erosive dermatitis with expanding papular rash is typical of pyotraumatic dermatitis. FIGURE 7-79 Flea Allergy Dermatitis. Severe lumbar and tail head dermatitis in a flea-allergic dog. FIGURE 7-81 Flea Allergy Dermatitis. Allergic alopecia on the caudal FIGURE 7-82 Flea Allergy Dermatitis. Eosinophilic plaque on the face flanks of a flea-allergic cat. of a flea-allergic cat. Severe, erythematous, erosive dermatitis with crust formation developed acutely after flea exposure.  Flea Allergy Dermatitis 215 FIGURE 7-83 Flea Allergy Dermatitis. Preauricular dermatitis with a FIGURE 7-84 Flea Allergy Dermatitis. Allergic alopecia on the focal eosinophilic plaque in a flea-allergic cat. abdomen of a flea-allergic cat. Lack of apparent cutaneous inflammation often leads to the misdiagnosis of psychogenic alopecia. Note the small eosinophilic plaque on the proximal region of the right inner thigh. FIGURE 7-85 Flea Allergy Dermatitis. An eosinophilic plaque caused FIGURE 7-86 Flea Allergy Dermatitis. An eosinophilic plaque caused by flea allergy dermatitis in a cat. Alopecic, moist, erosive dermatitis is by flea allergy dermatitis on the distal limb of the cat. apparent. FIGURE 7-87 Flea Allergy Dermatitis. Eosinophilic granulomas FIGURE 7-88 Flea Allergy Dermatitis. An oral eosinophilic granuloma affecting the chin and upper lips of this cat were caused by an underlying in a flea-allergic cat. Feline oral eosinophilic granulomas are often a flea allergy. The skin is alopecic, erythematous, and swollen, as is typical manifestation of flea allergy. of an eosinophilic granuloma. 216 CHAPTER 7 Hypersensitivity Disorders Flea Allergy Dermatitis—cont’d FIGURE 7-90 Flea Allergy Dermatitis. Hairs and flea dirt collected with a flea comb and placed on paper. FIGURE 7-89 Flea Allergy Dermatitis. Same cat as in Figure 7-88. Digested blood passed as feces forms a dark coagulate typical of “flea dirt.” FIGURE 7-91 Flea Allergy Dermatitis. An intradermal allergy test FIGURE 7-92 Flea Allergy Dermatitis. Characteristic lumbar dermatitis result using flea antigen (right) was positive in this flea-allergic dog. is demonstrated by visible alopecia covering the back half of this dog’s Histamine (left) and saline (middle) were used as positive and negative body. controls.  Flea Allergy Dermatitis 217 FIGURE 7-93 Flea Allergy Dermatitis. A focal lesion on the lumbar FIGURE 7-94 Flea Allergy Dermatitis. Close-up of the dog in Figure region of a dog. Note the similarity to a hot spot (pyotraumatic dermatitis) 7-93. The focal lesion clearly demonstrates erythema and mild crusting. but without the moist exudate. FIGURE 7-95 Flea Allergy Dermatitis. Severe erythema with a moist exudate starting to form, which likely will lead to the formation of a hot spot (pyotraumatic dermatitis). 218 CHAPTER 7 Hypersensitivity Disorders Feline Atopy Features b. Systemic antihistamines may reduce clinical symptoms in 40% to 70% of atopic cats. A beneficial effect should Feline atopy is a type 1 hypersensitivity reaction to environ- occur within 1 to 2 weeks of initiation of therapy mental antigens (allergens); a genetic or heritable predisposi- (Table 7-3). tion is suspected. It is uncommon in cats and is less common c. Oral essential fatty acid supplements may help control than flea hypersensitivity and food allergy. pruritus in 20% to 50% of cats. A beneficial effect Cats do not have a pattern unique to atopy. The primary should occur within 8 to 12 weeks of initiation of symptom is pruritus (chewing, scratching, excessive groom- therapy. A synergistic effect may be seen when essential ing), which may be seasonal or nonseasonal, depending on fatty acid supplements are administered in combina- the offending allergens. This pruritus may concentrate around tion with other therapies. the head, neck, and ears, or it may involve other areas such as d. Systemic glucocorticoids control pruritus but almost the ventral abdomen, caudal thighs, forelegs, or lateral thorax. always result in adverse effects ranging from mild to Self-trauma usually results in alopecia that can be bilaterally severe and may increase risk for MRS infections. Effec- symmetrical. Remaining hairs are broken off and do not tive therapies include the following: epilate easily. The alopecic skin may appear otherwise normal – Prednisolone 2 mg/kg PO q 24 hours until pruritus or may be secondarily excoriated. Miliary dermatitis, cerumi- and lesions resolve (≈2–8 weeks); then 2 mg/kg PO nous otitis externa, and eosinophilic granuloma complex q 48 hours for 2 to 4 weeks, tapered down to the lesions are common. With chronicity, secondary pyoderma or lowest possible alternate-day dosage if long-term peripheral lymphadenomegaly may develop. Atopy may be maintenance therapy is needed linked with chronic bronchitis or asthma in some cats. Many – Dexamethasone 2 mg PO q 1 to 3 days to reduce cats with self-induced excoriations have concurrent secondary pruritus and then tapered to the lowest possible bacterial infections. frequency required 3. Allergy treatment (immune modulation): Top Differentials a. The caregiver can reduce exposure to offending aller- gens by removing them from the environment, if pos- Differentials include flea allergy dermatitis, other hypersensi- sible. HEPA air and charcoal filters can be used to tivities (food, mosquito bite), dermatophytosis, ectoparasites reduce pollens, molds, and dust in the home. For (cheyletiellosis, ear mites, feline scabies, demodicosis), psy- house dust mite–sensitive cats, household treatments chogenic alopecia, pemphigus, and cutaneous lymphoma. of carpets, mattresses, and upholstery with the acari- cide benzyl benzoate once a month for approximately Diagnosis 3 months and then every 3 months thereafter may 1. Rule out other differentials, especially flea allergy derma- effectively eliminate house dust mites from the envi- titis, dermatophytosis, mites, and food allergy. ronment. Old cat beds should be discarded because 2. Allergy testing (intradermal, serologic): allergy testing can they may accumulate house dust mite antigens. Dehu- be highly variable according to the method used. Positive midifying the house to below 40% relative humidity reactions to grass, tree, mold, weed, insect, dander, feathers, decreases house dust mite, mold, and flea antigen or indoor environmental allergens are seen. False-negative loads. To achieve this, high-efficiency dehumidifiers reactions are common. False-positive reactions can occur. that are capable of pulling several liters of water per Systemic fluorescein administration may improve the diag- day from the air are required. nostic accuracy of intradermal skin testing in cats. b. Cyclosporine (Atopica) 7.5 mg/kg PO can be adminis- 3. Dermatohistopathology (nondiagnostic): variably mild to tered every 24 hours until beneficial effects are seen marked perivascular or diffuse inflammation with lym- phocytes, mast cell hyperplasia, and eosinophils. Epider- mal hyperplasia, spongiosis, erosions, ulcers, and TABLE 7-3 Antihistamine Therapy for Cats* serocellular crusts may be present. Antihistamine Dose Treatment and Prognosis Chlorpheniramine 2–4 mg/cat PO q 12–24 hours Amitriptyline 5–10 mg/cat PO q 12–24 hours 1. Infection prevention: any secondary pyoderma or otitis should be treated with appropriate therapies for 2 to 4 Clemastine 0.68 mg/cat PO q 12 hours weeks. Cyproheptadine 2 mg/cat PO q 12 hours 2. Symptomatic therapy (itch control): pruritus can be con- trolled with antihistamines, essential fatty acid supple- Hydroxyzine 5–10 mg/cat PO q 8–12 hours ments, and glucocorticoids. Diphenhydramine 2–4 mg/kg PO q 12 hours a. An integrated flea control program should be instituted Fexofenadine 30-60 mg/cat PO q 24 hours to prevent flea bites from aggravating the pruritus.  Feline Atopy 219 (≈4–6 weeks). Then try to taper down dosage fre- AUTHOR’S NOTE quency to every 48 to 72 hours. Many cats can be maintained on every-72-hour dosing, making this Although extremely common, long-acting inject- therapy extremely cost effective. Cats should be feline able steroids should be used only as a last resort leukemia virus (FeLV) and feline immunodeficiency because life-threatening cardiac effects have been virus (FIV) negative. The risk of toxoplasmosis infec- identified in up to 11% of cats, as have other better tion is a matter of concern; however; this risk seems to known medical risks, including diabetes and UTI. be very low as of this writing. Cyclosporine (Atopica) is extremely well toler- c. Immunotherapy (allergy vaccine) is indicated if ated in cats and has very few adverse effects. It is medical therapy is ineffective or unacceptable to the interesting to note that cyclosporine seems to be owner or if it results in undesirable adverse effects. able to control most of the immunologic causes of Overall, 50% to 70% of atopic cats show favorable feline dermatitis with the exception of flea allergy responses to immunotherapy. Clinical improvement is (when fleas are not being treated), dermatophyto- usually noted within 3 to 8 months but can take up to sis, and mites. 1 year in some cats. 4. The prognosis is good for most cats, but successful man- agement usually requires lifelong therapy. FIGURE 7-96 Feline Atopy. Allergic alopecia on the abdomen of a cat. FIGURE 7-97 Feline Atopy. Multifocal alopecia on the flank and lumbar Similar alopecic lesions with excessive grooming can be caused by flea area of a cat with atopy. allergy, food allergy, and mite infestations. FIGURE 7-98 Feline Atopy. Focal erythema with slight alopecia on the FIGURE 7-99 Feline Atopy. Allergic alopecia affecting almost the entire flank of an atopic cat. This lesion was a mild eosinophilic plaque. front limb of an atopic cat. Note the general absence of dermatitis (apparent inflammation), which often leads to the misdiagnosis of psychogenic alopecia. 220 CHAPTER 7 Hypersensitivity Disorders Feline Atopy—cont’d FIGURE 7-100 Feline Atopy. Small focal crusts typical of miliary FIGURE 7-101 Feline Atopy. Alopecia and early eosinophilic plaques dermatitis in an atopic cat. on the abdomen of an allergic cat. FIGURE 7-102 Feline Atopy. This intradermal allergy test result FIGURE 7-103 Feline Atopy. Close-up of the intradermal allergy test in demonstrates several positive reactions. Note the subtlety of the Figure 7-102. Positive reactions appear as erythematous macules. reactions, which is typical of allergy tests in cats. FIGURE 7-104 Feline Atopy. Generalized moth-eaten alopecia on the FIGURE 7-105 Feline Atopy. Allergic alopecia on the abdomen of an trunk of an atopic cat. atopic cat. Cutaneous inflammation can be mild and easily overlooked.  Feline Atopy 221 FIGURE 7-106 Feline Atopy. Allergic periocular dermatitis in an atopic cat. FIGURE 7-107 Feline Atopy. Positive intradermal allergy skin test result in a cat. Note the extreme subtly of the positive reactions compared with reactive canine tests. FIGURE 7-109 Feline Atopy. Normal perimammary tissue in a cat with atopy. Note cats with autoimmune skin disease often have severe perimammary dermatitis. FIGURE 7-108 Feline Atopy. Alopecia on the lumbar area of an atopic cat. Note that lumbar dermatitis is not pathognomonic for flea allergy dermatitis in cats. 222 CHAPTER 7 Hypersensitivity Disorders Feline Food Hypersensitivity Features c. Oral essential fatty acid supplements may help control pruritus in 20% to 50% of cats. A beneficial effect Feline food hypersensitivity is an adverse reaction to a food or should occur within 8 to 12 weeks of initiation of food additive. It can occur at any age. It is uncommon in therapy. A synergistic effect may be seen when essential cats—less common than flea hypersensitivity—but may be fatty acid supplements are administered in combina- more common than feline atopy. tion with other therapies. Cats do not have a unique pattern of food allergy. Feline d. Systemic glucocorticoids control pruritus but almost food hypersensitivity is characterized by nonseasonal pruritus always result in adverse effects ranging from mild to that may or may not respond to glucocorticoid therapy. Dis- severe and may increase risk for MRS infections. Effec- tribution of the pruritus may be localized to the head and tive therapies include the following: neck, or it may be generalized and involve the trunk, ventrum, – Prednisolone 2 mg/kg PO q 24 hours until pruritus and limbs. Skin lesions are variable and may include alopecia, and lesions resolve (≈2–8 weeks); then 2 mg/kg PO erythema, miliary dermatitis, eosinophilic granuloma complex q 48 hours for 2 to 4 weeks, tapered down to the lesions, excoriations, crusts, and scales. Malassezia or cerumi- lowest possible alternate-day dosage if long-term nous otitis externa may be seen. Concurrent GI symptoms maintenance therapy is needed (e.g., diarrhea, vomiting) may be reported. – Dexamethasone, 2 mg PO q 1 to 3 days to reduce the pruritus and then tapered to the lowest possible Top Differentials frequency required Differentials include flea allergy dermatitis, atopy, mosquito 3. Allergy treatment: bite hypersensitivity, dermatophytosis, ectoparasites (cheyleti- a. Offending dietary allergen(s) should be avoided. A bal- ellosis, ear mites, feline scabies, demodicosis), psychogenic anced home-cooked diet or a commercially prepared alopecia and pemphigus, and cutaneous lymphoma. hypoallergenic diet should be provided. b. Cyclosporine (Atopica) 7.5 mg/kg PO can be adminis- Diagnosis tered every 24 hours until beneficial effects are seen (≈4–6 weeks). Then try to taper down dosage fre- 1. Rule out other differentials, especially flea allergy derma- quency to every 48 to 72 hours. Many cats can be titis, dermatophytosis, mites, and atopy. maintained on every-72-hour dosing, making this 2. Dermatohistopathology (nondiagnostic)