Better Dermatology Appointment Compliance 10 Common Characteristics ofHighly Successful Practices Keith A Hnilica DVM, MS, DACVD

Who am I to decide: I am a veterinary dermatologist currently enrolled in an MBA program. During the last year, I have had the wonderful opportunity to visit dozens of great practices (through the Novartis LEAD and Pfizer’s Partners for Success programs). During these visits, I was able to learn many lessons from successful practices. In addition, I have listened to many practice managers, sales reps, and business people much smarter than myself. What I have learned is that there are common behaviors that are found in most of the truly great clinics: THIS is THAT list.

Immutable Lessons from the Road:

1. All staff members are motivated to solve specific client problems with practice specific protocols formulated to implement the “Best in Class” treatment options.

2. The mission statement includes a commitment to the highest quality of practice (not the cheapest).

3. Staff rounds are conducted to educate everyone in the clinic on the most common diseases and the practice’s protocols treatment.

4. All staff provides consistent client education and treatment recommendations: the same message from the front to the back of the practice.

5. The doctors are removed from all treatment cost discussions: decisions are made based on medical appropriateness not negotiated based on cost.

6. Follow up counts.

7. Technicians are used to their full potential: great knowledge, tremendous ability, and enthusiasm produce an effective patient advocate that functions like a physician’s assistant.

8. The receptions are recognized as the store front window of the practice.

9. Great emphasis is placed on disease prevention not just finding and fixing problems.

10. All employees play and hug the patients. Practice Considerations

Some of the simplest issues can have dramatic impact. The following are a few estimations of your client’s experience. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Sight:

Initial impression: 1 2 3 4 5 wow

Educational materials: 1 2 3 4 5 impressive

Clutter: 1 2 3 4 5 contained

Cleanliness: 1 2 3 4 5 immaculate

Sounds:

Noise level: 1 2 3 4 5 quite

Phones: 1 2 3 4 5 absent

Ability to eavesdrop: 1 2 3 4 5 limited

Smell:

Animal odor: 1 2 3 4 5 none

Fragrance level: 1 2 3 4 5 pleasant

Confidence Inspiring:

Attire: 1 2 3 4 5 professional

Lobby: 1 2 3 4 5 impressive

Exam rooms: 1 2 3 4 5 functional

KA Hnilica DVM, MS, DACVD www.itchnot.com Dermatology Fact Sheet

What are the Infections and Why are they there?

The 10 most common skin patterns in dogs with skin disease are: Folliculitis, Pododermatits, Otits, Yeast/Malassezia dermatitis Pruritus, Non-pruritic alopecia, Autoimmune disease, keratinization defects, lump/bumps/draining tracts, Weirdopathies.

All secondary infections of the skin and ears are triggered by allergies or endocrine disease causing changes in the normal structure and function of the skin (glands, thickness, turnover time, secretions, acidity, saltiness, dryness, IgA levels, temperature, etc)

The infectious causes of folliculitis are bacterial pyoderma, dermatophyte, and demodicosis.

Folliculitis looks like a mosquito bite rash (papular rash) with hair loss and crusting.

Severe folliculitis may result in ruptured follicles (furunculosis) and cellulitis.

Chin pyoderma and chin acne in dogs are usually caused by ingrown hairs.

Yeast dermatitis is caused by malassezia sp. and triggered by allergies or endocrine disease.

Yeast dermatitis looks like thickened lichenified skin - elephant skin in large plaques and smells like Fritos.

Yeast infections are usually in moist areas - arm pits, ventral neck, interdigital, inguinal skin and ears.

Eye margin dermatitis (blepharitis) is usually caused by yeast dermatitis.

Simple uninfected allergy patients will typically be below a 5 on the 0 - 10 itch scale.

Secondary infections cause the itch level to increase above 5 on the 0 - 10 itch scale.

Dogs with a 10 on the 0 - 10 itch scale often have yeast, scabies, or insect/flea infections.

Skin infection treatment duration is based on the typical epidermal turn-over time which is 21-28 days.

Most good skin antibiotics start with a “c” - cephalexin, Clavamoc, clindamycin, cefpodoxime.

The most common risk factor leading to MRStaph (multi-drug resistant Staph) is the use of fluoroquinolone antibiotics.

Cephalexin administered with ketoconazole makes dogs vomit.

Ketoconazole is the longest lasting anti-fungal drug in the glands and skin.

Terbinafine is the best anti-fungal drug for dermatophytes. Microsporum canis is usually from cats: M. gypsum and Trichophyton mentagrophytes are from soil or rodents.

General body pruritus is caused by atopy, food allergy or scabies.

Allergies are associated with increased IL-4 which increases Th2 lymphocytes and thus increases in IgE, mast cells, eosinophils and the chemicals these cells release.

The immune response is predominantly either Th1 cells (IgG, IgM, Neutrophils, macrophages) or Th2 cells (IgE, mast cells, eosinophils).

Foot licking is usually associated by atopy.

Lumbar dermatitis is usually caused by insect (mosquito) and flea allergy.

Perianal dermatitis and butt scooting are usually associated by food allergy.

Hot spots (pyotraumatic dermatitis) are caused by insect bites (fleas or mosquitoes usually).

50% of allergic dogs do not sleep through the night and itch.

Acral lick granulomas are usually caused by a neuropathy and not allergy.

Atopy should be treated with pollen avoidance, antihistamines, Cytopoint and Allergy vaccine.

Food allergic dogs should avoid all beef, dairy and chicken.

Cytopoint blocks only IL-31 while Apoquel blocks IL-31 and IL-2, TNF, EPO and more.

Steroids and Apoquel are the only drugs that can cause Demodicosis.

Apoquel has a 10% tumor risk in dogs.

Isoxazolines are the safest and best class of parasiticides and are the treatment of choice for Demodicosis and Insect allergies.

Sarcoptiform mites have round bodies and stubby legs and are often contagious and have a 21 day life cycle.

The only disease that causes a pinal-pedal reflex is scabies.

Lumps Bumps and Draining tracts are caused by infections, neoplasia, or immune mediated granulomas.

The best way to diagnose the cause of Lumps Bumps and Draining tracts is to perform cytology, DNA PCR or cultures, and biopsies.

Common infectious causes of Lumps Bumps and Draining tracts are staph, demodex, nocardia, mycobacterium, actinomyces, and deep fungal infections.

Big dogs usually get hypothyroidism (20%) and small dogs get Cushing’s (50%).

Melatonin is the only safe treatment for Cushing’s and follicular dysplasia/arrest. Otitis is usually triggered by allergies or endocrine disease and NOT swimming or conformation.

Ear cleaning and flushes should be used in the clinic and not sent home.

Otits should be treated with multimodal medications either every 1-3 days with short acting meds or every 1-2 weeks with long-acting medications.

Most allergic otitis starts as a sterile inflamed ear and over time developed a staph or yeast infection with a waxy exudate.

A purulent ear exudate (pus) is associated with mixed infection with Pseudomonas, proteus, staph and possible yeast. Pseudomonas otitis is caused by recurrent-episodic otitis when the treatment is started and stoped multiple times.

Otitis should be prevented by controlling the triggering primary disease and multimodal medications used every 3-7 days with short acting meds or every 2-3 weeks with long-acting medications.

Long-term otitis prevention does not lead to Pseudomonas otitis.

Ototoxicity (hearing loss or neuro signs) are extremely rare (1 in 10,000) and happen regardless of the tympanic membrane being intact or ruptured. Thus the treatment for otitis is the same regardless of the ear-drum status.

Autoimmune skin disease (Pemphigus and Lupus) usually (90%) cause lesions on the nasal planet, ear pinna, and foot pads (PPP) due to the velcro like proteins that hold the skin together being targeted by the immune system.

Autoimmune diseases are diagnoses based on clinical pattern, acantholytic cells on cytology, and skin biopsies.

Skin diseases associated with oral erosions or ulcers are BAD and usually caused by Pemphigus vulgarism, Lupus, drug reactions, or Cutaneous lymphoma (mycosis fungoides)

The treatment for autoimmune skin diseases consist of normalizing the skin and glands and immune modulating and suppressing therapies: baths, Vit A, Omega 3 FA, doxy/tetracycline, niacinamide, UV light, tacrolimus, topical steroids, Atopica, Apoquel, oral steroids, azathiaprine, chlorambucil, lomustine, dapsone, mycophenolate mofetil, steroid IV infusions.

Follicular casts are always associated with keratinization defects like sebaceous adenitis and Cocker seborrhea and Vitamin A is the best safest therapy.

Vitamin A therapy helps normalize the skin and ear glands and the epidermal turn-over time.

The most common skin tumors are sebaceous adenomas, follicular cysts, skin tags (acrocodons) apocrine cysts, lipoma, fibroma, hemangioma, melanocytoma, and mast cell tumors.

The 5 most common causes of round-cell tumors are lymphoma, mast cell, melanoma, histiocytoma, and TVT.

Acantholytic associated with pemphigus and look like round-cell tumor cytology but are from surface samples and not fine-needle aspirates. 4 EDITION

SMALL ANIMAL DERMATOLOGY A COLOR ATLAS AND THERAPEUTIC GUIDE

K EITH A. HNILICA , DVM, MS, MBA , DACVD The Itch Clinic Allergy, Dermatology, Otology Knoxville, Tennessee www.TheItchClinic.com www.itchnot.com

ADAM P. PATTERSON , DVM, DACVD Chief of Dermatology College of Veterinary Medicine & Biological Sciences Texas A&M University College Station, Texas

CHAPTER | | 1

Differential Diagnoses

■ Essential Questions ■ Papules ■ Ten Clinical Patterns ■ Miliary Dermatitis ■ What Are the Infections? ■ Plaques ■ W h y A r e T h e y T h e r e ? ■ Follicular Casts ■ D i ff erentials Based on Body Region ■ Epidermal Collarettes ■ Diseases Primarily Limited to the Face ■ Comedones ■ Diseases of Nasal Depigmentation ■ Lichenifi cation ■ Diseases with Oral Lesions ■ I n fl ammatory or Pruritic Alopecic Diseases ■ Ear Margin Dermatitis ■ Noninfl ammatory or Nonpruritic Alopecic Diseases ■ Nasodigital Hyperkeratosis ■ Cellulitis and Draining Lesions ■ Interdigital Pododermatitis ■ Nodular Diseases ■ Diseases of the Claw ■ Pruritic Diseases ■ Diseases of the Footpads ■ Seborrheic Diseases ■ D i ff erentials Based on Primary and Secondary ■ Hyperpigmentation Lesions ■ Hypopigmentation ■ Vesicular and Pustular Diseases ■ Breed Predispositions to Select Skin Conditions in ■ Erosive and Ulcerative Diseases Dog and Cats

Almost all dermatology patients have a primary or underlying After the origin of a patient’ s dermatosis is known, it is a simple disease that causes secondary infections. These infections must matter of therapeutic follow-through to resolve the problem. be eliminated and prevented but will recur rapidly unless the Recognition of basic patterns allows a practical approach primary disease is identifi ed and controlled. to most of the common skin diseases. Most skin cases seen in a veterinary practice can be success- fully managed if two essential questions can be answered: Ten Clinical Patterns (1) What are the secondary infections? and (2) Why are these What are the secondary infections? (always secondary) secondary infections there? 1. Folliculitis: Folliculitis is the most common “pattern” of Essential Questions disease mimicking other patterns. However, it is common for it to be concurrent with other disease patterns (e.g., 1. What are the infections? yeast dermatitis). The major differentials to consider for fol- ■ Folliculitis liculitis are superfi cial staphylococcal pyoderma or bacterial – Pyoderma folliculitis, demodicosis, and dermatophytosis. Pyoderma – Demodex is the mostly likely cause in the dog, with demodicosis a – Dermatophyte close second if not a concurrent factor. Juvenile-onset ■ Pododermatitis demodicosis may affect the patient in a symmetric fashion. – Bacterial A good rule of thumb is to consider all dermatologic – Yeast patients to have folliculitis until proven otherwise and ■ Otitis then search for predisposing underlying diseases (e.g., – Bacterial allergy, endocrinopathy, cornifi cation disorder or defect). – Yeast 2. Pododermatitis: Always scrape the dorsal pedal surface ■ Malassezia yeast dermatitis when it is alopecic because both demodicosis and allergic 2. Why are they there? skin disease may cause pododermatitis; steroids are not ■ Allergies appropriate for the former. Hemorrhagic bullae are mani- – Atopy festations of deep pyoderma; therefore, they should be – Food allergy cultured. A lesion on the paw pads is usually an indica- – Scabies tion to biopsy. P3 digit amputation is rarely needed ■ Endocrinopathy to make a diagnosis of symmetric lupoid onychodystro- – Hypothyroidism phy because the history with typical clinical fi ndings is – Cushing ’s suffi cient for a fi rm tentative diagnosis. 1 2 CHAPTER 1 ■ Differential Diagnoses

■ Single paw : trauma, foreign body, infection (e.g., bac- exfoliative dermatitis, plaques, nodules, depigmentation, teria, yeast), localized demodicosis, cutaneous horn, + /- lesions affecting nonhaired skin, consider cutaneous neoplasia, arteriovenous pedal fi stula T-cell lymphoma (CTCL) and biopsy. ■ Multiple paws: infection (e.g., bacteria, yeast, hook- Distribution patterns and differential diagnoses for worms, distemper, leishmaniasis), generalized demo- pruritus: dicosis, allergic skin disease, split paw pad disease, ■ Dorsum : pediculosis, cheyletiellosis, fl ea allergy der- palmar or plantar interdigital comedones and follicu- matitis (FAD), + /- AD in terriers lar cysts, autoimmune- or immune-mediated dermato- ■ Face, ears, paws, axillae, inguinum, and perineum: cuta- sis (e.g., pemphigus foliaceus, vasculitis, symmetric neous adverse food reaction (CAFR), AD lupoid onychodystrophy or onychomadesis), dermato- ■ Pinnal margins, elbows, hocks, and ventral trunk : sarcop- myositis, metabolic dermatosis (e.g., hepatocutaneous tic mange syndrome, zinc-responsive dermatosis, nasodigital ■ Rear or perineum : anal sacculitis, trichuriasis, FAD, hyperkeratosis), and sometimes neoplasia (e.g., cuta- CAFR, AD, psychocutaneous disorder neous lymphoma, subungual small cell carcinoma or ■ Sparsely haired body regions: allergic contact dermatitis melanoma in heavily pigmented dogs) (rare) 3. Otitis: Because the ear is just an extension of the skin, 6. Nonpruritic alopecia (endocrine): Always exclude fol- a good dermatologic examination of the skin may pro- liculitis when confronted with alopecia (especially when vide clues (other “patterns”) about potential causes of other typical lesions are present) because it is the most ear disease. Resolution of otitis externa is achievable if common reason for it and often a resultant feature of primary causes are identifi ed and managed. Similarly, other diseases within the pattern of “nonpruritic sym- otic cytology should be used on every case to initially metrical alopecia.” Consider an endocrinopathy as a determine the infection(s) present, as well as monitor cause of recurring infection when pruritus resolves with response to therapy during reexaminations. By and large, infection control. Exclude castration- or neuter-responsive correctly administered topical antimicrobial treatments dermatosis, hypothyroidism, and hyperadrenocorticism (volume and duration) are more effective for infected before considering alopecia X. Many alopecic conditions canals than systemic therapy. Rigid palpable canals (ossi- have breed predilections, so consult a text for a listing of fi ed) are usually beyond medical resolution and would these associations. be better removed (total ear canal ablation and bulla ■ Endocrinopathy : hypothyroidism, hyperadrenocorti- osteotomy). cism, sex hormone–related dermatoses Is the pinna or canal affected? ■ Follicular dysplasias: color dilution alopecia, black hair ■ Pinnae: trauma, aural hematoma, sarcoptic mange, fl y follicular alopecia, canine recurrent fl ank alopecia bite or strike hypersensitivity, allergic skin or ear (CRFA), breed-related follicular alopecia disease, ear margin seborrhea or dermatosis, vasculitis ■ Hair cycle arrest : Alopecia X, CRFA, defl uxions, canine or other autoimmune dermatoses, neoplasia pattern alopecia or baldness ■ Otitis externa : facets and differentials (chart below) 7. Autoimmune- or immune-mediated skin disease: Hepa- 4. Malassezia yeast dermatitis: The pattern is characteristic tocutaneous syndrome, zinc-responsive dermatosis, der- of Malassezia yeast, but any chronic pruritic skin disorder matomyositis, eosinophilic dermatitis with edema (Well’ s may resemble it, including folliculitis (superfi cial pyo- syndrome), mucocutaneous pyoderma, and some forms derma, demodicosis, dermatophytosis), ectoparasitism, of dermatophytosis may mimic this pattern of disease. and allergic skin disease. Yeast dermatitis is often over- Skin biopsy is useful to correctly diagnose the disease so looked as a cause of pruritic skin disease. The author ’s a reasonable prognosis can be offered to the client and a favorite way to fi nd yeast is with the use of acetate tape treatment plan tailored to the patient can be developed cytology. Just the fi nding of a single yeast from rep- (some autoimmune- or immune-mediated diseases do resentative lesions is signifi cant (yeast hypersensitivity?) not require systemic glucocorticoids). and warrants topical or systemic (or both) treatment based Distribution patterns and differential diagnoses for on the severity of pruritus. However, if cytology is “nega- autoimmune- or immune-mediated dermatoses: tive” for yeast when confronted with this pattern, assume ■ Face, pinnae, or nasal planum: pemphigus foliaceus, they are there, treat accordingly, and search for predispos- pemphigus erythematosus, discoid lupus erythemato- ing underlying diseases (e.g., allergy, endocrinopathy, cor- sus, vasculitis, uveodermatologic syndrome, drug nifi cation defect). reaction, vitiligo Why are they there? (the key to preventing relapse of ■ Oral cavity + /- other body areas: pemphigus vulgaris, infections) subepidermal blistering dermatosis, systemic lupus 5. Pruritus (allergies, mites, fl eas): When confronted with erythematosus, vasculitis, erythema multiforme, drug pruritus, always exclude infection and parasites fi rst! reaction Many times pruritus is reassessed after controlling for ■ Pads and elsewhere on the body : basically any of the microorganisms before determining the “next step.” aforementioned diseases Atopic dermatitis (AD) is a clinical diagnosis based on 8. Keratinization defects: Exclude secondary reasons for a the exclusion of other causes of pruritus; “allergy tests” scaling disorder before considering primary ones. Some do not diagnosis it. If you see pruritic erythroderma, hereditary cornifi cation defects are tardive, not being So, What Is the Solution? 3

recognized until the dog is 2 to 5 years old. Follicular What Are the Infections? casts are typical of a cornifi cation defect. ■ Primary scaling disorders : primary seborrhea (usually For every dermatitis case every time you evaluate the patient, of spaniels and terriers), ichthyosis, Schnauzer ask yourself, “What are the infections?” comedo syndrome, ear margin seborrhea or dermato- Unless you have microscopic vision, answering this ques- sis, nasal parakeratosis of Labrador retrievers, tail tion will require the use of cytology. Unfortunately, most gland hyperplasia, nasodigital hyperkeratosis general practices do not routinely perform skin and ear cytol- ■ Secondary scaling disorders : environmental, nutritional, ogy for dermatitis; instead they rely on the doctor’ s best guess. folliculitis, Malassezia dermatitis or otitis, ectoparasit- Sometimes this can be successful (even a broken clock is ism, leishmaniasis, allergic skin disease, endocrinopa- correct twice a day); however, a more precise method is avail- thy, follicular dysplasias, hair cycle arrest, sebaceous able. Use of diarrhea and the fecal examination as a compari- adenitis, autoimmune- or immune-mediated derma- son and as a model for improvement works well because both toses, metabolic dermatoses (e.g., hepatocutaneous skin cytology and fecal examinations involve the use of a syndrome, zinc-responsive dermatosis, vitamin A– microscope, can easily identify the type of infection, and can responsive dermatosis), neoplasia be performed by trained technical staff. 9. Lumps, bumps, and draining tracts: Wear gloves when ■ So why does your clinic perform fecal examinations? confronted with this pattern of disease because some ■ When is a fecal examination performed (before the doc- infectious agents are transmissible to people. Infectious tor ’s examination or during)? etiologies must be excluded when these lesions are ■ Who performs the fecal examination? present. Acral lick dermatitis (lick granuloma) is a form ■ Does the clinic charge for the fecal examination? of deep pyoderma; tissue culture (deep dermis with epi- The answers to these questions should be the same for skin dermis removed) is helpful. cytology: The minimum dermatologic database (skin scrap- ■ Infectious infl ammatory: bacterial, atypical bacterial, ings, impression smears, tape preps, and otic swabs). mycobacterial, fungal, oomycete, parasite The practical solution for determining the best method ■ Noninfectious infl ammatory: cyst, xanthoma, hygroma, by which to answer the question, “What are the infections?” cutaneous histiocytosis, pyogranuloma or granuloma is to implement a minimum database infection screening syndrome, sterile nodular panniculitis, perianal procedure to be performed by the technician before the veteri- fi stula narian examines the patient. Every dermatology patient should ■ Neoplasia : benign, malignant undergo otic cytology, skin cytology (an impression smear or ■ Mineral deposition: calcinosis circumscripta, calcinosis a tape prep), and a skin scrape at every examination (initially cutis and at every recheck visit). The three-slide technique (Figure 10. Weirdopathies: Commonly, this pattern is an unusual 1-1 ) can be performed easily and interpreted by a technician manifestation of an aforementioned “pattern” or is before the doctor completes an evaluation, which is exactly formed by several overlapping ones. After “folliculitis” how diarrhea and fecal examinations are handled in most has been excluded, skin biopsy (± culture) is usually clinics. Moving the cytologic evaluation to the beginning of warranted when confronted with an “oddopathy.” Several the dermatology appointment and thereby empowering the skin biopsies of representative lesions will help better technical staff to accomplish the evaluation optimizes the categorize the disease process—infectious, allergic, autoimmune- or immune-mediated, endocrine or fol- licular abnormality, cornifi cation defect, congenital, or neoplasia—assuming the proper technique is used and the pathologist is provided a detailed history with clinical fi ndings. Ideally, a dermatopathologist should be sought. Calcinosis cutis often appears as an oddopathy. A patient with an oddopathy might be best examined by a dermatologist.

So, What Is the Solution? A vast majority of dogs with allergy or endocrine disease have or will have a secondary bacterial or yeast infection. Yeast dermatitis is the most commonly missed diagnosis in general practice dermatology. Bacterial pyoderma is often identifi ed but is usually mistreated with too low doses of antibiotics administered for too short a time. Otitis is now recognized and treated better than it was in years past; however, treatment Skin scrape Skin cytology Ear cytology for otitis that is based on actual documented organism types (cocci/yeast) and relative counts on follow-up evaluations is a rare FIGURE 1-1 The Three-Slide Technique. Skin scrapes, cutaneous occurrence. cytology, and otic swabs. 4 CHAPTER 1 ■ Differential Diagnoses

dermatology appointment and provides essential information AUTHOR ’ S NOTE in the most effi cient manner. When an owner brings a pet into the clinic for a small Could clinical dermatology really be this easy? hairless spot, it would be appropriate to question the necessity Yes. Unfortunately, most of us were taught derma- for an otic cytology even when there is no sign of otitis and tology from the perspective of a NASA engineer when the hairless spot is the problem. However, the three- who is determined to address and eliminate every slide technique is most helpful in these exact types of cases. If possible scenario regardless of how rare its occur- focal pruritus occurs in a dog and the patient has a secondary rence. Based on any standard of logic, statistics, or otitis (which the technician identifi ed during the infection common sense, the most likely disease should be screen), the veterinarian should more aggressively discuss this addressed fi rst. It is illogical to perform diagnostic and work up the patient for possible allergy. If the patient did tests or therapeutic trials for rare or unlikely dis- not have otitis, the pruritus could be minimized in the hope eases as part of the initial dermatologic workup, yet that it was a short-term problem that is likely to self-resolve. this is exactly how most veterinarians are taught to Similarly, there is no excuse for mistreating a patient who diagnose atopy: “a diagnosis of exclusion.” If a has demodicosis. Lesions caused by demodicosis can look patient is seasonally foot licking, the most likely identical to folliculitis lesions caused by bacterial pyoderma diagnosis is atopy. and dermatophytosis. Clinical appearance is not an acceptable criterion for ruling in or ruling out demodicosis. When the technician performs a skin scrape as part of the infection screen, demodicosis can be identifi ed and treated easily and accurately. Optimizing owner understanding and compliance: Much of the problem that veterinarians face when treating an aller- Why Are They There? gic patient is the pet owner ’s lack of understanding and ability to adhere to long-term prevention and treatment Infections are always secondary to a primary disease; however, protocols. There is great information available regarding all too often, the patient is not evaluated or treated for the cognitive psychology that can optimize the human primary disease for three main reasons: (1) only the secondary factors that limit successful outcomes. Here are some infections are treated over and over again, (2) the nature of suggestions: the allergy is confusing, and (3) cheap steroids that have 1. Have the pet owner complete a patient history form. delayed repercussions are accessible. This allows the client to focus on the details of the skin Why are the infections there? This question should be disease and symptoms and primes the client to listen asked and answered for every dermatology patient if successful better and accept the diagnosis and information that outcomes are to be achieved. will be provided by the veterinarian. Most dermatology patients have allergy or endocrine 2. Try to avoid a rambling, stream-of-consciousness disease. Through signalment, a good patient history, and rec- approach to the discussion of allergy. Many of us have ognition of unique patterns of lesions, a prioritized differen- an “automatic” allergy spiel that only confuses the tial list can be formulated quickly. client and dose not focus on the specifi c problems of By knowing the most unique and frequent symptoms asso- the individual patient. ciated with each allergic disease, an astute clinician can deter- 3. Use simplifi ed charts and handouts to organize the mine the most likely allergy with approximately 85% accuracy; diagnosis and treatment phases of the allergy educa- this rate rivals many other diagnostic testing results for some tion discussion. These focus the educational message of the most common assays. and improve the understanding of the client. Addition- For example, a dog that is foot licking is likely atopic. If the ally, draw and write on these handouts and give owner reports a seasonal pattern to the podopruritus, then you them to the client to review later. This increases accep- have a reasonably accurate diagnosis—EASY. tance of the message and improves compliance with Atopy: foot licking; seasonal; when pruritus fi rst started, typi- therapy. cally between 1 and 3 years of age 4. Organize the diagnostic testing and treatment options Food allergy: perianal dermatitis (erythema, alopecia, licheni- into groups based on the severity of the patient and fi cation); gastrointestinal disease; younger than 1 year old response to previous treatments (mild patients need a, or older than 5 years of age when started; German breeds b, c; moderately severe patients need d, e, f; and severe Flea allergy: dermatitis predominantly affecting the lumbar patients need g, h, i). region (caudal to the last rib) 5. Assess the risk to the patient and family members Scabies: positive pinnal-pedal refl ex (ear scratch test) for methicillin-resistant Staphylococcus aureus (MRS) Hypothyroidism: large-breed dog that is disproportionately infections. Families at risk for MRS contagion and zoo- obese for food intake and has a poor hair coat with areas nosis must be willing to accept aggressive medical of alopecia over areas of friction management to reduce the risk. All three species of Cushing ’s disease: patient with a long history of steroid MRS can be transmitted from dogs to people and from abuse, or small-breed dog with polyphagia, polyuria (PU), people to dogs. If family members have a history of and polydipsia (PD), and symmetrical alopecia MRS, consider aggressively monitoring the patient with Why Are They There? 5 cultures because dogs can acquire MRS from humans. need the most aggressive diagnostic workup and treat- If family members are immunosuppressed, monitor ments achievable to protect the entire family from con- the patient for MRS pseudintermedius and MRS tagion and zoonosis. In these families, avoid the use of schleiferi , which can be a source of contagious infection steroids or fl uoroquinolone antibiotics, which can to at-risk, immunosuppressed people. These patients increase the risk of MRS.

Text continued on p. 12 Dermatology 101: A Pattern Approach to Clinical Dermatology What are the infections? and Why are they there? Keith A. Hnilica DVM, MS, DACVD University of Tennessee, Knoxville Tn

Almost all dermatology patients have a primary/underlying disease which causes secondary infections. The infections must be eliminated and prevented, but will recur unless the primary disease is identified and controlled.

Most skin cases seen in practice can be successfully managed if these 2 question can be answered. Once the etiology of a patients dermatosis is known, it is a simple matter of therapeutic followthrough to resolve the problem.

The recognition of the basic patterns allows a practical approach to most of the common skin diseases.

10 Clinical Patterns What are the infections? (Always secondary) 1. Folliculitis 2. Pododermatitis 3. Otitis 4. Yeast Dermatitis

Why are they there? (The key to preventing relapse of infections) 5. Pruritus 6. Nonpruritic Alopecia (endocrine) 7. Autoimmune Skin Disease 8. Keratinization Defects

9. Lumps, Bumps, and Draining Tracts 10. Weirdopathies ______Case example: 2 year old male Labrador that has seasonal pruritus (foot licking) and a moth- eaten hair coat. What are the Infections? Why are they there? “ Folliculitis Allergies

pyoderm a, demodex, dermatophyte “ Atopy

“ Pododermatitis “ Food allergy

bacterial, yeast “ Scabies “ Otitis bacterial, yeast Endocrinopathy

“ Yeast dermatitis “ Hypothyroidism

“ Cushing’s Skin Scrapes 31 require biopsy for identifi cation of mites within the hair fol- a 10× objective). A search of the entire slide ensures that if only licles. Hair plucks from an area of lesional skin may be used one or two mites are present (as is typical of scabies infection), to help fi nd follicular mites. This technique is especially the user will likely fi nd them. It may be helpful to lower the helpful in areas or situations when a skin scrape would be microscope condenser; this provides greater contrast to the diffi cult: around the eyes or excited puppies. mites, thereby enhancing their visibility. (One must be sure to Regardless of the collection technique used, the entire slide raise the condenser before looking for cells or bacteria on stained should be searched for mites with the use of low power (usually slides.)

BOX 2-1 What Are the Infections?

For every dermatitis case, every time you evaluate the and interpreted by a technician before the doctor com- patient, ask yourself, “What are the infections?” pletes an evaluation, which is exactly how diarrhea cases Using diarrhea and the microscopic fecal examination and fecal examinations are handled in most clinics. as a comparison works well because both skin cytology and fecal examinations involve the use of a microscope, can easily identify the type of infection, and can be per- formed by trained technical staff . So why does your clinic perform fecal examinations? When is a fecal examination performed (before the doctor’ s examination)? Who per- formed the fecal examination? Does the clinic charge for the fecal examination? The answers to these questions should be the same for skin cytology (skin scrapings, impression smears, tape preps, and otic swabs). The practical solution for determining the best method by which to answer the question, “What are the infec- tions?” is to implement a minimum database “infection screening” procedure to be performed by the technician before the veterinarian examines the patient. Every der- matology patient should undergo otic cytology, skin Skin scrape Skin cytology Ear cytology cytology (an impression smear or a tape prep), and a skin (cocci/yeast) scrape at every examination (initially and at every recheck FIGURE 2-1 The Three-Slide Technique. Skin scrapes, cutaneous visit). This three-slide technique can be performed easily cytology, and otic swabs.

TABLE 2-1 Diagnosing Common Cutaneous Parasites Mite Diagnostic Test Accuracy Other Tests Additional Tests Demodex canis Deep scrape High Biopsies may be needed with extremely thickened lesions Demodex cati Deep scrape High Demodex gatoi Superfi cial scrape Low Lime sulfur dip trial, response to Mites may be treatment diffi cult to fi nd Sarcoptes Superfi cial scrape Low (only 20%) Response to treatment Pinnal-pedal refl ex (80%) Otodectes Otic mineral oil prep, superfi cial High scrape Cheyletiella Flea comb, tape prep, superfi cial Moderate Vacuum collection techniques are Possible identifi cation of scrape, vacuum preferred by some veterinarians mites by fecal fl otation Lice Tape prep (usually grossly visible) High Notoedres cati Superfi cial scrape High Trombicula Targeted scrape on focal lesion Moderate WHAT IS MAKING MY DOG SO ITCHY?

Evaluation Form A thorough history can help us find the source of your dog’s itching more quickly. Please answer the following questions to help guide the diagnostic process. Date Pet owner name Name of dog Age Breed Weight

Physical Evaluation Please check any that describe your dog and circle problem areas on the drawing. ❑ Hair loss ❑ Foul odor ❑ Inflammation or redness ❑ Itching/Scratching CIRCLE PROBLEM AREAS (Itching, hair loss, lesions, etc.) ❑ Otitis (ear infections) ❑ Licking/Chewing ❑ Skin lesions (sores) ❑ Changes in skin (reddish brown stains, discolorations and/or areas that are thick and leathery) ❑ Other • Has your dog ever had ear problems? ❑ Yes ❑ No • Does your dog have any chronic gastrointestinal signs like diarrhea or vomiting? ❑ Yes ❑ No

Severity Evaluation On a scale of 0 to 10 rank the severity of your dog’s symptoms.

SEVERITY OF CONDITION OVERALL 0 1 2 3 4 5 6 7 8 9 10 No symptoms Severe SEVERITY OF SKIN LESIONS 0 1 2 3 4 5 6 7 8 9 10 No lesions Severe SEVERITY OF SCRATCHING/LICKING/CHEWING 0 1 2 3 4 5 6 7 8 9 10 No signs Severe

Onset and Seasonality Evaluation • Is this the first time your dog has experienced these symptoms? ❑ Yes ❑ No – If no, at what age did the symptoms first occur? ❑ <1 yr ❑ 1-3 yrs ❑ 4-7 yrs ❑ 7+ yrs – If no, has it occurred around the same time of year each time? ❑ Yes ❑ No – If no, approximate time of year symptoms occur. • How long have the current symptoms been going on? • Did the itch start gradually and over time become worse? ❑ Yes ❑ No • Did the itch come on suddenly without warning? ❑ Yes ❑ No • Was there a “rash” first or itching first? Or simultaneous? ❑ Rash first ❑ Itch first ❑ Simultaneous

Parasite Control • Is your dog on a flea/heartworm preventative? ❑ Yes ❑ No – If yes, what product(s)? • What months do you administer the preventative? • When was the last time you administered the parasite control?

Five Question Approach to Dermatology

1. Are they Itchy?

a. No i. Is there hair loss? 1. Big dogs – hypothyroidism 2. Small dogs Cushing’s 3. Blue or Grey - Color dilution alopecia

ii. Planum/Pinnae/Pads = pemphigus/Lupus

iii. Lumps/Bumps/Draining Tracts 1. infection – bacterial, fungal, parasitic 2. neoplasia- Round cell tumors (L/M/M/H) 3. sterile

iv. Keratinization defects = Vit A def, Sebaceous Adenitis, dysplasia

b. Yes – ask Q 2-5

2. Are most of the symptoms on the front half or back-half of the body? 1. Front-half = Atopy 2. Back-half = Insect or food

3. Do they lick their feet? 1. Yes = 90% Atopy

4. Is there a crusting rash? a. Rash with red papules or crusts = folliculitis i. Bacterial Infection – MRSA Risk? ii. Demodex iii. Dermatophyte

b. Lichenification/Leathery-Elephant skin – yeast infection

5. Do they stink? a. Fritos/Beer – yeast b. Rot – bacterial

6. Are the ears infected? a. Yes = must have Atopy/Food Allergy or Endocrine Dz The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

Patient’s Name: ______Age: Breed: Reason for Visit: Diet: Chronic: 1 2 3 4 5 6 7 8 9 10

Itch: 1 2 3 4 5 6 7 8 9 10

Odor : 1 2 3 4 5 6 7 8 9 10

Skin: 1 2 3 4 5 6 7 8 9 10

Lichen: 1 2 3 4 5 6 7 8 9 10

Crusts: 1 2 3 4 5 6 7 8 9 10

Rash: 1 2 3 4 5 6 7 8 9 10

Ears: 1 2 3 4 5 6 7 8 9 10

Feet: 1 2 3 4 5 6 7 8 9 10

Lumbar: 1 2 3 4 5 6 7 8 9 10

GI: 1 2 3 4 5 6 7 8 9 10

Sleeping at Night: Yes No Separation/Thunder Anxiety: Yes No Nodules: Yes No

The Itch Clinic 4 locations in East Tennessee (800) 621-1370 www.itchnot.com TheItchClinic.com The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

Cytology Results: Skin yeast cocci pollen A-cells

Ears yeast cocci rods

Scrape negative mites: ______

Secondary Infections:

Pyoderma: 1 2 3 4 5 6 7 8 9 10

Demodex: 1 2 3 4 5 6 7 8 9 10

Yeast: 1 2 3 4 5 6 7 8 9 10

Otitis: 1 2 3 4 5 6 7 8 9 10

Primary Disease:

Atopy: 1 2 3 4 5 6 7 8 9 10

Food Allergy: 1 2 3 4 5 6 7 8 9 10

Scabies: 1 2 3 4 5 6 7 8 9 10

Insect/Flea: 1 2 3 4 5 6 7 8 9 10

Hypothyroidism: 1 2 3 4 5 6 7 8 9 10

Cushing’s: 1 2 3 4 5 6 7 8 9 10

Lupus/PF: 1 2 3 4 5 6 7 8 9 10

MRSA/MRSP: 1 2 3 4 5 6 7 8 9 10

Dermatophyte: 1 2 3 4 5 6 7 8 9 10

Diagnosis: Treatment: Next Step:

The Itch Clinic 4 locations in East Tennessee (800) 621-1370 www.itchnot.com TheItchClinic.com The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

ALLERGY PREVENTION

1. POLLEN ALLERGIES – remove pollens BATHE every 3-7 days with a disinfecting shampoo to wash off pollens and kill bacteria and yeast. After shampoo apply a OATMEAL conditioner (Torb-D) to restore the epidermal barrier. Apply the disinfecting Torb-D lotion to red itchy spots in-between the baths to prevent infection. Treat the EARS with prevention therapy after every bath (warmed LETK or EpiOtic Flush) WIPE the feet, chin, and face folds with baby wipes at bedtime. Always wipe in the direction of hair growth to remove any ingrown hairs. 2. FOOD ALLERGENS REMOVE ALL BEEF, DAIRY, CHICKEN in the food and treats forever. (READ THE INGREDIENT LIST!!) Select Lamb, Rabbit, Duck, lean Pork or FISH/SALMON diet (see email list) OTC diets like Wellness Simple, Canidae, Natural Balance, Blue Basics, Natural Planet, Merrick, and Zignature work well. (email Food list available)

3. INSECTS ALLERGIES PLEASE make sure ALL pets are treated with a NEW generation (nonBeef/nonChicken) Flavor Tabs: Sentinel or Interceptor (old formula) milbemycin - heart-worm and intestinal parasite control SIMPARICA or BRAVECTO every 30 days to prevent mites, chiggers, mosquitoes, fleas, and ticks. Revolution Plus or Bravecto every 30 days for cats.

4. BLOCK HISTAMINE: Antihistamines help reduce the skin irritation and have few side effects. In the MORNING (and up to every 12 hours for severe itching) give ______generic Zyrtec, Allegra, or Claritin At BEDTIME (and up to 3 times each day for severe itching) give ______generic Benadryl (25mg).

5. PROMOTE SKIN AND GLAND HEALTH Essential Fatty Acid (EPA) (fish, flax, SALMON, krill oil) every day for allergies, Skin health, joint health, and general improved aging (1000mg EPA per 25 lbs weight). Vitamin A daily to prevent “Old Dog Warts” skin tumors and improve gland health (2,000 IU per 25 lbs). Melatonin for hair growth and rejuvenate geriatric conditions and behaviors (5mg or 10mg every 12 hours). Human Probiotic daily to prevent tear staining or for puppies to prevent allergies.

The Itch Clinic 3 locations in East Tennessee (800) 621-1370 www.TheItchClinic.com The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

TREATING ATOPY (ENVIRONMENTAL ALLERGIES) CAN BE VERY SUCCESSFUL BUT DOES INVOLVE WORK AND LONG-TERM TREATMENT.

1. ALLERGY PREVENTION THERAPY REMOVE POLLEN WITH FREQUENT BATHS AND WIPES AVOID FOOD ALLERGENS WITH A RESTRICTED DIET – NO BEEF, DAIRY, CHICKEN PREVENT INSECTS WITH MONTHLY SIMPARICA or BRAVECTO BLOCK HISTAMINE WITH DAILY GENERIC ANTIHISTAMINES PROMOTE SKIN/ GLAND HEALTH WITH OMEGA 3 FATTY ACID and VITAMIN A

2. AGGRESSIVE TREATMENT OPTIONS

A. STEROIDS MOST SIDE EFFECTS ON THE LIVER AND OTHER ORGANS MRSTAPH RISK AND URINARY INFECTIONS

B. APOQUEL – 80% EFFECTIVE IN 3 DAYS but NO CURE 10% RISK OF TUMORS, PNEUMONIA, DEMODEX MITES PLEASE READ THE COMPLETE LABEL MOSTSIDE EFFECTS

TREATMENT FOR POLLEN ALLERGIES 40 lb DOG

C. ATOPICA – 80% EFFECTIVE IN 6 WEEKS $80-160/MO NO ADVERSE EFFECTS EXCEPT RARE GI UPSET 5% ------

---- D. ALLERGY SKIN TESTING AND VACCINE $39/MO

--- 85% EFFECTIVE IN 4-6 WEEKS 60% CURE AFTER 2 YEARS $300 ALLERGY TEST 1% SIDE EFFECTS S A F E F A S

-- --

-- E. MONOCLONAL ANTIBODY THERAPY INJECTION (AMAT/CYTOPOINT)

-- 90% EFFECTIVE IN 48 HOURS REPEATED EVERY 2-3-6 MONTH $80/INJ

Injection stings but otherwise NO SIDE EFFECTS ------

The Itch Clinic 3 locations in East Tennessee (800) 621-1370 www.TheItchClinic.com DAILYITCHREPORTCARD

PATIENT:______DATE:______

DAY 1 0 1 2 3 4 5 6 7 8 9 10

DAY 2 0 1 2 3 4 5 6 7 8 9 10

DAY 3 0 1 2 3 4 5 6 7 8 9 10

DAY 4 0 1 2 3 4 5 6 7 8 9 10

DAY 5 0 1 2 3 4 5 6 7 8 9 10

DAY 6 0 1 2 3 4 5 6 7 8 9 10

DAY 7 0 1 2 3 4 5 6 7 8 9 10

DAY 8 0 1 2 3 4 5 6 7 8 9 10

DAY 9 0 1 2 3 4 5 6 7 8 9 10

DAY 10 0 1 2 3 4 5 6 7 8 9 10

DAY 11 0 1 2 3 4 5 6 7 8 9 10

DAY 12 0 1 2 3 4 5 6 7 8 9 10

DAY 13 0 1 2 3 4 5 6 7 8 9 10

DAY 14 0 1 2 3 4 5 6 7 8 9 10

DAY 15 0 1 2 3 4 5 6 7 8 9 10 DAILYITCHREPORTCARD

PATIENT:______DATE:______

DAY 16 0 1 2 3 4 5 6 7 8 9 10

DAY 17 0 1 2 3 4 5 6 7 8 9 10

DAY 18 0 1 2 3 4 5 6 7 8 9 10

DAY 19 0 1 2 3 4 5 6 7 8 9 10

DAY 20 0 1 2 3 4 5 6 7 8 9 10

DAY 21 0 1 2 3 4 5 6 7 8 9 10

DAY 22 0 1 2 3 4 5 6 7 8 9 10

DAY 23 0 1 2 3 4 5 6 7 8 9 10

DAY 24 0 1 2 3 4 5 6 7 8 9 10

DAY 25 0 1 2 3 4 5 6 7 8 9 10

DAY 26 0 1 2 3 4 5 6 7 8 9 10

DAY 27 0 1 2 3 4 5 6 7 8 9 10

DAY 28 0 1 2 3 4 5 6 7 8 9 10

DAY 29 0 1 2 3 4 5 6 7 8 9 10

DAY 30 0 1 2 3 4 5 6 7 8 9 10

Dr Icthy Pharmacy Dr Itchy’ s Medica l Tool box

Dr. Keith A Hnilica DVM, MS,ACVD, MBA

TheItchClinic.com 246 CHAPTER 8 ■ Autoimmune and Immune-Mediated Skin Disorders

Pemphigus Foliaceus—cont’d

TABLE 8-1 Immunosuppressive Therapies for Autoimmune and Immune-Mediated Skin Disease D r u g — S p e c i e s I n d u c t i o n D o s a g e M a i n t e n a n c e D o s a g e To p i c a l T h e r a p y Steroids (hydrocortisone, Applied every 12 hours Taper to lowest ef ective dose dexamethasone, triamcinolone, f uocinolone, betamethasone, mometasone, and so on) Tacrolimus Applied every 12 hours Taper to lowest ef ective dose Conservative Oral Treatments with Very Few Adverse Ef ects 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: 500 mg of each drug PO D o g s < 10 kg: 250 mg of each drug PO q 8 hours q 12–24 hours D o g s > 10 kg: 250 mg of each drug PO q 12–24 hours Doxycycline and minocycline may be 5–10 mg/kg q 12 hours Then taper to lowest ef ective dose substituted for tetracycline Cyclosporine (Atopica)—dogs and cats 5–12.5 mg/kg PO q 12–24 hours After remission is achieved, taper slowly to lowest ef ective dose R e l i a b l y E f ective Treatments, but Adverse Ef ects 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 Oclacitinib (Apoquel)—dogs and cats 0.4–0.6 mg/kg PO q 12 hours (higher doses may After remission, taper to lowest be needed especially in cats) ef ective dose Azathioprine—dogs only 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 ef ective dose Aggressive Treatments with Few Studies Documenting Ef cacy and Safety Methylprednisolone sodium succinate 1 mg/kg IV over a 3- to 4-hour period q 24 Alternate-day oral glucocorticosteroid (pulse therapy)—dogs and cats hours for 2–3 consecutive days Dexamethasone (pulse therapy)—dogs 1 mg/kg IV once or twice 24 hours apart Alternate-day oral glucocorticosteroid and cats Cyclophosphamide—dogs and cats 50 mg/m 2 (or 1.5 mg/kg) PO q 48 hours 25–50 mg/m 2 (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 ef ective dose Lef unomide 2 mg/kg q 12 hours Then taper to lowest ef ective dose

E PA , E i c o s a p e n t a e n o i c a c i d ; P O , o r a l ; q , e v e r y .

Feline Dermatology and Pruritis 28 CHAPTER 1 ■ Differential Diagnoses

Breed Predispositions to Select Skin Conditions in Dogs and Cats—cont’d Eosinophils Eosinophilic plaques, eosinophilic ulcers, and fat chin syndrome are all associated with numerous etiologies. Eosinophilic granuloma syndrome Cytology of lesions manifestations of eosinophilic dermatitis granulomas, linear indolent

Skin scrapes negative “Allergic” alopecia identified Alopecia with or without apparent cats with allergies or ectoparasites. ood’s lamp ood’s Algorithm for Working Up a Pruritic Cat. Cat. Up a Pruritic Working for Algorithm cutaneous inflammation is common in Feline dermatitis

W Cytology of lesions an important differential. Biopsy the skin lesion to confirm Rule out dermatophytosis Acantholytic cells and neutrophils the nipples and nail beds (paronychia). DTM fungal cultures, trichogram, possible pemphigus. Pemphigus in cats often causes an erosive dermatitis around ficient FIGURE 1-30 FIGURE Dermatophyte is the most common skin infection in cats and is zoonotic, making it Skin scrapes positive appropriate therapy for suf Treat the parasitic infestation with Treat duration to eliminate the parasites. Miliary dermatitis numerous conditions. This is the most common clinical Cytology of lesions presentation in cats and can be caused by Bacteria or Malassezia identified Treat these secondary infections with Treat topical and systemic treatments. Identify hyperthyroidism, allergies, ectoparasites). the primary/underlying disease (e.g., diabetes, Breed Predispositions to Select Skin Conditions in Dogs and Cats 29 disease. abdominal ultrasound Paraneoplastic Biopsy, consider Biopsy, adenocarcinoma or usually present with dermatitis caused by weight loss and other cutaneous lymphoma medical workup and occurs in old cats that evidence of metabolic hepatic and pancreatic can mimic allergies but . in cats except tolerated Atopica; well Very and treats etiologies, flea allergy most allergic cyclosporine Old cat with sudden onset of dermatitis , can Biopsy insect skin tests. flea and food Environmental FIGURE 1-30, cont’d 1-30, FIGURE lack of specific Allergy testing testing of cats is allergies. Allergy poor reactivity of less common than allergies, including hypersensitivity occur in cats but are (complete absence of inflammation). serum testing and the difficult because of the difficult Aggressive flea control confirming this diagnosis. Flea allergy dermatitis is the most the flea population is primary of control on all contact pets to eliminate fleas may not be apparent, aggressive flea common cause of feline dermatitis. Because ferential. Food trial this dif causes of feline 10–12 weeks will ingredient diet for Food allergy is one confirm or eliminate novel protein source of the more common dermatitis. Feeding a in an extreme limited- Young to middle-age cat Young This will identify the etiology or at least be able to suggest an infection (folliculitis or diffuse pyogranulomatous dermatitis), This will identify the etiology or at least be able to suggest an infection (folliculitis diffuse hypersensitivity reaction (eosinophils and mast cells), autoimmune skin disease (interface dermatitis), neoplasia, or psychogen ic any infections. Otodectes and Treatment with Treatment Demodex gatoi , Cheyletiella , and ficult to find on skin dermatitis and be avermectins will kill Cheyletiella but are Lime sulfur dip trial Otodectes can cause scrapes. Weekly dips scrapes. Weekly dif weeks should resolve Ectoparasites such as ineffective for D. gatoi. ineffective with lime sulfur for 4–6 CATS

Cats do NOT have the same patterns or secondary infections that dogs demonstrate.

Bacterial pyoderma can be self resolved in cats with out antibiotics, if the triggering disease is treated and controlled.

Convenia is the best antibiotic for cats.

Yeast dermatitis in cats is rare but usually triggered by metabolic disease (diabetes, hyperthyroidism).

Kittens and shelter cats are the most common source of dermatophytes (Microsporum canis) which is zoonotic.

Herpes virus dermatitis in cats is increasing in frequency and presents as erosive facial dermatitis. DNA PCR testing is the best diagnostic method to confirm the diagnosis.

Skin lesions around the nipples is almost always associated with pemphigus in cats.

Otits is rare in cats and usually caused by tumors or ceruminous gland cysts.

Most older cats will have increased dark waxy exudate which is not a disease or problem and should not be treated as treatment usually makes the situation worse.

Most inflammatory diseases in cats are caused by a lymphocytic, plasmacytic, eosinophilic immune response and Atopica (cyclosporine) is the safest and best long-term treatment option.

The allergy-pattern syndromes in cats are: allergic alopecia, bald belly, eosinophilic plaques, eosinophilic granulomas, indolent ulcers, fat chin syndrome, otitis, allergic asthma, stomatitis.

Any allergy (food, insect, pollen, mold) can trigger any of allergy-patterns in cats.

The infectious causes of the allergy-patterns in cats are: demodex cati, dermatophyte, herpes virus.

The best treatment progression for cats with the allergy-patterns would be to: 1. submit DNA PCR testing for Herpes, Demodex, dermatophyte 2. treat with an isoxazoline parasiticide to rule out insect allergy 3. start Atopica (cyclosporine) therapy for 1 month 4. consider skin biopsies and blood work 5. consider a home cooked food trial with pork or beef as the base protein 6. consider steroid therapy (oral or at-home injectable) every 3 days 7. consider allergy skin testing and allergy vaccine therapy

Injectable Depomedrol and Vetalog cause diabetes and heart failure in 20% of treated cats.

Cats with sudden onset of the allergy-pattern syndromes over the age of 10 years often have paraneoplastic syndrome with internal carcinoma of the liver, pancreases or lung. Radiographs and abdominal ultrasound are best to identify the source.

THERE WAS MINIMAL EVIDENCE OF INFECTION BASED ON CLINICAL EXAM AND MICROSCOPIC CYTOLOGY

DNA PCR TESTING SAMPLES WERE COLLECTED AND ARCHIVED TO IDENTIFY POSSIBLE HERPES VIRUS, MITES, F UNGAL DERMATOPH YTE INFECTION S

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ALLERGIC DERMATITIS CAN BE CAUSED BY MANY TRIGGERS (INSECTS, POLLENS, MOLDS, FOODS, ETC)

MOST RESPOND WELL BUT A PROGRESSIVE THERAPY TRIAL WILL BE USED EVERY 2 WEEKS TO FIND THE SAFEST M OST EFFECTIVE AND COST E FFE CTIVE TREATMENT PLAN

======

IF POSSIBLE APPLY GENESIS DROPS TO ANY RED ITCHY AREA EVERY 12-24 HOURS AND ALLOW 5 MINUTES BEFORE LICKING

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EVERY 2 WEEKS WE WILL PROGRESS UNTIL SIGNIFICANT BENEFIT IS OBSERVED

S UPER A GGRESS IVE INSECT CONTROL FOR ALL PARASITES

HEARTWORMS, INTESTINAL WORMS, MOSQUITOES, MITES, AND FLEAS

Apply Revolution Plus or Bravecto every 30 days

GIVE 1/2 - 1 TABLET OF CHLORPHENIRAMINE (4MG TABS) EVERY 12-24 HOURS TO CONTROL THE ALLERGIES

GIVE ATOPICA ORALLY EVERY DAY FOR 2-3 WEEKS THEN EVERY OTHER DAY. MIX IN YUMMY FOOD OR GIVE ORALLY WITH A YUMMY CHASER

GIVE ORAL DEX TABLETS OR ORAL LIQUID EVERY DAY FOR 3 DAYS THEN EVERY 2-3 DAYS FOR CONTROL

ORAL AMITRIPTYLINE 10MG EVERY 12 HOURS

GIVE INJECTABLE DEX EVERY 2-3 DAYS FOR LONG-TERM CONTROL AND PREVENTION

ALLERGY SKIN TESTING AND VACCINE THERAPY - GIVE WEEKLY VACCINE

GIVE APOQUEL ORALLY EVERY 12-24 HOURS - DISSOLVE WITH WATER AND ADD TO YUMMY TREAT

HOME COOKED RESTRICTED FOOD TRIAL

GIVE INJECTABLE CYCLOSPORINE EVERY DAY FOR 2 WEEKS THEN EVERY 2-3 DAYS FOR LONG-TERM CONTROL AND PREVENTION

SKIN BIOPSIES TO DIAGNOSIS AUTO-IMMUNE SKIN DISEASE OR CANCER

======Feline Dermatology and Pruritus

Feline pruritus is one of the most common dermatologic problems affecting cats. Mild cases often respond to empiric antipruritic treatments. Severe or chronic cases need a thorough workup to identify and control the primary etiology for long-term success. Since many etiologies can cause the 3 common clinical patterns (alopecia, miliary dermatitis, and eosinophilic granuloma complex) a prioritized differential list should be used to systematically work through the different etiologies. Flea allergy, insect hypersensitivity, Demodicosis, and food allergy are the most common pruritic diseases: however, dermatophytosis and other infectious causes of alopecia and miliary dermatitis should be eliminated.

Clinical Features: Regardless of the underlying cause, cats seem to react with 3 distinct clinical patterns. Alopecia is one of the most common presentations, especially on the abdomen and inner thighs. Often there are no skin lesions just alopecia. Miliary dermatitis and eosinophilic granuloma complex (eosinophilic plaque, linear granuloma, indolent ulcer, oral granuloma) are also common feline dermatologic patterns. Regardless of the clinical pattern, the differential list is similar.

THE NEW ERA: 5 Steps to success WITH OUT steroids

1. Rule out Flea allergy is the most common allergy in cats and most pruritic cats respond to an aggressive flea control trial. Cats commonly present with pruritic miliary dermatitis with secondary excoriations, crusting, and alopecia of the neck, dorsal lumbosacral area, caudomedial thighs and/or ventral abdomen. Other symptoms include symmetrical alopecia secondary to excessive grooming, and eosinophilic granuloma complex lesions. Many cats are extremely effective at removing fleas and flea dirt by grooming making it difficult to prove the existence of a flea infestation. Therefore, all pruritic cats should be treated aggressively for possible flea allergy dermatitis. Capstar administered every other day for 1 month effectively prevents flea feeding and eliminates the pets exposure to flea salivia. If the patient is better after 12-15 every other day doses of Capstar, FLEA exposure and FLEA ALLERGY has been confirmed. 2. Culture for RING WORM: Dermatophyte is the most common infectious skin disease in cats. The most common clinical lesion pattern is miliary dermatitis. Diagnosis is usually based on Wood=s lamp examination and cultures. Since ringworm can mimic so many other diseases, it should be considered and ruled out in all cats with skin lesions. 3. Eliminate Mites: Demodex gatoi may be the more common Demodex species (especially in the Southern states) and causes pruritic symptoms similar to allergic dermatitis. D. gatoi is the short bodied mite that inhabits the superficial skin structures and may be contagious to other cats. Generalized disease is characterized by variably pruritic, multifocal, patchy, regional, or symmetric alopecia with or without erythema, scaling, crusts, macules, and hyperpigmentation. Lesions usually involve the head, neck, limbs, flanks, and/or the ventrum. Ceruminous otitis externa and secondary pyoderma may be present. Notoedres cati is rare. Cheyletiella mites live on hair and fur and are usually fnadableo with tape preps, skin scrapes, flea comb surf examination, or fecal. 4. Consider a food trial if the Patient will comply: Food allergy is a nonseasonal pruritic dermatitis that may respond to steroids. The distribution of the pruritus and lesions may be localized to the head and neck, or it may be generalized and involve the trunk, ventrum, and limbs. Skin lesions are variable and may include alopecia, erythema, miliary dermatitis,

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com eosinophilic granuloma complex lesions, excoriations, crusts, and scales. Ceruminous otitis externa is often present. Concurrent gastrointestinal symptoms may be present. 5. Cyclosporine Therapy controls almost all other allergies or other caused of immune mediated dermatosis in cats. Insect hypersensitivity (Mosquitoes, moth, cockroach, ants, etc) is possibly the second most common cause of allergy in cats. Atopy symptoms may be seasonal or non- seasonal depending on the offending allergens. The pruritus may occur on the head, neck, and ears, or it may be in other areas such as the ventral abdomen, caudal thighs, forelegs, and/or the lateral thorax. Pemphigus is usually a nonpruritic disease with lesions that include superficial erosions, crusts, scales, epidermal collarettes, and alopecia. Occasionally, the cat grooms excessively which can be interpreted as pruritus. Lesions around the nail beds and nipples are common. 6. IF OVER 10 years of age at Onset: Paraneoplastic pruritus is a rare disorder but can be observed in older cats with certain tumors. Pruritus associated with systemic and cutaneous tumors is more common in aged cats. Too often, the diagnosis is only made after prolonged attempts to identify more common causes of pruritus.

Diagnostics: Perform appropriate diagnostics based on prioritized differential list.

Trichogram The microscopic examination of the hair (both the root and tip) may provide evidence of pruritus (fractured hair tips) or dermatophytosis (frayed root end).

Many cats are reluctant to groom in front of the pet owner; therefore, owners may not be aware of the pruritus. Fractured hair tips can provide crucial evidence to confirm pruritus and convince the owner to proceed with diagnostic testing and treatment.

Fungal Dermatophytosis is rarely pruritic; however, cats with miliary lesions may culture groom excessively.

Flea This should be one of the first diagnostic tests employed. Combing

The identification of fleas or flea dirt will confirm this common cause of feline skin disease.

The flea comb material may also be used for microscopic identification of other ectoparasites (Cheyletiella, ticks, and other mites)

Cytology The identification of bacterial (folliculitis), yeast, or acantholytic cells (pemphigus) will help guide additional diagnostics and treatments.

Eosinophils are commonly found regardless of the primary etiology.

Skin Scrapes The identification of Demodex (common), Cheyletiella, and Notoedres mites (uncommon) would confirm these diagnoses.

Fecal Examination will occasionally reveal ectoparasites (mites) that were not found

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com floatation on routine skin scrapings.

Flea Control Capstar administered every other day for 1 months effectively prevents flea Trial feeding and the pets exposure to flea saliva. Aggressive Flea control on all pets in the home. Often, cats will have no evidence of flea infestation but respond to aggressive flea control.

Therapeutic Since skin scrapes for Demodex gatoi can be falsely negative in infected cats, trial for a therapeutic trial consisting of 6 weeks of lime sulfur dips may be needed to Demodex confirm or rule out this differential.

Skin biopsy This is often the quickest way to collect the most information regarding a dermatosis. Even if not diagnostic, enough information can be gathered to guide additional diagnostic tests or therapeutic trials (allergic dermatitis compared to folliculitis compared to paraneoplastic dermatitis).

Food Trial Currently, a dietary food trial is the only way to confirm or eliminate food allergy dermatitis as a cause of pruritus. There are no in vitro testing methodologies that correlate with clinical disease.

The most allergen restricted yet palatable diets should be used for a 10-week trial.

Home-prepared diets provide better allergen restriction and are often more palatable than commercial diets, but are not balanced or complete.

Following the 10-week elimination food trial, a dietary challenge should be used to confirm the diagnosis of food allergy. Often other treatments are initialed during the 10-week period. A food challenge will confirm or eliminate the restricted diet as the cause of improvement and thus substantiate the diagnosis of food allergy.

Summary: Since flea allergy is the most common cause of skin lesions in cats, it is imperative to rule out flea allergy dermatitis through an aggressive flea control trial. The key to success is a thorough dermatologic workup. By considering and ruling out the more common or more easily treatable causes of feline dermatitis, success is easily achievable with out the need for steroids.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com FELINE SUBMISSION FORM Owner Name: Animal Name: Species: Age: Sex: Date: RESEAR CH ASSOCIATES LABOR ATORY Specimen Source (Please Circle) Blood Swab Phone: (972)960-2221 Fax: (972)960-1997 www.vetdna.com Acct # Check Enclosed Amount:______PAYMENT

ACCOUNT Name Credit Card Address AMEX Discover Master Card Visa On File City Exp. Date: ______/______State/ZIP Country ______Name On Card Phone# Email ______Credit Card Number Fax Specimen Requirements: Blood - 0.1 ml whole blood Swab - Dry sterile swab LIVE ANIMAL TESTING ENVIRONMENTAL TESTING POST MORTEM

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Rethinking Canine Allergy 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 simplifi ed 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 benefi cial new therapies, we continue to struggle to acceptance of the message and improves compliance fi nd 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 eff ective 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 immu no suppressed, 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 Staphy lococcus 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 specifi c prob- from contagion and zoonosis. In these families, avoid lems of the individual patient. the indiscriminate use of steroids or fl uoroquinolone 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-infl ammatory 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 signifi cant 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 identifi cation 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 ramifi cations 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 diff erent 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 eff ect. 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 diff er- 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 eff ects. itch quickly: 5. Give essential fatty acids every 12 to 24 hours to 1. For suspected or known atopic dogs, Canine Atopic decrease the infl ammatory 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 eff ects of IL-31. This injection is 6. For young allergic dogs, administration of nonfl avored highly eff ective at reducing pruritic atopic symp- h probiotic once each day may help delay or prevent toms with minimal adverse eff ects at the time of this the full eff ect 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 fl ares.

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 signifi cant adverse eff ects when used long term. These When the relative simple and easy prevention thera- treatments should only be used over extended time pies are insuffi cient, 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 eff ective, 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 fl ares. 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 eff ects of IL-31. This monthly injection is highly • Limit the use of repeated courses of antimicrobials. eff ective at reducing pruritic atopic symptoms with • Limit adverse events associated with allergy manage- minimal adverse eff ects 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 fi cation of the diagnosis and advanced medical a defi ned 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 Diff erentials months to 6 years. However, in most atopic dogs, symptoms Differentials include food allergy, scabies, Malassezia dermati- fi rst 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, (fl ea 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, fl anks, Diagnosis groin, axillae, face, and ears. Self-trauma often results in sec- 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 fi cation. Secondary pyoderma, Malassezia dermatitis, and mites) are causing the allergy, the foot licking may be otitis externa are common. Chronic acral lick dermatitis, nonseasonal. The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

ALLERGY PREVENTION

1. POLLEN ALLERGIES – remove pollens BATHE every 3-7 days with a disinfecting shampoo to wash off pollens and kill bacteria and yeast. After shampoo apply a OATMEAL conditioner (Torb-D) to restore the epidermal barrier. Apply the disinfecting Torb-D lotion to red itchy spots in-between the baths to prevent infection. Treat the EARS with prevention therapy after every bath (warmed LETK or EpiOtic Flush) WIPE the feet, chin, and face folds with baby wipes at bedtime. Always wipe in the direction of hair growth to remove any ingrown hairs. 2. FOOD ALLERGENS REMOVE ALL BEEF, DAIRY, CHICKEN in the food and treats forever. (READ THE INGREDIENT LIST!!) Select Lamb, Rabbit, Duck, lean Pork or FISH/SALMON diet (see email list) OTC diets like Wellness Simple, Canidae, Natural Balance, Blue Basics, Natural Planet, Merrick, and Zignature work well. (email Food list available)

3. INSECTS ALLERGIES PLEASE make sure ALL pets are treated with a NEW generation (nonBeef/nonChicken) Flavor Tabs: Sentinel or Interceptor (old formula) milbemycin - heart-worm and intestinal parasite control SIMPARICA or BRAVECTO every 30 days to prevent mites, chiggers, mosquitoes, fleas, and ticks. Revolution Plus or Bravecto every 30 days for cats.

4. BLOCK HISTAMINE: Antihistamines help reduce the skin irritation and have few side effects. In the MORNING (and up to every 12 hours for severe itching) give ______generic Zyrtec, Allegra, or Claritin At BEDTIME (and up to 3 times each day for severe itching) give ______generic Benadryl (25mg).

5. PROMOTE SKIN AND GLAND HEALTH Essential Fatty Acid (EPA) (fish, flax, SALMON, krill oil) every day for allergies, Skin health, joint health, and general improved aging (1000mg EPA per 25 lbs weight). Vitamin A daily to prevent “Old Dog Warts” skin tumors and improve gland health (2,000 IU per 25 lbs). Melatonin for hair growth and rejuvenate geriatric conditions and behaviors (5mg or 10mg every 12 hours). Human Probiotic daily to prevent tear staining or for puppies to prevent allergies.

The Itch Clinic 3 locations in East Tennessee (800) 621-1370 www.TheItchClinic.com The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

TREATING ATOPY (ENVIRONMENTAL ALLERGIES) CAN BE VERY SUCCESSFUL BUT DOES INVOLVE WORK AND LONG-TERM TREATMENT.

1. ALLERGY PREVENTION THERAPY REMOVE POLLEN WITH FREQUENT BATHS AND WIPES AVOID FOOD ALLERGENS WITH A RESTRICTED DIET – NO BEEF, DAIRY, CHICKEN PREVENT INSECTS WITH MONTHLY SIMPARICA or BRAVECTO BLOCK HISTAMINE WITH DAILY GENERIC ANTIHISTAMINES PROMOTE SKIN/ GLAND HEALTH WITH OMEGA 3 FATTY ACID and VITAMIN A

2. AGGRESSIVE TREATMENT OPTIONS

A. STEROIDS MOST SIDE EFFECTS ON THE LIVER AND OTHER ORGANS MRSTAPH RISK AND URINARY INFECTIONS

B. APOQUEL – 80% EFFECTIVE IN 3 DAYS but NO CURE 10% RISK OF TUMORS, PNEUMONIA, DEMODEX MITES PLEASE READ THE COMPLETE LABEL MOSTSIDE EFFECTS

TREATMENT FOR POLLEN ALLERGIES 40 lb DOG

C. ATOPICA – 80% EFFECTIVE IN 6 WEEKS $80-160/MO NO ADVERSE EFFECTS EXCEPT RARE GI UPSET 5% ------

---- D. ALLERGY SKIN TESTING AND VACCINE $39/MO

--- 85% EFFECTIVE IN 4-6 WEEKS 60% CURE AFTER 2 YEARS $300 ALLERGY TEST 1% SIDE EFFECTS S A F E F A S

-- --

-- E. MONOCLONAL ANTIBODY THERAPY INJECTION (AMAT/CYTOPOINT)

-- 90% EFFECTIVE IN 48 HOURS REPEATED EVERY 2-3-6 MONTH $80/INJ

Injection stings but otherwise NO SIDE EFFECTS ------

The Itch Clinic 3 locations in East Tennessee (800) 621-1370 www.TheItchClinic.com The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

DOCTOR UPDATES IN DERMATOLOGY: HUGE CHANGES AND IMPROVEMENTS

Due to the increasing liability veterinarians are facing (legally and ethically), the long-term use of steroids or Apoquel for the treatment of allergy should be stopped. 1. Steroids and Apoquel should only be used for acute flare management (2 weeks or less) a. If longer treatment is needed: i. Have the owner sign an informed consent form. ii. READ THE APOQUEL LABEL!!! iii. Check lab-work every 6 – 12 months. iv. Monitor for tumors and lymphadenopathy. v. Monitor for pneumonia and Demodicosis. vi. DO NOT USE IF MRSA INFECTION IS A RISK.

Cytopoint is finally available and should be the first treatment option for the control of itch and allergies. 1. Cytopoint is a monoclonal antibody with almost NO adverse effects. 2. Cytopoint usually controls symptoms for 4-8 weeks with minimal additional therapy. 3. DO NOT HEAT OR FREEZE THE PRODUCT. 4. Due to the multiple sizes and dose options, inventory can be frustrating.

Allergy skin testing and Desensitization vaccine is the next best, safest, and economical treatment option for allergies. 1. If Cytopoint fails or becomes too expensive, plan for allergy skin testing. 2. Allergy skin testing is 30% more successful than blood testing, a. Testing the target tissue (skin) is ideal. b. Including ALL reacting allergens increases efficacy. Most of the Itch Clinic Vaccines contain 25-35 allergens in the recipe. c. Giving a lower dose more often than company recommendations increases the efficacy of the desensitizing vaccine. d. IF MRSA IS A RISK FACTOR, THE VACCINE SHOULD CONTAIN A STAPHLYOCOCUS EXTRACT TO BOOST THE IMMUNE PROTECTION.

If Cytopoint or Allergy Skin testing are not successful or not a reasonable treatment option, home cooked food trials or Atopica are reasonable and safe treatments. 1. Due to the price and recent documentation of food contamination, prescription diets are less ideal. If a true food trial is needed, home cook diets provide the best diagnostics. 2. Atopica remains a safe and effective treatment for atopy. Useless the current rebates are used Atopica can be expensive.

The Itch Clinic 4 locations in East Tennessee (800) 621-1370 www.itchnot.com TheItchClinic.com The Itch Clinic Allergy, Dermatology, and Otology Dr. Keith A Hnilica DVM, MS, DACVD

Data summary for Hnilica’s experience with the Canine Atopy Monoclonal Antibody Immuno-Therapy (CADI, AMAT, Cytopoint)

Patients were treated and followed from October 2015 through July 2017.

Conclusions and Suggestions: 1. Cytopoint monoclonal antibody injections are an amazing therapy and EVERY itchy dog should be treated at least once to evaluate response and duration. a. Based on the response and cost consider alternative SAFE treatments i. Atopica ii. Food Trial iii. Allergy Desensitizing Vaccine Therapy based on allergy skin testing b. DO NOT RESORT TO STEROIDS or APOQUEL unless there are NO safe options. 2. True treatment failures are true failures and increasing the dose of treatment does not help improve response. 3. Every dog responds differently with regard to duration of therapy and there is no recommended schedule. 4. During the time period, NO dogs were cured or pushed into remission like we experience with allergy desensitization immunotherapy vaccine therapy based on skin testing (60% in 2 years). 5. During the time period, NO dogs developed tachyphylaxis or resistance to the monoclonal antibody treatment.

Data and Treatment Parameters: All patients had symptoms consistent with Atopy (environmental allergies) and ages ranged from 8 months to 14 years (average age was 5 years).

730 dogs were treated during the time period. Of these 730 dogs: 12 dogs (5.2%) failed to have any improvement even with repeated administration of the treatment.

229 dogs (31.4%) received only 1 treatment and elected to pursue other treatments due to the cost and lack of prolong effect. Most of these patients were large dogs with owners finding the cost of treatment too expensive or smaller dogs who did not demonstrate sufficient duration of treatment benefit.

501 dogs (68.6%) were treated with multiple doses over the duration of the study period. The average interval between treatments for this group was 3.9 months.

These dogs typically fell into 3 categories: 1. Small dogs receiving treatment every 2-3 months and doing well. 2. Large dogs receiving treatment every 4-8 months and doing well. 3. Small or large dogs receiving treatment every 1-2 months but failed other safe treatment options. The Itch Clinic 4 locations in East Tennessee (800) 621-1370 www.itchnot.com TheItchClinic.com ALLERGY SKIN TESTING ALLERGY DESENSITIZATION VACCINE

Allergy skin testing and Desensitization vaccine therapy is the GOLD STANDARD for treating Atopy (environmental allergies).

1. Allergy Skin Testing and Desensitization Vaccine works BETTER, FASTER, and is SAFER in dogs and cats than people.

2. The allergy skin test identifies any pollens, insects, house dust, dust mites, and indoor allergens that can cause the allergic symptoms.

3. Allergy skin testing is better than blood tests with the allergy vaccine resulting in superior response and cure rates.

4. 85% of patients demonstrate good to excellent improvement in the first 3 months.

5. 60% of patients can stop the allergy desensitization vaccine therapy after 2 years and are in long-term remission (cure).

6. The allergy desensitization vaccine is administered at home every 7-14 days.

7. Dogs and cats have very-very few adverse effects from the shots.

THE ITCH CLINIC

• ALLERGY • DERMATOLOGY • OTOLOGY • NEUROCHEMICAL and NEURO-IMMUNOLOGICAL ITCH

Dr. Keith A. Hnilica DVM, MS, DACVD

Helping YOU find more successful treatments for your allergic pet

Providing Specialized Veterinary Care for Your Pets ...

Allergies - Skin Infections / MRStaph Ear Disease - Hormonal Imbalances Auto-Immune Diseases ... and all other skin conditions

4 LOCATIONS IN EAST TENNESSEE (800) 621-1370 Ext. 2 • www.TheItchClinic.com Diagnosing and Treating Canine Allergy

Canine Atopy (environmental, pollen allergies)

Features Canine atopy is a hypersensitivity reaction to inhaled (possibly a historic theory) or cutaneously absorbed environmental antigens (allergens) in genetically predisposed individuals. It is common in dogs, with age of onset ranging from 6 months to 6 years. However, in most atopic dogs, symptoms first appear at between 1 and 3 years of age. Symptoms begin as skin erythema and pruritus (licking, chewing, scratching, rubbing), which may be seasonal or 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 secondary skin lesions, including salivary staining, alopecia, excoriations, scales, crusts, hyperpigmentation, and lichenification. Secondary pyoderma, Malassezia dermatitis, and otitis externa are common. Chronic acral lick dermatitis, recurrent pyotraumatic dermatitis, conjunctivitis, hyperhidrosis (sweating), and, rarely, allergic bronchitis or rhinitis may be seen.

Top Differentials Differentials include food allergy, scabies, Malassezia dermatitis, bacterial pyoderma, as well as other hypersensitivities (flea bite, contact), parasites (cheyletiellosis, pediculosis), and folliculitis (dermatophyte, Demodex).

Diagnosis 1. Seasonal foot-licking is the most unique and typical symptom of atopy. If year-round allergens (house dust mites) are causing the allergy, the foot-licking may be nonseasonal. 2. Allergy testing (intradermal, serologic): allergy testing can be highly variable according to the method used. Positive reactions to grass, weed, tree, mold, insect, dander, or indoor environmental allergens are seen. False-negative and false-positive reactions may occur. 3. Dermatohistopathology (nondiagnostic): superficial perivascular dermatitis that may be spongiotic or hyperplastic. Inflammatory cells are predominantly lymphocytes and histocytes. Eosinophils are uncommon. Neutrophils or plasma cells suggest secondary infection.

Treatment and Prognosis 1. Infection Prevention: a. Any secondary pyoderma, otitis externa, and Malassezia dermatitis should be treated with appropriate therapies. Controlling and preventing secondary infection is an essential component of managing atopic dogs. Bathing every 3 – 7 days and treating the ears after every bath helps wash off pollens and disinfect the skin and ear canals, preventing the secondary infections from recurring.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 2. Symptomatic Therapy (itch control): a An integrated flea control program should be instituted to prevent flea bites from aggravating the pruritus. b Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms. C Systemic antihistamine therapy reduces clinical symptoms in many cases (Table 7-1). Antihistamines can be used alone or in combination with glucocorticoids or essential fatty acids for a synergistic effect. One- to two-week long therapeutic trials with different antihistamines may be required to determine which is most effective. D Oral essential fatty acid supplements (180mg EPA/10 lb) help control pruritus in 20% to 50% of cases, but 8 to 12 weeks of therapy may be needed before beneficial effects are seen. Also, a synergistic effect is often noted when essential fatty acid supplements are administered in combination with glucocorticoids or antihistamines. E Dextromethorphan, an opioid antagonist, may also be a useful adjunct in managing the licking, chewing, and biting behaviors associated with allergic dermatitis in dogs. Dextromethorphan 2mg/kg PO should be administered every 12 hours. A beneficial effect should be seen within 2 weeks. F Systemic glucocorticoid therapy is often effective (75%) in controlling pruritus but almost always result in adverse effects ranging to mild (PU/PD) to severe (immuno-dysfunction, Demodicosis, and calcinosis cutis). It is a therapeutic option if the allergy season is very short but may result in unacceptable adverse effects, especially if used over the long term. 1. Potent, long acting injectable steroids are contraindicated for the treatment of allergies due to their comparatively short anti-inflammatory benefits ( 3 weeks) relative to the prolonged metabolic and immuno-depressive effects (6-10 weeks). 2. Injectable short acting steroids (dexamehtasone Sodium Phosphate, 0.5 – 1 mg/kg or prednisilone acetate 0.1mg – 1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if there are no concurrent secondary infection. This treatment option allows the clinician to more closely control and monitor the patients steroids use compared to oral treatments that are administered by the owner. 3. Temaril-P (trimeprizine and prednisilone combination) is a unique drug that provides significant antipruritic effects at a relatively lower dose of the prednisilone. One tablet should be administered per 10 to 20 kg every 24 to 48 hours. The dosage should be tapered to the lowest possible dose and frequency. 4. Prednisone 0.25 to 1mg/kg (or methylprednisolone 0.2-0.8mg/kg) PO should be administered every 24 to 48 hours for 3 to 7 days. The dosage should be tapered to the lowest possible dose and frequency. 5. All dogs treated with long-term steroids (more than 3 months) should be frequently monitored for liver disease and UTI. 8. Allergy Treatment (immune-modulation) a. Exposure to offending allergens should be reduced, if possible, by their removal from the environment. High-efficiency particulate (HEPA) air and charcoal filters should be used to reduce pollens, molds, and dust in the home. For house dust mite–sensitive dogs, household treatments for carpets, mattresses, and upholstery with the acaricide benzyl benzoate once a month for approximately 3 months, then every 3 months thereafter, may effectively eliminate house dust mites from the environment. Old dog beds should be discarded as these accumulate house dust mite antigens. Dehumidifying the house to below 40% relative

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com humidity decreases house dust mite, mold, and flea antigen loads. To achieve this, high- efficiency dehumidifiers that are capable of pulling several liters of water from the air per day are required.

b. Cyclosporine (Atopica) helps control pruritus in 75% of atopic dogs. A dose of 5mg/kg PO should be administered every 24 hours until beneficial effects are seen (approximately 4-6 weeks). Then, dosage frequency should be tapered down to every 48 to 72 hours. For long- term control, approximately 25% of dogs require daily dosing, 50% can be controlled with every-other-day dosing, and approximately 25% can be controlled with twice-weekly dosing. Glucocorticoids can be used initially to speed response. As of this writing, there are no statistically significant increases in tumor risk or severe infection resulting from the immune effects of cyclosporine.

c. With immunotherapy (allergy vaccine), 60% to 75% of atopic dogs show good (some medical therapy still needed) to excellent (no other therapy needed) response. Clinical improvement is usually noted within 3 to 5 months of initiation of immunotherapy, but it can take up to 1 year in some dogs.

11. The prognosis is good, although lifelong therapy for control is needed in most dogs. Relapses (pruritic flare-ups with/without secondary infections) are common, so individualized treatment adjustments to meet patient needs may be required periodically. In dogs that become poorly controlled, one should rule out secondary infection (e.g., that caused by bacteria or Malassezia); sarcoptic mange; demodicosis; concurrent food, flea bite, and recently acquired hypersensitivity to additional environmental allergens. Because a strong genetic component is present, the breeding of any male or female dog with clinical signs of atopic dermatitis should be discouraged.

Box Author’s Note Our profession has excelled at reducing the use of steroids for arthritis; however, we have failed to make similar achievements for allergic disease including atopy. Since both disease have many similarities, including chronicity and multimodal therapeutic options, our goal should be to minimize the use of steroids for allergic diseases through the use of alternative, safer treatment options. To achieve best medicine, the frequency of steroid use should be similar for patients with arthritis and allergy. The use of long-acting, injectable steroids should be stopped due to the profound impact on the metabolic and immune systems as well as the growing concern of legal liability for the practitioner.

Author’s Note The only real, long-term options for treating the allergic immune response to environmental allergens are avoidance, allergy vaccine, or cyclosporine (Atopica). Based on typical cgeneral practice demographics, every full time small animal veterinarian should have approximately 20-30 patients who are no longer controlled with symptomatic therapy and need more aggressive treatment (allergy vaccine or cyclosporine).

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com Canine Food Hypersensitivity

Features Canine food hypersensitivity is an adverse reaction to a food or food additive. It can occur at any age, from recently weaned puppies to elderly dogs that have been eating the same dog food for years. Approximately 30% of dogs diagnosed with food allergy are younger than 1 year of age. It is common in dogs. Canine food hypersensitivity is characterized by nonseasonal pruritus that may or may not respond to steroid therapy. The pruritus may be regional or generalized and usually involves the ears, feet, inguinal or axillary areas, face, neck, and perineum. Affected skin is often erythematous, and a papular rash may be present. Self-trauma–induced lesions include alopecia, excoriations, scales, crusts, hyperpigmentation, and lichenification. Secondary superficial pyoderma, Malassezia dermatitis, and otitis externa are common. Other symptoms that may be seen are acral lick dermatitis, chronic seborrhea, and recurring pyotraumatic dermatitis. Some dogs are minimally pruritic, with the only symptom being recurrent infection with pyoderma, Malassezia dermatitis, or otitis. In these cases, the pruritus is present only when secondary infections are left untreated. Occasionally, urticaria or angioedema may occur. Concurrent gastrointestinal signs (e.g., frequent bowel movements, vomiting, diarrhea, flatulence) are reported in 20%-30% of cases.

Top Differentials Differentials include atopy, scabies, Malassezia dermatitis, bacterial pyoderma, as well as other hypersensitivities (flea bite, contact), parasites (cheyletiellosis, pediculosis), and folliculitis (dermatophyte, Demodex).

Diagnosis 1. Perianal dermatitis with or without recurrent otitis is the most common and unique feature of food allergy. However, food allergy can manifest in many patterns and should be suspected for atypical pruritic patient including cases of recurrent infections without pruritus. 2. Dermatohistopathology (nondiagnostic): varying degrees of superficial perivascular dermatitis. Mononuclear cells or neutrophils may predominate. Eosinophils may be more numerous than in atopy 3. Food allergy testing (intradermal, serologic)(nondiagnostic): not recommended because test results are unreliable. Some dogs will have positive reactions to storage mite antigens, which may be clinically relevant, or they may be caused by cross-reactivity with other insects. Storage mites are ubiquitous, and their clinical significance is currently unknown. 4. Response to hypoallergenic diet trial: symptoms improve within 10 to 12 weeks of initiation of a strict home-cooked or commercially prepared restricted diet (one protein and one carbohydrate source). The hypoallergenic diet should not contain food ingredients previously administered in dog food, treats, or table scraps, nor should flavored heartworm preventative, flavored medications, nutritional supplements, or chewable treats (i.e., pig ears, cow hooves, rawhide, dog biscuits, table food such as cheese or peanut butter to hide pills in) be Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com administered during the hypoallergenic diet trial. Beef and dairy are the most common food allergens in dogs and avoiding these alone may result in clinical improvement. Other common food allergies include chicken, eggs, soy, corn, and wheat. 5. Provocative challenge: recurrence of symptoms within hours to days of reintroduction of suspect allergen into the diet.

Treatment and Prognosis 1. Infection Prevention: a. Any secondary pyoderma, otitis externa, and Malassezia dermatitis should be treated with appropriate therapies. Controlling and preventing secondary infection is an essential component of managing atopic dogs. Bathing every 3 – 7 days and treating the ears after every bath helps wash off pollens and disinfect the skin and ear canals, preventing the secondary infections from recurring. 2. Symptomatic Therapy (itch control) is variably effective for food allergy: a An integrated flea control program should be instituted to prevent flea bites from aggravating the pruritus. b Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms. C Systemic antihistamine therapy reduces clinical symptoms in many cases (Table 7-1). One- to two-week long therapeutic trials with different antihistamines may be required to determine which is most effective. D Oral essential fatty acid supplements (180mg EPA/10 lb) help control pruritus in 20% to 50% of cases, but 8 to 12 weeks of therapy may be needed before beneficial effects are seen. Also, a synergistic effect is often noted when essential fatty acid supplements are administered in combination with glucocorticoids or antihistamines. E Dextromethorphan, an opioid antagonist, may also be a useful adjunct in managing the licking, chewing, and biting behaviors associated with allergic dermatitis in dogs. Dextromethorphan 2mg/kg PO should be administered every 12 hours. A beneficial effect should be seen within 2 weeks. F Systemic glucocorticoid therapy is only variably effective (unpredictable minimal to good response) in controlling pruritus cause by the food allergy; but almost always result in adverse effects ranging to mild (PU/PD) to severe (immuno-dysfunction, Demodicosis, and calcinosis cutis). (see Atopy section) 1. Potent, long acting injectable steroids are contraindicated for the treatment of allergies due to their comparatively short anti-inflammatory benefits ( 3 weeks) relative to the prolonged metabolic and immuno-depressive effects (6-10 weeks). 2. Injectable short acting steroids (dexamehtasone Sodium Phosphate, 0.5 – 1 mg/kg or prednisilone acetate 0.1mg – 1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if there are no concurrent secondary infection. This treatment option allows the clinician to more closely control and monitor the patient’s steroids use compared to oral treatments that are administered by the owner. 3. All dogs treated with long-term steroids (more than 3 months) should be frequently monitored for liver disease and UTI.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 8. Food Allergy Treatment a. Offending dietary allergen(s) should be avoided. A balanced home-cooked diet or a commercial hypoallergenic diet should be provided. b. To identify offending substances to be avoided (challenge phase after food allergy has been confirmed with the dietary trial) one new food item should be added to the hypoallergenic diet every 2 to 4 weeks. If the item is allergenic, clinical symptoms will recur within 7 to 10 days. Note: Some dogs (approximately 20%) should be fed home-cooked diets to remain symptom-free. For these dogs, commercial hypoallergenic diets are ineffective, presumably because their hypersensitivity relates to a food preservative or dye. c. Ancedotal reports suggest that higher doses (10mg/kg) of cyclosporine (Atopica) may ne beneficial in reducing the allergic immune response and symptoms of food allergy. 8. The prognosis is good. In dogs that are poorly controlled, owner noncompliance should be ruled out, along with development of hypersensitivity to an ingredient in the hypoallergenic diet, secondary infection (caused by bacteria, Malassezia, dermatophyte), scabies, demodicosis, atopy, flea allergy dermatitis, and contact hypersensitivity.

Author’s Note Due to recent food industry changes, there has been an explosion of products available through prescription or over-the-counts and the listing is beyond the scope of this text. Many of the over-the-counter diets are sufficiently restricted and of high enough quality to produce clinical benefit when a food allergic patient restricted to one of the nonBeef and nondairy products. Food allergy is responsible for most of the very unusual clinical symptom patterns in dogs with recurrent infections (with or without pruritus). Poor owner compliance should be expected making the long-term management of food allergic patients difficult and frustrating; repeated lapses in diet result in flare-ups in the pruritus and secondary infections.

Author’s Note The use of long-acting, injectable steroids should be stopped due to the profound impact on the metabolic and immune systems as well as the growing concern of legal liability for the practitioner.

Flea Allergy Dermatitis (flea bite hypersensitivity)

Features Flea allergy dermatitis is a common skin disease in dogs and cats sensitized to flea salivia proteins through repeated and intermittent flea bites. Symptoms are usually seasonal (warm weather months and in the fall) in temperate zones and often nonseasonal in subtropical and tropical areas. Fall is often the most severe season relating to when the first cold snap occurs. Dogs The distribution typically involves the caudodorsal lumbosacral area, dorsal tail head, caudomedial thighs, abdomen, and flanks. Lesions include pruritic, papular, crusting eruptions

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com with secondary erythema, seborrhea, alopecia, excoriations, pyoderma, hyperpigmentation, and lichenification. Cats Cats do not have a pattern unique to flea allergy dermatitis. Patients commonly present with pruritic miliary dermatitis with secondary excoriations, crusting, and alopecia of the neck, dorsal lumbosacral area, caudomedial thighs, and ventral abdomen. Other symptoms include symmetrical alopecia secondary to excessive grooming and eosinophilic granuloma complex lesions.

Top Differentials Differentials include atopy, food hypersensitivity, other ectoparasites (scabies, cheyletiellosis, pediculosis, demodicosis), superficial pyoderma, dermatophytosis, demodicosis, and Malassezia dermatitis.

Diagnosis 1. Lumbar dermatitis in the dog is the most consistent and unique feature of flea allergy dermatitis. In cats, flea allergy should be highly suspected in any cat with skin disease. 2. Visualization of fleas or flea excreta on body: may be difficult on flea-allergic animals as flea- allergic animals are very effective at removing fleas through grooming 3. Allergy testing (intradermal, serologic): positive skin test reaction to flea antigen or positive serum immunoglobulin (Ig)E antiflea antibody titer is highly suggestive, but false-negative results are possible 4. Dermatohistopathology (nondiagnostic): varying degrees of superficial or deep perivascular to interstitial dermatitis, with eosinophils often predominating 5. Response to aggressive flea control (nitenpyram administered every other day for 1 month): symptoms resolve

Treatment and Prognosis 1. Integrated flea management program (Insect growth regulator combined with an adulticide combined with environmental treatments) is essential due to the progressive tolerance of the flea to available adulticides. With time, specific active ingredients typically loose efficacy due to the chronic exposure and genetic drift of the flea. 2. Topical or systemic insect growth regulators (lufenuron, piriproxyfen, methoprene) may be effective alone or used in combination with adulticidal therapy. 3. Affected and all in-contact dogs and cats should be treated with adulticidal flea sprays, spot-on solutions, orals, or dips every 7 to 30 days, as instructed on the label. Products that contain spinosid , imidocloprid, selamectin, or fipronil are especially effective when used topically every 2 to 4 weeks. In heavily flea-infested environments, fleas may continue to be found on animals for several months in spite of topical flea control. In these cases, affected animals should also be administered nitenpyram at a minimum dose of 1mg/kg PO every 24 to 48 hours for 2 to 4 weeks, or until fleas are no longer seen. The environment should be treated (see number 5 below).

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 4. Flea-allergic animals should be treated prophylactically with nitenpyram, minimum dose 1mg/kg PO, on any day that an encounter is planned with other potentially flea-infested animals (e.g., a visit to the groomer, veterinary hospital, park, another household with animals). No more than one treatment with nitenpyram should be administered per day. 5. In heavily flea-infested environments, areas where pets spend the most time should be treated. Indoor premises should be treated with an insecticide and an insect growth regulator (e.g., methoprene, piriproxyfen). The outdoor environment should be treated with insecticidal or biologic products designed for such use. 6. Flea control therapy should be continued from spring until first snowfall in temperate areas and year-round in warm climates. Year-round flea infestations can be perpetuated indoors and on wildlife despite extreme cold outdoors. 7. Symptomatic Therapy (itch control): a Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms. b Systemic antihistamine therapy reduces clinical symptoms in many cases (Table 7-1). c Systemic glucocorticoid therapy is often effective (75%) in controlling pruritus but almost always result in adverse effects ranging to mild (PU/PD) to severe (immuno-dysfunction, Demodicosis, and calcinosis cutis). It is a therapeutic option if the allergy season is very short but may result in unacceptable adverse effects, especially if used over the long term. 1. Potent, long acting injectable steroids are contraindicated for the treatment of allergies due to their comparatively short anti-inflammatory benefits ( 3 weeks) relative to the prolonged metabolic and immuno-depressive effects (6-10 weeks). 2. Injectable short acting steroids (dexamehtasone Sodium Phosphate, 0.5 – 1 mg/kg or prednisilone acetate 0.1mg – 1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if there are no concurrent secondary infection. This treatment option allows the clinician to more closely control and monitor the patients steroids use compared to oral treatments that are administered by the owner. 3. Temaril-P (trimeprizine and prednisilone combination) is a unique drug that provides significant antipruritic effects at a relatively lower dose of the prednisilone. One tablet should be administered per 10 to 20 kg every 24 to 48 hours. The dosage should be tapered to the lowest possible dose and frequency. 4. Prednisone 0.25 to 1mg/kg (or methylprednisolone 0.2-0.8mg/kg) PO should be administered every 24 to 48 hours for 3 to 7 days. The dosage should be tapered to the lowest possible dose and frequency. 5. All dogs treated with long-term steroids (more than 3 months) should be frequently monitored for liver disease and UTI.

8. The prognosis is good if strict flea control is practiced. Fleas may infest other in-contact animals and humans. They may carry blood-borne diseases in a manner similar to ticks.

Author’s note The use of long-acting, injectable steroids should be stopped due to the profound impact on the metabolic and immune systems as well as the growing concern of legal liability for the practitioner.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com Any dog with lumbar dermatitis or any cat with skin disease should be highly suspected of having flea allergy dermatitis even if the patient has been treated with seemingly good flea control therapies. A nitenpyram trial (every other day for 1 month) is the most efficient and cost effective way to convince the owner and yourself of the role of flea allergy in a pruritic patient.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com Acral Dermatitis

Primary Disease Allergy Secondary Neuropathy Bacterial Hypothyroidism Blasto infection Neoplasia

Amitriptyline Allergy, Behavior Pain Hydrocodone Pain Endorphins Behavior Antibiotics 2nd infection Use ALL 3 for 1 month then taper or DC 1 by 1

Rethinking Otitis Otitis in 3 Steps

1. Dirty – Waxy ears with minimal symptoms – itch or pain and rare occurrences a. Clean the ears in the clinic if possible i. EpiOtic Advanced best-safest product currently ii. No acids, No alcohol, herbals iii. Fill ear canal – let shake dry – repeat until clean

2. Otitis a. Allergy or Endocrine disorder as the trigger b. Mild non-infected otitis will eventually become infected c. Treatment i. Multimodal ointment (100s of products) 1. Place in the ear every 24-72 hours 2. Make sure volume is adequate: .5ml – 1.5 ml 3. Use a syringe or pump bottle for easy dosing 4. 1/10,000 ototoxicity rate ii. Long-term Ear Pack 1. LETK – lanolin, enrofloxacin, triamcinolone, ketoconazole a. Must be warmed to prevent ear plug b. Can be used every 1-2 weeks c. Cheap but messy 2. Osurnia and Claro a. Same active ingredients b. Osurnia is alcohol free bioactive gel c. Claro is alcohol base with quicker kill d. Both are effective for 2-3 weeks and can be repeated.

d. Prevention i. Use which ever ear product at longer intervals 1. Multimodal ointments use every 3-7 days 2. Long-term Ear Pack use every 2-3-4 weeks

3. Severe purulent ulcerated and painful otitis a. Usually mixed bacteria – cocci and rods – Pseudomonas, Proteus, Ecoli b. Liquid purulent exudate and discharge c. Painful, ulcerated ears d. Tympanic membrane is usually ruptured but often can’t see it anyway e. Oral antibiotics do not achieve high enough concentration at the ear tissue f. Severe swelling and pain may require 1 week of high dose steroids g. Bacteria cultures are usually not necessary h. TrisEDTA 4 oz with 1200mg enrofloxacin and 40 mg of Dex SP i. Fill ear canal completely every 12-24 hours ii. Should resolve infection in 2 weeks iii. Then switch to prevention therapy i. If not successful, consider culture guided therapy or TECA

Diagnosing and Treating Otitis

Features Otitis externa is an acute or chronic inflammatory disease of the external ear canal. Its causes are numerous and almost always have an underlying, primary disease (Table 15.1) that alters the normal structure and function of the canal resulting in a secondary infection (Table 15.2). Otitis externa is common in cats and dogs, with Cocker spaniels especially at risk for developing severe and chronic disease. Otic pruritus or pain is a common symptom of otitis externa. Head rubbing, ear scratching, head shaking, aural hematomas, and a head tilt, with the affected ear tilted down, may be noted. An otic discharge that may be malodorous is often present. In acute cases, the inner ear pinna and ear canal are usually erythematous and swollen. The ear canal may also be eroded or ulcerated. Pinnal alopecia, excoriations, and crusts are common. In chronic cases, pinnal hyperkeratosis, hyperpigmentation, and lichenification, as well as ear canal stenosis from fibrosis or ossification, are common. Decreased hearing may be noted. Concurrent otitis media should be suspected if otitis externa has been present for 2 months or longer, even if the tympanic membrane appears to be intact and no clinical signs of otitis media (drooping or inability to move ear or lip, drooling, decreased or absent palpebral reflex, exposure keratitis) are evident. Rarely, symptoms of otitis interna (head tilt, nystagmus, ataxia) may be present. Oral examination may reveal pain (severe otitis media), inflammation, or masses (especially polyps in cats). Depending on the underlying cause, concurrent skin disease may be seen.

Diagnosis 1. Based on history and clinical findings 2. Otoscopic examination: assess degree of inflammation, ulceration, stenosis, and proliferative changes; amount and nature of debris and discharge; presence of foreign bodies, ectoparasites, and masses; and integrity of tympanic membrane 3. Mineral oil prep (ear swab): look for otodectic and demodectic mites and ova 4. Cytology (ear swab): look for bacteria, yeasts, fungal hyphae, cerumen, leukocytes, and neoplastic cells 5. Bacterial culture (external or middle ear exudate): indicated when bacteria are found on cytology in spite of antibiotic therapy, or when otitis media is suspected 6. Fungal culture: indicated when dermatophytic otitis is suspected, especially in long-haired cats that have ceruminous otitis 7. Radiography (bulla series), computed tomography (CT), magnetic resonance imaging (MRI): evidence of bullous involvement (sclerosis, opacification) is seen in approximately 75% of otitis media cases 8. Dermatohistopathology: may be indicated to identify primary cause (e.g., autoimmune disease, sebaceous adenitis, erythema multiforme), if neoplasia is suspected (ear canal mass), or if ear canal resection or ablation is performed because of end-stage otitis

Treatment and Prognosis 1. Primary causes of the otitis should be identified and corrected, if possible (Table 15-1). 2. For swimmer’s ear, maceration of ear canals can be prevented by prophylactic instillation of a drying agent after the dog gets wet (swimming, bathing), or two to three times per week in very humid climates. Effective products are ear products that contain astringents/alcohol 3. For allergic otitis, long-term management includes control of underlying allergies, resolution of any secondary bacterial and yeast otitis, and institution of ear cleaning and treatment every 3-7 days to prevent the recurrence. In animals whose underlying allergies cannot be identified or completely controlled, the judicious use of steroid-containing otic preparations as infrequently as needed may prevent otitis flare-ups

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

4. For mild/acute otitis, at home, the owner should perform ear cleaning every 2 to 7 days with a ceruminolytic agent (that does not need to be flushed out) to prevent earwax and debris from accumulating. Lifelong ear cleaning every 3 – 7 days may be necessary to prevent relapses of otitis. The use of cotton swabs (which may damage the epithelium) is not recommended. 5. For severe/chronic otitis, in-hospital ear cleaning and flushing should be performed to remove accumulated exudate and debris from the vertical and horizontal ear canals (under sedation or anesthesia if necessary). The procedure should be repeated every 2 to 7 days until all debris has been removed. Products that can be used for ear flushing include the following: n Water or saline n DSS diluted in warm water or saline Non-ototoxic ear cleaning product n Povidone-iodine 0.2%-1% solution (may be ototoxic) n Chlorhexidine 0.05%-0.2% solution (may be ototoxic) n Pretreatment (5 minutes before lavage) with a urea peroxide cleaning product is very effective at dissolving exudate but MUST be flushed out of the canal(may be ototoxic) 6. Systemic glucocorticoids should be administered if the ear is painful or the canal is stenotic from tissue swelling or proliferation. For dogs, prednisone 0.25 to 0.5mg/kg PO should be administered every 12 hours for 5 to 10 days. For cats, prednisolone 0.5-1.0mg/kg PO should be administered every 12 hours for 7 to 14 days.

Individual Diseases 7. For ear mites, affected and all in-contact dogs and cats should be treated. When otic treatments are used, additional treatment to eliminate ectopic mites should be concurrently administered. Effective therapies for ear mites include the following: n Otic miticide as per label directions (ivermectin and milbemycin products are safe and highly effective) n Selemectin 6-12mg/kg topically on skin twice 2-4 weeks apart (dogs) n Tresaderm 0.125-0.25 mL AU q 12 hours for 2-3 weeks n Ivermectin 0.3mg/kg PO q 7 days for 3-4 treatments, or 0.3mg/kg SC q 10-14 days for 2-3 treatments n Fipronil 0.1-0.15 mL AU q 14 days for two to three treatments (based on anecdotal reports) 8. For demodectic otitis, Effective therapies for ear mites include the following: n Otic miticide as per label directions (ivermectin and milbemycin products are safe and highly effective) An alternative treatment is to use 1% injectable ivermectin solution 0.1 to 0.15 mL instilled AU every 24 hours, continuing at least 2 weeks past complete clinical resolution with no evidence of mites on follow-up ear smears. 9. For yeast otitis, antifungal-containing ear preparations should be repackaged into a bottle to provide more accurate dosing; dropper bottle, brown amber bottle, etc. Then, 0.2 to 0.4 mL 1 1 ( /4- /2 dropperful) should be instilled in the affected ear every 12 hours for at least 2 to 4 weeks. Treatment should be continued until follow-up ear smears are cytologically negative for microorganisms, the external canals are no longer edematous or inflamed, and the ear canal epithelium has normalized. Effective products include the following: n Clotrimazole n Miconazole n Thiabendazole n Nystatin 10. For severe refractory yeast otitis externa or otitis media, in addition to topical antifungal treatment, systemic antifungal therapy may be helpful if administered for at least 3 to 4 weeks, then continued 1 to 2 weeks beyond complete clinical cure. Effective therapies include the following: n Ketoconazole 5mg/kg PO q 12 hours, or 10mg/kg PO q 24 hours with food n Fluconazole 5mg/kg PO q 12 hours, or 10mg/kg PO q 24 hours with food n Itraconazole 5-10mg/kg PO q 24 hours with food

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

n Pulse itraconazole 5-10mg/kg PO q 24 hours with food on 2 consecutive days each week 11. For bacterial otitis, antibiotic-containing ear preparations should be repackaged into to provide more accurate dosing; dropper bottle, brown amber bottle, etc. Then, 0.2 to 0.4 mL 1 1 ( /4- /2 dropperful) should be instilled in affected ears every 8 to 12 hours for at least 2 to 4 weeks. Treatment should be continued until follow-up ear smears are cytologically negative for microorganisms, the external canals are no longer edematous or inflamed, and the ear canal epithelium has normalized. Effective products include the following: n Gentamicin n Neomycin n Polymixin B and neomycin n Polymixin E and neomycin 12. For bacterial otitis media, Systemic antibiotics may not achieve sufficient tissue concentrations to kill Pseudomonas and to prevent antibiotic resistance, the highest possible dose of antibiotic that is safe should be administered with concurrent high-concentration topical therapy of the same antibiotic. If topical has been used aggressively and has been unsuccessful, systemic antibiotics may be indicated, based on culture and sensitivity results, for a minimum of 4 weeks, and continued 2 weeks beyond complete clinical cure. Antibiotics include the following: n Ormetoprin-sulfadimethoxine 27.5mg/kg PO q 24 hours n Trimethoprim-sulfa 22mg/kg PO q 12 hours n Cephalexin, cephradine, or cefadroxil 22mg/kg PO q 8 hours n Ciprofloxacin 5-15mg/kg PO q 12 hours n Enrofloxacin 20mg/kg PO q 24 hours (may increase the risk of resistant bacteria) n Orbifloxacin 7.5mg/kg PO q 24 hours (may increase the risk of resistant bacteria) n Marbofloxacin 5.5mg/kg PO q 24 hours (may increase the risk of resistant bacteria)

13. For Pseudomonas otitis, aggressive treatment should be provided for at least 2-4 weeks, then continued 2 weeks beyond complete clinical cure. All underlying/primary diseases should be identified and addressed. Currently, the most effective treatments include tris– ethylenediaminetetra-acetic acid (EDTA) solutions with high concentrations of antibiotics instilled in high volumes (to ensure deep penetration and prevent dilution by exudate). Antibiotics should be selected according to culture and sensitivity results. Systemic antibiotics may not achieve sufficient tissue concentrations (mutation prevention concentration) to kill Pseudomonas and prevent antibiotic resistance. If systemic antibiotics are used, the highest possible dose that is safe should be administered, along with concurrent high-concentration topical therapy of the same antibiotic.

n The tris–ethylenediaminetetra-acetic acid (EDTA) solution should be combined with enrofloxacin to make a 10- to 20-mg/mL solution. The solution should be used q 12-24 hours to completely fill the ear canal. Even as the sole therapy, the surfactants in T8 Solution act to clean the ear while allowing the high concentration of enrofloxacin to penetrate into the deep canal. This treatment is 80% effective in chronic, recurrent otitis cases, even if the bacteria are reported to be resistant to enrofloxacin (because of the tris-EDTA and high concentration of antibiotic)

n Tris-EDTA solution (with/without enrofloxacin 10mg/mL, gentamicin 3mg/mL, or amikacin 9mg/mL) 0.4 mL instilled q 8-12 hours n Combination 3 mL enrofloxacin (Baytril Injectable 22.7mg/mL) plus 4mg dexamethasone sodium phosphate plus 12 mL ear cleanser: 0.2-0.4 mL instilled q 12 hours n Amikacin sulfate (Amiglyde V Injectable 50mg/mL), undiluted, 0.1-0.2 mL instilled q 12 hours 1 n Silver sulfadiazine (Silvadene) 0.1% solution (mix 1.5 mL [ /3 tsp]) of Silvadene Cream with 13.5 mL distilled water, or mix 0.1 g silver sulfadiazine powder with 100 mL distilled water), and instill 0.5 mL q 12 hours

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

n Ticarcillin equine intrauterine infusion (Ticillin), undiluted, 0.2-0.3 mL q 8 hours n Ticarcillin powder for injection (vial should be reconstituted as directed, then frozen in TB syringes as 1-mL aliquots). New syringe should be thawed each day and kept refrigerated. A dose of 0.2 to 0.3 mL should be instilled into affected ears q 8 hours

For End-Stage Ears 14. For chronic proliferative otitis, aggressive medical therapy is needed. Weekly ear cleaning should be instituted. For bacterial/yeast otitis externa and media, long-term (minimum, 4 weeks) systemic and topical antibiotics or antifungal medications should be administered, then continued 2 weeks beyond complete clinical resolution of the infection. To reduce tissue proliferation, prednisone 0.5mg/kg PO should be administered every 12 hours for 2 weeks; then, 0.5mg/kg PO should be administered every 24 hours for 2 weeks, followed by 0.5mg/kg PO every 48 hours for 2 weeks. These ears rarely return to complete normalcy, so long-term maintenance therapy with steroid-containing otic preparations, as described for allergic otitis, is almost always necessary. 15. For end-stage ears, indications for surgery include the following: n Traction-avulsion or surgical resection of inflammatory polyps/masses n Lateral ear canal resection, which aids in ventilation and drainage and allows for easier application of medication but rarely results in cure because a large amount of diseased tissue is still present n Vertical ear canal ablation, if proliferative changes are present in the vertical canal but the horizontal canal is not affected. Total ear canal ablation and lateral bulla osteotomy is usually indicated to alleviate chronic pain and discomfort when end-stage otitis externa and otitis media are no longer responsive to medical management 16. The prognosis is variable, depending on whether the underlying cause can be identified and corrected, and on the chronicity and severity of the otitis externa. Because Cocker spaniels are especially at risk for chronic and severe otitis externa, early and aggressive management of primary otitis externa and secondary inflammation is warranted in this breed.

Author’s Note:

The most important component for successful long-term treatment of otitis are

1. Identify and control the underlying, primary disease; infectious otitis is secondary and recurrence can only be prevented if the primary disease is treated.

2. Use sufficient volumes of otic medications to completely coat and penetrate the ear canal; most patients need a minimum of 0.25 ml to provide enough medication.

3. Don’t treat and stop; treat and stop but rather use frequent (every 3-7 days) cleaning or treatment to prevent otitis recurrence.

It is extremely important to base treatment decisions on cytology (initial and recheck) and clinical impression together.

The most consistently successful and least ototoxic treatment for Pseudomonas otitis is a high concentration enrofloxcin solution mixed into a trisEDTA (making a 10mg/ml final solution). If the infection is not improving, consider a deep otic lavage and evaluation of the otic bullae. Systemic antibiotics do NOT seem to improve treatment efficacy beyond the topical solution alone.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

Top 11 Dematoses

Atopy W2825-Ch007.qxd 8/12/2005 11:08 Page 162

162 CHAPTER 7 Hypersensitivity Disorders

Canine Atopy (allergic inhalant dermatitis)

Features Treatment and Prognosis Canine atopy is a type 1 hypersensitivity reaction to 1. Exposure to offending allergens should be inhaled or cutaneously absorbed environmental anti- reduced, if possible, by their removal from the gens (allergens) in genetically-predisposed individu- environment. High-efficiency particulate (HEPA) als. It is common in dogs, with age of onset ranging air and charcoal filters should be used to reduce from 3 months to 7 years. However, in most atopic pollens, moulds, and dust in the home. For house dogs, symptoms first appear at between 1 and 3 years dust mite–sensitive dogs, household treatments of age. for carpets, mattresses, and upholstery with the Symptoms begin as skin erythema and pruritus acaricide, benzyl benzoate, once a month for (licking, chewing, scratching, rubbing), which may be approximately 3 months, then every 3 months seasonal or nonseasonal, depending on the offending thereafter, may effectively eliminate house dust allergen. The distribution of the pruritus usually mites from the environment. Old dog beds should involves the feet, flanks, groin, axillae, face, and ears. be discarded as these accumulate house dust Self-trauma often results in secondary skin lesions, mite antigens. Dehumidifying the house to below including salivary staining, alopecia, excoriations, 40% relative humidity decreases house dust mite, scales, crusts, hyperpigmentation, and lichenification. mould, and flea antigen loads. To achieve this, Secondary pyoderma, Malassezia dermatitis, and otitis high-efficiency dehumidifiers that are capable of externa are common. Chronic acral lick dermatitis, pulling several liters of water from the air are recurrent pyotraumatic dermatitis, conjunctivitis, required. hyperhidrosis (sweating), and, rarely, allergic bronchi- 2. Any secondary pyoderma, otitis externa, and tis or rhinitis may be seen. Malassezia dermatitis should be treated with appropriate therapies. Controlling secondary infection is an essential component of managing Top Differentials atopic dogs. Differentials include other hypersensitivities (food, 3. A flea control program should be instituted to flea bite, contact), parasites (scabies, cheyletiellosis, prevent flea bites from aggravating the pruritus. pediculosis), folliculitis (bacteria, dermatophyte, 4. Pruritus should be controlled with topical therapy Demodex), and Malassezia dermatitis. and systemic therapies such as antihistamines, essential fatty acid supplements, glucocorticoids, cyclosporine, or immunotherapy (see Numbers 5 Diagnosis through 14 below). 1. Usual basis: history and clinical findings, rule out 5. Topical therapy with shampoos, conditioners, and other differentials sprays (i.e., those containing oatmeal, pramoxine, 2. Allergy testing (intradermal, serologic): allergy aloe vera, antihistamines, or glucocorticoids) testing can be highly variable according to the applied every 2 to 7 days or as needed may help method used. Positive reactions to grass, weed, tree, reduce clinical symptoms. mould, insect, dander, or indoor environmental 6. Systemic antihistamine therapy reduces clinical allergens are seen. False-negative and false-positive symptoms in 20% to 35% of cases (Table 7-1). Anti- reactions may occur. Some dogs have positive reac- histamines can be used alone or in combination tions to storage mite antigens, which may be clini- with glucocorticoids or essential fatty acids for a cally relevant, or they may exhibit cross-reactivity synergistic effect. One- to two-week-long thera- with other insects. Storage mites are ubiquitous, peutic trials with different antihistamines may be and their clinical significance is currently unknown. required to determine which one is most effective. 3. Dermatohistopathology (nondiagnostic): superfi- 7. Oral essential fatty acid supplements (180 mg/ cial perivascular dermatitis that may be spongiotic 10 lb) (various commercial products with different or hyperplastic. Inflammatory cells are predomi- omega-6:3 ratios) help control pruritus in 20% to nantly lymphocytes and histocytes. Eosinophils are 50% of cases, but 8 to 12 weeks of therapy may be uncommon. Neutrophils or plasma cells suggest needed before beneficial effects are seen. Also, a secondary infection. synergistic effect is often noted when essential fatty acid supplements are administered in combi- N nation with glucocorticoids or antihistamines. W2825-Ch007.qxd 8/12/2005 11:08 Page 163

Canine Atopy 163

TABLE 7-1 12. Cyclosporine (Atopica, Neoral) helps control pru- ritus in 60% to 75% of atopic dogs. A dose of 5 mg/ 16 Antihistamine Therapy in Dogs kg PO should be administered every 24 hours until beneficial effects are seen (approximately 4-6 Antihistamine Dose weeks). Then, dosage frequency should be tapered down to every 48 to 72 hours. For long-term Chlorpheniramine 0.2-3 mg/kg PO q 8-12 hours control, approximately 25% of dogs require daily Diphenhydramine 1-4 mg/kg PO q 8 hours dosing, 50% can be controlled with every-other- Hydroxyzine 3-7 mg/kg PO q 8 hours day dosing, and approximately 25% can be con- Amitriptyline 1-2 mg/kg PO q 12 hours trolled with twice-weekly dosing. Glucocorticoids Cyproheptadine 0.1-2 mg/kg PO q 8-12 hours can be used initially to speed response or con- Trimeprazine 0.5-5 mg/kg PO q 8-12 hours currently on a long-term basis to minimize Brompheniramine 0.5-2 mg/kg PO q12 hours cyclosporine dosage. ?Clemastine 0.05-1.5 mg/kg PO q 12 hours 13. With immunotherapy (allergy shots), 50% to 75% 4 ?Terfenadine 0.25-10 mg/kg PO q 12-24 hours of atopic dogs show good (some medical therapy Astemizole 1 mg/kg PO q 12-24 hours still needed) to excellent (no other therapy needed) Promethazine 1-2.5 mg/kg PO q 12 hours response. Clinical improvement is usually noted Loratadine 0.5 mg/kg PO q 24 hours within 6 to 8 months of initiation of immunother- Cetirizine 0.5-1 mg/kg PO q 24 hours apy, but it can take up to 1 year in some dogs. Doxepin 0.5-1 mg/kg PO q 8-12 hours 14. The prognosis is good, although lifelong therapy Dimenhydrinate 8 mg/kg PO q 8 hours for control is needed in most dogs. Relapses (pru- Tripelennamine 1 mg/kg PO q 12 hours ritic flare-ups with/without secondary infections) Clomipramine 1-3mg/kg PO q 24 hours are common, so individualized treatment adjust- ?Azatadine 1 mg/dog PO q 24 hours ments to meet patient needs may be required peri- odically. In dogs that become poorly controlled, one should rule out secondary infection (e.g., that 8. Pentoxifylline, although not necessarily effective caused by bacteria, Malassezia, dermatophyte); by itself, may be useful as an adjunctive treatment sarcoptic mange; demodicosis; concurrent food, to decrease the frequency of glucocorticoid admin- flea bite, or contact hypersensitivities; and recently istration. Pentoxifylline 10 to 15 mg/kg PO should acquired hypersensitivity to additional environ- be administered every 8 to 12 hours. mental allergens. Because a strong genetic compo- 9. Another alternative therapy that may help control nent is present, the breeding of any male or female pruritus in some dogs is misoprostol 6 mg/kg PO dog with clinical signs of atopic dermatitis should every 8 hours. be discouraged. 10. Dextromethorphan, an opioid antagonist, may also be a useful adjunct in managing the licking, chewing, and biting behaviors associated with allergic dermatitis in dogs. Dextromethorphan 2 mg/ kg PO should be administered every 12 hours. A beneficial effect should be seen within 2 weeks. 3 11. Systemic glucocorticoid therapy is often effective in controlling pruritus. It is a therapeutic option if the allergy season is short (<4 months) but may result in unacceptable adverse effects, especially if used over the long term. Prednisone 0.25 to 0.5 mg/ kg (or methylprednisolone 0.2-0.4 mg/kg) PO should be administered every 12 hours until pruritus ceases (approximately 3-10 days). Then, prednisone 0.5 to 1.0 mg/kg (methylprednisolone 0.4-0.8 mg/kg) PO should be administered every 48 hours for 3 to 7 days. The dosage should be tapered until <0.5 mg/kg prednisone (<0.4 mg/kg methylprednisolone) is being administered every FIGURE 7-8 Canine Atopy. Alopecia, erythema, and 48 hours, if long-term maintenance therapy is excoriations on the face, extremities, and flank of an adult needed. Shar pei. N

Demodex W2825-Ch005.qxd 8/4/2005 14:09 Page 102

102 CHAPTER 5 Parasitic Skin Disorders

Canine Localized Demodicosis

Features 7. The prognosis is good. Most cases resolve within 4 Skin lesions occur when there is a localized overpop- to 8 weeks, but a few may progress to generalized ulation of Demodex canis, a normal commensal inhabi- demodicosis. Systemic therapy or total body dips tant of canine skin. Demodectic overgrowth is often should not be used in intact animals as this may associated with a predisposing factor such as endo- mask the development of generalized demodicosis, parasitism, poor nutrition, immunosuppressive drug which is thought to be an inherited disease. D. canis therapy, or transient stress (e.g., estrus, pregnancy, is not considered contagious to other dogs (except surgery, boarding). Canine localized demodicosis is for newborn puppies), to cats, or to humans. common in dogs, with highest incidence reported in puppies 3 to 6 months old. Canine localized demodicosis may appear as one to five patchy areas of alopecia with variable erythema, hyperpigmentation, and scaling localized to one region of the body. Lesions are most common on the face, but they can be anywhere on the body. Lesions are not usually pruritic unless they are secondarily infected.

Top Differentials Differentials include superficial pyoderma, dermato- phytosis, and trauma.

Diagnosis FIGURE 5-3 Canine Localized Demodicosis. 1. Microscopy (deep skin scrapes): many demodectic Multiple alopecic papular lesions on the face of an adult adults, nymphs, larvae, or ova Shetland Sheep dog. (Courtesy D. Angarano.) 2. Dermatohistopathology: intrafollicular demodectic mites with varying degrees of perifolliculitis, folli- culitis, or furunculosis

Treatment and Prognosis 1. Any predisposing factors and secondary pyoderma should be identified and treated. 2. Lesions should be treated topically with 2.5% to 3% benzoyl peroxide shampoo, lotion, cream, or gel every 24 hours. 3. Miticidal treatment may not be necessary because many cases resolve spontaneously. 4. Rotenone-containing products or benzyl benzoate lotion may be miticidal when applied to lesions every 24 hours. 5. Alternatively, 0.03% to 0.05% amitraz solution applied to lesions every 24 hours is often effective. FIGURE 5-4 Canine Localized Demodicosis. Focal 6. Topical therapy is continued until follow-up skin area of alopecia and hyperpigmentation typical of a scrapings are negative and lesions have resolved. folliculitis.

N W2825-Ch005.qxd 8/4/2005 14:09 Page 103

Canine Localized Demodicosis 103

FIGURE 5-5 Canine Localized Demodicosis. FIGURE 5-6 Canine Localized Demodicosis. Numerous comedones on the abdomen of a dog with Microscopic image of demodex Demodex mites as seen with hyperadrenocorticism. Comedones are often caused by a 10¥ objective. demodicosis or Cushing’s.

FIGURE 5-7 Canine Localized Demodicosis. This FIGURE 5-8 Canine Localized Demodicosis. Focal circular area of alopecia with central hair regrowth typical area of papular dermatitis caused by demodex. of folliculitis is often misdiagnosed as dermatophytosis.

FIGURE 5-9 Canine Localized Demodicosis. A focal FIGURE 5-10 Canine Localized Demodicosis. area of alopecia on the muzzle of a young dog. (Courtesy Papular dermatitis with hyperpigmentation typical of D. Angarano.) Demodicosis.

N W2825-Ch005.qxd 8/4/2005 14:09 Page 104

104 CHAPTER 5 Parasitic Skin Disorders

Canine Generalized Demodicosis

Features D. injai infestations are typically characterized by Canine generalized demodicosis may appear as a gen- greasy seborrhea (seborrhea oleosa), especially over eralized skin disease that may have genetic tendencies the dorsum of the trunk. Other skin lesions may and can be caused by three different species of demod- include alopecia, erythema, hyperpigmentation, and ectic mites: D. canis, D. injai, and an unnamed short- comedones. bodied Demodex mite. D. canis, a normal resident of the canine pilosebaceous unit (hair follicle, sebaceous duct, and sebaceous gland), is primarily transmitted Top Differentials from the mother to neonates during the first 2 to 3 days Differentials include pyoderma (superficial or deep), of nursing, but adult-to-adult transmission may rarely dermatophytosis, hypersensitivity (flea bite, food, occur. D. injai, a recently described, large, long-bodied atopy), and autoimmune skin disorders. Demodex mite, is also found in the pilosebaceous unit, but its mode of transmission is unknown. Mode of transmission is also unknown for the short-bodied Diagnosis unnamed Demodex mite, which, unlike the other two 1. Microscopy (deep skin scrapes): many demodectic species, lives in the stratum corneum. Depending on adults, nymphs, larvae, and ova are typically found the dog’s age at onset, generalized demodicosis is clas- with D canis and the short-bodied, unnamed sified as juvenile-onset or adult-onset. Both forms are demodectic mite, although D canis may be difficult common in dogs. Juvenile-onset generalized demodi- to find in fibrotic lesions and in feet. With D. injai, cosis may be caused by D. canis and the short-bodied mites may be low in number (e.g., 1-2 mites per high unnamed Demodex mite. It occurs in young dogs, power field) usually between 3 and 18 months of age, with highest 2. Dermatohistopathology: minimal to mild suppura- incidence in medium-sized and large purebred dogs. tive perivascular dermatitis with mites in stra- Adult-onset generalized demodicosis can be caused by tum corneum, or intrafollicular demodectic mites all three mite species and occurs in dogs older than 18 with varying degrees of perifolliculitis, folliculitis, months of age, with highest incidence in middle-aged or furunculosis to older dogs that are immunocompromised because of an underlying condition such as endogenous or iatrogenic hyperadrenocorticism, hypothyroidism, Treatment and Prognosis immunosuppressive drug therapy, diabetes mellitus, 1. If adult-onset, any underlying conditions should or neoplasia. To date, only adult-onset disease has be identified and corrected. Spontaneous resolu- been reported with D. injai, with highest incidence tion of generalized demodicosis after treatment of noted in terrier breeds and their crosses, especially underlying hypothyroidism without miticidal West Highland White terriers. treatment has been reported in one dog with D Clinical signs of infestation with either D. canis or injai infestation. the unnamed Demodex mite are variable. Generalized 2. Intact dogs, especially females, should be neutered demodicosis is defined as five or more focal lesions, or because estrus or pregnancy may trigger relapse. two or more body regions affected. Usually, patchy, 3. Any secondary pyoderma should be treated with regional, multifocal, or diffuse alopecia is observed appropriate long-term (minimum 3-4 weeks) sys- with variable erythema, silvery grayish scaling, temic antibiotics that are continued at least 1 week papules or pruritus. Affected skin may become licheni- beyond clinical resolution of the pyoderma. fied, hyperpigmented, pustular, eroded, crusted, or 4. Traditional miticidal treatment entails the ulcerated from secondary superficial or deep pyo- following: derma. Lesions can be anywhere on the body, includ- Total body hair coat clip if dog is medium- to ing the feet. Pododemodicosis is characterized by any long-haired combination of interdigital pruritus, pain, erythema, Weekly bath with 2.5% to 3% benzoyl peroxide alopecia, hyperpigmentation, lichenification, scaling, shampoo, followed by a total body application swelling, crusts, pustules, bullae, and draining tracts. of 0.03% to 0.05% amitraz solution. The cure rate Peripheral lymphadenomegaly is common. Systemic ranges from 50% to 86%. signs (e.g., fever, depression, anorexia) may be seen if 5. For demodectic pododermatitis, in addition to N secondary bacterial sepsis develops. weekly amitraz dips, foot soaks in 0.125% amitraz solution should be performed every 1 to 3 days. W2825-Ch005.qxd 8/4/2005 14:09 Page 105

Canine Generalized Demodicosis 105

6. Alternatively, treatment with ivermectin 0.6 mg/ kg PO every 24 hours is often effective against gen- eralized demodicosis. Initially, ivermectin 0.1 mg/ kg PO is administered on day 1, then 0.2 mg/kg PO is administered on day 2, with oral daily incre- ments of 0.1 mg/kg until 0.6 mg/kg/day is being administered, assuming that no signs of toxicity develop. If the dog cannot tolerate a 0.6-mg/ kg/day dosage, treatment with 0.4 mg/kg/day can be attempted. The cure rate for 0.6 mg/kg/day ivermectin is 85% to 90%. 7. Another effective alternative therapy is milbe- mycin oxime, 0.5 to 2 mg/kg PO every 24 hours. The cure rate is 85% to 90%, with the prognosis for cure being better for juvenile-onset cases than for FIGURE 5-11 Canine Generalized Demodicosis. adult-onset cases. Generalized alopecia and papules with crusts and scales on 8. Doramectin is also reported to be effective against the head and neck of a juvenile dog. canine demodicosis at a dose of 0.6 mg/kg SC once weekly. The cure rate is approximately 85%. Adverse effects are uncommon but include, as for ivermectin, dilated pupils, lethargy, blindness, and coma. 9. For dogs £20 kg, the use of 9% amitraz collars may be effective. The dog’s neck is shaved to ensure that the collar is in close contact with the skin, and the collar is replaced every 2 weeks for the dura- tion of treatment. In small dogs, use of 9% amitraz collars alone may be as effective as ivermectin (0.6 mg/kg/day PO). Also, the combined use of oral ivermectin and 9% amitraz collars may be more effective than either oral ivermectin or 9% amitraz collars alone. 10. Moxidectin 1% injectable for cattle has been FIGURE 5-12 Canine Generalized Demodicosis. reported effective when administered at a dosage Multifocal alopecia over the head, trunk, and extremities of of 0.4 mg/kg PO every 24 to 72 hours. However, an adult dog with generalized Demodicosisdemodicosis. adverse effects are common, especially when the drug is administered SC. 11. Regardless of the miticidal treatment chosen, therapy is administered over the long term (weeks to months). Treatments should be continued for at least 1 month beyond the time when follow-up skin scrapings become negative for mites. 12. The prognosis is good to fair. Relapses may occur, requiring periodic or lifelong treatment in some dogs. The use of glucocorticosteroids in any dog that has been diagnosed with demodicosis should be avoided. Because of its hereditary predisposi- tion, neither female nor male dogs with juvenile- onset generalized demodicosis should be bred. D canis is not considered contagious to cats or to humans. It is transmitted from bitch to newborn puppies during the first 2 to 3 days of nursing, and FIGURE 5-13 Canine Generalized Demodicosis. possibly between adult dogs that are close cohab- Close-up of the dog in Figure 5-12. The multifocal areas of alopecia with mild hyperpigmentation are apparent. itants. The mode of transmission for D injai and the unnamed short-bodied Demodex mite is unknown. N W2825-Ch005.qxd 8/4/2005 14:10 Page 109

Feline Demodicosis 109

Feline Demodicosis

Features corneum, or intrafollicular mites with varying Feline demodicosis is a skin disease that can be caused degrees of perifolliculitis and folliculitis by two different species of demodectic mites—D cati, a normal commensal of cat skin, and D gatoi, a short-bodied Demodex mite whose normal habitat is Treatment and Prognosis unknown. Skin disease may be localized or general- 1. Any predisposing factors should be identified and ized. D gatoi is a relatively recently recognized infec- corrected. tion that is contagious and usually causes pruritic skin 2. D gatoi may be difficult to find on microscopy but disease. D cati infections are often associated with an respond well to lime sulfur dips. underlying immunosuppressive or metabolic disease a. 2%-4% lime sulfur dips applied q 3-7 days for 4-8 such as feline immunodeficiency virus (FIV), feline weeks. Clinical improvement is often observed leukemia virus (FeLV), toxoplasmosis, systemic lupus within 3-4 weeks, but therapy should be con- erythematosus, neoplasia, or diabetes mellitus. Local- tinued for a total of 6-8 weeks to resolve the ized or generalized demodicosis caused by D cati infec- infection tion is rare in cats. D gatoi infections are emerging as a b. Anecdotal reports suggest that ivermectin and common cause of pruritic skin disease in cats, espe- milbemycin may be variably effective, but cially in the southern United States. studies are lacking Localized disease is characterized by a variably pru- 3. D cati: localized lesions may resolve spontaneously ritic ceruminous otitis externa or by focal patchy alope- without treatment. cia and erythema that may be scaly or crusty. Localized a. For localized lesions, topical therapies that may skin lesions are most common around the eyes, on the be effective when applied q 24 hours include the head, or on the neck. Generalized disease is character- following: ized by variably pruritic, multifocal, patchy, regional, Rotenone or symmetrical alopecia, with or without erythema, 0.025%-0.03% amitraz solution scaling, crusts, macules, and hyperpigmentation. b. For generalized lesions, treatments that may be Lesions usually involve the head, neck, limbs, flanks, effective include the following: or ventrum. Ceruminous otitis externa and secondary 2% lime sulfur solution applied to the entire pyoderma may be present. body q 7 days Doramectin 0.6 mg/kg SC once weekly 0.015%-0.025% amitraz solution applied to entire Top Differentials body q 1-2 weeks. Note: Do not use amitraz on Differentials include dermatophytosis, other ectopara- diabetic cats sites (Cheyletiella, Notoedres, ear mites), hypersensitiv- c. For both localized and generalized disease, treat- ity (flea bite, food, atopy), psychogenic alopecia, and ments should be continued until lesions have other causes of otitis externa. resolved and follow-up skin scrapings are nega- tive for mites (approximately 3-4 weeks) 4. The prognosis for localized demodicosis is good. Diagnosis The prognosis for generalized demodicosis is good 1. Microscopy (deep and superficial skin scrapings, to guarded, depending on the underlying cause. ear swabs): demonstration of demodectic adults, D cati is not considered contagious to other cats nymphs, larvae, or ova. D gatoi may be difficult (except for newborn kittens), to dogs, or to humans. to find The mode of transmission for D gatoi is unknown, 2. D gatoi: history, clinical signs, and response to but reports of unrelated household cats being weekly lime sulfur dips simultaneously affected suggest that it may be con- 3. Dermatohistopathology: minimal to mild suppura- tagious between adult cats. tive perivascular dermatitis with mites in stratum

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Flea Allergy Dermatitis 173

Flea Allergy Dermatitis (flea bite hypersensitivity)

Features Treatment and Prognosis Flea allergy dermatitis is a common skin disease in 1. Affected and all in-contact dogs and cats should be dogs and cats sensitized to flea bites. Symptoms are treated with adulticidal flea sprays, spot-on solu- usually seasonal (warm weather months and in the tions, or dips every 7 to 30 days, as instructed on fall) in temperate zones and often nonseasonal in sub- the label. Products that contain fipronil, imidoclo- tropical and tropical areas. prid, or selamectin are especially effective when used topically every 3 to 4 weeks. In heavily flea- Dogs infested environments, fleas may continue to be Lesions include pruritic, papular, crusting eruptions found on animals in spite of topical flea control. In with secondary erythema, seborrhea, alopecia, excori- these cases, affected animals should also be admin- ations, pyoderma, hyperpigmentation, and licheni- istered nitenpyram at a minimum dose of 1 mg/kg fication. The distribution typically involves the PO every 24 to 48 hours for 1 to 2 weeks, or until caudodorsal lumbosacral area, dorsal tail head, cau- fleas are no longer seen, and the environment domedial thighs, abdomen, and flanks. should be treated (see Number 5 below). 7 2. Topical or systemic insect growth regulators (lufen- Cats uron, piriproxyfen, methoprene) may be effective Patients commonly present with pruritic miliary alone or used in combination with adulticidal dermatitis with secondary excoriations, crusting, therapy. and alopecia of the neck, dorsal lumbosacral area, 3. Flea control therapy should be continued from caudomedial thighs, and ventral abdomen. Other spring until first snowfall in temperate areas and symptoms include symmetrical alopecia secondary to year-round in warm climates. excessive grooming and eosinophilic granuloma 4. Flea-allergic animals should be treated prophylacti- complex lesions. cally with nitenpyram, minimum dose 1 mg/kg PO, on any day that an encounter is planned with other potentially flea-infested animals (e.g., a visit Top Differentials to the groomer, veterinary hospital, park, another Differentials include atopy, food hypersensitivity, household with animals). No more than one treat- other ectoparasites (scabies, cheyletiellosis, pediculo- ment with nitenpyram should be administered per sis, demodicosis), superficial pyoderma, dermatophy- day. 8 tosis, demodicosis, and Malassezia dermatitis. 5. In heavily flea-infested environments, areas where pets spend the most time should be treated. Indoor premises should be treated with an insecticide Diagnosis and an insect growth regulator (e.g., methoprene, 1. Usual basis: history and clinical findings; rule out piriproxyfen). The outdoor environment should other differentials be treated with insecticidal or biologic products 2. Visualization of fleas or flea excreta on body: may designed for such use. be difficult on flea-allergic animals 6. To help resolve pruritus, one should consider glu- 3. Aggressive flea control as flea-allergic animals are cocorticoid therapy. Oral prednisone 0.5 mg/kg 6 very effect at removing fleas through grooming (dogs) or 1.0 mg/kg (cats) should be administered 4. Allergy testing (intradermal, serologic): positive every 12 hours for 3 to 7 days, then every 24 hours skin test reaction to flea antigen or positive serum for 3 to 7 days, then every 48 hours for 3 to 7 days. immunoglobulin (Ig)E antiflea antibody titer is Alternatively, cats may be given repositol methyl- highly suggestive, but false-negative results are prednisolone acetate 20 mg/cat or 4 mg/kg SC possible once or twice at a 2- to3-week interval. 9 5. Dermatohistopathology (nondiagnostic): varying 7. For secondary pyoderma, appropriate systemic degrees of superficial or deep perivascular to antibiotics should be administered for at least 3 to interstitial dermatitis, with eosinophils often 4 weeks. predominating 8. The prognosis is good if strict flea control is prac- 6. Response to flea control: symptoms resolve ticed. Fleas may infest other in-contact animals and humans. They may carry blood-borne diseases in a manner similar to ticks. N W2825-Ch007.qxd 8/12/2005 11:10 Page 174

174 CHAPTER 7 Hypersensitivity Disorders

Flea Allergy Dermatitis (flea bite hypersensitivity)—cont’d

FIGURE 7-38 Flea Allergy Dermatitis. Moth-eaten FIGURE 7-39 Flea Allergy Dermatitis. Lumbar alopecia on the lumbar and caudal flank area is typical of dermatitis caused by a flea allergy. Most lesions in flea allergy dermatitis in dogs. flea-allergic patients are caudal to the rib cage.

FIGURE 7-40 Flea Allergy Dermatitis. Severe lumbar FIGURE 7-41 Flea Allergy Dermatitis. Same dog as in and tail head dermatitis in a flea-allergic dog. Figure 7-39. The lumbar dermatitis was caused by flea allergy. Note that the lesions are caudal to the last rib.

FIGURE 7-42 Flea Allergy Dermatitis. Hot spots FIGURE 7-43 Flea Allergy Dermatitis. Allergic (pyotraumatic dermatitis) are usually caused by exposure alopecia on the caudal flanks of a flea-allergic cat. to fleas. The severe, erythematous, moist, erosive dermatitis with expanding papular rash is typical of pyotraumatic dermatitis. N

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34 CHAPTER 3 Bacterial Skin Diseases

Superficial Pyoderma (superficial bacterial folliculitis)

Features emerging as a common canine isolate in patients with Superficial pyoderma is a superficial bacterial infection chronic infections and previous antibiotic exposure. Ad- involving hair follicles and the adjacent epidermis. The ditionally, methicillin-resistant Staphylococcus aureus infection usually occurs secondary to an underlying (human MRSA) may be becoming more common cause; allergies and endocrine disease are the most among veterinary species. common causes (Box 3-3). Superficial pyoderma is common in dogs and rare in cats. Superficial pyoderma is characterized by focal, mul- Top Differentials tifocal, or generalized areas of papules, pustules, Differentials include demodicosis, dermatophytosis, crusts, and scales, epidermal collarettes, or circum- scabies, and autoimmume skin diseases. scribed areas of erythema and alopecia that may have hyperpigmented centers. Short-coated dogs often present with a “moth-eaten” patchy alopecia, small Diagnosis tufts of hair that stand up, or reddish brown discol- 1. Rule out other differentials oration of white hairs. In long-coated dogs, symptoms 2. Cytology (pustule): neutrophils and bacterial cocci can be insidious and may include a dull, lusterless hair 3. Dermatohistopathology: epidermal microabscesses, coat, scales, and excessive shedding. In both short- and nonspecific superficial dermatitis, perifolliculitis, long-coated breeds, primary skin lesions are often and folliculitis. Intralesional bacteria may be diffi- obscured by remaining hairs but can be readily appre- cult to find ciated if an affected area is clipped. Pruritus is variable, 4. Bacterial culture: Staphylococcus species ranging from none to intense levels. Bacterial infec- tions secondary to endocrine disease may cause pruri- tus, thereby mimicking allergic skin disease. Treatment and Prognosis Staphylococcus intermedius is the most common bac- 1. The underlying cause should be identified and terium isolated from canine pyoderma and is usually corrected. limited to dogs. Staphylococcus schleiferi is a relatively 2. Systemic antibiotics (minimum 3-4 weeks) should new bacterial species in dogs and humans that is be administered and continued 1 week beyond complete clinical resolution (see Box 3-1). 3. Concurrent bathing every 2 to 7 days with an BOX 3-3 antibacterial shampoo that contains chlorhexidine, ethyl lactate, or benzoyl peroxide is helpful. Causes of Secondary Superficial and 4. If lesions recur within 7 days of antibiotic discon- Deep Pyoderma tinuation, the duration of therapy was inadequate and antibiotics should be reinstituted for a longer ■ Demodicosis, scabies, Pelodera time period. ■ Hypersensitivity (e.g., atopy, food, flea bite) 5. If lesions do not completely resolve during antibi- ■ Endocrinopathy (e.g., hypothyroidism, otic therapy, or if they recur weeks to months later, hyperadrenocorticism, sex hormone imbalance, alopecia X) an underlying cause should be sought (see Box 3-3). ■ Immunosuppressive therapy (e.g., glucocorticoids, progestational compounds, cytotoxic drugs) 6. No response to antibiotic therapy suggests anti- ■ Autoimmune and immune-mediated disorders biotic resistance or a nonbacterial skin disease. ■ Trauma or bite wound 7. If lesions resolve but pruritus persists, underlying ■ Foreign body ectoparasitism or an allergy is probably present. ■ Poor nutrition 8. The prognosis is good if the underlying cause can be identified and corrected or controlled.

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Superficial Pyoderma 35

FIGURE 3-24 Superficial Pyoderma. The alopecia, FIGURE 3-25 Superficial Pyoderma. The papular papules, and crusts around the eye of this allergic Irish rash on the abdomen of an allergic dog caused by multi- setter are typical of bacterial folliculitis. drug-resistant Staphylococcus schleiferi. The papular rash typical of pyoderma persisted despite high high-dose antibiotic therapy, suggesting the antibiotic antibiotic- resistant nature of the organism.

FIGURE 3-26 Superficial Pyoderma. FIGURE 3-27 Superficial Pyoderma. This papular Close-up of the papular rash in figure Figure 3-25. dermatitis forms coalescing lesions as demonstrated by the erythematous plaque. Note the early epidermal collarettes associated with some papules.

FIGURE 3-28 Superficial Pyoderma. FIGURE 3-29 Superficial Pyoderma. Severe Close-up of the N erythematous dermatitis with large epidermal collarettes dog in figure Figure 3-28. The erythematous dermatitis caused by a multi-drug-resistant infection. with epidermal collarettes formation is apparent. W2825-Ch003.qxd 8/4/2005 13:33 Page 29

Mucocutaneous Pyoderma 29

Mucocutaneous Pyoderma

Features Box 3-1 Mucocutaneous pyoderma is a bacterial infection of mucocutaneous junctions. It is uncommon in dogs; Oral Antibiotics for Bacterial German shepherds and their crosses are possibly Skin Infection predisposed. Lesions are characterized by mucocutaneous Antibiotic-Dose swelling, erythema, and crusting that may be bilater- First-Line Drugs ally symmetrical. Affected areas may be painful or ■ Cefadroxil 22 mg/kg q 8-12 hours pruritic and self-traumatized, and they may become ■ Cefpodoxime 5-10 mg/kg q 12-24 hours exudative, eroded, ulcerated, fissured, and depig- ■ Cephalexin 22 mg/kg q 8 hours, or 30mg/kg q 12 hours mented. The margins of the lips, especially at the com- ■ Cephradine 22 mg/kg q 8 hours missures, are most frequently affected, but the nares ■ Clavulanated amoxicillin 12.5-22 mg/kg q 8-12 hours and, less commonly, the eyelids, vulva, prepuce, and ■ Ormetoprim/sulfadimethoxine 55 mg/kg once on day 1, then 27.5 mg/kg q 24 hours anus are sometimes involved. Concurrent axillary or ■ Oxacillin 22 mg/kg q 8 hours inguinal ulcerations may be present. ■ Trimethoprim/sulfadiazine 22-30 mg/kg q 12 hours ■ Trimethoprim/sulfamethoxazole 22-30 mg/kg q 12 hours

Top Differentials Second-Line Drugs Differentials include superficial pyoderma, lip fold ■ Chloramphenicol 50 mg/kg q 8 hours dermatitis, demodicosis, dermatophytosis, Malassezia ■ Ciprofloxacin 5-15 mg/kg q 12 hours dermatitis, candidiasis, autoimmune skin disorders, ■ Clindamycin hydrochloride 5.5-11 mg/kg q 12 hours and epitheliotropic lymphoma. ■ Enrofloxacin 10-20 mg/kg q 12-24 hours ■ Erythromycin 10-15 mg/kg q 8 hours ■ Ibafloxacin 15mg/kg q 24 hours Diagnosis ■ Marbofloxacin 2.75-5.5 mg/kg q 12-24 hours 1. Usual basis: history, clinical findings, and rule out ■ Orbifloxacin 5-7.5 mg/kg q 24 hours other differentials 2. Cytology (impression smear): bacterial cocci or rods 3. Dermatohistopathology: epidermal hyperplasia, 2. For severe lesions, in addition to topical therapy, superficial epidermal pustules, crusting, and appropriate systemic antibiotics should be admin- lichenoid dermatitis with preservation of base- istered for 3 weeks (Box 3-1). ment membrane. Dermal infiltrates are often 3. Prognosis is good, but lifelong maintenance therapy predominantly composed of plasma cells, with is often needed. If regularly-applied, topical anti- varying numbers of lymphocytes, neutrophils, and biotics do not maintain remission; however, pulse macrophages. therapy with systemic antibiotics may be effective. Cephalexin 30 mg/kg PO every 12 hours, or clavu- lanated amoxicillin 22 mg/kg PO every 12 hours, Treatment and Prognosis should be administered until lesions have com- 1. For mild to moderate lesions, affected areas should pletely resolved (for approximately 3-6 weeks, then be clipped and cleaned with shampoo that con- with long-term twice-weekly pulse therapy of tains benzoyl peroxide or chlorhexidine. Topical either cephalexin 30 mg/kg PO every 12 hours, or mupirocin ointment or cream should be applied clavulanated amoxicillin 22 mg/kg PO every 12 every 12 to 24 hours for 1 week, then every 3 to 7 hours, on 2 consecutive days each week [see Box days for maintenance therapy, as needed. 3-1]). 1

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Otitis Eliminating Otitis in 4 Steps with 6 Products

Four Steps

Find the underlying disease.

Most chronic cases of otitis are caused by the changes in the micro environment that normally protects the ear canal from opportunistic yeast and bacterial overgrowth. When the tissue becomes inflamed as with allergy or the glands and normal defense mechanisms are altered as with endocrine diseases, the bacteria and yeast rapidly populate the canal leading to secondary infections. Foreign bodies, neoplasia, and polyps can act as a nidus for recurrent infections.

Conformational changes are often blamed for causing the recurrent otitis. In actuality, abnormal ear conformation is rare and typically not the cause of secondary infections.

Use High concentration Topical products

Systemic antimicrobials do not achieve high enough concentrations in the ear tissue to kill pseudomonas. Yeast and bacteria (with lower MICs) may be effectively treated with systemic treatments but topicals usually work fine.

Use High volumes and Frequent Applications of therapeutics

One of the most common causes of treatment failures is the use of too small volumes of cleaners or treatment solutions. Enough topical solution must be used to coat the entire ear canal thus saturating the organisms with the antimicrobial.

Dropper bottles provide an easy method that allows the owner to treat the ear more quickly yet ensuring adequate volume has been used. Many products are dispensed in bottles that conceal the applicator making it impossible to visualize the solution during the treatment procedure. This results in too little medicine being instilled and thus treatment failures.

Treating the active otitis requires instilling enough of the therapeutic every 12 hours until the infection resolves.

Don't Just Stop but Taper Frequency

One of the most common problems is stopping the medications all at once when the infection has resolved. Because otitis is caused by underlying/primary diseases (allergies, endocrinopathies, etc.) continuing ear treatments to prevent infection recurrence is crucial. Often the frequency of otic cleaning and/or treatment can be reduced to every 2-7 days (after weekly bath works well). When the underlying disease has been corrected, the ear maintenance treatments can be reduced even further.

Eliminating Otitis in 4 Steps with 6 Products

6 Products (Hnilica's list)

1. Alcohol based ear cleaner (Vet Solutions Ear Cleaner) Cases selection: normal ears of swimming dogs Benefits: Clean, dry, and disinfect the ear canal (like swimmer's ear therapies) Adverse effects: Pain if broken skin, ototoxic if ruptured ear drum

In dogs that swim often, an alcohol based ear cleaner is useful to clean, disinfect, and dry the ear after swimming. Alcohol ear cleaners are usually inexpensive.

Alcohol will cause PAIN if used in ears that have lesions or active inflammation. Additionally, if the tympanic membrane is ruptured, alcohol ear cleaners should not be used.

2. Epiotic (Virbac) Case selection: Any dirty ear Benefits: One of the best yet mild ear cleaners for wax or pus Adverse effects: none

Any dirty ear that needs cleaning should be flushed by filling the entire ear canal; massaging the canal and letting the patient shake. No swabs should be used as these are like "Brilo pads on a stick" and irritate the canal. Ear cleaning solutions can be irritating if used more often than every other day. Epiotic has mild antibacterial and anti yeast effects.

3. Otomax® (Schering) Case selection: 98% of infectious otitis cases can be successfully treated with Otomax® bid Benefits: Thin ointment that helps dissolve wax with a moderately potent steroid, new generation antifungal, and gentamycin. Adverse effects: Few: ototoxic in less than 1% of cases.

Otomax® is thin enough to penetrate the deep ear canal in most otitis cases. It has multivalent antimicrobial effect (yeast and bacteria) with a moderately potent steroid to help normalize the inflammation in the ear canal. Most otitis cases will respond to Otomax® therapy with in 10-14 days. Otomax® can also be used for chronic/recurrent cases to prevent the infections from returning (instilled every 2- 7 days as needed to prevent infection and control inflammation). Stopping otic therapy completely is a common mistake in dogs with recurrent otitis associated with an underlying/primary disease.

Dropper bottles should be used to ensure sufficient volume is used to coat the entire ear canal (1/3 dropper in small dogs and ½ dropper in big dogs). BID dosing is best.

4. LA Baytril 100 Injectable (Bayer) Case selection: Pseudomonas Otitis Benefits: High concentrations of enrofloxacin can be achieved with less volume Adverse effects: contains benzyl and butyl alcohol

Use the injectable enrofloxacin to make 1% - 2% ear treatment solutions (10- 20mg/ml final concentration)

5. T8 Solution (DVM Pharmaceuticals) Case selection: Pseudomonas Otitis Benefits: Contains surfactants to clean the ear and benzyl alcohol to help kill pseudomonas Adverse effects: none documented even when used with ruptured ear drums

The emerging best in class therapy for chronic and recurrent otitis caused by secondary Pseudomonas infections relies on the use of tris-EDTA compounded treatments. Tris-EDTA alters the bacteria’s normal defensive mechanisms and has a synergistic effect when used in combination with topical antibiotics. With the recent introduction of new otic preparations; the use of tris-EDTA has become more common. Anecdotal reports suggest good efficacy against Pseudomonas otitis when tris-EDTA is combined with high concentrations of enrofloxacin even when used without systemic antibiotics.

T8 Solution® contains surfactants (nonoxynol 12), tris-EDTA, benzyl alcohol and buffers to make a final solution with a pH of 8.5. The surfactant provides a mild cleaning action that helps remove the otic exudate without irritating the otic canal tissue. The tris-EDTA in a buffered solution makes it possible to compound enrofloxacin into the solution without the inactivation of the fluoroquinolone caused by the acidic pH in acid otic cleaners. Benzyl alcohol is an FDA approved aromatic alcohol. Studies evaluating the ototoxicity of benzyl alcohol are lacking; however, benzyl alcohol is a bacteriostatic preservative in many pharmaceuticals, ophthalmic and otic solutions (including Cipro HC Otic and Baytril Otic), cough syrup, bacteriostatic water for injection, and other intravenously medications. Additionally benzyl alcohol has been shown to be an effective topical local anesthetic. A recent study demonstrated that a tris EDTA solution containing benzyl alcohol significantly reduced the bacterial counts of Staphylococcus intermedius and Pseudomonas aeruginosa where as a tris EDTA solution without benzyl alcohol had no effect on Staphylococcus intermedius and Pseudomonas aeruginosa counts. The authors concluded that the addition of benzyl alcohol was necessary to significantly reduced Staphylococcus intermedius and Pseudomonas aeruginosa counts.

6. Steroids (oral or MometamaxR) Case selection: Severely Swollen, stenotic, and painful ears Benefits: Reduce the inflammation, pain, and swelling: also allow the topical medications to penetrate the deep ear canal better Adverse effects: Iatrogenic Cushing's disease

Potent steroid therapy greatly improves the clinical symptoms of severe otitis. The swelling and pain commonly seen can be greatly reduced with steroid therapy making it easer for the owner to medicate the ear canal. Additionally, the ear canals usually open significantly allowing the topical treatments to penetrate into the deep canal better.

Several treatment options are available. Oral steroids provide an effective inside-out treatment with out complicating the topical treatment protocols. High antiinflammatory doses should be used for 7-14 days.

Alternatively, potent topical steroids may be used (Synotic, Mometamax). These products contain extremely potent steroids that penetrate the ear tissue causing a local effect as wells as deep tissue and systemic steroidal effects. These products should be used and assumed to be absorbed systemically. Therefore, short durations of bid dosing should be administered in severe otitis cases when the clinician would be willing to use systemic steroid therapy. Using topical steroids complicates the topical antimicrobial treatment. Compounding (mixing) too many ingredients in bottles or in the ear canal creates interactions that can decrease the efficacy of the treatments.

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Canine Food Hypersensitivity 167

Canine Food Hypersensitivity (canine cutaneous adverse food reaction)

Features a strict home-cooked or commercially prepared Canine food hypersensitivity is an adverse reaction to restricted diet (one protein and one carbohydrate a food or food additive. It can occur at any age, in source). The hypoallergenic diet should not contain recently weaned puppies to elderly dogs that have food ingredients previously administered in dog been eating the same dog food for years. Approxi- food, treats, or table scraps (Table 7-2), nor should mately 30% of dogs diagnosed with food allergy are flavored heartworm preventative, flavored medica- younger than 1 year of age. It is common in dogs. tions, nutritional supplements, or chewable treats Canine food hypersensitivity is characterized by (i.e., pig ears, cow hooves, rawhide, dog biscuits, nonseasonal pruritus that may or may not respond to table food such as cheese or peanut butter to hide steroid therapy. This pruritus may be regional or gen- pills in) be administered during the hypoallergenic eralized and usually involves the ears, feet, inguinal diet trial. Beef and dairy are the most common food or axillary areas, face, neck, and perineum. Affected allergens in dogs. skin is often erythematous, and a papular rash may be 5. Provocative challenge: recurrence of symptoms present. Self-trauma–induced lesions include alopecia, within hours to days of reintroduction of suspect excoriations, scales, crusts, hyperpigmentation, and allergen into the diet. lichenification. Secondary superficial pyoderma, Malassezia dermatitis, and otitis externa are common. Other symptoms that may be seen are acral lick der- Treatment and Prognosis matitis, chronic seborrhea, and recurring pyotraumatic 1. Any secondary pyoderma, otitis externa, and dermatitis. Some dogs are minimally pruritic, with Malassezia dermatitis should be treated with appro- the only symptom being recurrent infection with priate therapies. Controlling secondary infection is pyoderma, Malassezia dermatitis, or otitis. In these an essential component of managing food-allergic cases, the pruritus is present only when secondary dogs. infections are left untreated. Occasionally, urticaria or 2. A flea control program should be instituted to angioedema may occur. Concurrent gastrointestinal prevent flea bites from aggravating the pruritus. signs (e.g., frequent bowel movements, vomiting, diar- 3. Offending dietary allergen(s) should be avoided. rhea, flatulence) are occasionally reported. A balanced home-cooked diet or a commercial hypoallergenic diet should be provided. 4. To identify offending substances to be avoided, one Top Differentials new food item should be added to the hypoaller- Differentials include other hypersensitivities (atopy, genic diet every 2 to 4 weeks. If the item is aller- flea bite, contact), parasites (scabies, cheyletiellosis, genic, clinical symptoms will recur within 7 to 10 pediculosis), folliculitis (caused by bacteria, dermato- days. Note: Some dogs (approximately 20%) should phyte, Demodex), and Malassezia dermatitis. be fed home-cooked diets to remain symptom-free. For these dogs, commercial hypoallergenic diets are ineffective, presumably because their hypersensi- Diagnosis tivity relates to a food preservative or dye. 1. Rule out other differentials. 5. Alternatively, medical therapy alone with systemic 2. Dermatohistopathology (nondiagnostic): varying glucocorticoids, antihistamines, fatty acids, or degrees of superficial perivascular dermatitis. topical therapies as described for canine atopy can Mononuclear cells or neutrophils may predominate. be attempted. However, response is variable. Eosinophils may be more numerous than in 6. For some dogs whose only symptom is recurring atopy superficial pyoderma, control may be achieved 3. Food allergy testing (intradermal, serologic): not with long-term, low-dose antibiotic therapy alone. recommended because test results are unreliable. Cephalexin 20 mg/kg PO is administered every Some dogs will have positive reactions to storage 8 hours, or 30 mg/kg every 12 hours (minimum, 4 mite antigens, which may be clinically relevant, or weeks), and is continued at least 1 week beyond they may exhibit cross-reactivity with other insects. complete clinical resolution of the pyoderma. Storage mites are ubiquitous, and their clinical sig- Cephalexin is then continued as maintenance nificance is currently unknown. therapy at 30 mg/kg PO every 24 hours. 5 4. Response to hypoallergenic diet trial: symptoms 7. For recurrent otitis, the owner should perform at- N improve within 10 to 12 weeks of initiation of home ear cleaning every 2 to 7 days with a cerumi- W2825-Ch007.qxd 8/12/2005 11:09 Page 168

168 CHAPTER 7 Hypersensitivity Disorders

Canine Food Hypersensitivity (canine cutaneous adverse food reaction)—cont’d

TABLE 7-2 Commercial Hypoallergenic Diets for Dogs

Manufacturer Product How Supplied Main Ingredients

Hills Prescription Diet Canine Canned Rice, lamb, lamb liver, rice flour, powdered cellulose, d/d Lamb and Rice vegetable oil Prescription Diet Canine Canned Whitefish, rice, rice flour, animal fat, powdered d/d Whitefish and Rice cellulose, vegetable oil Prescription Diet Canine Dry Brewers’ rice, salmon, rice protein concentrate, d/d Rice and Salmon animal fat, vegetable oil, sucrose Prescription Diet Canine Dry Brewers’ rice, duck by-products, rice protein con d/d Rice and Duck centrate, animal fat, vegetable oil, sucrose Prescription Diet Canine Dry Brewers’ rice, dried egg product, animal fat, veg d/d Rice and Egg etable oil, sucrose Prescription Diet Canine z/d Dry Dried potato products, hydrolyzed chicken liver, potato starch, vegetable oil, hydrolyzed chicken Prescription Diet Canine z/d Dry Starch, hydrolyzed chicken liver, vegetable oil, Ultra hydrolyzed chicken Iams Eukanuba Veterinary Diets Canned Catfish, herring meal, modified potato starch, dried Response FP Formula beet pulp, corn oil Dry Potato, herring meal, catfish, animal fat, dried beet pulp, fish digest Eukanuba Response KO Dry Oat flour, kangaroo, canola meal, animal fat, dried Kangaroo and Oatmeal beet pulp, fish oil Innovative Veterinary Limited Ingredient Lamb Canned Potato, lamb stock, lamb, lamb by-products, canola Diets and Potato oil, salmon oil Dry Dehydrated potatoes, lamb, lamb meal, potato protein, canola oil, potato fiber, salmon oil Limited Ingredients Venison Danned Potato, venison stock, venison, venison by-products, and Potato canola oil, salmon oil Dry Dehydrated potatoes, venison, potato protein, canola oil, potato fiber, salmon oil Limited Ingredient Rabbit Canned Potato, rabbit, rabbit stock, rabbit by- products, and Potato canola oil, salmon oil Dry Dehydrated potatoes, rabbit, potato protein, canola oil, potato fiber, salmon oil Limited Ingredient Duck Canned Potatoes, duck, duck stock, duck by-products, and Potato canola oil, salmon oil Dry Dehydrated potatoes, duck, duck meal, potato fiber, canola oil, salmon oil Limited Ingredient Canned Potatoes, whitefish, fish stock, canola oil, salmon Whitefish and Potato stock Innovative Pet Nature’s Recipe Easy-to- Canned Lamb stock, lamb, soybean meal, ground rice, Foods Digest Lamb, Lamb Meal, potaoes, carrots, lamb by-products, canola oil, Rice and Barley Formula lamb liver, ground barley Dry Lamb meal, ground rice, cracked pearl barley, animal fat, natural flavor, tomato puree Nature’s Recipe Allergy Canned Soybean meal, ground rice, carrots, potatoes, Vegetarian Formula ground barley, canola oil Dry Ground rice, soy flour, cracked pearl barley, canola oil Nature’s Recipe Allergy Canned Venison stock, venison meal, venison by-products, Venison Meal and Rice potatoes, carrots, ground rice, canola oil, peas, Formula ground barley Pet Products Plus, Sensible Choice With Lamb Canned Lamb, brewers’ rice Inc and Rice Dry Lamb meal, brewers’ rice, rice flour, rice gluten, poultry fat Sensible Choice Lamb Meal Dry Lamb meal, brewers’ rice, rice gluten, rice flour, and Rice Puppy poultry fat N W2825-Ch007.qxd 8/12/2005 11:09 Page 169

Canine Food Hypersensitivity 169

TABLE 7-2 Commercial Hypoallergenic Diets for Dogs—cont’d

Manufacturer Product How Supplied Main Ingredients

Purina CNM HA-Formula Dry Corn starch, modified isolated soy protein, coconut oil, canola oil CNM LA-Formula Dry Brewers’ rice, salmon meal, trout, canola meal, tallow, brewer’s dried yeast, canola oil, fish oil Waltham Waltham Veterinary Diet Canned Lamb by-products, lamb, rice Selected Protein With Lamb and Rice Waltham Veterinary Diet Dry Rice, catfish meal, rice gluten, cellulose powder, Selected Protein With catfish, vegetable oil Rice and Catfish Nutro Products, Inc Natural Choice Lamb and Canned Lamb broth, lamb, lamb liver, rice gluten, ground Rice Formula rice, dried egg product Dry Lamb meal, ground rice, rice bran, rice flour, sun flower oil, rice gluten, dried egg product Natural Choice Lite Lamb Canned Lamb broth, lamb, barley, defatted rice bran, rice and Rice Formula gluten, ground rice, peas, lamb liver Dry Rice flour, lamb meal, rice bran, ground rice, sunflower oil, dried egg product, rice gluten Natural Choice Puppy, Canned Lamb broth, lamb liver, lamb, lamb kidney, dried egg Lamb and Rice Formula product, ground rice, rice gluten

nolytic agent (that does not need to be flushed 8. The prognosis is good. In dogs that are poorly con- out) to prevent accumulation of ear wax and debris. trolled, owner noncompliance should be ruled out, Lifelong weekly ear cleaning may be necessary along with development of hypersensitivity to an to prevent relapses of otitis. The use of cotton ingredient in the hypoallergenic diet, secondary swabs (which may damage the epithelium) is not infection (caused by bacteria, Malassezia, dermato- recommended. phyte), scabies, demodicosis, atopy, flea allergy dermatitis, and contact hypersensitivity.

FIGURE 7-24 Canine Food Hypersensitivity. FIGURE 7-25 Canine Food Hypersensitivity. Severe periocular dermatitis (alopecia, erythema, and Alopecia, erythema, and excoriations around the eye and hyperpigmentation) is a common finding in allergic ear. The crusting papular rash is due to a secondary dogs. superficial pyoderma associated with the allergic disease.

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Canine Hypothyroidism 241

Canine Hypothyroidism

Features If present, dermal mucinosis is highly suggestive of This endocrinopathy is most often associated with hypothyroidism, but this can be a normal finding in primary thyroid dysfunction caused by lymphocytic some breeds (e.g., Shar pei)

thyroiditis or idiopathic thyroid atrophy. It is common 4. Serum total thyroxine (TT4), free thyroxine (FT4) in dogs, with highest incidence in middle-aged to by equilibrium dialysis, and endogenous thyroid-

older dogs. Young adult large and giant-breed dogs are stimulating hormone (TSH) assays: low TT4, low also occasionally affected. Congenital hypothyroidism FT4, and high TSH are highly suggestive of is extremely rare. hypothyroidism, but false-positive and false-nega-

A variety of cutaneous symptoms can be seen. tive results can occur, especially with TT4 and TSH. Alopecia on the bridge of the nose occurs in some For example, although TT4 is a good screening test, dogs. The hair coat may be dull, dry, and brittle. Bilat- it should not be used alone to make a diagnosis erally symmetrical alopecia that spares the extremities because its serum level can be artificially increased may occur, with easily epilated hairs. Alopecic skin or decreased by several factors, such as nonthy- may be hyperpigmented, thickened, or cool to the roidal illness, autoantibodies, and drug therapy touch. Thickened and droopy facial skin from dermal (Table 9-1) mucinosis, chronic seborrhea sicca or oleosa, or ceru- minous otitis externa may be present. Seborrheic skin and ears may be secondarily infected with yeast or Treatment and Prognosis bacteria. In some dogs, the only symptom is recurrent 1. Any secondary seborrhea, pyoderma, Malassezia or antibiotic-resistant pyoderma or adult-onset gener- dermatitis, or demodicosis can be treated with alized demodicosis. Pruritus is not a primary feature appropriate topical and systemic therapies. of hypothyroidism and, if present, reflects secondary pyoderma, Malassezia infection, or demodicosis. Non- TABLE 9-1 cutaneous symptoms of hypothyroidism are variable and may include aggression, lethargy or mental Factors and Drugs That May Affect dullness, exercise intolerance, weight gain or obesity, thermophilia (cold intolerance), bradycardia, vague Total Thyroxine (TT4) Serum Levels neuromyopathic or gastrointestinal signs, central in Dogs nervous system involvement (e.g., head tilt, nystag- mus, hemiparesis, cranial nerve dysfunction, hyper- Reduced TT4 Values Increased TT4 Values metria), and reproductive problems (e.g., decreased Normal hourly fluctuations Normal hourly fluctuations libido, prolonged anestrus, infertility). Puppies with Nonthyroidal illness Recovery phase of illness congenital hypothyroidism are disproportionate Prolonged fasting Age <3 months dwarfs with short limbs and neck relative to their body Age >7 years Obesity length. Breed = Greyhounds Autoantibodies Autoantibodies Diestrus, pregnancy Top Differentials Phenobarbital Estrogen Furosemide Progesterone Differentials include other causes of endocrine alope- Glucocorticoids Insulin cia and seborrhea, superficial pyoderma, Malassezia Sulfonamides Narcotic analgesics dermatitis, and demodicosis. Nonsteroidal Anti-inflammatories (e.g., Rimadyl, Diagnosis Etogesic) Salicylates 1. Rule out other differentials Tricyclic antidepressants 2. Hemogram and serum biochemistry panel: nonspe- Phenylbutazone cific findings may include a mild, nonregenerative Mitotane anemia, hypercholesterolemia, or elevated creatine General anesthesia kinase NOTE: When hypothyroidism is suspected, both TT (total T ) and fT (free T [by 3. Dermatohistopathology: usually, nonspecific 4 4 4 4 equilibrium dialysis]) should be measured. Compared with TT4,fT4—the small endocrine changes or findings consistent with pyo- portion of thyroxine that is not protein bound—is less affected by nonthyroidal N derma, Malassezia dermatitis, or seborrhea are seen. illness, autoantibodies, and drug therapy; the exception is sulfonamides. W2825-Ch009.qxd 8/12/2005 11:16 Page 242

242 CHAPTER 9 Hereditary, Congenital, and Acquired Alopecias

Canine Hypothyroidism—cont’d

2. Levothyroxine 0.02 mg/kg PO should be adminis- tered every 12 hours until symptoms resolve (approximately 8-16 weeks). Some dogs can then be maintained with 0.02 mg/kg PO every 24 hours; others require lifelong twice-daily dosing to main- tain remission. 3. Dogs with concurrent heart disease should be started on levothyroxine more gradually. Treatment should begin with 0.005 mg/kg PO every 12 hours; dosage should be increased by 0.005 mg/kg every 2 weeks until 0.02 mg/kg every 12 hours is being administered.

4. After 2 to 4 months of therapy, the serum TT4 level should be measured 4 to 6 hours after medication administration and should be in the high normal to FIGURE 9-38 Canine Hypothyroidism. Generalized supranormal range. If the level is low or within the truncal alopecia in an adult collie. normal range and minimal clinical improvement has been seen, the dosage of levothyroxine should

be increased and the serum TT4 level checked 2 to 4 weeks later. If the level is >7.5 mg/dL, the levothy- roxine dose should be reduced. 5 5. If signs of thyrotoxicosis from oversupplementation (e.g., anxiety, panting, polydipsia, polyuria) occur,

the serum TT4 level should be evaluated. If the level is markedly elevated, medication should be tem- porarily stopped until adverse effects abate; it should then be reinstituted at a lower dose or a less frequent dosage schedule. 6. The prognosis is good with lifelong replacement thyroxine therapy, although hypothyroidism- induced neuromuscular abnormalities may not completely resolve. FIGURE 9-39 Canine Hypothyroidism. Mild alopecia on the bridge of the nose may be an early lesion of hypothyroidism.

FIGURE 9-37 Canine Hypothyroidism. An obese Rottweiler with hypothyroidism. Note that the hair coat FIGURE 9-40 Canine Hypothyroidism. Alopecia lacks the bilaterally symmetrical alopecia that is considered and hyperpigmentation with no evidence of secondary characteristic of this disease. superficial pyoderma on the trunk. N W2825-Ch009.qxd 8/12/2005 11:16 Page 232

232 CHAPTER 9 Hereditary, Congenital, and Acquired Alopecias

Canine Hyperadrenocorticism (Cushing’s disease)

Features Diagnosis Spontaneously occurring hyperadrenocortism is asso- 1. Hemogram: neutrophilia, lymphopenia, and ciated with the excessive production of endogenous eosinopenia are often seen steroid hormones (principally glucocorticoids, but 2. Serum biochemistry panel: an elevated alkaline sometimes mineralocorticoids or sex hormones) by the phosphatase enzyme level is typical. There may also adrenal cortex. The disease is caused by a hyperfunc- be mildly to markedly elevated alanine transami- tioning adrenal tumor (15%-20% of cases) or pituitary nase activity, as well as elevated cholesterol, triglyc- tumor (80%-85% of cases). Pituitary-dependent hyper- eride, or glucose levels adrenocortism (PDH) is caused by the excessive 3. Urinalysis: the specific gravity is usually low, and production of adrenocorticotropic hormone (ACTH), there may be bacteriuria, proteinuria, or glucosuria usually from a pituitary microadenoma or macro- 4. Urine cortisol/creatinine ratio: usually elevated. A adenoma. Iatrogenically induced disease occurs nonspecific screening test that is not diagnostic by secondary to excessive administration of exogenous itself because false-positive results are common glucocorticoids. Iatrogenic hyperadrenocorticism (stress-induced, seen with many other illnesses). can occur at any age and is common, especially in To minimize the effects of stress, a home-collected chronically pruritic dogs and dogs with immune- urine sample should be used, instead of one mediated disorders that are controlled with long-term obtained at the veterinary hospital glucocorticoids. Spontaneously occurring hypera- 5. Dermatohistopathology: often shows nondiagnos- drenocorticism is also common and tends to occur in tic changes consistent with any endocrinopathy. middle-aged to older dogs, with an increased inci- Dystrophic mineralization (calcinosis cutis), thin dence noted in Boxers, Boston terriers, Dachshunds, dermis, and absent erector pili muscles are highly Poodles, and Scottish terriers. suggestive of hyperadrenocorticism, but these The hair coat often becomes dry and lusterless, and changes are not always present slowly progressing, bilaterally symmetrical alopecia is 6. Abdominal ultrasonography: may demonstrate common. The alopecia may become generalized, but it adrenal tumor or hyperplasia usually spares the head and limbs. Remaining hairs 7. Computed tomography (CT) or magnetic resonance are easily epilated, and alopecic skin is often thin, imaging (MRI): may detect a pituitary mass hypotonic, and hyperpigmented. Cutaneous striae and 8. Adrenal function tests: comedones may be seen on the ventral abdomen. The Adrenocorticotropic hormone (ACTH) stimulation skin may be mildly seborrheic (fine, dry scales), bruise test (cortisol): an exaggerated poststimulation easily, and exhibit poor wound healing. Chronic sec- cortisol level is highly suggestive of endogenous ondary superficial or deep pyoderma, dermatophyto- hyperadrenocortism, but false-negative and false- sis, or demodicosis is common and may be the client’s positive results can occur. In iatrogenic cases, primary complaint. Calcinosis cutis (whitish, gritty, an inadequate response to ACTH stimulation is firm, bonelike papules and plaques) may develop, typical. Note: Reconstituted cosyntropin (ACTH especially on the dorsal midline of the neck or ventral solution) can be stored frozen at -20∞C in plastic abdomen, or in the inguinal area. syringes for up to 6 months with no adverse Polyuria and polydipsia (water intake > 00 mL/kg/ effects on its bioactivity day) and polyphagia are common. Muscle wasting or ACTH stimulation test (17-hydroxyprogesterone): weakness, a pot-bellied appearance (from hepato- exaggerated basal and poststimulation 17- megaly, fat redistribution, and weakened abdominal hydroxyprogesterone levels may be seen in muscles), increased susceptibility to infection (con- endogenous hyperadrenocortism, but false- junctival, skin, urinary tract, lung), excessive panting, negative and false-positive results can occur. 17- and variable behavioral or neurologic signs (expand- Hydroxyprogesterone, a progestin, is an adrenal ing pituitary tumor) are often present. gland–produced precursor of cortisol Low-dose (0.01 mg/kg) dexamethasone suppres- sion test: inadequate cortisol suppression is Top Differentials highly suggestive of endogenous hyperadreno- Differentials include other causes of endocrine cortism, but false-negative and false-positive alopecia, superficial pyoderma, demodicosis, and results can occur. Suppression at 4 hours followed N dermatophytosis. by escape from suppression at 8-hour sampling is characteristic of PDH W2825-Ch009.qxd 8/12/2005 11:16 Page 233

Canine Hyperadrenocorticism 233

High-dose (0.1 mg/kg) dexamethasone suppres- water and food intake before and during induction sion test: used to help differentiate between may be useful. Water and food intake often adrenal neoplasia and pituitary-dependent markedly decreases when adequate adrenal sup- hyperadrenocorticism. A lack of cortisol suppres- pression has been achieved. If signs of adrenal sion is suggestive of adrenal neoplasia, whereas insufficiency (e.g., anorexia, depression, vomiting, cortisol suppression suggests pituitary disease diarrhea, ataxia, disorientation) develop, mitotane Endogenous ACTH assay: used to help differenti- therapy should be stopped and hydrocortisone 0.5 ate between adrenal neoplasia and pituitary- to 1.0 mg/kg PO every 12 hours administered, dependent hyperadrenocorticism. An elevated until symptoms resolve. ACTH level is suggestive of pituitary disease, 7. To maintain remission following mitotane induc- whereas a depressed ACTH level is suggestive of tion, mitotane PO with food 50 mg/kg should be adrenal neoplasia administered once weekly, or 25 mg/kg twice weekly. Dogs that relapse during maintenance Treatment and Prognosis therapy should be reinduced with daily mitotane 1. Any concurrent infections (e.g., pyoderma, for 5 to 14 days or until recontrolled, then main- demodicosis, urinary tract infection) should be tained with 62 to 75 mg/kg once weekly, or 31 to treated with appropriate therapies. 37.5 mg/kg twice weekly. A great deal of patient 2. Treatment of choice for iatrogenically induced variability occurs, requiring close monitoring. cases is to progressively taper, then discontinue 8. An alternative medical treatment for PDH is glucocorticoid therapy. trilostane (not currently available in the United 3. Treatment of choice for adrenal neoplasia is States). At this writing, its optimal dosing regimen adrenalectomy. has not yet been determined, but many investiga- 4. Dogs with inoperable adrenal tumors or metas- tors are using the following protocol: tases may benefit from mitotane or trilostane Dogs <5 kg: give 30 mg PO with food q 24 hours therapy. Dogs between 5 and 20 kg: give 60 mg PO with Mitotane: One should give 50 mg/kg PO every food q 24 hours 24 hours with food for 7 to 14 days. An ACTH Dogs between 20 and 40 kg: give 120 mg PO with stimulation test is performed every 7days. If food q 24 hours inadequate cortisol suppression persists, one Dogs >40 kg: give 240 mg PO with food q 24 hours should increase the mitotane dosage to 75 to One can assess efficacy by monitoring clinical 100 mg/kg/day for an additional 7 to 14 days, signs and evaluating results of ACTH stimula- monitoring with ACTH stimulation tests weekly. tion tests 10 days, 4 weeks, and 12 weeks When adequate adrenal suppression is demon- after the start of therapy, then every 3 months strated, maintenance mitotane therapy is initi- thereafter. ACTH stimulation tests should be ated as described below (see Number 7) performed 4 to 6 hours after trilostane dosing. Trilostane: Therapy should be initiated and main- A post-ACTH cortisol level <150 nmol/L (but tained as described below (see Number 8) >20 nmol/L) is usually consistent with good 1 5. An effective treatment (where available) for PDH control. However, optimal clinical control has is microsurgical transsphenoidal hypophysectomy. also been reported with post-ACTH cortisol This procedure requires a highly skilled neurosur- concentrations between 150 and 250 nmol/L, so geon and specialized veterinary facilities that blood work results should always be interpreted have access to advanced pituitary imaging tech- alongside clinical signs. If the dog is not clini- niques. Postoperative complications may include cally well controlled and post-ACTH cortisol hypernatremia, keratoconjunctivitis sicca, diabetes concentrations are >150 nmol/L, the dose of insipidus, and secondary hypothyroidism. trilostane should be increased. Dose adjustments 6. The traditional medical treatment of choice for should be made in increments of 20 to 30 mg/ PDH is mitotane 50 mg/kg PO administered every dog. A wide range of trilostane doses to induce 24 hours with food. The daily dosage is continued and maintain remission have been reported in until the basal serum or plasma cortisol level nor- dogs, with the therapeutic dose for most dogs malizes and does not increase following ACTH being between 4 and 20 mg/kg/day. Some dogs stimulation. Control is usually achieved within 5 may require twice-daily dosing if duration to 10 days of initiation of therapy, so the patient of effect is inadequate. Clinical signs such as should be closely monitored with ACTH stimula- polydipsia/polyuria/polyphagia often start to tion tests performed every 2 to 3days. Monitoring improve within the first 10 days of treatment,

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234 CHAPTER 9 Hereditary, Congenital, and Acquired Alopecias

Canine Hyperadrenocorticism (Cushing’s disease)—cont’d

but alopecia and other skin changes may take 3 or more months to improve. If signs of adrenal insufficiency (depression, inappetence, vomit- ing, diarrhea) develop at any time during therapy, or if post-ACTH cortisol concentrations (measured 4-6 hours after trilostane dosing) are <20 nmol/L, trilostane should be stopped for 5 to 7 days, then reinstituted at a lower dose. Note: Although trilostane appears to be well tolerated by most dogs, sudden death has been reported in dogs with concurrent heart problems. Trilostane is also contraindicated in pregnant and lactating dogs, dogs with primary hepatic 2 disease, and dogs with renal insufficiency. 9. Other alternative, but less consistently successful, FIGURE 9-12 Canine Hyperadrenocorticism. An medical treatments for PDH include the following: adult Labrador with an adrenal tumor, demonstrating severe muscle wasting that causes the abnormal body Ketoconazole 15 mg/kg PO with food q 12 hours confirmation. Selegiline (L-deprenyl) 1-2 mg/kg PO q 24 hours 3 10. For calcinosis cutis, adjunctive topical treatment with dimethyl sulfoxide (DMSO) gel every 24 hours may help resolve the lesions. During DMSO therapy, serum calcium levels should be monitored periodically because hypercalcemia is a potential adverse effect of this treatment. 11. The prognosis ranges from good to poor, depend- ing on the cause and severity of the disease, with the average survival time for dogs with PDH being approximately 2.5 years after diagnosis.

FIGURE 9-13 Canine Hyperadrenocorticism. Same dog as in Figure 9-12. The potbellied appearance and alopecia are apparent.

FIGURE 9-11 Canine Hyperadrenocorticism. An adult Labrador demonstrates the typical potbellied appearance. Generalized muscle wasting, which causes the abnormal posture, is also seen. Note that the hair coat is generally in good condition and does not demonstrate bilaterally symmetrical alopecia.

FIGURE 9-14 Canine Hyperadrenocorticism. Same dog as in Figure 9-12. Generalized seborrhea sicca can be N secondary to numerous underlying diseases but was caused by hyperadrenocorticism in this dog.

Acral Lick Granuloma W2825-Ch013.qxd 8/23/2005 9:09 Page 328

328 CHAPTER 13 Miscellaneous Cutaneous Disorders of the Dog

Acral Lick Dermatitis (lick granuloma, acral pruritic nodule)

Features 2. Dermatohistopathology: ulcerative and hyperplas- Acral lick dermatitis is first noted as excessive, com- tic epidermis, mild neutrophilic and mononuclear pulsive licking at a focal area on a limb, resulting in perivascular dermatitis, and varying degrees of a firm, proliferative, ulcerative, alopecic lesion. The dermal fibrosis causes of the licking are multifactorial, and, although 3. Bacterial culture (exudates, biopsy specimen): environmental stress (e.g., boredom, confinement, Staphylococcus is often isolated. Mixed gram- loneliness, separation anxiety) may be a contributor, positive and gram-negative infections are common other factors are usually more important (Box 13-1). This dermatitis is common in dogs, with the highest incidence in middle-aged to older, large-breed dogs, Treatment and Prognosis especially Doberman pinschers, Great Danes, Golden 1. The underlying causes should be identified and cor- retrievers, Labrador retrievers, German shepherds, rected (see Box 13-1). and Boxers. 2. One should treat for secondary bacterial infection The lesion usually begins as a small area of der- with long-term systemic antibiotics (minimum, 6-8 matitis that slowly enlarges because of persistent weeks, and as long as 4-6 months in some dogs). licking. The affected area becomes alopecic, firm, Antibiotic therapy should be continued at least 3 to raised, thickened, and plaquelike to nodular, and it 4 weeks beyond regression of the lesion. The antibi- may be eroded or ulcerated. With chronicity, extensive otic should be selected according to bacterial culture fibrosis, hyperpigmentation, and secondary bacterial and sensitivity results. infection are common. Lesions are usually single but 3. Topical applications of analgesic, steroidal, or bad- may be multiple, and they are most often found on tasting medications every 8 to 12 hours may help the dorsal aspect of the carpus, metacarpus, tarsus, or stop the licking. metatarsus. 4. Anecdotal reports suggest good efficacy with combined antibiotic, amitriptyline (2 mg/kg q 12 hours), and hydrocodone (0.25 mg/kg q 8-12 hours) Top Differentials administered until lesions resolve. Then, one drug Differentials include demodicosis, dermatophyte should be discontinued every 2 weeks until it can kerion, fungal or bacterial granuloma, and neoplasia. be determined which drug (if any) may be required for maintenance therapy. 1 5. When no underlying cause can be found, treatment Diagnosis with behavior-modifying drugs may be beneficial 1. Usually based on history, clinical findings, and in some dogs (Table 13-1). Trial treatment periods of ruling out other differentials up to 5 weeks should be used until the most effec- tive drug is identified. Lifelong treatment is often necessary. 6. Laser ablation may be beneficial. BOX 13-1 7. Mechanical barriers such as wire muzzles and ban- daging, Elizabethan collars, and side braces are also Underlying Causes of Acral helpful. Lick Dermatitis 8. Surgical excision is not recommended because postoperative complications, especially wound ■ Hypersensitivity (atopy, food) dehiscence, are common. ■ Fleas 9. The prognosis is variable. Chronic lesions that are ■ Trauma (cut, bruise) unresponsive or extensively fibrotic and those for ■ Foreign body reaction which no underlying cause can be found have ■ Infection (bacterial, fungal) a poor prognosis for resolution. Although this ■ Demodicosis disease is rarely life threatening, its course may be ■ Hypothyroidism intractable. ■ Neuropathy ■ Osteopathy ■ N Arthritis W2825-Ch013.qxd 8/23/2005 9:09 Page 329

Acral Lick Dermatitis 329

TABLE 13-1 Drugs for Psychogenic Dermatoses in Dogs

Drug Dose

Anxiolytics Phenobarbital 2-6 mg/kg PO q 12 hours Diazepam (Valium) 0.2 mg/kg PO q 12 hours Hydroxyzine (Atarax) 2.2 mg/kg PO q 8 hours

Tricyclic Antidepressants Fluoxetine (Prozac) 1 mg/kg PO q 24 hours Amitriptyline (Elavil) 1-3 mg/kg PO q 12 hours FIGURE 13-2 Acral Lick Dermatitis. A focal alopecic Imipramine (Tofranil) 2-4 mg/kg PO q 24 hours erosive lesion demonstrating the raised infiltrative nature Clomipramine (Clomicalm, 1-3 mg/kg PO q 24 hours Anafranil) typical of this disease.

Endorphin Blocker Naltrexone (ReVia) 2 mg/kg PO q 24 hours

Endorphin Substitute Hydrocodone (Hycodan) 0.25 mg/kg PO q 8 hours

Topical Products Fluocinolone acetonide (Synotic) 16 + flunixin meglumine (Banamine) 17 Deep Heet + Bitter Apple

FIGURE 13-3 Acral Lick Dermatitis. A focal area of alopecia and thickening on the distal extremity.

FIGURE 13-1 Acral Lick Dermatitis. This focal FIGURE 13-4 Acral Lick Dermatitis. A focal area of alopecic erosive lesion on the medial aspect of the distal alopecia with tissue thickening and minimal erosion. leg is typical of this disease.

N

Scabies W2825-Ch005.qxd 8/4/2005 14:11 Page 112

112 CHAPTER 5 Parasitic Skin Disorders

Canine Scabies (sarcoptic mange)

Features bodies may persist for several months after treat- Canine scabies manifests as a disease that is caused by ment cessation Sarcoptes scabiei var. canis, a superficial burrowing skin 5. Dermatohistopathology (usually nondiagnostic): mite. Mites secrete allergenic substances that elicit varying degrees of epidermal hyperplasia and an intensely pruritic hypersensitivity reaction in superficial perivascular dermatitis with lympho- sensitized dogs. Canine scabies is common in dogs. cytes, mast cells, and eosinophils. Mite segments are Affected dogs often have a previous history of being rarely found within the stratum corneum in an animal shelter, having contact with stray dogs, or visiting a grooming or boarding facility. In multiple- dog households, more than one dog is usually affected. Treatment and Prognosis Canine scabies is a nonseasonal intense pruritus 1. Affected and all in-contact dogs should be treated that responds poorly to corticosteroids. Lesions with a scabicide. include papules, alopecia, erythema, crusts, and 2. Traditional therapy involves bathing dogs with an excoriations. Initially, less-hairy skin is involved, such antiseborrheic shampoo to remove crusts, followed as on the hocks, elbows, pinnal margins, and ventral by a total body application of a topical scabicide abdomen and chest. With chronicity, lesions may every 7 days for at least 5 weeks (note that systemic spread over the body, but the dorsum of the back is treatments are generally more effective than topical usually spared. Peripheral lymphadenomegaly is often products). Effective topical products include the present. Secondary weight loss may occur. Heavily following: infested dogs may develop severe scaling and crust- 2%-3% lime sulfur solution ing. Some dogs may present with intense pruritus but Organophospates (malathion, phosmet, mercap- no or minimal skin lesions. Although they are uncom- tomethyl phtalimide). Organophosphates are the mon, asymptomatic carrier states are possible in dogs. most toxic and least effective therapies available 3. Selamectin is the only systemic treatment licensed for canine scabies. The manufacturer’s recommen- Top Differentials dation is to topically apply 6 to 12 mg/kg twice 1 Differentials include hypersensitivity (flea bite, food, month apart, but application of 6 to 12 mg/kg every atopy), pyoderma, demodicosis, dermatophytosis, 2 weeks at least four times may be more effective. Malassezia dermatitis, and contact dermatitis. 4. Alternative treatments include the following: 0.025%-0.03% amitraz solution applied to the entire body three times at 2-week intervals, or once Diagnosis weekly for 2-6 weeks 1. Usual basis: history, clinical findings, and response Fipronil spray 3 mL/kg, applied as pump spray to to scabicidal treatment the entire body three times at 2-week intervals, or 2. Pinnal-pedal reflex: rubbing of the ear margin 6 mLl/kg applied as sponge-on once weekly for between thumb and forefinger may elicit a scratch 2 weeks reflex. This reflex is highly suggestive but not Ivermectin 0.2-0.4 mg/kg PO q 7 days, or SC q 14 pathognomonic for scabies days, for 4-6weeks 3. Microscopy (superficial skin scrapings): detection of Milbemycin oxime 0.75 mg/kg PO q 24 hours for 30 sarcoptic mites, nymphs, larvae. or ova. False- days, or 2 mg/kg PO q 7 days for 3-5 weeks negative results are common because mites are Moxidectin 1% injectable for cattle 0.2-0.25 mg/kg extremely difficult to find PO or SC q 7 days for 3-6 weeks. Note: Adverse 4. Serology (enzyme-linked immunosorbent assay effects are common, especially when moxidectin [ELISA]): detection of circulating immunoglobulin is administered SC (Ig)G antibodies against Sarcoptes antigens. This is a 5. If the animal is severely pruritic and mites have highly specific and sensitive test, but false-negative been identified, prednisone 0.5-1.0 mg/kg PO every results can occur in young puppies and in dogs 24 hours for the first 2 to 5 days of scabicidal treat- receiving corticosteroid therapy. Also, false-positive ment may be helpful. Use of steroids without the results may be seen in dogs that have been suc- finding of mites makes it impossible for the practi- cessfully treated for scabies because detectable anti- tioner to determine response to scabicidal therapy. N W2825-Ch005.qxd 8/4/2005 14:11 Page 113

Canine Scabies 113

6. For secondary pyoderma, appropriate systemic 8. The prognosis is good. S scabei is a highly conta- antibiotics should be administered for 3 to 4 weeks. gious parasite of dogs that can also transiently 7. In kennel situations, bedding should be disposed of infest humans and, rarely, cats. and the environment thoroughly cleaned and treated with parasiticidal sprays.

FIGURE 5-42 Canine Scabies. Generalized alopecia FIGURE 5-43 Canine Scabies. Generalized alopecia with a crusting papular dermatitis affecting the head and and crusts affecting a pruritic puppy. The alopecic ear neck of a young adult dog. Note that the ear margins are pinnae are characteristic of scabies. severely affected.

FIGURE 5-45 Canine Scabies. Alopecia and crusting on the lateral elbow of a dog with scabies.

FIGURE 5-44 Canine Scabies. Alopecia and crusting dermatitis on the ear pinnae margin of this dog is characteristic of scabies.

FIGURE 5-46 Canine Scabies. A positive pinnal pinnal-pedal reflex is highly suggestive of scabies. N

Dermatophytosis W2825-Ch004.qxd 8/4/2005 14:05 Page 71

Dermatophytosis 71

Dermatophytosis (ringworm)

Features 4. Dermatohistopathology: variable findings may Dermatophytosis is an infection of hair shafts and include perifolliculitis, folliculitis, furunculosis, stratum corneum caused by keratinophilic fungi. It superficial perivascular or interstitial dermatitis, occurs commonly in dogs and cats, with highest inci- epidermal and follicular orthokeratosis or paraker- dences reported in kittens, puppies, immunocompro- atosis, or suppurative epidermitis. Fungal hyphae mised animals, and long-haired cats. Persian cats and arthrospores in stratum corneum or hair shafts and Yorkshire and Jack Russell terriers appear to be may be difficult to find without special fungal stains predisposed. 5. Fungal culture: Microsporum or Trichophyton spp Skin involvement may be localized, multifocal, or generalized. Pruritus, if present, is usually minimal to mild but occasionally may be intense. Lesions usually Treatment and Prognosis include areas of circular, irregular, or diffuse alopecia 1. If the lesion is focal, a wide margin should be with variable scaling. Remaining hairs may appear clipped around it and topical antifungal medica- stubbled or broken off. Other symptoms in dogs and tion applied every 12 hours until the lesion cats include erythema, papules, crusts, seborrhea, resolves. (Some dermatologists believe that clip- and paronychia or onychodystrophy of one or more ping is beneficial; others believe that it spreads digits. Rarely, cats present with miliary dermatitis or lesions onto animals and further contaminates the dermal nodules (see “Dermatophytic Granulomas and environment.) Effective topicals for localized treat- Pseudomycetomas”). Other cutaneous manifestations ment include the following: in dogs include facial folliculitis and furunculosis 1% terbinafine cream resembling nasal pyoderma, kerions (acutely develop- 1% clotrimazole cream, lotion, or solution ing, alopecic, and exudative nodules) on the limb or 2% enilconazole cream face, and truncal dermal nodules (see “Dermatophytic 2% ketoconazole cream Granulomas and Pseudomycetomas”). Asymptomatic 1%-2% miconazole cream, spray, or lotion carrier states (subclinical infection) are common in 4% thiabendazole solution cats, especially among long-haired breeds. Asympto- 2. If response to localized treatment is poor, the matic disease, although rare in dogs, has been reported animal should be treated for generalized in Yorkshire terriers. dermatophytosis. 3. For animals with multifocal or generalized lesions, Top Differentials the entire hair coat should be clipped if the animal is medium- to long-haired. (Some dermatologists Dogs believe that clipping is beneficial; others believe Differentials in dogs include demodicosis and superfi- that it spreads lesions onto animals and further cial pyoderma. If nodular, neoplasia and acral lick der- contaminates the environment.) Topical antifungal matitis should be included. rinse or dip should be applied to the entire body one or two times per week (minimum 4-6 weeks) Cats until follow-up fungal culture results are negative. Differentials in cats include parasites, allergies, and Bathing the animal with a shampoo that contains feline psychogenic alopecia. chlorhexidine and miconazole or ketoconazole immediately preceding the antifungal dip may be helpful. Dogs with generalized dermatophytosis Diagnosis may be cured with topical therapy alone, whereas 1. Rule out other differentials cats almost always require concurrent systemic 2. Ultraviolet (Wood’s lamp) examination: hairs fluo- therapy. Effective topical antifungal solutions resce yellow-green with some Microsporum canis include the following: strains. This is an easy screening test, but false- Enilconazole 0.2% solution negative and false-positive results are common Lime sulfur 2%-4% solution 3. Microscopy (hairs or scales in potassium hydroxide 4. For cats with generalized dermatophytosis and preparation): Search for hair shafts infiltrated with dogs that are unresponsive to topical therapy hyphae and arthrospores. Fungal elements are often alone, topical therapy for generalized infection difficult to find should be combined with long-term (minimum 4-6 N W2825-Ch004.qxd 8/4/2005 14:05 Page 72

72 CHAPTER 4 Fungal Skin Diseases

Dermatophytosis (ringworm)—cont’d

weeks) systemic antifungal therapy and continued BOX 4-1 until 3 to 4 weeks beyond negative follow-up fungal culture results. Effective systemic antifun- Treating Dermatophytosis in gal drugs include the following: Multianimal Homes, Catteries, and Microsized griseofulvin at least 50 mg/kg/day PO with fat-containing meal Animal Facilities Ultramicrosized griseofulvin 5-10 mg/kg/day PO ■ Culture all animals to determine the extent and location with fat-containing meal of animal infections. Itraconazole (Sporonox) 5-10 mg/kg PO q 24 ■ Culture the environment (cages, counters, furniture, hours with food floors, fans, ventilation units, etc) to map the infected Terbinafine 30-40 mg/kg PO q 24 hours areas to be disinfected. Ketoconazole 10 mg/kg PO q 24 hours with food ■ Treat all infected animals with systemic antifungals until they have 2each animal has two negative fungal cultures 5. Alternatively, itraconazole (Sporonox) pulse taken at least 1 month apart. therapy has been shown to be effective and should ■ Treat all infected and exposed animals with topical 2% be continued until two consecutive follow- to -4% lime sulfur solution every 3- to 7 days to prevent up fungal cultures taken 2 to 4 weeks apart are contagion and zoonosis. Continue until all animals have 2 two negative fungal cultures taken at least 1 month negative. apart. Do not clip cats as this contaminates the clippers Protocol 1: The practitioner should give itracona- and facility and worsens the risk of contagion. zole (Sporonox) 10 mg/kg PO with food once ■ Dispose of all infected infected material. Remove any daily for 1 month, then on an alternate-week clutter from animal facilities or other infected areas. regi1men (1 week off, 1 week on). ■ Clean and disinfect all surface areas every 3 days. Continue until all animals have 2 two negative fungal Protocol 2: The practitioner should give itracona- cultures taken at least 1 month apart. Enilconazole 2 zole (Sporonox) 10 mg/kg orally with food once (Clinafarm EC disinfectant, American Scientific daily for 2 weeks, then on 2 consecutive days Laboratories, Union, NJ) is a very effective environmental disinfectant, but it is licensed only for each week (e.g., every Monday and Tuesday). poultry farm use in the United States. Household 6. All infected animals, including asymptomatic car- chlorine laundry bleach (5% sodium hypochlorite) riers, should be identified and treated. diluted 1:10 in water, is an effective, inexpensive environmental disinfectant. 7. Exposed, noninfected cats and dogs should be treated prophylactically with weekly topical anti- fungal rinse or dip for the duration of treatment of the infected animals. 8. The environment should be thoroughly vacuumed (vacuums may further contaminate the environ- ment) and disinfected. 9. For endemic infections involving multianimal homes, catteries, or animal facilities, treatment should be provided according to the treatment rec- ommendations outlined in Box 4-1. 10. Lufenuron has not demonstrated consistent effi- cacy in treating or preventing infection. 11. The prognosis is generally good, except for endemically infected multicat households and cat- teries. Animals with underlying immunosuppres- sive diseases also have a poorer prognosis for cure. FIGURE 4-26 Dermatophytosis. Focal alopecia and Dermatophytosis is contagious to other animals crusting on the muzzle of the cat caused by Microsporum and to humans. canis. (Courtesy of J. MacDonald.)

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FIGURE 4-49 Dermatophytosis. Microscopic FIGURE 4-50 Dermatophytosis. A new toothbrush examination of a trichogram demonstrating an infected can be used to collect hairs from a patient without hair with fungal ectothrix as seen with a 10¥ objective. cutaneous lesions (McKinsey’s toothbrush technique). The hairs should then be disbursed onto dermatophyte test medium (DTM) culture media.

FIGURE 4-51 Dermatophytosis. A folded gauze can FIGURE 4-52 Dermatophytosis. DTM culture media be used to wipe the fur of a patient or surface to collect demonstrating the typical white colony growth that is material that can then be disbursed onto DTM culture temporally associated with an immediate red color change. media. Note the individual learned the importance of wearing gloves when one is dealing with a potential a zoonotic disease.

FIGURE 4-53 Dermatophytosis. Close-up of a DTM FIGURE 4-54 Dermatophytosis. Microsporum canis fungal culture demonstrating the typical white colony macroconidia as observed with a 10¥ objective. Note the growth and red color change. This is suggestive of pointed ends and six or more divisions. dermatophytosis, but microscopic identification visualization should be performed to identify N Microsporum canis.

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64 CHAPTER 4 Fungal Skin Diseases

Malasseziasis (Malassezia dermatitis)

Features Diagnosis Malassezia pachydermatis is a yeast that is normally 1. Rule out other differentials found in low numbers in the external ear canals, in 2. Cytology (tape preparation, skin imprint): yeast perioral areas, in perianal regions, and in moist skin overgrowth is confirmed by the finding of more folds. Skin disease occurs in dogs when a hyper- than 2 round-to-oval, budding yeasts per high sensitivity reaction to the organisms occurs, or when power field (100¥). In yeast hypersensitivity, organ- there is cutaneous overgrowth. In dogs, Malassezia isms may be difficult to find overgrowth is almost always associated with an 3. Dermatohistopathology: superficial perivascular- underlying cause, such as atopy, food allergy, endo- to-interstitial lymphohistiocytic dermatitis with crinopathy, keratinization disorder, metabolic disease, yeasts and occasionally pseudohyphae in keratin. or prolonged therapy with corticosteroids. In cats, Organisms may be few in number and difficult to skin disease is caused by Malassezia overgrowth that find may occur secondary to an underlying disease (e.g., 4. Fungal culture: M. pachydermatis feline immunodeficiency virus, diabetes mellitus) or an internal malignancy. In particular, generalized Malassezia dermatitis may occur in cats with thymoma- Treatment and Prognosis associated dermatosis or paraneoplastic alopecia. 1. Any underlying cause must be identified and cor- Malasseziasis is common in dogs, especially among rected. West Highland White terriers, Dachshunds, English 2. For mild cases, topical therapy alone is often effec- setters, Basset hounds, American cocker spaniels, Shih tive. The patient should be bathed every 2 to 3 days tzus, Springer spaniels, and German shepherds. These with shampoo that contains 2% ketoconazole breeds may be predisposed. Malasseziasis is rare in (dogs only), 1% ketoconazole/2% chlorhexidine, 2% cats. miconazole, 2% to 4% chlorhexidine, or 1% selenium sulfide (dogs only). For added effect, baths can be Dogs followed by an application of 2% lime sulfur dip, Moderate to intense pruritus is seen, with regional or 0.2% enilconazole dip, or 1:1 dilution of white generalized alopecia, excoriations, erythema, and seb- vinegar in water. Treatment should be continued orrhea. With chronicity, affected skin may become until the lesions resolve and follow-up skin cytology lichenified, hyperpigmented, and hyperkeratotic. An reveals no organisms (approximately 2-4 weeks). unpleasant body odor is usually present. Lesions may 3. The treatment of choice for moderate to severe cases involve the interdigital spaces, ventral neck, axillae, is ketoconazole 5 to 10 mg/kg PO with food every perineal region, or leg folds. Paronychia with dark 12 to 24 hours, itraconazole (Sporonox) 5 to 10 mg/ brown nail bed discharge may be present. Concurrent kg PO with food every 24 hours, or pulse itracona- yeast otitis externa is common. zole (Sporonox) (dogs) 5 to 10 mg/kg with food on 2 consecutive days each week. Treatment should be Cats continued until lesions resolve and follow-up skin Symptoms include black, waxy otitis externa, chronic cytology reveals no organisms (approximately 2-4 chin acne, alopecia, and multifocal to generalized ery- weeks). thema and seborrhea. 4. Alternatively, treatment with terbinafine 30 mg/kg PO every 24 hours for 2 to 4 weeks may be effective. 5. The prognosis is good if the underlying cause can Top Differentials be identified and corrected. Otherwise, regular once- Differentials include other causes of pruritus and seb- or twice-weekly antifungal shampoo baths may be orrhea, such as demodicosis, superficial pyoderma, needed to prevent relapse. This disease is not con- dermatophytosis, ectoparasites, and allergies. sidered contagious to other animals or to humans, except for immunocompromised individuals.

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FIGURE 4-1 Malassezia. Severe alopecia, lichenification, and hyperpigmentation on the entire ventrum of a West Highland White Terrier. The yeast infection was secondary to allergic dermatitis.

FIGURE 4-2 Malassezia. Alopecia, erythema, and lichenification on the ventral neck of an allergic dog.

FIGURE 4-3 Malassezia. Pododermatitis caused by a secondary yeast infection demonstrates the alopecia and lichenification typical of Malassezia dermatitis. FIGURE 4-4 Malassezia. Severe pododermatitis demonstrating the intense inflammatory response caused by the hypersensitivity reaction to the Malassezia organisms. The severe erythema, alopecia, and lichenification is are apparent.

FIGURE 4-5 Malassezia. The interdigital dermatitis in this patient was caused by the secondary Malassezia FIGURE 4-6 Malassezia. The brown discoloration infection. The greasy, alopecic, inflamed skin in between around the base of the nails is a unique change typical of N the footpads is typical of yeast pododermatitis. secondary Malassezia infections. #1 Canine Atopy (environmental, pollen allergies)

Features Canine atopy is a hypersensitivity reaction to inhaled (possibly a historic theory) or cutaneously absorbed environmental antigens (allergens) in genetically predisposed individuals. It is common in dogs, with age of onset ranging from 6 months to 6 years. However, in most atopic dogs, symptoms first appear at between 1 and 3 years of age. Symptoms begin as skin erythema and pruritus (licking, chewing, scratching, rubbing), which may be seasonal or 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 secondary skin lesions, including salivary staining, alopecia, excoriations, scales, crusts, hyperpigmentation, and lichenification. Secondary pyoderma, Malassezia dermatitis, and otitis externa are common. Chronic acral lick dermatitis, recurrent pyotraumatic dermatitis, conjunctivitis, hyperhidrosis (sweating), and, rarely, allergic bronchitis or rhinitis may be seen.

Top Differentials Differentials include food allergy, scabies, Malassezia dermatitis, bacterial pyoderma, as well as other hypersensitivities (flea bite, contact), parasites (cheyletiellosis, pediculosis), and folliculitis (dermatophyte, Demodex).

Diagnosis 1. Seasonal foot-licking is the most unique and typical symptom of atopy. If year-round allergens (house dust mites) are causing the allergy, the foot-licking may be nonseasonal. 2. Allergy testing (intradermal, serologic): allergy testing can be highly variable according to the method used. Positive reactions to grass, weed, tree, mold, insect, dander, or indoor environmental allergens are seen. False-negative and false-positive reactions may occur. 3. Dermatohistopathology (nondiagnostic): superficial perivascular dermatitis that may be spongiotic or hyperplastic. Inflammatory cells are predominantly lymphocytes and histocytes. Eosinophils are uncommon. Neutrophils or plasma cells suggest secondary infection.

Treatment and Prognosis 1. Infection Prevention: a. Any secondary pyoderma, otitis externa, and Malassezia dermatitis should be treated with appropriate therapies. Controlling and preventing secondary infection is an essential component of managing atopic dogs. Bathing every 3 – 7 days and treating the ears after every bath helps wash off pollens and disinfect the skin and ear canals, preventing the secondary infections from recurring. 2. Symptomatic Therapy (itch control): a An integrated flea control program should be instituted to prevent flea bites from aggravating the pruritus.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com b Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms. C Systemic antihistamine therapy reduces clinical symptoms in many cases (Table 7-1). Antihistamines can be used alone or in combination with glucocorticoids or essential fatty acids for a synergistic effect. One- to two-week long therapeutic trials with different antihistamines may be required to determine which is most effective. D Oral essential fatty acid supplements (180mg EPA/10 lb) help control pruritus in 20% to 50% of cases, but 8 to 12 weeks of therapy may be needed before beneficial effects are seen. Also, a synergistic effect is often noted when essential fatty acid supplements are administered in combination with glucocorticoids or antihistamines. E Dextromethorphan, an opioid antagonist, may also be a useful adjunct in managing the licking, chewing, and biting behaviors associated with allergic dermatitis in dogs. Dextromethorphan 2mg/kg PO should be administered every 12 hours. A beneficial effect should be seen within 2 weeks. F Systemic glucocorticoid therapy is often effective (75%) in controlling pruritus but almost always result in adverse effects ranging to mild (PU/PD) to severe (immuno-dysfunction, Demodicosis, and calcinosis cutis). It is a therapeutic option if the allergy season is very short but may result in unacceptable adverse effects, especially if used over the long term. 1. Potent, long acting injectable steroids are contraindicated for the treatment of allergies due to their comparatively short anti-inflammatory benefits ( 3 weeks) relative to the prolonged metabolic and immuno-depressive effects (6-10 weeks). 2. Injectable short acting steroids (dexamehtasone Sodium Phosphate, 0.5 – 1 mg/kg or prednisilone acetate 0.1mg – 1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if there are no concurrent secondary infection. This treatment option allows the clinician to more closely control and monitor the patients steroids use compared to oral treatments that are administered by the owner. 3. Temaril-P (trimeprizine and prednisilone combination) is a unique drug that provides significant antipruritic effects at a relatively lower dose of the prednisilone. One tablet should be administered per 10 to 20 kg every 24 to 48 hours. The dosage should be tapered to the lowest possible dose and frequency. 4. Prednisone 0.25 to 1mg/kg (or methylprednisolone 0.2-0.8mg/kg) PO should be administered every 24 to 48 hours for 3 to 7 days. The dosage should be tapered to the lowest possible dose and frequency. 5. All dogs treated with long-term steroids (more than 3 months) should be frequently monitored for liver disease and UTI. 8. Allergy Treatment (immune-modulation) a. Exposure to offending allergens should be reduced, if possible, by their removal from the environment. High-efficiency particulate (HEPA) air and charcoal filters should be used to reduce pollens, molds, and dust in the home. For house dust mite–sensitive dogs, household treatments for carpets, mattresses, and upholstery with the acaricide benzyl benzoate once a month for approximately 3 months, then every 3 months thereafter, may effectively eliminate house dust mites from the environment. Old dog beds should be discarded as these accumulate house dust mite antigens. Dehumidifying the house to below 40% relative humidity decreases house dust mite, mold, and flea antigen loads. To achieve this, high- efficiency dehumidifiers that are capable of pulling several liters of water from the air per day are required. Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

b. Cyclosporine (Atopica) helps control pruritus in 75% of atopic dogs. A dose of 5mg/kg PO should be administered every 24 hours until beneficial effects are seen (approximately 4-6 weeks). Then, dosage frequency should be tapered down to every 48 to 72 hours. For long- term control, approximately 25% of dogs require daily dosing, 50% can be controlled with every-other-day dosing, and approximately 25% can be controlled with twice-weekly dosing. Glucocorticoids can be used initially to speed response. As of this writing, there are no statistically significant increases in tumor risk or severe infection resulting from the immune effects of cyclosporine.

c. With immunotherapy (allergy vaccine), 60% to 75% of atopic dogs show good (some medical therapy still needed) to excellent (no other therapy needed) response. Clinical improvement is usually noted within 3 to 5 months of initiation of immunotherapy, but it can take up to 1 year in some dogs.

11. The prognosis is good, although lifelong therapy for control is needed in most dogs. Relapses (pruritic flare-ups with/without secondary infections) are common, so individualized treatment adjustments to meet patient needs may be required periodically. In dogs that become poorly controlled, one should rule out secondary infection (e.g., that caused by bacteria or Malassezia); sarcoptic mange; demodicosis; concurrent food, flea bite, and recently acquired hypersensitivity to additional environmental allergens. Because a strong genetic component is present, the breeding of any male or female dog with clinical signs of atopic dermatitis should be discouraged.

Box Author’s Note Our profession has excelled at reducing the use of steroids for arthritis; however, we have failed to make similar achievements for allergic disease including atopy. Since both disease have many similarities, including chronicity and multimodal therapeutic options, our goal should be to minimize the use of steroids for allergic diseases through the use of alternative, safer treatment options. To achieve best medicine, the frequency of steroid use should be similar for patients with arthritis and allergy. The use of long-acting, injectable steroids should be stopped due to the profound impact on the metabolic and immune systems as well as the growing concern of legal liability for the practitioner.

Author’s Note The only real, long-term options for treating the allergic immune response to environmental allergens are avoidance, allergy vaccine, or cyclosporine (Atopica). Based on typical cgeneral practice demographics, every full time small animal veterinarian should have approximately 20-30 patients who are no longer controlled with symptomatic therapy and need more aggressive treatment (allergy vaccine or cyclosporine).

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com #2 Canine Generalized Demodicosis

Features Canine generalized demodicosis may appear as a generalized skin disease that may have genetic tendencies and can be caused by three different species of demodectic mites: D. canis, D. injai, and an unnamed short-bodied Demodex mite. D. canis, a normal resident of the canine pilosebaceous unit (hair follicle, sebaceous duct, and sebaceous gland), is primarily transmitted from the mother to neonates during the first 2 to 3 days of nursing, but adult-to-adult transmission may rarely occur. D. injai, a recently described, large, long-bodied Demodex mite, is also found in the pilosebaceous unit, but its mode of transmission is unknown. Mode of transmission is also unknown for the short-bodied unnamed Demodex mite, which, unlike the other two species, lives in the stratum corneum. Depending on the dog’s age at onset, generalized demodicosis is classified as juvenile-onset or adult-onset. Both forms are common in dogs. Juvenile-onset generalized demodicosis may be caused by D. canis and the short-bodied unnamed Demodex mite. It occurs in young dogs, usually between 3 and 18 months of age, with highest incidence in medium-sized and large purebred dogs. Adult-onset generalized demodicosis can be caused by all three mite species and occurs in dogs older than 18 months of age, with highest incidence in middle-aged to older dogs that are immunocompromised because of an underlying condition such as endogenous or iatrogenic hyperadrenocorticism, hypothyroidism, immunosuppressive drug therapy, diabetes mellitus, or neoplasia. To date, only adult-onset disease has been reported with D. injai, with highest incidence noted in terriers. Clinical signs of infestation with either D. canis or the unnamed Demodex mite are variable. Generalized demodicosis is defined as five or more focal lesions, or two or more body regions affected. Usually, patchy, regional, multifocal, or diffuse alopecia is observed with variable erythema, silvery grayish scaling, papules, or pruritus. Affected skin may become lichenified, hyperpigmented, pustular, eroded, crusted, or ulcerated from secondary superficial or deep pyoderma. Lesions can be anywhere on the body, including the feet. Pododemodicosis is characterized by any combination of interdigital pruritus, pain, erythema, alopecia, hyperpigmentation, lichenification, scaling, swelling, crusts, pustules, bullae, and draining tracts. Peripheral lymphadenomegaly is common. Systemic signs (e.g., fever, depression, anorexia) may be seen if secondary bacterial sepsis develops. D. injai infestations are typically characterized by a focal areas of greasy seborrhea (seborrhea oleosa), especially over the dorsum of the trunk. Other skin lesions may include alopecia, erythema, hyperpigmentation, and comedones. Small breeds and terriers seem to predisoosed to Demodex injai infections.

Diagnosis 1. Microscopy (deep skin scrapes): many demodectic adults, nymphs, larvae, and ova are typically found with D. canis and the short-bodied, unnamed demodectic mite, although D. canis may be difficult to find in fibrotic lesions and in feet. With D. injai, mites may be low in number and difficult to find requiring skin biopsies.

Treatment and Prognosis

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 1. If adult-onset, any underlying conditions should be identified and corrected. All steroid containing therapies should be discontinued as steroid administration is the mostcommon cause of adult onset demidicosis. 2. Intact dogs, especially females, should be neutered. Estrus or pregnancy may trigger relapse. 3. Any secondary pyoderma should be treated with appropriate long-term (minimum 3-4 weeks) systemic antibiotics that are continued at least 1 week beyond clinical resolution of the pyoderma. 4. Topical shampoo therapy using a 1-3% benzoyl peroxide shampoo every 3-7 days will help speed resolution and enhance the mitacidal treatments. 5. Effective Mitacidal therapies include the following: *Ivermectin 0.2-0.6mg/kg PO every 24 hours is often effective against generalized demodicosis. Initially, ivermectin 0.1mg/kg PO is administered on day 1, then 0.2mg/kg PO is administered on day 2, with oral daily increments of 0.1mg/kg until 0.2-0.6mg/kg/day is being administered, assuming that no signs of toxicity develop. The cure rate for 0.4mg/kg/day ivermectin is 85% to 90%. *Milbemycin oxime, 0.5 to 2mg/kg PO every 24 hours. The cure rate is 85% to 90%. *Doramectin is also reported to be effective against canine demodicosis at a dose of 0.6mg/kg SC once weekly. The cure rate is approximately 85%. Adverse effects are uncommon but include, as for ivermectin, dilated pupils, lethargy, blindness, and coma. *For dogs £20kg, the use of 9% amitraz collars may be effective. In small dogs, use of 9% amitraz collars alone may be as effective as ivermectin (0.6mg/kg/day PO). * Topical application of Promeris (topical metaflumizone and amitraz solution) (topical metaflumizone and amitraz solution) every two weeks has demonstrated good efficacy. *Moxidectin has demonstrated variable efficacy when applied every 2-4 weeks. Historical Treatment Include: Traditional miticidal treatment entails the following:

n Total body hair coat clip if dog is medium- to long-haired

n Weekly bath with 2.5% to 3% benzoyl peroxide shampoo, followed by a total body application of 0.03% to 0.05% amitraz solution. The cure rate ranges from 50% to 86%. * For demodectic pododermatitis, in addition to weekly amitraz dips, foot soaks in 0.125% amitraz solution should be performed every 1 to 3 days. 6. Regardless of the miticidal treatment chosen, therapy is administered over the long term (weeks to months). Treatments should be continued for at least 1 month beyond the time when the first follow-up skin scrapings becomes negative for mites (total of two negative skin scrapings). 7. The prognosis is good to fair. Relapses may occur, requiring periodic or lifelong treatment in some dogs. The use of glucocorticosteroids in any dog that has been diagnosed with demodicosis should be avoided. Because of its hereditary predisposition, neither female nor male dogs with juvenile-onset generalized demodicosis should be bred. D canis is not considered contagious to cats or to humans. It is transmitted from bitch to newborn puppies during the first 2 to 3 days of nursing, and possibly between adult dogs that are close cohabitants. The mode of transmission for D injai and the unnamed short-bodied Demodex mite is unknown.

Author’s Note: Steroids are the most common cause of adult onset Demodicosis. Products containing amitraz tend to be the most toxic usually due to the product vehicle. Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com Aggressive treatment should be tried for up to six months before giving up. One of the most common causes of treatment failure is that the patient will look greatly improved before negative skin scrapes are achieved. Many owners will discontinue treatment prematurely resulting in relapse. The average time to achieve clinical improvement is 4-6 weeks; the first negative skin scrape usually occurs around 6-8 weeks; and most patients need approximately 3 months of treatment to resolve the infection based on two negative skin scrapes at least 3 weeks apart.

#3 Flea Allergy Dermatitis

Features Flea allergy dermatitis is a common skin disease in dogs and cats sensitized to flea salivia proteins through repeated and intermittent flea bites. Symptoms are usually seasonal (warm weather months and in the fall) in temperate zones and often nonseasonal in subtropical and tropical areas. Fall is often the most severe season relating to when the first cold snap occurs. Dogs The distribution typically involves the caudodorsal lumbosacral area, dorsal tail head, caudomedial thighs, abdomen, and flanks. Lesions include pruritic, papular, crusting eruptions with secondary erythema, seborrhea, alopecia, excoriations, pyoderma, hyperpigmentation, and lichenification. Cats Cats do not have a pattern unique to flea allergy dermatitis. Patients commonly present with pruritic miliary dermatitis with secondary excoriations, crusting, and alopecia of the neck, dorsal lumbosacral area, caudomedial thighs, and ventral abdomen. Other symptoms include symmetrical alopecia secondary to excessive grooming and eosinophilic granuloma complex lesions.

Top Differentials Differentials include atopy, food hypersensitivity, other ectoparasites (scabies, cheyletiellosis, pediculosis, demodicosis), superficial pyoderma, dermatophytosis, demodicosis, and Malassezia dermatitis.

Diagnosis 1. Lumbar dermatitis in the dog is the most consistent and unique feature of flea allergy dermatitis. In cats, flea allergy should be highly suspected in any cat with skin disease. 2. Visualization of fleas or flea excreta on body: may be difficult on flea-allergic animals as flea- allergic animals are very effective at removing fleas through grooming

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 3. Allergy testing (intradermal, serologic): positive skin test reaction to flea antigen or positive serum immunoglobulin (Ig)E antiflea antibody titer is highly suggestive, but false-negative results are possible 4. Dermatohistopathology (nondiagnostic): varying degrees of superficial or deep perivascular to interstitial dermatitis, with eosinophils often predominating 5. Response to aggressive flea control (nitenpyram administered every other day for 1 month): symptoms resolve

Treatment and Prognosis 1. Integrated flea management program (Insect growth regulator combined with an adulticide combined with environmental treatments) is essential due to the progressive tolerance of the flea to available adulticides. With time, specific active ingredients typically loose efficacy due to the chronic exposure and genetic drift of the flea. 2. Topical or systemic insect growth regulators (lufenuron, piriproxyfen, methoprene) may be effective alone or used in combination with adulticidal therapy. 3. Affected and all in-contact dogs and cats should be treated with adulticidal flea sprays, spot-on solutions, orals, or dips every 7 to 30 days, as instructed on the label. Products that contain spinosid , imidocloprid, selamectin, or fipronil are especially effective when used topically every 2 to 4 weeks. In heavily flea-infested environments, fleas may continue to be found on animals for several months in spite of topical flea control. In these cases, affected animals should also be administered nitenpyram at a minimum dose of 1mg/kg PO every 24 to 48 hours for 2 to 4 weeks, or until fleas are no longer seen. The environment should be treated (see number 5 below). 4. Flea-allergic animals should be treated prophylactically with nitenpyram, minimum dose 1mg/kg PO, on any day that an encounter is planned with other potentially flea-infested animals (e.g., a visit to the groomer, veterinary hospital, park, another household with animals). No more than one treatment with nitenpyram should be administered per day. 5. In heavily flea-infested environments, areas where pets spend the most time should be treated. Indoor premises should be treated with an insecticide and an insect growth regulator (e.g., methoprene, piriproxyfen). The outdoor environment should be treated with insecticidal or biologic products designed for such use. 6. Flea control therapy should be continued from spring until first snowfall in temperate areas and year-round in warm climates. Year-round flea infestations can be perpetuated indoors and on wildlife despite extreme cold outdoors. 7. Symptomatic Therapy (itch control): a Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms. b Systemic antihistamine therapy reduces clinical symptoms in many cases (Table 7-1). c Systemic glucocorticoid therapy is often effective (75%) in controlling pruritus but almost always result in adverse effects ranging to mild (PU/PD) to severe (immuno-dysfunction, Demodicosis, and calcinosis cutis). It is a therapeutic option if the allergy season is very short but may result in unacceptable adverse effects, especially if used over the long term. 1. Potent, long acting injectable steroids are contraindicated for the treatment of allergies due to their comparatively short anti-inflammatory benefits ( 3 weeks) relative to the prolonged metabolic and immuno-depressive effects (6-10 weeks).

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 2. Injectable short acting steroids (dexamehtasone Sodium Phosphate, 0.5 – 1 mg/kg or prednisilone acetate 0.1mg – 1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if there are no concurrent secondary infection. This treatment option allows the clinician to more closely control and monitor the patients steroids use compared to oral treatments that are administered by the owner. 3. Temaril-P (trimeprizine and prednisilone combination) is a unique drug that provides significant antipruritic effects at a relatively lower dose of the prednisilone. One tablet should be administered per 10 to 20 kg every 24 to 48 hours. The dosage should be tapered to the lowest possible dose and frequency. 4. Prednisone 0.25 to 1mg/kg (or methylprednisolone 0.2-0.8mg/kg) PO should be administered every 24 to 48 hours for 3 to 7 days. The dosage should be tapered to the lowest possible dose and frequency. 5. All dogs treated with long-term steroids (more than 3 months) should be frequently monitored for liver disease and UTI.

8. The prognosis is good if strict flea control is practiced. Fleas may infest other in-contact animals and humans. They may carry blood-borne diseases in a manner similar to ticks.

Author’s note The use of long-acting, injectable steroids should be stopped due to the profound impact on the metabolic and immune systems as well as the growing concern of legal liability for the practitioner. Any dog with lumbar dermatitis or any cat with skin disease should be highly suspected of having flea allergy dermatitis even if the patient has been treated with seemingly good flea control therapies. A nitenpyram trial (every other day for 1 month) is the most efficient and cost effective way to convince the owner and yourself of the role of flea allergy in a pruritic patient.

#4 Superficial Pyoderma

Features Superficial pyoderma is a superficial bacterial infection involving hair follicles and the adjacent epidermis. The infection is almost alwayss secondary to an underlying cause; allergies and endocrine disease are the most common causes (Box 3-3). Superficial pyoderma is one of the most common skin diseases in dogs but rare in cats. Superficial pyoderma is characterized by focal, multifocal, or generalized areas of papules, pustules, crusts, and scales, epidermal collarettes, or circumscribed areas of erythema and alopecia that may have hyperpigmented centers. Short-coated dogs often present with a “moth- eaten” patchy alopecia, small tufts of hair that stand up, or reddish brown discoloration of white hairs. In long-coated dogs, symptoms can be insidious and may include a dull, lusterless hair coat, scales, and excessive shedding. In both short- and long-coated breeds, primary skin lesions are often obscured by remaining hairs but can be readily appreciated if an affected area is

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com clipped. Pruritus is variable, ranging from none to intense levels. Bacterial infections secondary to endocrine disease may cause pruritus, thereby mimicking allergic skin disease. Staphylococcus pseudintermedius (previously Staphylococcus intermedius)is the most common bacterium isolated from canine pyoderma and is usually limited to dogs. Staphylococcus schleiferi is a bacterial species in dogs and humans that is emerging as a common canine isolate in patients with chronic infections and previous antibiotic exposure. Both Staphylococcus pseudintermedius and Staphylococcus schleiferi may develop methacillin-resistence especially if subtherapeutic doses of antibiotics or flouroquinilone antibiotics have been previously used in the patient. Additionally, methicillin-resistant Staphylococcus aureus (human MRSA) is becoming more common among veterinary species. All three Staphylococcus may be zoonotic, moving from humans to canines or from canine to human; immunosuppressed individuals are at most risk.

Causes of Secondary Superficial and Deep Pyoderma

n Demodicosis, scabies, Pelodera

n Hypersensitivity (e.g., atopy, food, flea bite)

n Endocrinopathy (e.g., hypothyroidism, hyperadrenocorticism, sex hormone imbalance, alopecia X)

n Immunosuppressive therapy (e.g., glucocorticoids, progestational compounds, cytotoxic drugs)

n Autoimmune and immune-mediated disorders

n Trauma or bite wound

n Foreign body

n Poor nutrition

Treatment and Prognosis 1. The underlying cause must be identified and controlled. 2. Systemic antibiotics (minimum 3-4 weeks) should be administered and continued 1 week beyond complete clinical and cytological resolution (see Box 3-1). 3. Concurrent bathing every 2 to 7 days with an antibacterial shampoo that contains chlorhexidine or benzoyl peroxide is helpful. 4. If lesions recur within 7 days of antibiotic discontinuation, the duration of therapy was inadequate and antibiotics should be reinstituted for a longer time period and better attempts to identify and control the underlying disease should occur. 5. If lesions do not completely resolve during antibiotic therapy or if there is no response to the antibiotics, antibiotic resistance should be assumes and a bacterial culture and sensitivity submitted. 7. If antibiotics resistance is suspected or confirmed, frequent bathing (up to daily) and the frequent application of topical chlorhexidine solutions combined with the simultaneous administration of two different class antibiotics at high doses seem to produce the best results. Monitoring the infection with cytology and cultures with antibiotic sensitivities is important to determine when the treatments can be stopped. Premature discontinuation of therapy, not completely controlling the primary disease, and the use of fluoroquinilone antibiotics will likely perpetuate the resistant infection. 8. The prognosis is good if the underlying cause can be identified and corrected or controlled.

Author's Note:

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com ** Superficial Pyoderma is one of the most common skin diseases in dogs and almost always has an underlying cause (allergies or endocrine disease). ** Cefpodoxime, Ormetoprim/sulfadimethoxine (Primor), and Convenia provide the most consistent compliance which seem to help reduce the development of resistance when used at high doses. ** MRSA, MRSS, MRSI, and MRSP are becoming an emerging problem in some regions of the US. >>The most likely risk factors include previous exposure to fluoroquinilone antibiotics, sub-therapeutic antibiotic dosing, and concurrent steroid therapy. >> Daily baths and topical treatments can be very beneficial in the resolution of the infection. >> Maximize the dose of antibiotics and consider using two antibiotics simultaneously to protect additional resistance from developing. >> Practice good hygiene (HAND WASHING) to prevent zoonosis. ** Consider screening dogs who visit the elderly or sick to prevent zoonosis. Cultures from the nose, lips, ears, axilla, and perianal areas are best for screening patients for MRS.

#5 Otitis

Features Otitis externa is an acute or chronic inflammatory disease of the external ear canal. Its causes are numerous and almost always have an underlying, primary disease (Table 15.1) that alters the normal structure and function of the canal resulting in a secondary infection (Table 15.2). Otitis externa is common in cats and dogs, with Cocker spaniels especially at risk for developing severe and chronic disease. Otic pruritus or pain is a common symptom of otitis externa. Head rubbing, ear scratching, head shaking, aural hematomas, and a head tilt, with the affected ear tilted down, may be noted. An otic discharge that may be malodorous is often present. In acute cases, the inner ear pinna and ear canal are usually erythematous and swollen. The ear canal may also be eroded or ulcerated. Pinnal alopecia, excoriations, and crusts are common. In chronic cases, pinnal hyperkeratosis, hyperpigmentation, and lichenification, as well as ear canal stenosis from fibrosis or ossification, are common. Decreased hearing may be noted. Concurrent otitis media should be suspected if otitis externa has been present for 2 months or longer, even if the tympanic membrane appears to be intact and no clinical signs of otitis media (drooping or inability to move ear or lip, drooling, decreased or absent palpebral reflex, exposure keratitis) are evident. Rarely, symptoms of otitis interna (head tilt, nystagmus, ataxia) may be present. Oral examination may reveal pain (severe otitis media), inflammation, or masses (especially polyps in cats). Depending on the underlying cause, concurrent skin disease may be seen.

Diagnosis 1. Based on history and clinical findings 2. Otoscopic examination: assess degree of inflammation, ulceration, stenosis, and proliferative changes; amount and nature of debris and discharge; presence of foreign bodies, ectoparasites, and masses; and integrity of tympanic membrane 3. Mineral oil prep (ear swab): look for otodectic and demodectic mites and ova 4. Cytology (ear swab): look for bacteria, yeasts, fungal hyphae, cerumen, leukocytes, and neoplastic cells Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 5. Bacterial culture (external or middle ear exudate): indicated when bacteria are found on cytology in spite of antibiotic therapy, or when otitis media is suspected 6. Fungal culture: indicated when dermatophytic otitis is suspected, especially in long-haired cats that have ceruminous otitis 7. Radiography (bulla series), computed tomography (CT), magnetic resonance imaging (MRI): evidence of bullous involvement (sclerosis, opacification) is seen in approximately 75% of otitis media cases 8. Dermatohistopathology: may be indicated to identify primary cause (e.g., autoimmune disease, sebaceous adenitis, erythema multiforme), if neoplasia is suspected (ear canal mass), or if ear canal resection or ablation is performed because of end-stage otitis

Treatment and Prognosis 1. Primary causes of the otitis should be identified and corrected, if possible (Table 15-1). 2. For swimmer’s ear, maceration of ear canals can be prevented by prophylactic instillation of a drying agent after the dog gets wet (swimming, bathing), or two to three times per week in very humid climates. Effective products are ear products that contain astringents/alcohol 3. For allergic otitis, long-term management includes control of underlying allergies, resolution of any secondary bacterial and yeast otitis, and institution of ear cleaning and treatment every 3-7 days to prevent the recurrence. In animals whose underlying allergies cannot be identified or completely controlled, the judicious use of steroid-containing otic preparations as infrequently as needed may prevent otitis flare-ups 4. For mild/acute otitis, at home, the owner should perform ear cleaning every 2 to 7 days with a ceruminolytic agent (that does not need to be flushed out) to prevent earwax and debris from accumulating. Lifelong ear cleaning every 3 – 7 days may be necessary to prevent relapses of otitis. The use of cotton swabs (which may damage the epithelium) is not recommended. 5. For severe/chronic otitis, in-hospital ear cleaning and flushing should be performed to remove accumulated exudate and debris from the vertical and horizontal ear canals (under sedation or anesthesia if necessary). The procedure should be repeated every 2 to 7 days until all debris has been removed. Products that can be used for ear flushing include the following: n Water or saline n DSS diluted in warm water or saline Non-ototoxic ear cleaning product n Povidone-iodine 0.2%-1% solution (may be ototoxic) n Chlorhexidine 0.05%-0.2% solution (may be ototoxic) n Pretreatment (5 minutes before lavage) with a urea peroxide cleaning product is very effective at dissolving exudate but MUST be flushed out of the canal(may be ototoxic) 6. Systemic glucocorticoids should be administered if the ear is painful or the canal is stenotic from tissue swelling or proliferation. For dogs, prednisone 0.25 to 0.5mg/kg PO should be administered every 12 hours for 5 to 10 days. For cats, prednisolone 0.5-1.0mg/kg PO should be administered every 12 hours for 7 to 14 days.

Individual Diseases 7. For ear mites, affected and all in-contact dogs and cats should be treated. When otic treatments are used, additional treatment to eliminate ectopic mites should be concurrently administered. Effective therapies for ear mites include the following: n Otic miticide as per label directions (ivermectin and milbemycin products are safe and highly effective) n Selemectin 6-12mg/kg topically on skin twice 2-4 weeks apart (dogs) n Tresaderm 0.125-0.25 mL AU q 12 hours for 2-3 weeks n Ivermectin 0.3mg/kg PO q 7 days for 3-4 treatments, or 0.3mg/kg SC q 10-14 days for 2-3 treatments n Fipronil 0.1-0.15 mL AU q 14 days for two to three treatments (based on anecdotal reports) 8. For demodectic otitis, Effective therapies for ear mites include the following:

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com n Otic miticide as per label directions (ivermectin and milbemycin products are safe and highly effective) An alternative treatment is to use 1% injectable ivermectin solution 0.1 to 0.15 mL instilled AU every 24 hours, continuing at least 2 weeks past complete clinical resolution with no evidence of mites on follow-up ear smears. 9. For yeast otitis, antifungal-containing ear preparations should be repackaged into a bottle to provide more accurate dosing; dropper bottle, brown amber bottle, etc. Then, 0.2 to 0.4 mL 1 1 ( /4- /2 dropperful) should be instilled in the affected ear every 12 hours for at least 2 to 4 weeks. Treatment should be continued until follow-up ear smears are cytologically negative for microorganisms, the external canals are no longer edematous or inflamed, and the ear canal epithelium has normalized. Effective products include the following: n Clotrimazole n Miconazole n Thiabendazole n Nystatin 10. For severe refractory yeast otitis externa or otitis media, in addition to topical antifungal treatment, systemic antifungal therapy may be helpful if administered for at least 3 to 4 weeks, then continued 1 to 2 weeks beyond complete clinical cure. Effective therapies include the following: n Ketoconazole 5mg/kg PO q 12 hours, or 10mg/kg PO q 24 hours with food n Fluconazole 5mg/kg PO q 12 hours, or 10mg/kg PO q 24 hours with food n Itraconazole 5-10mg/kg PO q 24 hours with food n Pulse itraconazole 5-10mg/kg PO q 24 hours with food on 2 consecutive days each week 11. For bacterial otitis, antibiotic-containing ear preparations should be repackaged into to provide more accurate dosing; dropper bottle, brown amber bottle, etc. Then, 0.2 to 0.4 mL 1 1 ( /4- /2 dropperful) should be instilled in affected ears every 8 to 12 hours for at least 2 to 4 weeks. Treatment should be continued until follow-up ear smears are cytologically negative for microorganisms, the external canals are no longer edematous or inflamed, and the ear canal epithelium has normalized. Effective products include the following: n Gentamicin n Neomycin n Polymixin B and neomycin n Polymixin E and neomycin 12. For bacterial otitis media, Systemic antibiotics may not achieve sufficient tissue concentrations to kill Pseudomonas and to prevent antibiotic resistance, the highest possible dose of antibiotic that is safe should be administered with concurrent high-concentration topical therapy of the same antibiotic. If topical has been used aggressively and has been unsuccessful, systemic antibiotics may be indicated, based on culture and sensitivity results, for a minimum of 4 weeks, and continued 2 weeks beyond complete clinical cure. Antibiotics include the following: n Ormetoprin-sulfadimethoxine 27.5mg/kg PO q 24 hours n Trimethoprim-sulfa 22mg/kg PO q 12 hours n Cephalexin, cephradine, or cefadroxil 22mg/kg PO q 8 hours n Ciprofloxacin 5-15mg/kg PO q 12 hours n Enrofloxacin 20mg/kg PO q 24 hours (may increase the risk of resistant bacteria) n Orbifloxacin 7.5mg/kg PO q 24 hours (may increase the risk of resistant bacteria) n Marbofloxacin 5.5mg/kg PO q 24 hours (may increase the risk of resistant bacteria)

13. For Pseudomonas otitis, aggressive treatment should be provided for at least 2-4 weeks, then continued 2 weeks beyond complete clinical cure. All underlying/primary diseases should be identified and addressed. Currently, the most effective treatments include tris– ethylenediaminetetra-acetic acid (EDTA) solutions with high concentrations of antibiotics instilled in high volumes (to ensure deep penetration and prevent dilution by exudate). Antibiotics should be selected according to culture and sensitivity results. Systemic

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com antibiotics may not achieve sufficient tissue concentrations (mutation prevention concentration) to kill Pseudomonas and prevent antibiotic resistance. If systemic antibiotics are used, the highest possible dose that is safe should be administered, along with concurrent high-concentration topical therapy of the same antibiotic.

n The tris–ethylenediaminetetra-acetic acid (EDTA) solution should be combined with enrofloxacin to make a 10- to 20-mg/mL solution. The solution should be used q 12-24 hours to completely fill the ear canal. Even as the sole therapy, the surfactants in T8 Solution act to clean the ear while allowing the high concentration of enrofloxacin to penetrate into the deep canal. This treatment is 80% effective in chronic, recurrent otitis cases, even if the bacteria are reported to be resistant to enrofloxacin (because of the tris-EDTA and high concentration of antibiotic)

n Tris-EDTA solution (with/without enrofloxacin 10mg/mL, gentamicin 3mg/mL, or amikacin 9mg/mL) 0.4 mL instilled q 8-12 hours n Combination 3 mL enrofloxacin (Baytril Injectable 22.7mg/mL) plus 4mg dexamethasone sodium phosphate plus 12 mL ear cleanser: 0.2-0.4 mL instilled q 12 hours n Amikacin sulfate (Amiglyde V Injectable 50mg/mL), undiluted, 0.1-0.2 mL instilled q 12 hours 1 n Silver sulfadiazine (Silvadene) 0.1% solution (mix 1.5 mL [ /3 tsp]) of Silvadene Cream with 13.5 mL distilled water, or mix 0.1 g silver sulfadiazine powder with 100 mL distilled water), and instill 0.5 mL q 12 hours n Ticarcillin equine intrauterine infusion (Ticillin), undiluted, 0.2-0.3 mL q 8 hours n Ticarcillin powder for injection (vial should be reconstituted as directed, then frozen in TB syringes as 1-mL aliquots). New syringe should be thawed each day and kept refrigerated. A dose of 0.2 to 0.3 mL should be instilled into affected ears q 8 hours

For End-Stage Ears 14. For chronic proliferative otitis, aggressive medical therapy is needed. Weekly ear cleaning should be instituted. For bacterial/yeast otitis externa and media, long-term (minimum, 4 weeks) systemic and topical antibiotics or antifungal medications should be administered, then continued 2 weeks beyond complete clinical resolution of the infection. To reduce tissue proliferation, prednisone 0.5mg/kg PO should be administered every 12 hours for 2 weeks; then, 0.5mg/kg PO should be administered every 24 hours for 2 weeks, followed by 0.5mg/kg PO every 48 hours for 2 weeks. These ears rarely return to complete normalcy, so long-term maintenance therapy with steroid-containing otic preparations, as described for allergic otitis, is almost always necessary. 15. For end-stage ears, indications for surgery include the following: n Traction-avulsion or surgical resection of inflammatory polyps/masses n Lateral ear canal resection, which aids in ventilation and drainage and allows for easier application of medication but rarely results in cure because a large amount of diseased tissue is still present n Vertical ear canal ablation, if proliferative changes are present in the vertical canal but the horizontal canal is not affected. Total ear canal ablation and lateral bulla osteotomy is usually indicated to alleviate chronic pain and discomfort when end-stage otitis externa and otitis media are no longer responsive to medical management 16. The prognosis is variable, depending on whether the underlying cause can be identified and corrected, and on the chronicity and severity of the otitis externa. Because Cocker spaniels are especially at risk for chronic and severe otitis externa, early and aggressive management of primary otitis externa and secondary inflammation is warranted in this breed.

Author’s Note:

The most important component for successful long-term treatment of otitis are Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com 1. Identify and control the underlying, primary disease; infectious otitis is secondary and recurrence can only be prevented if the primary disease is treated.

2. Use sufficient volumes of otic medications to completely coat and penetrate the ear canal; most patients need a minimum of 0.25 ml to provide enough medication.

3. Don’t treat and stop; treat and stop but rather use frequent (every 3-7 days) cleaning or treatment to prevent otitis recurrence.

It is extremely important to base treatment decisions on cytology (initial and recheck) and clinical impression together.

The most consistently successful and least ototoxic treatment for Pseudomonas otitis is a high concentration enrofloxcin solution mixed into a trisEDTA (making a 10mg/ml final solution). If the infection is not improving, consider a deep otic lavage and evaluation of the otic bullae. Systemic antibiotics do NOT seem to improve treatment efficacy beyond the topical solution alone.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

#6 Canine Food Hypersensitivity

Features Canine food hypersensitivity is an adverse reaction to a food or food additive. It can occur at any age, from recently weaned puppies to elderly dogs that have been eating the same dog food for years. Approximately 30% of dogs diagnosed with food allergy are younger than 1 year of age. It is common in dogs. Canine food hypersensitivity is characterized by nonseasonal pruritus that may or may not respond to steroid therapy. The pruritus may be regional or generalized and usually involves the ears, feet, inguinal or axillary areas, face, neck, and perineum. Affected skin is often erythematous, and a papular rash may be present. Self-trauma–induced lesions include alopecia, excoriations, scales, crusts, hyperpigmentation, and lichenification. Secondary superficial pyoderma, Malassezia dermatitis, and otitis externa are common. Other symptoms that may be seen are acral lick dermatitis, chronic seborrhea, and recurring pyotraumatic dermatitis. Some dogs are minimally pruritic, with the only symptom being recurrent infection with pyoderma, Malassezia dermatitis, or otitis. In these cases, the pruritus is present only when secondary infections are left untreated. Occasionally, urticaria or angioedema may occur. Concurrent gastrointestinal signs (e.g., frequent bowel movements, vomiting, diarrhea, flatulence) are reported in 20%-30% of cases.

Top Differentials Differentials include atopy, scabies, Malassezia dermatitis, bacterial pyoderma, as well as other hypersensitivities (flea bite, contact), parasites (cheyletiellosis, pediculosis), and folliculitis (dermatophyte, Demodex).

Diagnosis 1. Perianal dermatitis with or without recurrent otitis is the most common and unique feature of food allergy. However, food allergy can manifest in many patterns and should be suspected for atypical pruritic patient including cases of recurrent infections without pruritus. 2. Dermatohistopathology (nondiagnostic): varying degrees of superficial perivascular dermatitis. Mononuclear cells or neutrophils may predominate. Eosinophils may be more numerous than in atopy 3. Food allergy testing (intradermal, serologic)(nondiagnostic): not recommended because test results are unreliable. Some dogs will have positive reactions to storage mite antigens, which may be clinically relevant, or they may be caused by cross-reactivity with other insects. Storage mites are ubiquitous, and their clinical significance is currently unknown. 4. Response to hypoallergenic diet trial: symptoms improve within 10 to 12 weeks of initiation of a strict home-cooked or commercially prepared restricted diet (one protein and one carbohydrate source). The hypoallergenic diet should not contain food ingredients previously administered in dog food, treats, or table scraps, nor should flavored heartworm preventative, flavored medications, nutritional supplements, or chewable treats (i.e., pig ears, cow hooves, rawhide, dog biscuits, table food such as cheese or peanut butter to hide pills in) be Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

administered during the hypoallergenic diet trial. Beef and dairy are the most common food allergens in dogs and avoiding these alone may result in clinical improvement. Other common food allergies include chicken, eggs, soy, corn, and wheat. 5. Provocative challenge: recurrence of symptoms within hours to days of reintroduction of suspect allergen into the diet.

Treatment and Prognosis 1. Infection Prevention: a. Any secondary pyoderma, otitis externa, and Malassezia dermatitis should be treated with appropriate therapies. Controlling and preventing secondary infection is an essential component of managing atopic dogs. Bathing every 3 – 7 days and treating the ears after every bath helps wash off pollens and disinfect the skin and ear canals, preventing the secondary infections from recurring. 2. Symptomatic Therapy (itch control) is variably effective for food allergy: a An integrated flea control program should be instituted to prevent flea bites from aggravating the pruritus. b Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms. C Systemic antihistamine therapy reduces clinical symptoms in many cases (Table 7-1). One- to two-week long therapeutic trials with different antihistamines may be required to determine which is most effective. D Oral essential fatty acid supplements (180mg EPA/10 lb) help control pruritus in 20% to 50% of cases, but 8 to 12 weeks of therapy may be needed before beneficial effects are seen. Also, a synergistic effect is often noted when essential fatty acid supplements are administered in combination with glucocorticoids or antihistamines. E Dextromethorphan, an opioid antagonist, may also be a useful adjunct in managing the licking, chewing, and biting behaviors associated with allergic dermatitis in dogs. Dextromethorphan 2mg/kg PO should be administered every 12 hours. A beneficial effect should be seen within 2 weeks. F Systemic glucocorticoid therapy is only variably effective (unpredictable minimal to good response) in controlling pruritus cause by the food allergy; but almost always result in adverse effects ranging to mild (PU/PD) to severe (immuno-dysfunction, Demodicosis, and calcinosis cutis). (see Atopy section) 1. Potent, long acting injectable steroids are contraindicated for the treatment of allergies due to their comparatively short anti-inflammatory benefits ( 3 weeks) relative to the prolonged metabolic and immuno-depressive effects (6-10 weeks). 2. Injectable short acting steroids (dexamehtasone Sodium Phosphate, 0.5 – 1 mg/kg or prednisilone acetate 0.1mg – 1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if there are no concurrent secondary infection. This treatment option allows the clinician to more closely control and monitor the patient’s steroids use compared to oral treatments that are administered by the owner. 3. All dogs treated with long-term steroids (more than 3 months) should be frequently monitored for liver disease and UTI. 8. Food Allergy Treatment

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

a. Offending dietary allergen(s) should be avoided. A balanced home-cooked diet or a commercial hypoallergenic diet should be provided. b. To identify offending substances to be avoided (challenge phase after food allergy has been confirmed with the dietary trial) one new food item should be added to the hypoallergenic diet every 2 to 4 weeks. If the item is allergenic, clinical symptoms will recur within 7 to 10 days. Note: Some dogs (approximately 20%) should be fed home-cooked diets to remain symptom-free. For these dogs, commercial hypoallergenic diets are ineffective, presumably because their hypersensitivity relates to a food preservative or dye. c. Ancedotal reports suggest that higher doses (10mg/kg) of cyclosporine (Atopica) may ne beneficial in reducing the allergic immune response and symptoms of food allergy. 8. The prognosis is good. In dogs that are poorly controlled, owner noncompliance should be ruled out, along with development of hypersensitivity to an ingredient in the hypoallergenic diet, secondary infection (caused by bacteria, Malassezia, dermatophyte), scabies, demodicosis, atopy, flea allergy dermatitis, and contact hypersensitivity.

Author’s Note Due to recent food industry changes, there has been an explosion of products available through prescription or over-the-counts and the listing is beyond the scope of this text. Many of the over-the-counter diets are sufficiently restricted and of high enough quality to produce clinical benefit when a food allergic patient restricted to one of the nonBeef and nondairy products. Food allergy is responsible for most of the very unusual clinical symptom patterns in dogs with recurrent infections (with or without pruritus). Poor owner compliance should be expected making the long-term management of food allergic patients difficult and frustrating; repeated lapses in diet result in flare-ups in the pruritus and secondary infections.

Author’s Note The use of long-acting, injectable steroids should be stopped due to the profound impact on the metabolic and immune systems as well as the growing concern of legal liability for the practitioner.

#7 Canine Hypothyroidism

Features This endocrinopathy is most often associated with primary thyroid dysfunction caused by lymphocytic thyroiditis or idiopathic thyroid atrophy. It is common in dogs, with highest incidence in middle-aged to older dogs. Young adult large and giant-breed dogs are also occasionally affected. Congenital hypothyroidism is extremely rare. A variety of cutaneous symptoms can be seen. Alopecia on the bridge of the nose occurs in some dogs as an early symptom. The hair coat may be dull, dry, and brittle. Bilaterally symmetrical alopecia that spares the extremities may occur, with easily epilated hairs. Alopecic skin may be hyperpigmented, thickened, or cool to the touch. Thickened and droopy facial skin from dermal mucinosis, chronic seborrhea sicca or oleosa, or ceruminous otitis externa may be present. Seborrheic skin and ears may be secondarily infected with yeast or bacteria. In some dogs, the only symptom is recurrent pyoderma or adult-onset generalized demodicosis. Pruritus is not a primary feature of hypothyroidism and, if present, reflects secondary pyoderma, Malassezia infection, or demodicosis. Noncutaneous symptoms of hypothyroidism are variable Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

and may include aggression, lethargy or mental dullness, exercise intolerance, weight gain or obesity, thermophilia (cold intolerance), bradycardia, vague neuromyopathic or gastrointestinal signs, central nervous system involvement (e.g., head tilt, nystagmus, hemiparesis, cranial nerve dysfunction, hypermetria), and reproductive problems (e.g., decreased libido, prolonged anestrus, infertility). Puppies with congenital hypothyroidism are disproportionate dwarfs with short limbs and neck relative to their body length.

Top Differentials Differentials include other causes of endocrine alopecia, superficial pyoderma, Malassezia dermatitis, and demodicosis.

Diagnosis 1. Rule out other differentials 2. Hemogram and serum biochemistry panel: nonspecific findings may include a mild, nonregenerative anemia, hypercholesterolemia, or elevated creatine kinase 3. Dermatohistopathology: usually, nonspecific endocrine changes or findings consistent with pyoderma, Malassezia dermatitis, or seborrhea are seen. If present, dermal mucinosis is highly suggestive of hypothyroidism, but this can be a normal finding in some breeds (e.g., Shar pei) 4. Serum total thyroxine (TT4), free thyroxine (FT4) by equilibrium dialysis, and endogenous thyroid-stimulating hormone (TSH) assays: low TT4, low FT4, and high TSH are highly suggestive of hypothyroidism, but false-positive and false-negative results can occur, especially with TT4 and TSH. For example, although TT4 is a good screening test, it should not be used alone to make a diagnosis because its serum level can be artificially increased or decreased by several factors, such as nonthyroidal illness, autoantibodies, and drug therapy (Table 9-1)

Treatment and Prognosis 1. Any secondary seborrhea, pyoderma, Malassezia dermatitis, or demodicosis should be treated with appropriate topical and systemic therapies. 2. Levothyroxine 0.02mg/kg PO should be administered every 12 hours until symptoms resolve (approximately 8-16 weeks). Some dogs can then be maintained with 0.02mg/kg PO every 24 hours; others require lifelong twice-daily dosing to maintain remission. 3. Dogs with concurrent heart disease should be started on levothyroxine more gradually. Treatment should begin with 0.005mg/kg PO every 12 hours; dosage should be increased by 0.005mg/kg every 2 weeks until 0.02mg/kg every 12 hours is being administered. 4. After 2 to 4 months of therapy, the serum TT4 level should be measured 4 to 6 hours after medication administration and should be in the high normal to supranormal range. If the level is low or within the normal range and if minimal clinical improvement has been seen, the dosage of levothyroxine should be increased and the serum TT4 level checked 2 to 4 weeks later. 5. If signs of thyrotoxicosis from oversupplementation (e.g., anxiety, panting, polydipsia, polyuria) occur, the serum TT4 level should be evaluated. If the level is markedly elevated, medication should be temporarily stopped until adverse effects abate; it should then be reinstituted at a lower dose or a less frequent dosage schedule. 6. The prognosis is good with lifelong replacement thyroxine therapy, although hypothyroidism- induced neuromuscular abnormalities may not completely resolve.

#7 Canine Hyperadrenocorticism (Cushing’s disease)

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

Features Spontaneously occurring hyperadrenocorticism is associated with the excessive production of endogenous steroid hormones (principally glucocorticoids, but sometimes mineralocorticoids or sex hormones) by the adrenal cortex. The disease is caused by a hyperfunctioning adrenal tumor (15%-20% of cases) or pituitary tumor (80%-85% of cases). Pituitary-dependent hyperadrenocorticism (PDH) is caused by the excessive production of adrenocorticotropic hormone (ACTH), usually from a pituitary microadenoma or macroadenoma. Iatrogenically induced disease occurs secondary to excessive administration of exogenous glucocorticoids. Iatrogenic hyperadrenocorticism can occur at any age and is common, especially in chronically pruritic dogs and dogs with immune-mediated disorders that are controlled with long-term glucocorticoids. Spontaneously occurring hyperadrenocorticism is also common and tends to occur in middle-aged to older dogs, with an increased incidence noted in Boxers, Boston terriers, Dachshunds, Poodles, and Scottish terriers. The hair coat often becomes dry and lusterless, and slowly progressing, bilaterally symmetrical alopecia is common. The alopecia may become generalized, but it usually spares the head and limbs. Remaining hairs are easily epilated, and alopecic skin is often thin, hypotonic, and hyperpigmented. Cutaneous striae and comedones may be seen on the ventral abdomen. The skin may be mildly seborrheic (fine, dry scales), bruise easily, and exhibit poor wound healing. Chronic secondary superficial or deep pyoderma, dermatophytosis, or demodicosis is common and may be the client’s primary complaint. Calcinosis cutis (whitish, gritty, firm, bonelike papules and plaques) may develop, especially on the dorsal midline of the neck or ventral abdomen, or in the inguinal area. Polyuria and polydipsia (water intake > 100mL/kg/day) and polyphagia are common. Muscle wasting or weakness, a pot-bellied appearance (from hepatomegaly, fat redistribution, and weakened abdominal muscles), increased susceptibility to infection (conjunctival, skin, urinary tract, lung), excessive panting, and variable behavioral or neurologic signs (expanding pituitary tumor) are often present.

Top Differentials Differentials include other causes of endocrine alopecia, follicular dysplasia, alopecia X, superficial pyoderma, demodicosis, and dermatophytosis.

Diagnosis 1. Hemogram: neutrophilia, lymphopenia, and eosinopenia are often seen 2. Serum biochemistry panel: an elevated alkaline phosphatase enzyme level is typical (90% of cases). There may also be mildly to markedly elevated alanine transaminase activity, as well as elevated cholesterol, triglyceride, or glucose levels 3. Urinalysis: the specific gravity is usually low, and there may be bacteriuria, proteinuria, or glucosuria. Subclinical urinary tract infections are common 4. Urine cortisol/creatinine ratio: usually elevated. A nonspecific screening test that is not diagnostic by itself because false-positive results are common (stress-induced, seen with many other illnesses). To minimize the effects of stress, a home-collected urine sample should be used, instead of one obtained at the veterinary hospital 5. Dermatohistopathology: often shows nondiagnostic changes consistent with any endocrinopathy. Dystrophic mineralization (calcinosis cutis), thin dermis, and absent erector pili muscles are highly suggestive of hyperadrenocorticism, but these changes are not always present 6. Abdominal ultrasonography: may demonstrate adrenal hyperplasia or tumor 7. Computed tomography (CT) or magnetic resonance imaging (MRI): may detect a pituitary mass 8. Adrenal function tests: n ACTH stimulation test (cortisol): an exaggerated poststimulation cortisol level is highly suggestive of endogenous hyperadrenocorticism, but false-negative and false-positive results can occur. In iatrogenic cases, an inadequate response to ACTH stimulation is typical. Note: Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

Reconstituted cosyntropin (ACTH solution) can be stored frozen at -20°C in plastic syringes for up to 6 months with no adverse effects on its bioactivity n ACTH stimulation test (17-hydroxyprogesterone): exaggerated basal and poststimulation 17- hydroxyprogesterone levels may be seen in endogenous hyperadrenocorticism, but false- negative and false-positive results can occur. 17-Hydroxyprogesterone, a progestin, is an adrenal gland–produced precursor of cortisol n Low-dose (0.01mg/kg) dexamethasone suppression test: inadequate cortisol suppression is highly suggestive of endogenous hyperadrenocorticism, but false-negative and false-positive results can occur. Suppression at 4 hours followed by escape from suppression at 8-hour sampling is characteristic of PDH n High-dose (0.1mg/kg) dexamethasone suppression test: used to help differentiate between adrenal neoplasia and pituitary-dependent hyperadrenocorticism. A lack of cortisol suppression is suggestive of adrenal neoplasia, whereas cortisol suppression suggests pituitary disease n Endogenous ACTH assay: used to help differentiate between adrenal neoplasia and pituitary-dependent hyperadrenocorticism. An elevated ACTH level is suggestive of pituitary disease, whereas a depressed ACTH level is suggestive of adrenal neoplasia Treatment and Prognosis 1. Any concurrent infections (e.g., pyoderma, demodicosis, urinary tract infection) should be treated with appropriate therapies. Any secondary pyoderma, otitis externa, and Malassezia dermatitis should be treated with appropriate therapies. Controlling and preventing secondary infection is an essential component of managing atopic dogs. Bathing every 3 – 7 days and treating the ears after every bath helps disinfect the skin and ear canals, preventing the secondary infections from recurring. 2. Treatment of choice for iatrogenic Cushing's cases is to progressively taper, then discontinue glucocorticoid therapy. 3. Treatment of choice for adrenal neoplasia is adrenalectomy. a. Dogs with inoperable adrenal tumors or metastases may benefit from mitotane or trilostane therapy. n Mitotane for adrenal tumors: One should give 50mg/kg PO every 24 hours with food for 7 to 14 days. An ACTH stimulation test is performed every 7 days. If inadequate cortisol suppression persists, increase the mitotane dosage to 75 to 100mg/kg/day for an additional 7 to 14 days, monitoring with ACTH stimulation tests weekly. When adequate adrenal suppression is demonstrated, maintenance mitotane therapy is initiated as described below 4. The traditional (historic) medical treatment of choice for PDH is mitotane 50mg/kg PO administered every 24 hours with food. The daily dosage is continued until the basal serum or plasma cortisol level normalizes and does not increase following ACTH stimulation. Control is usually achieved within 5 to 10 days of initiation of therapy, so the patient should be closely monitored with ACTH stimulation tests performed every 7 days. Monitoring water and food intake before and during induction may be useful. Water and food intake often markedly decreases when adequate adrenal suppression has been achieved. If signs of adrenal insufficiency (e.g., anorexia, depression, vomiting, diarrhea, ataxia, disorientation) develop, mitotane therapy should be stopped and hydrocortisone 0.5 to 1.0mg/kg PO every 12 hours administered, until symptoms resolve. To maintain remission following mitotane induction, mitotane PO with food 50mg/kg administered once weekly, or 25mg/kg twice weekly. Dogs that relapse during maintenance therapy should be reinduced with daily mitotane for 5 to 14 days or until recontrolled, then maintained with 62 to 75mg/kg once weekly, or 31 to 37.5mg/kg twice weekly. A great deal of patient variability occurs, requiring close monitoring. 5. A more recent treatment option and the current recommendation for the medical treatment of PDH is trilostane. At this writing, its optimal dosing regimen has not yet been determined, but many investigators are using the following protocol: n Dogs <5kg: give 30mg PO with food q 24 hours n Dogs between 5 and 20kg: give 60mg PO with food q 24 hours n Dogs between 20 and 40kg: give 120mg PO with food q 24 hours

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

n Dogs >40kg: give 240mg PO with food q 24 hours Assess efficacy by monitoring clinical signs and evaluating results of ACTH stimulation tests 10 days, 4 weeks, and 12 weeks after the start of therapy, then every 3 months thereafter. ACTH stimulation tests should be performed 4 to 6 hours after trilostane dosing. A post- ACTH cortisol level <150 nmol/L (but >20nmol/L) is usually consistent with good control. However, optimal clinical control has also been reported with post-ACTH cortisol concentrations between 150 and 250 nmol/L, so blood work results should always be interpreted alongside clinical signs. If the dog is not clinically well controlled and post-ACTH cortisol concentrations are >150 nmol/L, the dose of trilostane should be increased. Dose adjustments should be made in increments of 20 to 30mg/dog. A wide range of trilostane doses to induce and maintain remission have been reported in dogs, with the therapeutic dose for most dogs being between 4 and 20mg/kg/day. Some dogs may require twice-daily dosing if duration of effect is inadequate. Clinical signs such as polydipsia/polyuria/polyphagia often start to improve within the first 10 days of treatment, but alopecia and other skin changes may take 3 or more months to improve. If signs of adrenal insufficiency (depression, inappetence, vomiting, diarrhea) develop at any time during therapy, or if post-ACTH cortisol concentrations (measured 4-6 hours after trilostane dosing) are <20 nmol/L, trilostane should be stopped for 5 to 7 days, then reinstituted at a lower dose. Note: Although trilostane appears to be well tolerated by most dogs, sudden death has been reported in dogs with concurrent heart problems. Trilostane is also contraindicated in pregnant and lactating dogs, dogs with primary hepatic disease, and dogs with renal insufficiency. 6. Other alternative, but less consistently successful, medical treatments for PDH include the following: Ketoconazole 15mg/kg PO with food q 12 hours or Selegiline (L-deprenyl) 1-2mg/kg PO q 24 hours 7. An effective treatment (where available) for PDH is microsurgical transsphenoidal hypophysectomy. This procedure requires a highly skilled neurosurgeon and specialized veterinary facilities that have access to advanced pituitary imaging techniques. Postoperative complications may include hypernatremia, keratoconjunctivitis sicca, diabetes insipidus, and secondary hypothyroidism. 8. For calcinosis cutis, adjunctive topical treatment with dimethyl sulfoxide (DMSO) gel every 24 hours may help resolve the lesions. During DMSO therapy, serum calcium levels should be monitored periodically because hypercalcemia is a potential adverse effect of this treatment. 9. The prognosis ranges from good to poor, depending on the cause and severity of the disease, with the average survival time for dogs with PDH being approximately 2.5 years after diagnosis.

#8 Acral Lick Dermatitis (lick granuloma)

Features Acral lick dermatitis is first noted as excessive, compulsive licking at a focal area on a limb, resulting in a firm, proliferative, ulcerative, alopecic lesion. The causes of the licking are multifactorial, and, although environmental stress (e.g., boredom, confinement, loneliness, separation anxiety) may be a contributor, other factors are usually more important (Box 13-1). This dermatitis is common in dogs, with the highest incidence in middle-aged to older, large- breed dogs, especially Doberman pinschers, Great Danes, Golden retrievers, Labrador retrievers, German shepherds, and Boxers. The lesion usually begins as a small area of dermatitis that slowly enlarges because of persistent licking. The affected area becomes alopecic, firm, raised, thickened, and plaquelike to nodular, and it may be eroded or ulcerated. With chronicity, extensive fibrosis, hyperpigmentation, and secondary bacterial infection are common. Lesions are usually single but Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

may be multiple, and they are most often found on the dorsal aspect of the carpus, metacarpus, tarsus, or metatarsus.

Top Differentials Differentials include demodicosis, dermatophyte kerion, fungal or bacterial granuloma, and neoplasia.

Diagnosis 1. Usually based on history, clinical findings, and ruling out other differentials

BOX 13- 1 Underlying Causes of Acral Lick Dermatitis

n Hypersensitivity (atopy, food)

n Fleas

n Trauma (cut, bruise)

n Foreign body reaction

n Infection (bacterial, fungal)

n Demodicosis

n Hypothyroidism

n Neuropathy

n Osteopathy

n Arthritis

2. Dermatohistopathology: ulcerative and hyperplastic epidermis, mild neutrophilic and mononuclear perivascular dermatitis, and varying degrees of dermal fibrosis 3. Bacterial culture (exudates, biopsy specimen): Staphylococcus is often isolated. Mixed gram- positive and gram-negative infections are common

Treatment and Prognosis 1. The underlying causes should be identified and corrected (see Box 13-1). 2. One should treat for secondary bacterial infection with long-term systemic antibiotics (minimum, 6-8 weeks, and as long as 4-6 months in some dogs). Antibiotic therapy should be continued at least 3 to 4 weeks beyond regression of the lesion. The antibiotic should be selected according to bacterial culture and sensitivity results. 3. Anecdotal reports suggest good efficacy with combined antibiotic, amitriptyline (2mg/kg q 12 hours), and hydrocodone (0.25mg/kg q 8-12 hours) administered until lesions resolve. Then, one drug should be discontinued every 2 weeks until it can be determined which drug (if any) may be required for maintenance therapy. 4. Topical applications of analgesic, steroidal, or bad-tasting medications every 8 to 12 hours may help stop the licking but response is unpredictable and often disappointing.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

5. When no underlying cause can be found, treatment with behavior-modifying drugs may be beneficial in some dogs (Table 13-1). Trial treatment periods of up to 5 weeks should be used until the most effective drug is identified. Lifelong treatment is often necessary. 6. Alternative medical treatments such as cold laser therapy or acupuncture have been beneficial in some patients. 7. Mechanical barriers such as wire muzzles and bandaging, Elizabethan collars, and side braces may be helpful. 8. Surgical excision or laser ablation is not recommended because postoperative complications, especially wound dehiscence, are common. Laser ablation may help sterilize the lesion and deaden nerve endings; however, response is highly variable. 9. The prognosis is variable. Chronic lesions that are unresponsive or extensively fibrotic and those for which no underlying cause can be found have a poor prognosis for resolution. Although this disease is rarely life threatening, its course may be intractable.

TABLE 13- 1 Drugs for Psychogenic Dermatoses in Dogs

Drug Dose

Anxiolytics Phenobarbital 2-6 mg/kg PO q 12 hours Diazepam 0.2 mg/kg PO q 12 hours Hydroxyzine 2.2 mg/kg PO q 8 hours

Tricyclic Antidepressants Fluoxetine 1 mg/kg PO q 24 hours Amitriptyline 1-3 mg/kg PO q 12 hours Imipramine 2-4 mg/kg PO q 24 hours Clomipramine 1-3 mg/kg PO q 24 hours

Endorphin Blocker Naltrexone 2 mg/kg PO q 24 hours

Endorphin Substitute Hydrocodone 0.25 mg/kg PO q 8 hours

Topical Products Fluocinolone acetonide + flunixin meglumine Deep Heet + Bitter Apple

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

#9 Canine Scabies (sarcoptic mange)

Features Canine scabies manifests as a disease that is caused by Sarcoptes scabiei var. canis, a superficial burrowing skin mite. Mites secrete allergenic substances that elicit an intensely pruritic hypersensitivity reaction in sensitized dogs. Canine scabies is common in dogs. Affected dogs often have a previous history of being in an animal shelter, having contact with stray dogs, or visiting a grooming or boarding facility. Wildlife such as fox and coyotes are often the source of initial infection and possible repeated infections. In multiple-dog households, more than one dog is usually affected. Canine scabies is a nonseasonal intense pruritus that responds only variably to corticosteroids. Lesions include papules, alopecia, erythema, crusts, and excoriations. Initially, less-hairy skin is involved, such as on the hocks, elbows, pinnal margins, and ventral abdomen and chest. With chronicity, lesions may spread over the body, but the dorsum of the back is usually spared. Peripheral lymphadenomegaly is often present. Secondary weight loss may occur. Heavily infested dogs may develop severe scaling and crusting. Some dogs may present with intense pruritus but no or minimal skin lesions. Although they are less common, asymptomatic carrier states are possible in dogs; however, in multiple-dog households, a range of symptoms (severe to nonpruritic) may exist..

Top Differentials Differentials include hypersensitivity (food, atopy, flea), Malassezia dermatitis, pyoderma, demodicosis, dermatophytosis, and contact dermatitis.

Diagnosis 1. History, clinical findings, and response to scabicidal treatment 2. Pinnal-pedal reflex: rubbing of the ear margin between thumb and forefinger may elicit a scratch reflex. This reflex is highly suggestive of a scabies infection with approximately 80% accuracy. 3. Microscopy (superficial skin scrapings): detection of sarcoptic mites, nymphs, larvae. or ova. False-negative results are common because mites are extremely difficult to find; approximately 20% accurate. 4. Serology (enzyme-linked immunosorbent assay [ELISA]): detection of circulating immunoglobulin (Ig)G antibodies against Sarcoptes antigens. This is a highly specific and sensitive test, but false-negative results can occur in young puppies and in dogs receiving corticosteroid therapy. Also, false-positive results may be seen in dogs that have been successfully treated for scabies because detectable antibodies may persist for several months after treatment cessation 5. Dermatohistopathology (usually nondiagnostic): varying degrees of epidermal hyperplasia and superficial perivascular dermatitis with lymphocytes, mast cells, and eosinophils. Mite segments are rarely found within the stratum corneum

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

Treatment and Prognosis 1. Affected and all in-contact dogs should be treated with a scabicide. Failure to treat all dogs results in reinfection and persistent pruritus. 2. Any secondary pyoderma should be treated with appropriate long-term (minimum 3-4 weeks) systemic antibiotics that are continued at least 1 week beyond clinical resolution of the pyoderma. 4. Topical shampoo therapy using a antimicrobial shampoo every 3-7 days will help speed resolution and enhance the mitacidal treatments. 5. Systemic treatments are the most effective due to the accurate dosing and better compliance. Effective systemic treatments include the following: *Selamectin applied 6 to 12mg/kg every 2 weeks at least four times may be more effective.

n Ivermectin 0.2-0.4mg/kg PO q 7 days, or SC q 14 days, for 4-6weeks * Doramectin 0.2-0.6 mg/kg SQ q 7 days for 4-6 weeks.

n Milbemycin oxime 0.75mg/kg PO q 24 hours for 30 days, or 2mg/kg PO q 7 days for 3-5 weeks n Moxidectin applied every 2-4 weeks for 4-6 weeks; frequent application may lead to increased adverse effects. 6. Topical treatments may be effective but due to the poorer compliance, treatment failures are more common. Effective topical products include the following:

*n 0.025%-0.03% amitraz solution applied to the entire body three times at 2-week intervals, or once weekly for 2-6 weeks n Fipronil spray 3 mL/kg, applied as pump spray to the entire body three times at 2-week intervals, or 6 ml/kg applied as sponge-on once weekly for 4-6 weeks

n 2%-3% lime sulfur solution

n Organophospates (malathion, phosmet, mercaptomethyl phtalimide). Organophosphates are the most toxic and least effective therapies available 5. If the animal is severely pruritic and mites have been identified, steroids may be used for the first 2 to 5 days of scabicidal treatment may be helpful. Use of steroids without the finding of mites makes it impossible for the practitioner to determine response to scabicidal therapy. 6.. In kennel situations, bedding should be disposed of and the environment thoroughly cleaned and treated with parasiticidal sprays. 8. The prognosis is good. S scabei is a highly contagious parasite of dogs that can also transiently infest humans and, rarely, cats. Reinfection can occur leading to chronic pruritic disease.

Author’s Note: Scabies infections can very closely mimic food allergy and atopy. The pinnal-pedal reflex (ear scratch test) is the easiest and most suggestive test for scabies. If reinfection is suspected, long-term scabicidal therapy may be beneficial unless the source can be identified and treated.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

# 10 Dermatophytosis (ringworm)

Features Dermatophytosis is an infection of hair shafts and stratum corneum caused by keratinophilic fungi. It occurs commonly in dogs and cats, with highest incidences reported in kittens, puppies, immunocompromised animals, and long-haired cats. Persian cats and Yorkshire and Jack Russell terriers appear to be predisposed. Skin involvement may be localized, multifocal, or generalized. Pruritus, if present, is usually minimal to mild but occasionally may be intense. Lesions usually include areas of circular, irregular, or diffuse alopecia with variable scaling. Remaining hairs may appear stubbled or broken off. Other symptoms in dogs and cats include erythema, papules, crusts, seborrhea, and paronychia or onychodystrophy of one or more digits. Rarely, cats present with miliary dermatitis or dermal nodules (see “Dermatophytic Granulomas and Pseudomycetomas”). Other cutaneous manifestations in dogs include facial folliculitis and furunculosis resembling nasal pyoderma, kerions (acutely developing, alopecic, and exudative nodules) on the limb or face, and truncal dermal nodules (see “Dermatophytic Granulomas and Pseudomycetomas”). Asymptomatic carrier states (subclinical infection) are common in cats, especially among long- haired breeds. Asymptomatic disease, although rare in dogs, has been reported in Yorkshire terriers.

Top Differentials Dogs Differentials in dogs include demodicosis and superficial pyoderma. If nodular, neoplasia and acral lick dermatitis should be included. Cats Differentials in cats include parasites, allergies, and feline psychogenic alopecia.

Diagnosis 1. Rule out other differentials 2. Ultraviolet (Wood’s lamp) examination: hairs fluoresce yellow-green with some Microsporum canis strains. This is an easy screening test, but false-negative and false-positive results are common 3. Trichogram (hairs or scales in potassium hydroxide preparation): Search for hair shafts infiltrated with hyphae and arthrospores. Fungal elements are often difficult to find 4. Dermatohistopathology: variable findings may include perifolliculitis, folliculitis, furunculosis, superficial perivascular or interstitial dermatitis, epidermal and follicular orthokeratosis or parakeratosis, or suppurative epidermitis. Fungal hyphae and arthrospores in stratum corneum or hair shafts. 5. Fungal culture: Microsporum or Trichophyton spp 6. PCR analysis may simplify the diagnosis where available. Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

Treatment and Prognosis 1. If the lesion is focal, a wide margin should be clipped around it and topical antifungal medication applied every 12 hours until the lesion resolves. (Some dermatologists believe that clipping spreads lesions onto animals and further contaminates the environment.) Effective topicals for localized treatment include products that contain the following:

n terbinafine cream

n clotrimazole cream, lotion, or solution

n enilconazole cream

n ketoconazole cream

n miconazole cream, spray, or lotion

2. If response to localized treatment is poor, the animal should be treated for generalized dermatophytosis. 3. Topical antifungal rinse or dip should be applied to the entire body one or two times per week (minimum 4-6 weeks) until follow-up fungal culture results are negative. Bathing the animal with a shampoo that contains chlorhexidine and (miconazole or ketoconazole) immediately preceding the antifungal dip may be helpful. Dogs with generalized dermatophytosis may be cured with topical therapy alone, whereas cats almost always require concurrent systemic therapy. Effective topical antifungal solutions include the following:

n Enilconazole 0.2% solution

n Lime sulfur 2%-4% solution 4. For cats with dermatophytosis and dogs that are unresponsive to topical therapy alone, topical therapy for generalized infection should be combined with long-term systemic antifungal therapy and continued until 3 to 4 weeks beyond negative follow-up fungal culture results. The average duration of therapy is 8-12 weeks. Effective systemic antifungal drugs include the following:

n Terbinafine 30-40mg/kg PO q 24 hours

n Ketoconazole 10mg/kg PO q 24 hours with food (dogs) Fluconazole 10mg/kg PO q 24 hours with food.

n Itraconazole (Sporonox) 5-10mg/kg PO q 24 hours with food Less effective systemic antifungal drugs include the following:

n Microsized griseofulvin at least 50mg/kg/day PO with fat-containing meal

n Ultramicrosized griseofulvin 5-10mg/kg/day PO with fat-containing meal 5. Alternatively, pulse therapy may be almost as effective and multiple protocols have been published using various drugs. Pulse treatments should be continued until two consecutive follow-up fungal cultures taken 2 to 4 weeks apart are negative. 6. All infected animals, including asymptomatic carriers, should be identified and treated. Exposed, noninfected cats and dogs should be treated prophylactically with weekly topical antifungal rinse or dip for the duration of treatment of the infected animals. 7. The environment should be thoroughly cleaned by removing all contaminated materials and disinfected with bleach (vacuums may further contaminate the environment). 8. For endemic infections involving multianimal homes, catteries, or animal facilities, treatment should be provided according to the recommendations outlined in Box 4-1. 9. Lufenuron has not demonstrated consistent efficacy in treating or preventing infection.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

10. The prognosis is generally good, except for endemically infected multicat households and catteries. Animals with underlying immunosuppressive diseases also have a poorer prognosis for cure. Dermatophytosis is contagious to other animals and to humans.

BOX 4 - 1 Treating Dermatophytosis in Multianimal Homes, Catteries, and Animal Facilities

n Culture all animals to determine the extent and location of animal infections.

n Culture the environment (cages, counters, furniture, floors, fans, ventilation units, etc) to map the infected areas to be disinfected.

n Treat all infected animals with systemic antifungals until each animal has two negative fungal cultures taken at least 1 month apart.

n Treat all infected and exposed animals with topical 2% to 4% lime sulfur solution every 3 to 7 days to prevent contagion and zoonosis. Continue until all animals have two negative fungal cultures taken at least 1 month apart. Do not clip cats as this contaminates the clippers and facility and worsens the risk of contagion.

n Dispose of all infected material. Remove any clutter from animal facilities or other infected areas.

n Clean and disinfect all surface areas every 3 days. Continue until all animals have two negative fungal cultures taken at least 1 month apart. Enilconazole (Clinafarm EC disinfectant, American Scientific Laboratories, Union, NJ) is a very effective environmental disinfectant, but it is licensed only for poultry farm use in the United States. Household chlorine laundry bleach (5% sodium hypochlorite) diluted 1:10 in water is an effective, inexpensive environmental disinfectant.

BOX Author’s Note: ** Microsporum canis is one of the most common zoonotic diseases in veterinary medicine. ** Adopted kittens should be screened for infection during the first veterinary wellness visit. ** Chronicly infected animals likely have contaminated the home requiring aggressive cleaning and disinfection of the environment. ** Even long-standing and severe infections can be resolved with aggressive and persistent treatments. ** The discontinuation of therapy MUST be based on negative cultures.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

#11 Malasseziasis

Features Malassezia pachydermatis is a yeast that is normally found in low numbers in the external ear canals, in perioral areas, in perianal regions, and in moist skin folds. Skin disease occurs in dogs when a hypersensitivity reaction to the organisms develops, or when there is cutaneous overgrowth. In dogs, Malassezia overgrowth is almost always associated with an underlying cause, such as atopy, food allergy, endocrinopathy, keratinization disorder, metabolic disease, or prolonged therapy with corticosteroids. In cats, skin disease is caused by Malassezia overgrowth that may occur secondary to an underlying disease (e.g., feline immunodeficiency virus, diabetes mellitus or an internal malignancy). In particular, generalized Malassezia dermatitis may occur in cats with thymoma-associated dermatosis or paraneoplastic alopecia. Malasseziasis is common in dogs, especially among West Highland White terriers, Dachshunds, English setters, Basset hounds, American cocker spaniels, Shih tzus, Springer spaniels, and German shepherds. These breeds may be predisposed. Malasseziasis is rare in cats.

Moderate to severe pruritus is seen, with regional or generalized alopecia, excoriations, erythema, and seborrhea. With chronicity, affected skin may become lichenified, hyperpigmented, and hyperkeratotic (leathery or elephant-like skin). An unpleasant body odor is usually present. Lesions may involve the interdigital spaces, ventral neck, axillae, perineal region, or leg folds. Paronychia with dark brown nail bed discharge may be present. Concurrent yeast otitis externa is common.

Diagnosis 1. Rule out other differentials 2. Cytology (tape preparation, impression smear): yeast overgrowth is confirmed by the finding round-to-oval, budding yeasts per high power field (100´). In yeast hypersensitivity, organisms may be difficult to find

Treatment and Prognosis 1. Any underlying cause (allergies, endocrinopathy, keratinization defect) must be identified and corrected. 2. For mild cases, topical therapy alone is often effective. The patient should be bathed every 2 to 3 days with shampoo that contains 2% ketoconazole, 1% ketoconazole/2% chlorhexidine, 2% miconazole, 2% to 4% chlorhexidine, or 1% selenium sulfide (dogs only). Shampoos that have two active ingredients provide better efficacy. Treatment should be continued until the lesions resolve and follow-up skin cytology reveals no organisms (approximately 4 weeks). 3. The treatment of choice for moderate to severe cases is ketoconazole (dogs) or fluconazole 10mg/kg PO with food every 24 hours, Treatment should be continued until lesions resolve and follow-up skin cytology reveals no organisms (approximately 4 weeks).

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com

4. Alternatively, treatment with terbinafine 5-40mg/kg PO every 24 hours or itraconazole (Sporonox) 5-10mg/kg every 24 hours for 4 weeks may be effective. 5. Pulse therapy protocols have been published using several drugs and a variety of schedules; however, these often take longer to resolve the active infection. 5. The prognosis is good if the underlying cause can be identified and corrected. Otherwise, regular once- or twice-weekly antiyeast shampoo baths may be needed to prevent relapse. This disease is not considered contagious to other animals or to humans, except for immunocompromised individuals.

Authors’s Note: ** Yeast dermatitis is currently the most commonly missed diagnosis in US general practices. Any patient with leathery, elephant-skin like lesions on the ventrum should be suspected of having Malassezia dermatitis. ** Cutaneous cytology is not always successful for finding Malassezia organisms requiring the clinician to rely on clinical lesion patterns to make a tentative diagnosis. ** Yeast dermatitis is severely pruritic with owners reporting an itch level of 10 on a 0-10 visual analog scale.

Dr. Keith A Hnilica, DVM, MS, MBA, DACVD Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 3rd Edition 2010 itchnot.com