Dermatology PDF

Dermatology 13 CH A P TE R Elizabeth Rustemeyer May...

Dermatology 13 CH A P TE R Elizabeth Rustemeyer May 7. Bulla: A vesicle larger than 1 cm in diameter GENERAL ASSESSMENT OF 8. Wheal: Circumscribed, raised lesion consist- THE DERMATOLOGY PATIENT ing of edema that appears in minutes to I. Signalment: Age, breed, sex, color hours. The lesion will pit with digital pressure A. Age: Congenital-hereditary conditions 9. Nodule: A small circumscribed solid elevation B. Breeds: Terriers, atopy; American cocker greater than 1 cm in diameter that results spaniels, seborrhea from massive infiltration of inflammatory or C. Sex: Reproductive hormone endocrinopathies neoplastic cells into the dermis or subcutane- D. Color: Color-dilution alopecias ous (SC) tissue II. Primary complaint: What is the owner’s primary rea- 10. Tumor: Neoplastic enlargement of any struc- son for consulting a veterinarian? Be sure to address ture of the skin this via diagnostics, treatments, and client education 11. Cyst: Epithelial lined cavity filled with fluid or III. History solid material, such as keratin or sebaceous A. A thorough and accurate history provides useful secretions information that will aid in diagnosis D. Primary or secondary lesions. Primary if main B. Obtain history in chronological order: Are the clinical sign is directly caused by the disease pro- symptoms seasonal or nonseasonal? Which cess, secondary if not specifically caused by the symptoms were present first—the itching or disease process but secondary to self-trauma or the alopecia? Have things changed since the inflammation symptoms were initially noticed? 1. Alopecia: Baldness or absence of hair from an IV. Physical examination area of skin where it is normally present. This A. Properly using the correct dermatologic terms for is a primary lesion in endocrinopathies but a lesions is crucial, as is a thorough physical exami- secondary lesion to pyoderma nation. Be sure to examine the ears, feet, mucous 2. Scale: Accumulation of loose fragments of the membranes, lymph nodes, claws, and footpads. stratum corneum (keratinocytes). This is a pri- Note whether the lesions appear symmetrical or mary lesion in seborrhea but secondary to self- nonsymmetrical trauma or inflammation B. Differentiate between primary and secondary 3. Follicular casts: Accumulation of follicular ma- lesions terial adhered to the hair shaft C. Primary lesions: Main clinical sign directly caused 4. Crust: Dried exudate made up of serum, white by a disease process blood cells (WBCs), red blood cells, and 1. Macule: Circumscribed flat spot up to 1 cm in keratin diameter characterized by a change in color 5. Hyperpigmentation: Increased epidermal or 2. Patch: A macule greater than 1 cm in diameter; dermal melanin not palpable 6. Hypopigmentation: Loss of epidermal melanin 3. Papule: A solid elevation up to 1 cm in diame- 7. Comedo (comedones): Dilated hair follicle ter. This represents infiltration of cells, edema, filled with keratin and sebaceous secretions or hypertrophy of the epidermis. It can be (blackhead) palpated and is often erythematous E. Secondary lesions: Not specific for the underlying 4. Plaque: Larger flat- topped elevation formed by disease process; may be caused by self-trauma or extension or collection of papules other inflammatory processes 5. Pustule: Small circumscribed elevation of skin 1. Epidermal collarettes: Circular rim of loosely filled with pus attached keratin (scale); usually indicative of 6. Vesicle: Circumscribed lesion up to 1 cm filled a staphylococcal infection with clear fluid. These are rare and fragile. 2. Scar: An area of fibrous tissue that has They are intraepidermal or subepidermal. replaced damaged dermal or SC tissue Most are associated with autoimmune skin 3. Excoriation: Erosion or ulcer formed by the diseases (small animal) or viral diseases removal of superficial epidermis in a linear (large animal) fashion by scratching, biting 189 190 SECTION II SMALL ANIMAL 4. Erosion: Interruption of the epidermis that 2. The site of cell division and production of does not penetrate the basement membrane daughter cells to supply the upper layers of zone; will heal without scarring the epidermis 5. Ulcer: Deeper interruption of the epidermis 3. Attached to the basement membrane zone that exposes the underlying dermis; will heal III. Epidermal turnover time: 21 to 28 days in most with scarring species. Some diseases can shorten cell turnover 6. Lichenification: “Elephant skin”; thickened, time, thus forcing keratinocytes to mature too firm skin with exaggerated superficial skin quickly, resulting in seborrhea markings; results from constant friction or IV. Cells of the epidermis inflammation A. Keratinocytes 7. Hyperkeratosis: Increased thickness of the 1. Most numerous stratum corneum 2. Produce keratin—involved in the process of 8. Fissure: Linear defect into the epidermis or keratinization dermis caused by disease or injury 3. Produce lipid for the barrier layer 9. Callus: Thickened hyperkeratotic lichenified 4. Produce important cell-signaling cytokines, area over bony prominences as a result of thus involved in the immune response to pressure or chronic low-grade friction allergy or injury V. Differential diagnosis: Separate each problem and list B. Melanocytes differential diagnoses for each 1. Basal layer of the epidermis VI. Diagnostic plan: Each diagnostic test is chosen to 2. Produce melanin pigment granules rule in or rule out the differential diagnoses listed for C. Langerhans cells: Responsible for immune each problem surveillance and antigen presentation, especially VII. Therapeutic plan: Formulation of a plan based on important in the development of allergies results from the thorough physical examination as D. Other cells well as results from each diagnostic test performed. 1. Merkel cell Avoid “shotgun” therapy with multiple classes of 2. Inflammatory cells (neutrophils, eosinophils, drugs (i.e., both antibiotics and steroids) lymphocytes, etc.) when skin is diseased VIII. Client education: A crucial portion of treating the V. Hair follicles and hair dermatologic patient. Clear, concise instructions and A. Phases of growth explanations will ensure that the owner follows 1. Anagen  hair growth phase directions as expected 2. Catagen  transition phase 3. Telogen  hair resting phase; most of an animal’s hair is in this phase STRUCTURE AND FUNCTION OF THE SKIN B. Hair growth is affected by the following: I. Skin structure 1. Hormones. Thyroid hormones, cortisol, sex A. Epidermis hormones B. Dermal-epidermal junction 2. Nutrition C. Dermis 3. Day length D. Hypodermis or subcutis (SC tissue) C. Types of hair follicles E. Epidermally derived appendages 1. Simple  1 hair per hair follicle opening. Cattle 1. Pilosebaceous structures and horses have this type of follicle 2. Eccrine sweat glands 2. Compound  Multiple hairs from one hair 3. Claws follicle opening. Dogs, cats, sheep, and goats II. Epidermis have this type of follicle A. Stratum corneum VI. Epidermal glands 1. Several layers of anuclear cornified cells A. Sebaceous glands. Sebum secretion affected by separated by lipids 1. Sex hormones 2. Major barrier to the outside world 2. Thyroid hormone 3. Hyperkeratosis describes thickening of this 3. Cortisol layer. 4. Malnourishment B. Stratum granulosum 5. Fatty acid deficiency 1. One layer thick in haired skin; additional layers B. Sweat glands in thinly haired skin 1. Apocrine glands 2. Granules in this layer contribute to formation a. Secretion empties into the hair follicle of the intercellular lipids in the stratum b. Most domestic animals have this type of corneum. gland throughout the body C. Stratum spinosum 2. Eccrine glands 1. Variable number of layers, typically one to a. Secretion empties onto the surface of the three layers in haired skin skin (“sweating”) 2. The beginning of cellular differentiation b. Found on the footpads of dogs and cats (keratinization) occurs here VII. Dermis D. Stratum basale A. Main support structure for the epidermis 1. One layer of columnar cells and melanocytes B. Thickest part of the skin  CHAPTER 13 Dermatology 191 C. Made up of collagen, elastic fibers, some muscles (arrector pili muscles), blood vessels, and nerves VIII. Functions of the skin A. Barrier: Physical protection from the environ- ment, including regulation of water loss as well as protection from microbial invasion B. Communication 1. Senses of touch, pain, itch 2. Immune system communicates from the skin to the lymphatic system C. Temperature regulation 1. The hair coat provides warmth 2. Blood vessels of the skin dilate or constrict to allow for cooling or preservation of heat 3. Sweat 4. SC fat Figure 13-1 Demodex canis. (From Birchard SJ, Sherding RG. Saunders Manual of Small Animal Clinical Practice, 3rd ed. St Louis, D. Secretion. Sweat, phermones, lipid barrier 2006, Saunders.) E. Storage. Electrolytes, water, vitamins, protein, carbohydrates F. Pigmentation. Ultraviolet light protection B. Localized demodicosis G. Vitamin D production 1. Age younger than1 year, usually 3 to 6 months 2. Lesions consist of localized areas of alopecia, usually minimal pruritus (mild clinical disease) FOLLICULITIS 3. The face, especially the periocular and com- I. Inflammation of the hair follicle. The clinical missures of mouth, and forelegs are most lesion reflects this and is typically a circular area of commonly affected areas alopecia with scale and hyperpigmentation. Papules, 4. 90% resolve spontaneously in 6 to 8 weeks pustules, and epidermal collarettes are also associ- 5. Optimize health (deworm, improve plane of ated with folliculitis nutrition) II. The three main differential diagnoses for folliculitis 6. This is not genetic or a genetic defect include bacterial pyoderma, demodicosis, and 7. Reexamine and rescrape in 3 weeks dermatophytosis a. If increase in numbers of mites, new lesions, A. Demodicosis lymphadenopathy—may be developing 1. Inflammatory parasitic skin disease caused by generalized condition the follicular mite Demodex canis or two b. A small number of localized cases progress other newly recognized variants to generalized demodicosis 2. D. canis found in small numbers in healthy C. Generalized demodicosis normal dog skin 1. Juvenile onset (3 to 12 months) 3. In the disease state, these mites are present a. Usually starts as localized lesions, which in much larger numbers than in normal progress to generalized lesions affecting all individuals parts of the body if not treated adequately 4. Demodicosis can be very difficult to cure and or do not resolve spontaneously thus very frustrating for the owner b. Most animals appear to have a hereditary 5. The demodex mite spends its entire life on disposition the skin of its host 2. Adult onset (usually older than 5 years) 6. Four stages a. May be associated with internal disease, a. Fusiform egg malignancy, or chronic corticosteroid use b. Six-legged larvae b. Can be associated with hypothyroidism c. Eight-legged nymph and spontaneous or iatrogenic hyperadre- d. Eight-legged adult (Figure 13-1) nocorticism 7. Life cycle takes 20 to 35 days c. If no cause is found, the odds of success- 8. Mites spread from bitch in the first 3 days fully treating are decreased of life 3. Clinical signs of generalized demodicosis 9. Nursing provides direct contact for transmis- a. Large areas of alopecia, usually nonpruritic sion; therefore, muzzle and forelegs are first b. Major differentials include pyoderma and sites of infestation dermatophytosis 10. Not a contagious disease; mites are difficult to c. Mild to severe erythema transfer to dogs older than a few days d. Usually skin becomes gray or hyperpig- 11. There is an assumed weak link in the immune mented from chronic inflammation as well system of dog with demodicosis as large groups of comedones 12. The current belief is that these dogs have a (1) Often there is secondary pyoderma— T-cell function abnormality superficial or deep, usually caused by 192 SECTION II SMALL ANIMAL Staphylococcus pseudintermedius, d. Recheck these animals in 3 to 4 weeks; if Proteus spp., or Pseudomonas spp. lesions are spreading or mite counts are (2) Clinically looks like papules, pustules, increasing, the disease is progressing crusts, exudation (nodular form in toward becoming generalized bulldogs) 3. Generalized demodicosis (3) A peripheral lymphadenopathy is often a. Correct any nutritional, parasitic, or other present if a pyoderma is present concurrent problems (4) Depending on the severity of the b. Dogs with adult-onset demodicosis should secondary pyoderma, the animal may receive full workups to look for underlying be systemically ill (immunosuppressive) diseases; that is, get 4. Chronic demodectic pododermatitis a minimum database (Complete blood cell a. This is a form of generalized demodicosis count, serum biochemistries, urinalysis, b. May have persistent foot lesions after ther- heartworm and fecal checks, and usually apy for generalized demodicosis thyroid and Cushing evaluation) c. Demodicosis may only have been present c. Start on appropriate antibiotic therapy on the feet based on culture and sensitivity. Use a d. Often refractory to therapy bactericidal antibiotic for 3 to 6 weeks 5. Otitis. Demodicosis may occasionally occur as d. Bathe the dog with an antibacterial and an erythematous, ceruminous otitis externa, keratolytic shampoo (e.g., benzoyl peroxide) especially in cats to open the hair follicles and remove crusts D. Diagnosis (Figure 13-2) before applying Mitaban dip if using 1. Deep skin scrapings or hair plucks e. Mitaban dips (trichograms) to visualize mites (1) Mitaban used every 2 weeks is the only 2. Squeeze the affected area to extrude mites Food and Drug Administration (FDA)- from the hair follicles approved treatment for canine 3. Take multiple scrapings, a minimum of three demodicosis scrapings from lesional skin (2) Dipping weekly improves the efficacy E. Therapy of Mitaban, but it is important to realize 1. Do not use corticosteroids in these patients! that this is an off-label use of the 2. Localized demodicosis product a. Spontaneous remission in 90% of cases so (3) Amitraz is a monoamine oxidase inhibi- treatment not usually needed; avoid using tor (MAOI). Do not dip if the dog is Amitraz (Mitaban dip) for this type of taking Anipryl or other MAOI inhibitors. demodicosis Antidote for Mitaban is yohimbine b. Benzoyl peroxide gel or shampoo for the (4) Monitor response to therapy with follicular flushing action and to prevent monthly skin scrapings Continue dipping secondary bacterial infections 1-2 months beyond two negative skin c. Improve nutrition; remove intestinal scrapings 1 month apart parasites or other stress factors (fecal and (5) Dogs should not be stressed while on heartworm test) this therapy. Female dogs should be spayed when the disease is under control because their estrus cycle may cause a relapse of the disease as well as to prevent pyometra and reduce the risk of mammary neoplasia f. Ivermectin (1) This is not an FDA-approved treatment (2) Bovine injectable ivomec (1% solution  10 mg/mL) (3) Treatment dose is much higher than the standard Heartgard dose. Use only in dogs proven negative for heartworms! (4) Use caution when considering use in collies, shelties or their crosses, or Old English sheepdogs especially, even those that have been tested for the mdr-1 gene deletion. Figure 13-2 Skin scrape. For deep skin scrapes, once capillary oozing (5) Reserve this treatment for Mitaban is initiated, the skin is usually squeezed before a final scrape is performed failures or if Mitaban is not a feasible to collect the material. (From Medleau L, Hnilica KA. Small Animal Der- treatment matology: A Color Atlas and Therapeutic Guide, 2nd ed. St Louis, 2006, (6) Side effects: Mydriasis, ataxia, coma, Saunders.) and death  CHAPTER 13 Dermatology 193 g. Milbemycin (Interceptor) G. Pyoderma (1) This is not an FDA approved treatment 1. Bacterial folliculitis and furunculosis are very (2) Treatment dose is higher than the stan- common in dogs dard dose for heartworm prevention. 2. Less common in cats Use only in dogs proven negative for 3. Secondary to an underlying disease process, heartworms! usually an allergic disease or endocrinopathy h. Client Education: Generalized demodicosis 4. Most commonly isolated organism is (1) Guarded prognosis Staphylococcus pseudintermedius (2) Long course of therapy 5. Pyoderma classifications (3) Juvenile-onset cases should not be bred! a. Surface pyoderma F. Feline demodicosis (1) Erosion with secondary colonization of 1. Demodex cati: Follicular mite similar to surface only Demodex canis except it is smaller and the (2) Usually secondary to self-trauma ova are slim and oval, rather than b. Superficial pyoderma spindle-shaped (1) Restricted to the stratum corneum or 2. Localized form opening of hair follicles a. Lesions are variably pruritic alopecic areas (2) Papules, crusted papules, pustules, affecting the nose, eyelids, and periocular epidermal collarettes skin c. Deep pyoderma b. Erythema and scaling may also be present (1) Infections of the deeper region of the c. Ceruminous otitis with demodex mites hair follicle resulting in rupture of the present may be seen without other lesions hair follicle (furunculosis) with exten- 3. Generalized form sion into the dermis and subcutis a. Similar to localized except more body (2) Nodules with draining serosanguineous regions are affected fluid b. Generalized form usually associated with 6. Treatment systemic disease and immunodeficiency a. Surface pyoderma state (1) Clip and clean lesion with dilute 4. Diagnosis chlorhexidine a. Skin scrapings (2) Avoid occlusive ointments b. Minimum database for generalized disease, (3) Topical antipruritics including feline leukemia virus and feline b. Superficial pyoderma immunodeficiency virus testing (1) Oral antibiotics 5. Differential diagnoses (a) Cephalosporins (such as cephalexin a. Dermatophytosis or Clavamox) 22 to 33 mg/kg every b. Pyoderma (rare in cats) 12 hours for a minimum of 21 days c. Causes of miliary dermatitis (b) Continue therapy for a minimum of d. Causes of pruritus 7 days beyond complete clinical 6. Treatment remission of lesions a. Localized form  lime sulfur spray or dip (2) Topical antimicrobials. Chlorhexidine or b. Generalized form benzoyl peroxide containing shampoos (1) Dependent on presence of underlying every 2-3 days disease (3) Avoid steroids (2) A consistent successful therapy has not c. Deep pyoderma been reported (1) Oral antibiotics for 4 to 8 weeks; treat for (3) Weekly lime sulfur dips at least 14 days beyond clinical remission (4) Treat underlying disease (2) Base antibiotic choice on culture and 7. Demodex gatoi sensitivity results a. Not a follicular mite; lives in the stratum (3) Hydrotherapy and topical antimicrobial corneum shampoos b. Broad blunted abdomen rather than a slim 7. Dermatophytosis elongated one a. Fungal organisms invade keratinized c. This is a contagious (to other cats) and structures pruritic mite b. This can be a self-limiting disease, depen- 8. Diagnosis dent on the immune status of the host a. Broad superficial skin scrapings c. These infections are zoonotic b. Negative skin scrapings do not rule out d. This is not a common infection in dogs, but D. gatoi as a differential diagnosis in a it is very common in cats pruritic cat e. Transmission via contact with an infected 9. Treatment host, fomite, or contaminated environment a. 6 weekly lime sulfur dips f. Clinical signs b. Treat all cats in the household (i.e., all (1) Minimal to extensive inflammation with in-contact cats) scaling and alopecia 194 SECTION II SMALL ANIMAL (2) Fungal kerions (dermatophytic 3. Hair loss in areas of friction or wear (collar, furunculosis) can also occur harness, over pressure points where the dog g. Microsporum canis is the most commonly lays down, etc.) isolated species. Infections can also be 4. Loss of guard hairs with retention of under caused by Microsporum gypseum or coat Trichophyton mentagrophytes 5. Myxedema: Increased skin thickness. Tragic h. Cats can be asymptomatic carriers facial expression i. Treatment 6. Recurrent pyoderma or otitis externa (1) Single lesions: Clip and treat with E. Diagnosis and treatment: See small animal topical antifungal agents. Avoid endocrinology section combination products containing III. Hyperadrenocorticism corticosteroids! A. Middle-aged to older dogs (2) Cats require whole body treatments! B. Dermatologic clinical signs Do not spot-treat cats 1. Cutaneous atrophy (thin epidermis and (3) Multiple lesions; weekly whole-body dermis) with prominent blood vessels treatments required 2. Calcinosis cutis (a) Lime sulfur dip 3. Poor wound healing (b) Chlorhexidine 4. Recurrent nonpruritic pyoderma. (c) Miconazole or ketoconazole “Self-medication” with endogenous cortisol shampoos 5. Comedones a frequent finding (d) Systemic therapy 6. Bruising or petechia noted in some cases i. Oral ketoconazole or itraconazole following venipuncture for dogs C. Diagnosis and treatment: See small animal ii. Oral itraconazole or terbinafine endocrinology section for cats IV. Sex hormone dermatoses iii. Griseofulvin is also used but has A. Hyperestrogenism many side effects 1. Estrogen source: Cystic ovaries or testicular (e) Treat for 2 weeks beyond clinical tumors (Sertoli cell tumor) cure and two negative fungal 2. Iatrogenic via estrogen supplementation for cultures 1 week apart urinary incontinence (4) Environmental decontamination is also 3. Females important a. Can have enlarged nipples or vulva in addition to a noninflammatory alopecia b. Irregular heat cycles ENDOCRINE AND ALOPECIC DERMATOSES 4. Males: Feminization I. Alopecia is usually symmetrical and bilateral sparing B. Hyperandrogenism the head and extremities. This is a noninflammatory 1. Usually from testicular tumors alopecia 2. Hyperplasia of perianal and tail glands II. Endocrine alopecias are not common in the cat; V. Alopecia X (follicular arrest) look for pruritus as a cause for this type of alopecia A. Not associated with systemic illness in the cat B. Common in poodles, Pomeranians, plush-coated A. The hair coat is dull and dry and easily epilated breeds with failure to regrow following clipping C. Progressive alopecia with hyperpigmentation of B. Skin can be hyperpigmented the skin C. Seborrhea present D. Diagnosed by ruling out other endocrine D. Comedones present alopecias E. Secondary bacterial or yeast infections are VI. Cyclic flank alopecia common. These conditions are nonpruritic unless A. Truncal alopecia that occurs seasonally and infections are present is typically seen in boxers, English bulldogs, F. Ceruminous otitis externa a common sequela Airedales III. Hypothyroidism B. Usually occurs during the winter months with A. Medium- to large-breed dogs hair regrowth in the warmer months B. Frequently middle-aged dogs; however, high-risk VII. Color-dilution alopecia breeds with autoimmune thyroiditis can be A. Associated with diluted coat colors diagnosed at a younger age B. Abnormal melanization resulting in a weak hair C. General clinical signs shaft that breaks with minimal trauma 1. Mental dullness 2. Lethargy PRURITIC SKIN DISORDERS 3. Obesity without increased food intake 4. Exercise intolerance I. Parasitic disorders D. Dermatologic clinical signs A. Flea allergy dermatitis 1. Alopecia 1. Major cause of skin disease in dogs 2. Alopecic “rat” tail 2. Most common cause of pruritus in cats  CHAPTER 13 Dermatology 195 3. Ctenocephalides felis: Common flea of dogs and cats 4. Thought to be a hypersensitivity reaction to flea saliva 5. Reaction pattern is due to both type I and type IV hypersensitivity reactions 6. Clinical signs a. Dogs (1) Pruritus (2) Tail-head region extending cranially on the dorsum (3) Inner and caudal thighs (4) Flexures of the elbows (5) Typically a primary papular eruption (6) Secondary pyoderma is extremely common due to self-trauma associated with pruritus b. Cats (1) Miliary dermatitis (2) Commonly affecting the neck, head, and tail base (3) Can be generalized Figure 13-3 Sarcoptes scabiei. (From Birchard SJ, Sherding RG. Saunders Manual of Small Animal Clinical Practice, 3rd ed. St Louis, 2006, (4) May only see alopecia with self-trauma/ Saunders.) excessive grooming 7. Diagnosis a. Compatible clinical signs 8. Treatment b. Presence of fleas or flea dirt a. Systemic therapy c. Presence of tapeworm segments (1) Revolution (selamectin) d. Positive reaction to flea saliva with (2) Ivermectin SC or orally (avoid use in intradermal injection at-risk breeds or dogs with heartworm e. This condition cannot be ruled out with the disease) absence of fleas; an aggressive flea control (3) Interceptor (milbemycin) program must be instituted in order to rule b. Topical therapy: Lime sulfur dip (LymDip); out this condition this is both antiparasitic and antipruritic 8. Treatment c. Treat all in-contact dogs a. Eliminate the flea exposure. Adulticidal plus C. Pediculosis (lice infestation) larvacidal or ovacidal flea control products 1. Lice are species specific b. Control pruritus and treat secondary infec- a. Linognathus setosus—dog-sucking louse tions with appropriate antibiotic therapy b. Trichodectes canis—dog-biting louse B. Scabies c. Felicola subrostratus—cat-biting louse 1. Sarcoptes scabiei var. canis mite 2. Transmitted via direct contact 2. Species varieties are host-specific but short- 3. Easily diagnosed with direct visualization or lived infestation can occur following transmis- tape cytology and microscopic examination sion to a host of a different species (i.e., dog to 4. Treatment human). Extremely contagious between same a. Most flea-control products will kill lice species animals by direct contact! b. Treat all in-contact animals 3. Epidermal burrowing mite D. Trombiculosis (chigger infestation) 4. Entire life cycle spent on the host 1. Adults are free living, but the bright orange 5. Life cycle is 17 to 21 days colored larvae will cause pruritus 6. Clinical signs 2. Seasonal distribution: Spring-fall a. Extremely pruritic 3. Transmitted via direct contact with vegetation b. Mites can be difficult to find with superficial 4. Pruritus and lesions typically associated skin scrapings with body areas in contact with leaf matter/ c. Ear margins, lateral hocks and elbows, vegetation ventral abdomen, chest 5. Diagnosis by visualization of the mites d. Lesions secondary to self trauma: Crusts, 6. Treatment excoriations, lichenification a. Frontline (fipronil) spray 7. Diagnosis b. Most flea sprays or dips are also effective a. This condition can mimic allergic skin E. Cheyletiellosis (walking dandruff) disease 1. Infects dogs, cats, and rabbits b. Multiple superficial skin scrapings a. Cheyletiella yasguri (Figure 13-3) b. Cheyletiella blakei c. Response to therapy is often diagnostic c. Cheyletiella parasitovorax 196 SECTION II SMALL ANIMAL 2. These mites are very large with large pinching 5. Diagnosis mouthparts a. Demonstrated organisms on cytology 3. Highly contagious b. Compatible clinical signs 4. Clinical signs 6. Treatment a. Mild-moderate pruritus a. Topical or oral antifungal agents b. Excessive scaling (seborrhea), especially b. Antiseborrheic shampoos along the dorsum c. Address the underlying cause 5. Diagnosis: Broad superficial skin scrapings B. Staphylococcal pyoderma. See folliculitis 6. Treatment III. Allergic disorders a. Treat all animals A. Atopy (atopic dermatitis) b. Environmental decontamination 1. Inherited predisposition for the development c. Frontline (fipronil) spray of hypersensitivities to environmental d. Revolution (selamectin) allergens associated with the production of e. Lime sulfur dip (LymDip) allergen specific immunoglobulin E (IgE) 7. Can cause intense pruritus in humans antibodies F. Notoedric mange: Notoedres cati 2. Type I hypersensitivity disorder 1. Sarcoptiform mite 3. Allergen exposure is thought to be mostly 2. Highly contagious among cats via direct percutaneous; previously inhalation was contact believed to be the main route of exposure 3. Severe pruritus of the head and neck 4. Allergic animals respond to allergen exposure 4. Diagnosed by superficial skin scrapings; mites by producing more IgE than a non allergic are easy to find compared with the canine animal produces scabies mite 5. Clinical signs typically noted between 1 and 5. Treatment 3 years of age a. Treat all in-contact cats a. Development of clinical signs requires a b. Lime sulfur dip (LymDip) second exposure (the challenge) following c. Revolution (selamectin) the initial exposure (sensitization) d. Ivermectin SC or orally b. Allergen-specific IgE is produced in II. Infectious disorders response to exposure to a previously A. Malassezia dermatitis (Figure 13-4) encountered allergen 1. Secondary yeast infections are extremely c. Allergen-specific IgE cross-links receptors common and intensely pruritic on mast cells causing degranulation of 2. This condition is always secondary to another mast cells and resulting in clinical signs of underlying condition atopy 3. Caused by Malassezia pachydermatis 6. Clinical signs 4. Clinical signs a. Seasonal to nonseasonal pruritus a. Intense pruritus b. Typically, face and feet are primarily b. Skin is lichenified and hyperpigmented affected, but these animals can be pruritic c. Affects the axilla, groin, ventral neck, and ab- in multiple body regions domen in particular (any moist warm area) c. Chronic otitis externa d. Most lesions secondary to self-trauma e. Secondary bacterial and yeast infections are extremely common 7. Diagnosis a. Pruritus is the hallmark of this disease b. Rule out other pruritic causes of skin disease c. This is a diagnosis of exclusion d. Allergy testing (intradermal or serum testing) is used to determine what the animal is allergic to, not to diagnose atopy 8. Treatment a. Avoid the allergen if possible (house dust mite) b. Hyposensitization vaccine therapy c. Corticosteroids are very effective when used correctly and judiciously d. Antihistamines can be used in combination with fatty acids or corticosteroids in order to use lower doses of corticosteroids in Figure 13-4 Cytology. Microscopic image of Malassezia yeast as viewed some animals with a 100 (oil) objective. (From Medleau L, Hnilica KA. Small Animal e. Topical antipruritic and bathing therapy will Dermatology: A Color Atlas and Therapeutic Guide, 2nd ed. St Louis, 2006, help decrease allergen exposure Saunders.) f. Cyclosporine  CHAPTER 13 Dermatology 197 B. Adverse reaction to food (food allergy) 6. Treatment 1. Mechanism of disease is not currently known a. Remove the irritating substance by bathing 2. Typically caused by the protein source in the b. Avoid the irritating substance diet and rarely occurs following a change in diet 3. Clinical signs KERATINIZATION AND METABOLIC a. Nonseasonal pruritus SKIN DISORDERS b. Variable response to corticosteroids c. Lesions secondary to self-trauma I. Keratinization disorders d. Secondary yeast and bacterial skin and ear A. Primary keratinization disorders infections very common B. Primary idiopathic seborrhea e. Some animals will also have gastrointestinal 1. Hereditary or genetic tendency (GI) signs 2. Young age of onset f. Can occur in animals of any age 3. Idiopathic form is most common 4. Diagnosis 4. Cocker spaniels, springer spaniels, West a. Elimination diet trial Highland white terriers b. Decrease in pruritus of 50% or more 5. Clinical signs c. Diagnosis confirmed by increase in pruritus a. Excessive dry or greasy scale with food challenge b. Malodor 5. Treatment 6. Diagnosis a. Avoid the offending dietary allergen a. Signalment and clinical signs b. Some animals will respond to antihistamine b. Histopathology or fatty acid therapy c. Response to treatment c. Corticosteroids or cyclosporine can be 7. Treatment considered but less successful with food a. Topical antiseborrheic shampoos and rinses allergy versus atopy b. Vitamin A therapy or synthetic retinoid d. Topical antipruritic therapy therapy e. Control secondary infections C. Schnauzer comedo syndrome C. Contact dermatitis 1. Primary localized keratinization disorder 1. Rare cause of skin disease 2. Adult onset 2. Typically occurs in thinly haired body regions 3. Multiple plugged hair follicles along the because hair provides excellent protection dorsum; secondary bacterial infections are 3. Cell mediated hypersensitivity reaction common (type IV) requiring prior sensitization to the 4. Treatment: Topicals that address the follicular allergen seborrhea as well as bacterial component 4. Clinical signs D. Feline acne a. Mild to moderate pruritus 1. Idiopathic localized primary keratinization b. Secondary lesions and pyoderma from disorder self-trauma 2. Secondary infections common in area with 5. Diagnosis abundant sebaceous secretions a. Rule out other causes via history, clinical 3. Treatment: Oral with or without topical signs, distribution of lesions antibiotic therapy, topical antiseborrheic b. Identify substances to perform patch agents testing or a challenge with based on E. Secondary keratinization disorders environmental history 1. Common 6. Treatment 2. Secondary to any allergic or endocrine a. Avoid the allergen disorder b. Topical corticosteroids if required 3. Address the underlying cause to eliminate c. Treat the secondary bacterial infection if clinical signs present II. Zinc deficiency d. Pentoxifylline administered orally A. Nordic breeds have an inherent inability to D. Irritant contact dermatitis absorb zinc from the GI tract 1. Considered an inflammatory reaction to an B. Any breed can demonstrate clinical signs if irritating substance rather than an immuno- consuming foods that bind zinc in the logic reaction like contact allergy GI tract and prevent absorption 2. Much more common than contact allergy 1. Plant-based proteins (e.g., corn or soy protein) 3. Irritating substances associated with irritant 2. Excess dietary calcium supplementation contact dermatitis include acids, detergents, C. Clinical signs insecticides 1. Crusting and ulceration on the face and 4. Clinical signs footpads a. Thinly haired areas 2. Animals may also be pyrexic and anorexic b. May be painful rather than pruritic D. Diagnosis 5. Diagnosis is based on history and physical 1. Signalment, history, and clinical signs examination 2. Histopathology 198 SECTION II SMALL ANIMAL E. Treatment B. Pemphigus vulgaris 1. Amino acid complexed zinc supplementation 1. Rare in dogs and cats 2. Some cases require corticosteroid therapy 2. Oral cavity plus epidermal involvement as well 3. Serious, often fatal disease 3. Avoid food sources known to bind zinc in the 4. Deep erosions down to the basal layer of the GI tract epidermis III. Hepatocutaneous syndrome 5. Cytology  acantholytic cells and neutrophils A. Cutaneous manifestation of end-stage liver 6. ANA negative disease C. Pemphigus erythematosus B. Associated with glucagonoma in humans 1. Considered a “benign” variation of pemphigus C. Clinical signs foliaceus as it affects the face only 1. Older dogs 2. This disease also has some similar 2. Severe crusting of the footpads, elbows, histopathologic and clinical features of commissures of the mouth lupus 3. Systemically ill; associated with liver 3. Lesions are pustules and crusts disease 4. ANA may be positive D. Diagnosis V. Bullous diseases: Bullous pemphigoid 1. Signalment and clinical signs A. This is a bullous disease with separation of the 2. Histopathology epidermis from the dermis 3. Evidence of liver failure B. Clinically identical to pemphigus vulgaris, a E. Treatment serious, often fatal, disease 1. Typically unsuccessful; extremely guarded C. Deep lesions that involve the basement prognosis membrane zone 2. Correct the liver disease if possible D. Lesions are ulcers and crusts; acantholytic cells 3. Nutritional management are not found on cytology or histopathology with bullous diseases E. ANA negative AUTOIMMUNE SKIN DISORDERS VI. Lupus I. These diseases are similar in that they are different A. Mechanism of disease: Presence of antibodies manifestations of autoimmunity, or loss of tolerance against nuclear antigens for “self” tissues B. Diagnosis is made using the results of skin biopsy II. Lesions are typically crusts covering erosions or ulcers for histopathology as well as screening lab work III. Common areas of the body affected include the nasal with or without ANA testing planum, the ear pinnae, and the footpads. Some C. Discoid lupus erythematosus diseases also have oral cavity or mucous membrane 1. Common autoimmune disorder, especially involvement in dogs IV. Diagnosis is made via skin biopsy for histopathology 2. No systemic signs; cutaneous lesions only with or without additional lab work in diseases with 3. Lesions are crusts and erosions with systemic signs hypopigmentation affecting the nasal V. Treatment planum and possibly the eyelids, footpads, A. Immunosuppressive doses of corticosteroids or scrotum B. Azathioprine: Dogs only 4. ANA negative C. Chlorambucil: Typically used in cats 5. Diagnosis D. Other immunosuppressive agents, such as a. Histopathology cyclosporine or gold salts b. Must rule out systemic illness with VI. Pemphigus complex. Mechanism of disease: IgG screening lab work directed at particular adhesion molecules within the 6. Treatment epidermis, resulting in acantholysis of keratinocytes. a. Doxycycline or niacinamide orally Lesions vary from pustules to superficial or deep b. Topical therapy erosions to ulcers (1) Tacrolimus (Protopic) A. Pemphigus foliaceus (2) Water-resistant titanium based 1. Most common of the autoimmune skin disorders sunscreen (avoid ultraviolet light) 2. Epidermal involvement only (3) Topical steroids have also been used 3. Planum, pinnae, footpads, and other body successfully areas can be affected D. Systemic lupus erythematosus 4. Characterized by subcorneal to intraepidermal 1. This is a systemic illness. Polyarthritis, pustules: Superficial layers of the epidermis, pyrexia, renal disease and WBC abnormalities resulting in crusts are some of the more common systemic 5. Because this disease is usually pustular, it can signs mimic pyoderma 2. Cutaneous lesions are extremely variable 6. Pustule cytology  acantholytic cells and 3. Oral lesions may be present neutrophils 4. Diagnosis 7. Antinuclar antibody (ANA) negative a. Histopathology  CHAPTER 13 Dermatology 199 b. Evidence of systemic disease from screening E. Treatment lab work 1. Systemic antibiotics for bacterial skin infection (1) Proteinuria with or without azotemia 2. Corticosteroid therapy also required (2) Hyperproteinemia IV. Erythema multiforme and toxic epidermal necrolysis (3) Frequently pancytopenia A. Unknown mechanism. Thought to be caused by c. ANA positive an antigen that could be a drug, toxin produced by a neoplasm, or related to vaccination B. Clinical signs IMMUNE-MEDIATED DISORDERS 1. Vesicular to ulcerative skin lesions I. Uveodermatologic syndrome (Vogt-Koyanagi-Harada, 2. May be systemically ill or VKH) C. Diagnosis A. Intense immune-mediated response targeting 1. History, clinical signs melanocytes 2. Skin biopsy for histopathology B. Melanocytes present in hair, skin, and retinal D. Treatment tissue 1. Identify the underlying cause and avoid it C. Melanocytes are eventually destroyed 2. Supportive therapy D. Clinical signs 3. Immunosuppressive therapy may be 1. Young adult dogs required 2. Nordic breeds typically V. Sebaceous adenitis 3. Acute onset of uveitis A. Immune-mediated destruction of the sebaceous 4. Hypopigmentation of the skin, usually noted glands on the face B. Eventual destruction of the sebaceous glands E. Diagnosis C. Breed disposition: Standard poodle, Akita, 1. Signalment and clinical signs Samoyed, vizsla 2. Skin biopsy for histopathology D. Clinical signs 3. Histopathology often performed on the ocular 1. Excessive scale with evidence of follicular tissue if enucleation is performed casts and patchy alopecia F. Treatment 2. Secondary bacterial and yeast infections 1. Treat the uveitis common 2. Skin lesions are cosmetic, and eventually all 3. Typically nonpruritic melanocytes will be destroyed E. Diagnosis: Histopathology is diagnostic II. Dermatomyositis F. Treatment A. Inherited disorder seen in Collies and Shetland 1. Antiseborrheic therapy sheepdogs 2. Topical treatments aimed at “replacing” the B. Inflammatory response targeting the hair follicles sebum and muscles of mastication resulting in muscle VI. Plasma cell pododermatitis atrophy and scarring A. Thought to be immune mediated, but the exact C. Clinical signs mechanism is unknown 1. Onset typically before 1 year of age B. Soft, painless swelling of the footpads 2. Alopecia, erythema, erosions to ulcers with in cats crusts C. Affects multiple footpads and multiple feet 3. Myopathy: Not present in all patients D. Diagnosis D. Diagnosis 1. Clinical signs 1. Breed and clinical signs 2. Histopathology 2. Histopathology, skin and muscle E. Treatment E. Treatment 1. Doxycycline orally 1. Pentoxifylline with or without 2. Corticosteroids corticosteroids 3. May spontaneously regress 2. Recommend against breeding III. Juvenile cellulitis NODULAR SKIN DISORDERS A. Commonly referred to as “puppy strangles” B. Immune-mediated process seen in young I. The main differential diagnoses for these lesions dogs. The trigger is unknown; however, most include infectious causes, neoplasia, or sterile animals have a concurrent staphylococcal inflammatory causes infection II. Diagnosis C. Clinical signs A. Deep skin biopsy for histopathology; must 1. Pustules, crusts, cellulitis usually affecting the include the subcutis for evaluation head and neck B. Tissue culture to rule out infectious 2. Regional lymphadenopathy causes 3. Pyrexia, lethargy, depression III. Infectious causes D. Diagnosis A. Bacterial infections 1. Signalment and clinical signs B. Fungal infections 2. Rule out other causes of folliculitis C. Atypical mycobacterial infections 200 SECTION II SMALL ANIMAL IV. Neoplasia 4. Otitis media V. Sterile diseases 5. Chronic pathologic changes: Hyperplasia, A. Sterile granuloma stenosis, and altered glandular secretions B. Sterile nodular panniculitis within the ear favoring microbial colonization VI. Treatment depends entirely upon the diagnosis and poor healing 6. Treatment errors E. Diagnosis OTITIS 1. Physical examination I. Histologically the ear is an extension of the skin 2. Otic examination II. Conditions that affect the skin will also affect the 3. Otic cytology external ear canals 4. Culture and sensitivity when indicated III. Cerumen: Waxy debris found in the ear canal pro- F. Management duced by sebaceous and apocrine glands lining the 1. Resolve primary factors if possible canals. It functions to trap foreign material and can 2. Reduce inflammation complicate treatment and resolution of otitis when 3. Treat any secondary infections present produced in abnormal amounts 4. Identify and treat the underlying problem IV. Otitis externa V. Otitis media, interna A. Inflammation of the external ear canal A. Inflammation of the middle ear B. Primary causes B. Anatomy of the middle ear includes the tympanic 1. Parasites membrane, bullous cavity, auditory tube, and a. Otodectes cyanotis  ear mites auditory ossicles b. Otobius megnini  spinous ear tick C. Usually an extension of otitis externa through a c. Demodex mites damaged tympanic membrane d. Eutrombicula alfreddugesi  chiggers D. May see extension via the auditory tube or e. Sarcoptes scabiei hematogenous spread. Auditory tube extension f. Poultry mites more common in cats with upper respiratory 2. Allergic disorders infections a. Most common cause for chronic otic E. Diagnosis inflammation in dogs 1. Observation of abnormal tympanic membrane b. Atopy 2. Radiographic or computed tomography scan c. Adverse reaction to food (food allergy) changes in the bulla d. Contact dermatitis or irritant contact 3. Pain upon opening the mouth dermatitis 4. Myringotomy and aspiration of fluid for 3. Foreign bodies cytology and culture and sensitivity 4. Keratinization disorders 5. Neurologic abnormalities: Facial nerve a. Primary seborrhea paralysis, Horner syndrome b. Hypothyroidism F. Treatment 5. Neoplasia of the ear canal 1. Long-term oral antibiotic therapy based on 6. Autoimmune disorders culture and sensitivity results C. Predisposing causes 2. Nonototoxic topical antibiotic 1. Factors that alter the microenvironment 3. Ear flushing under general anesthesia may be 2. Conformation required to remove excessive cerumen and a. Breeds with increased numbers of cerumi- debris nous glands (e.g., cocker spaniels) b. Breeds with stenotic ear canals Supplemental Reading (e.g., shar-pei, chow chow) c. Pendulous pinnae may restrict aeration of Campbell KL. Small Animal Dermatology Secrets. the canal Philadelphia, 2004, Hanley & Belfus. 3. Excessive moisture Medleau L, Hnilica KA. Small Animal Dermatology: a. Frequent swimming A Color Atlas and Therapeutic Guide, 2nd ed. b. Improper cleaning St Louis, 2006, Saunders. c. Obstruction of the ear canal Rhodes KH. The 5-Minute Veterinary Consult Clinical D. Perpetuating factors Companion: Small Animal Dermatology. Philadelphia, 1. Always secondary to a primary problem 2002, Lippincott Williams & Wilkins. 2. Yeast otitis: Malassezia pachydermatis Scott DW, et al. Muller and Kirk’s Small Animal 3. Bacterial otitis: Staphylococcus pseudintermedius, Dermatology, 6th ed. Philadelphia, 2001, Pseudomonas aeruginosa most common Saunders.