CHAPTER 13. Dermatology
Elizabeth Rustemeyer May
GENERAL ASSESSMENT OF THE DERMATOLOGY PATIENT
I. Signalment: Age, breed, sex, color
A. Age: Congenital-hereditary conditions
B. Breeds: Terriers, atopy; American cocker spaniels, seborrhea
C. Sex: Reproductive hormone endocrinopathies
D. Color: Color-dilution alopecias
II. Primary complaint: What is the owner’s primary reason for consulting a veterinarian? Be sure to address this via diagnostics, treatments, and client education
III. History
A. A thorough and accurate history provides useful information that will aid in diagnosis
B. Obtain history in chronological order: Are the symptoms seasonal or nonseasonal? Which symptoms were present first—the itching or the alopecia? Have things changed since the symptoms were initially noticed?
IV. Physical examination
A. Properly using the correct dermatologic terms for lesions is crucial, as is a thorough physical examination. Be sure to examine the ears, feet, mucous membranes, lymph nodes, claws, and footpads. Note whether the lesions appear symmetrical or nonsymmetrical
B. Differentiate between primary and secondary lesions
C. Primary lesions: Main clinical sign directly caused by a disease process
1. Macule: Circumscribed flat spot up to 1 cm in diameter characterized by a change in color
2. Patch: A macule greater than 1 cm in diameter; not palpable
3. Papule: A solid elevation up to 1 cm in diameter. This represents infiltration of cells, edema, or hypertrophy of the epidermis. It can be palpated and is often erythematous
4. Plaque: Larger flat- topped elevation formed by extension or collection of papules
5. Pustule: Small circumscribed elevation of skin filled with pus
6. Vesicle: Circumscribed lesion up to 1 cm filled with clear fluid. These are rare and fragile. They are intraepidermal or subepidermal. Most are associated with autoimmune skin diseases (small animal) or viral diseases (large animal)
7. Bulla: A vesicle larger than 1 cm in diameter
8. Wheal: Circumscribed, raised lesion consisting of edema that appears in minutes to hours. The lesion will pit with digital pressure
9. Nodule: A small circumscribed solid elevation greater than 1 cm in diameter that results from massive infiltration of inflammatory or neoplastic cells into the dermis or subcutaneous (SC) tissue
10. Tumor: Neoplastic enlargement of any structure of the skin
11. Cyst: Epithelial lined cavity filled with fluid or solid material, such as keratin or sebaceous secretions
D. Primary or secondary lesions. Primary if main clinical sign is directly caused by the disease process, secondary if not specifically caused by the disease process but secondary to self-trauma or inflammation
1. Alopecia: Baldness or absence of hair from an area of skin where it is normally present. This is a primary lesion in endocrinopathies but a secondary lesion to pyoderma
2. Scale: Accumulation of loose fragments of the stratum corneum (keratinocytes). This is a primary lesion in seborrhea but secondary to self-trauma or inflammation
3. Follicular casts: Accumulation of follicular material adhered to the hair shaft
4. Crust: Dried exudate made up of serum, white blood cells (WBCs), red blood cells, and keratin
5. Hyperpigmentation: Increased epidermal or dermal melanin
6. Hypopigmentation: Loss of epidermal melanin
7. Comedo (comedones): Dilated hair follicle filled with keratin and sebaceous secretions (blackhead)
E. Secondary lesions: Not specific for the underlying disease process; may be caused by self-trauma or other inflammatory processes
1. Epidermal collarettes: Circular rim of loosely attached keratin (scale); usually indicative of a staphylococcal infection
2. Scar: An area of fibrous tissue that has replaced damaged dermal or SC tissue
3. Excoriation: Erosion or ulcer formed by the removal of superficial epidermis in a linear fashion by scratching, biting
5. Ulcer: Deeper interruption of the epidermis that exposes the underlying dermis; will heal with scarring
6. Lichenification: “Elephant skin”; thickened, firm skin with exaggerated superficial skin markings; results from constant friction or inflammation
7. Hyperkeratosis: Increased thickness of the stratum corneum
8. Fissure: Linear defect into the epidermis or dermis caused by disease or injury
9. Callus: Thickened hyperkeratotic lichenified area over bony prominences as a result of pressure or chronic low-grade friction
V. Differential diagnosis: Separate each problem and list differential diagnoses for each
VI. Diagnostic plan: Each diagnostic test is chosen to rule in or rule out the differential diagnoses listed for each problem
VII. Therapeutic plan: Formulation of a plan based on results from the thorough physical examination as well as results from each diagnostic test performed. Avoid “shotgun” therapy with multiple classes of drugs (i.e., both antibiotics and steroids)
VIII. Client education: A crucial portion of treating the dermatologic patient. Clear, concise instructions and explanations will ensure that the owner follows directions as expected
STRUCTURE AND FUNCTION OF THE SKIN
I. Skin structure
A. Epidermis
B. Dermal-epidermal junction
C. Dermis
D. Hypodermis or subcutis (SC tissue)
E. Epidermally derived appendages
1. Pilosebaceous structures
2. Eccrine sweat glands
3. Claws
II. Epidermis
A. Stratum corneum
1. Several layers of anuclear cornified cells separated by lipids
2. Major barrier to the outside world
3. Hyperkeratosis describes thickening of this layer.
B. Stratum granulosum
1. One layer thick in haired skin; additional layers in thinly haired skin
2. Granules in this layer contribute to formation of the intercellular lipids in the stratum corneum.
C. Stratum spinosum
1. Variable number of layers, typically one to three layers in haired skin
2. The beginning of cellular differentiation (keratinization) occurs here
D. Stratum basale
1. One layer of columnar cells and melanocytes
2. The site of cell division and production of daughter cells to supply the upper layers of the epidermis
3. Attached to the basement membrane zone
III. Epidermal turnover time: 21 to 28 days in most species. Some diseases can shorten cell turnover time, thus forcing keratinocytes to mature too quickly, resulting in seborrhea
IV. Cells of the epidermis
A. Keratinocytes
1. Most numerous
2. Produce keratin—involved in the process of keratinization
3. Produce lipid for the barrier layer
4. Produce important cell-signaling cytokines, thus involved in the immune response to allergy or injury
B. Melanocytes
1. Basal layer of the epidermis
2. Produce melanin pigment granules
C. Langerhans cells: Responsible for immune surveillance and antigen presentation, especially important in the development of allergies
D. Other cells
1. Merkel cell
2. Inflammatory cells (neutrophils, eosinophils, lymphocytes, etc.) when skin is diseased
V. Hair follicles and hair
A. Phases of growth
1. Anagen = hair growth phase
2. Catagen = transition phase
3. Telogen = hair resting phase; most of an animal’s hair is in this phase
B. Hair growth is affected by the following:
1. Hormones. Thyroid hormones, cortisol, sex hormones
2. Nutrition
3. Day length
C. Types of hair follicles
1. Simple = 1 hair per hair follicle opening. Cattle and horses have this type of follicle
2. Compound = Multiple hairs from one hair follicle opening. Dogs, cats, sheep, and goats have this type of follicle
VI. Epidermal glands
A. Sebaceous glands. Sebum secretion affected by
1. Sex hormones
2. Thyroid hormone
3. Cortisol
4. Malnourishment
5. Fatty acid deficiency
B. Sweat glands
1. Apocrine glands
a. Secretion empties into the hair follicle
b. Most domestic animals have this type of gland throughout the body
2. Eccrine glands
a. Secretion empties onto the surface of the skin (“sweating”)
b. Found on the footpads of dogs and cats
VII. Dermis
A. Main support structure for the epidermis
B. Thickest part of the skin
VIII. Functions of the skin
A. Barrier: Physical protection from the environment, 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
D. Secretion. Sweat, phermones, lipid barrier
E. Storage. Electrolytes, water, vitamins, protein, carbohydrates
F. Pigmentation. Ultraviolet light protection
G. Vitamin D production
FOLLICULITIS
I. Inflammation of the hair follicle. The clinical lesion reflects this and is typically a circular area of alopecia with scale and hyperpigmentation. Papules, pustules, and epidermal collarettes are also associated with folliculitis
II. The three main differential diagnoses for folliculitis include bacterial pyoderma, demodicosis, and dermatophytosis
A. Demodicosis
1. Inflammatory parasitic skin disease caused by the follicular mite Demodex canis or two other newly recognized variants
2. D. canis found in small numbers in healthy normal dog skin
3. In the disease state, these mites are present in much larger numbers than in normal individuals
4. Demodicosis can be very difficult to cure and thus very frustrating for the owner
5. The demodex mite spends its entire life on the skin of its host
6. Four stages
a. Fusiform egg
b. Six-legged larvae
c. Eight-legged nymph
d. Eight-legged adult (Figure 13-1)
 |
| Figure 13-1 Demodex canis. (From Birchard SJ, Sherding RG. Saunders Manual of Small Animal Clinical Practice, 3rd ed. St Louis, 2006, Saunders.) |
7. Life cycle takes 20 to 35 days
8. Mites spread from bitch in the first 3 days of life
9. Nursing provides direct contact for transmission; therefore, muzzle and forelegs are first sites of infestation
10. Not a contagious disease; mites are difficult to transfer to dogs older than a few days
11. There is an assumed weak link in the immune system of dog with demodicosis
12. The current belief is that these dogs have a T-cell function abnormality
B. Localized demodicosis
1. Age younger than1 year, usually 3 to 6 months
2. Lesions consist of localized areas of alopecia, usually minimal pruritus (mild clinical disease)
3. The face, especially the periocular and commissures of mouth, and forelegs are most commonly affected areas
4. 90% resolve spontaneously in 6 to 8 weeks
5. Optimize health (deworm, improve plane of nutrition)
6. This is not genetic or a genetic defect
7. Reexamine and rescrape in 3 weeks
a. If increase in numbers of mites, new lesions, lymphadenopathy—may be developing generalized condition
b. A small number of localized cases progress to generalized demodicosis
C. Generalized demodicosis
1. Juvenile onset (3 to 12 months)
a. Usually starts as localized lesions, which progress to generalized lesions affecting all parts of the body if not treated adequately or do not resolve spontaneously
b. Most animals appear to have a hereditary disposition
2. Adult onset (usually older than 5 years)
a. May be associated with internal disease, malignancy, or chronic corticosteroid use
b. Can be associated with hypothyroidism and spontaneous or iatrogenic hyperadrenocorticism
c. If no cause is found, the odds of successfully treating are decreased
3. Clinical signs of generalized demodicosis
a. Large areas of alopecia, usually nonpruritic
b. Major differentials include pyoderma and dermatophytosis
c. Mild to severe erythema
d. Usually skin becomes gray or hyperpigmented from chronic inflammation as well as large groups of comedones
(1) Often there is secondary pyoderma—superficial or deep, usually caused by Staphylococcus pseudintermedius, Proteus spp., or Pseudomonas spp.
(2) Clinically looks like papules, pustules, crusts, exudation (nodular form in bulldogs)
(3) A peripheral lymphadenopathy is often present if a pyoderma is present
(4) Depending on the severity of the secondary pyoderma, the animal may be systemically ill
4. Chronic demodectic pododermatitis
a. This is a form of generalized demodicosis
b. May have persistent foot lesions after therapy for generalized demodicosis
c. Demodicosis may only have been present on the feet
d. Often refractory to therapy
5. Otitis. Demodicosis may occasionally occur as an erythematous, ceruminous otitis externa, especially in cats
D. Diagnosis (Figure 13-2)
 |
| Figure 13-2 Skin scrape. For deep skin scrapes, once capillary oozing is initiated, the skin is usually squeezed before a final scrape is performed to collect the material. (From Medleau L, Hnilica KA. Small Animal Dermatology: A Color Atlas and Therapeutic Guide, 2nd ed. St Louis, 2006, Saunders.) |
1. Deep skin scrapings or hair plucks (trichograms) to visualize mites
2. Squeeze the affected area to extrude mites from the hair follicles
3. Take multiple scrapings, a minimum of three scrapings from lesional skin
E. Therapy
1. Do not use corticosteroids in these patients!
2. Localized demodicosis
a. Spontaneous remission in 90% of cases so treatment not usually needed; avoid using Amitraz (Mitaban dip) for this type of demodicosis
b. Benzoyl peroxide gel or shampoo for the follicular flushing action and to prevent secondary bacterial infections
c. Improve nutrition; remove intestinal parasites or other stress factors (fecal and heartworm test)
d. Recheck these animals in 3 to 4 weeks; if lesions are spreading or mite counts are increasing, the disease is progressing toward becoming generalized
3. Generalized demodicosis
a. Correct any nutritional, parasitic, or other concurrent problems
b. Dogs with adult-onset demodicosis should receive full workups to look for underlying (immunosuppressive) diseases; that is, get a minimum database (Complete blood cell count, serum biochemistries, urinalysis, heartworm and fecal checks, and usually thyroid and Cushing evaluation)
c. Start on appropriate antibiotic therapy based on culture and sensitivity. Use a bactericidal antibiotic for 3 to 6 weeks
d. Bathe the dog with an antibacterial and keratolytic shampoo (e.g., benzoyl peroxide) to open the hair follicles and remove crusts before applying Mitaban dip if using
e. Mitaban dips
(1) Mitaban used every 2 weeks is the only Food and Drug Administration (FDA)-approved treatment for canine demodicosis
(2) Dipping weekly improves the efficacy of Mitaban, but it is important to realize that this is an off-label use of the product
(3) Amitraz is a monoamine oxidase inhibitor (MAOI). Do not dip if the dog is taking Anipryl or other MAOI inhibitors. Antidote for Mitaban is yohimbine
(4) Monitor response to therapy with monthly skin scrapings Continue dipping 1-2 months beyond two negative skin scrapings 1 month apart
(5) Dogs should not be stressed while on 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.
(5) Reserve this treatment for Mitaban failures or if Mitaban is not a feasible treatment
(6) Side effects: Mydriasis, ataxia, coma, and death
(1) This is not an FDA approved treatment
(2) Treatment dose is higher than the standard dose for heartworm prevention. Use only in dogs proven negative for heartworms!
h. Client Education: Generalized demodicosis
(1) Guarded prognosis
(2) Long course of therapy
(3) Juvenile-onset cases should not be bred!
F. Feline demodicosis
1. Demodex cati: Follicular mite similar to Demodex canis except it is smaller and the ova are slim and oval, rather than spindle-shaped
2. Localized form
a. Lesions are variably pruritic alopecic areas affecting the nose, eyelids, and periocular skin
b. Erythema and scaling may also be present
c. Ceruminous otitis with demodex mites present may be seen without other lesions
3. Generalized form
a. Similar to localized except more body regions are affected
b. Generalized form usually associated with systemic disease and immunodeficiency state
4. Diagnosis
a. Skin scrapings
b. Minimum database for generalized disease, including feline leukemia virus and feline immunodeficiency virus testing
5. Differential diagnoses
a. Dermatophytosis
b. Pyoderma (rare in cats)
c. Causes of miliary dermatitis
d. Causes of pruritus
6. Treatment
a. Localized form = lime sulfur spray or dip
b. Generalized form
(1) Dependent on presence of underlying disease
(2) A consistent successful therapy has not been reported
(3) Weekly lime sulfur dips
(4) Treat underlying disease
7. Demodex gatoi
a. Not a follicular mite; lives in the stratum corneum
b. Broad blunted abdomen rather than a slim elongated one
c. This is a contagious (to other cats) and pruritic mite
8. Diagnosis
a. Broad superficial skin scrapings
b. Negative skin scrapings do not rule out D. gatoi as a differential diagnosis in a pruritic cat
9. Treatment
a. 6 weekly lime sulfur dips
b. Treat all cats in the household (i.e., all in-contact cats)
G. Pyoderma
1. Bacterial folliculitis and furunculosis are very common in dogs
2. Less common in cats
3. Secondary to an underlying disease process, usually an allergic disease or endocrinopathy
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
