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96 Cards in this Set

  • Front
  • Back
Hyperkeratosis -
increase in thickness of the stratum corneum
Orthokeratotic hyperkeratosis
(cells are anuclear)
Basket-weave (primary idiopathic seborrhea of cocker spaniel)
Compact (nonspecific responses to chronic stimuli)
Parakeratotic hyperkeratosis
(cells contain nuclei)
Zinc-responsive dermatosis
Hepatocutaneous syndrome (superficial necrolytic dermatopathy)
Nonspecific responses to chronic stimuli
hyperplasia of the stratum spinosum
Epitheliogenesis imperfecta
Aplasia - failure of epithelial and adnexal development (hereditary/congenital)
Acantholysis -
loss of cohesion between epidermal cells
Anti-desmosomal antibodies (pemphigus)
Desmosomal lysis by inflammatory proteases (pyoderma)
Pustule -
vesicles filled with inflammatory cells
Crust -
dried exudate on the epidermal surface (serous, hemorrhagic, cellular)
Perifolliculitis -
inflammation around the follicle
Folliculitis -
inflammation of a hair follicle (wall and/or lumen)
Etiology: parasites (Demodex), bacteria (Staphylococci), dermatophytes (Microsporum, Trichophyton)
Furunculosis -
perforating folliculitis
Released hair shafts, keratin, and sebum cause a foreign body-type response in the surrounding dermis.
Secondary to: folliculitis, pruritic dermatoses, keratin plug of the follicular orifice…
Macule is a
flat non-palpable spot (less than 1cm in diameter) characterized by a change in color from the surrounding skin.
Patch is a
macule over 1 cm in size.
Macule and patch
hypopigmentation (vitiligo), hyperpigmentation, petechiae, ecchymoses
Papule is a
small solid (palpable) raised spot on the skin up to 1 cm in diameter
solid (palpable) larger flat topped elevation on the skin > 1 cm in diameter.
Papule and Plaque Examples:
edema, infiltration of inflammatory cells (allergic dermatitis, superficial bacterial folliculitis, calcinosis circumscripta)
Wheal is
an irregular elevated edematous white to pink skin area which usually changes in size and shape (within hours). If distensible areas (eyelids or lips) are affected, it is called angioedema.
Wheal Examples:
urticaria, insect bite, and positive reaction to allergy skin test.
Nodule is a
circumscribed, solid elevation greater than 1 cm that usually extends into the deeper layers of the skin and it is larger than a papule.
Nodule Examples:
neoplasia, hyperplasia, inflammation, and deposition (e.g. calcium)
Vesicle (blister) is an
intra- or subepidermal saccule filled with clear fluid.
Bulla is a

(intra- or subepidermal saccule filled with clear fluid)

over 1 cm in size.
Vesicle and Bulla
auto-immune, irritant, burn, and viral etiology.
Pustule is an
intra- or subepidermal saccule (vesicle) filled with pus (inflammatory cells). A pustule can be sterile or infectious.
Pustule Examples:
pemphigus, impetigo (superficial pyoderma)
Cyst is an
epithelium-lined cavity containing fluid or sometimes semisolid material (keratin).
Alopecia is
loss of hair and may vary form partial to complete.
Primary: endocrine dermatoses, follicular dysplasia
Secondary: trauma, inflammation
Scale is an
accumulation of loose fragments (flakes) of the stratum corneum (cornified cells) on the skin.
Primary: primary idiopathic seborrhea, endocrine dermatoses
Secondary: chronic inflammation
Crust is
formed when dried exudate, serum, pus, blood, cells, scales, or medications adhere to the surface of the skin.
Primary: primary idiopathic seborrhea, zinc-responsive dermatosis
Secondary: pyoderma, chronic pruritic dermatoses
Hyperkeratosis (Orthokeratotic and Parakeratotic):
Hyperkeratosis is an increase in thickness of the horny layer of the epidermis.
Primary: vitamin A-responsive dermatoses, primary idiopathic seborrhea, zinc-responsive dermatosis
Secondary: chronic inflammation
Follicular cast is an
accumulation and adherence of keratin and follicular material to the hair shafts above follicular ostia.
Primary: vitamin A-responsive dermatoses, primary idiopathic seborrhea, sebaceous adenitis
Secondary: demodicosis, dermatophytosis
Comedo is a dilated hair follicle filled with cornified cell and sebaceous material.
Primary: Cushing’s dz., feline acne
Secondary: seborrhea, demodicosis, dermatophytosis
Increase in epidermal and/or dermal melanin.
Examples: chronic inflammation, melanoma, lentigo
Erosion is a
partial loss of epidermis with intact basement membrane.
Examples: epidermal diseases, self-trauma
The epidermis is lost with exposure of the underlying dermis.
Examples: burns, deep pyoderma, and vasculitis
Scar is an
area of fibrous tissue that has replaced the damaged dermis or subcutaneous tissue.
It is usually atrophic, alopecic and depigmented or hyperpigmented.
Examples: burns, deep pyoderma
Excoriations are
erosions and ulcers caused by scratching, biting, rubbing or any other self-trauma (sometimes with linear pattern).
Fissure is a
linear crack or split in the epidermis or epidermis and dermis
Lichenification is a
thickening and hardening (leather) of the skin resulting in exaggeration of normal skin line markings.
Examples: chronic inflammation, friction
Callus is a
thickened, rough, hyperkeratotic, alopecic, often lichenified plaque on the skin (usually over bony prominences).
Examples: chronic low-grade friction
Epidermal collarette
Epidermal collarette is a special type of scale arranged in a circular rim of loose keratin flakes or peeling keratin.
Examples: secondary to ruptured vesicles or pustules
Biopsy sampling is recommended when:6
1. The therapy for the skin disorder is associated with significant side effects (to confirm the clinical diagnosis before starting therapy).
2. A nodular lesion, ulcer, or nonhealing wound might represent a tumor (so ,that surgical excision of the tumor can be performed as early as possible).
3. Lesions develop suddenly, are severe, or are unusual (to help identify a serious disease so that therapy can be instituted early).
4. Lesions develop during the course of therapy (to identify a potential adverse reaction to drug therapy).
5. When lesions are active and before use of therapy that might alter the histologic appearance of the lesions (NB - antiinflammatory therapy can alter lesions) and when there are multiple clinical differential diagnoses.
6. When a skin disorder fails to respond to apparently appropriate therapy or when the disorder responds to therapy but recurs when therapy is stopped (to establish the correct diagnosis, or evaluate for predisposing factors).
Acral lick dermatitis
(lick granuloma) in dogs is a relatively common dermatitis usually localized to a leg due to persistent licking as a consequence of psychogenic/behavioral problem or underlying polyneuropathy that incites sensation of pruritus.
Lesions: circumscribed, hairless, erythematous areas, sometimes ulcerated
Feline phychogenic alopecia –
breaking of hairs by persistent licking
Pyotraumatic dermatitis
(acute moist dermatitis, hot spots, traumatic deep pyoderma)
Common in dogs
Self-inflicted trauma of biting or scratching because of pain and/or pruritus (allergies, parasites, matted hair, and irritant chemicals) that is subsequently infected by bacteria (usually Staphylococcus sp.)

Gross lesions: exudative ulcerative/erosive dermatitis with red edges, and alopecia
macules, papules, vesicles, umbilicated pustules, crusts and scars
Contagious ecthyma
(contagious pustular dermatitis, orf, sore mouth)
 Parapoxvirus infection of predominantly young sheep and goats
 High morbidity and low mortality
 Lesions: proliferative, crusting dermatitis (macules, papules, vesicles, umbilicated pustules, crusts and scars) begins at the commissures of the mouth, and spread to the lips, oral mucosa, eyelids, and feet.
 Economic importance due to weight loss in lambs
 Zoonosis
Pseudocowpox (parapoxvirus)
Common skin lesions on the teats and udder of milking cows
 Characteristic rign or horseshoe-shaped crusts
 Zoonosis (milker's nodules)
Bovine papular stomatitis (Parapoxvirus)
- Target lesions in mouth of young cattle, but could be also affecting teats and muzzles of calves
- Zoonosis (lesions similar to “milker's nodules”)
Bovine herpes mammillitis (Bovine herpesvirus 2)
Mammillitis – inflammation of the nipple
 Pseudolumpy-skin disease, but in the USA and Canada it is localized disease and affected skin of mammary glands of milking cows.
 Virus cannot penetrate intact skin so previous trauma is usually present
 Economic significance due to decreased milk production
Nasodigital hyperkeratosis
Canine distemper
(hard pad disease)
Pyodermas are usually
secondary diseases
Superficial pyodermas
Proliferation of bacteria in the superficial and infundibular follicular epidermis produces an acute inflammatory response in which neutrophils migrate from the superficial vessels into the dermis and through the epidermis. It usually heals without scaring.
Gross: erythema, alopecia, pustules, crusts
Superficial pustular dermatitis (impetigo)
Coagulase-positive Staphylococcus
Neutrophilic pustules that develop into crusts in dogs and cats
Dermatophilus congolensis infection associated with prolonged wetting of the skin
Occurs in cattle, sheep, and horses more often than dogs, cats, pigs, and goats
Lesions: multilaminated crusts with matted hair over the back and distal extremities
Exudative epidermitis of pigs
(greasy pig disease)
Staphylococcus hyicus
Acute, often fatal dermatitis of neonatal piglets and a mild disease in older piglets.
Lesions: greasy brown-yellow malodorous exudate and crusts over the red underlying skin
Deep pyodermas
Deep bacterial infections involve the entire infundibular, isthmic and/or inferior portion of the hair follicles +/- surrounding dermis and subcutis.
 It is often secondary to immunosuppression, demodicosis (dogs), disorders associated with follicular hyperkeratosis or a sequela to superficial bacterial folliculitis.
 Lesions may vary: folliculitis, furunculosis, nodular to diffuse dermatitis or panniculitis with pustules, alopecia, nodules, ulcers, fistulas or hemorrhagic areas.
 Staphylococcal (S. intermedius) folliculitis and furunculosis develop most commonly in dogs.
 Subcutaneous abscesses (Pasteurella multocida & Streptococcus sp.) are common in cats.
Bacterial granulomatous dermatitis
 Feline leprosy (Mycobacterium lepraemurium) in cats living along the Pacific coast
 Atypical cutaneous mycobacteriosis – saprophytic Mycobacteria sp.
 Diffuse or nodular infiltrative granulomatous inflammation which may ulcerate and drain to the skin surface via fistula(e).
Virulent: ovine
Benign: ovine and bovine
– Trouma & moisture + Bacteroides nodosus and other bacteria such as Fusobacterium necrophorum
 B. nodosus produces potent proteolytic enzymes enabling deep bacterial penetration and F. necrophorum is predominantly responsible for necrosis resulting in separation and sloughing of hooves.
Ovine: Fusobacterium necrophorum – similar to benign footrot

Bovine (foul-in-the-foot): Fusobacterium necrophorum and Bacteroides melaninogenicus
Papillomatous digital dermatitis
(footwarths or hairy heel warts)
Associated with spirochetes
Erysipelas in pigs
(diamond disease) - rhomboidal, firm, raised, pink to dark purple papules/patches secondary to vasculitis, thrombosis and infection.

Erysipelothrix rushipathie vasculitis
Purpura in horses as a sequela of
S. equi.vasculitis
Superficial cutaneous mycosis:
Dermatophytoses (ringworm)
 Microsporum and Trichophyton fungi affect wide range of species
 Invade keratinized tissues (stratum corneum, hair shafts, and nails) by producing proteolytic enzymes.
 Fungal products and products released from damaged keratinocytes result in epidermal hyperplasia (hyperkeratosis, parakeratosis, acanthosis) and inflammation.
 Exocytosis of inflammatory cells to superficial and follicular epidermis results in folliculitis and, if follicular wall is destroyed, in furunculosis.
 Hair loss is due to broken hair shafts and loss of hairs from inflamed follicles.
 Fungi die in the central areas of inflammation and are viable peripherally forming the peripheral red ring (ringworm).
 Lesions: circular or irregular, scaly to crusty patches of alopecia surrounded by hyperemic ring.
Systemic mycosis
The respiratory tract is almost invariably the primary portal of entry and infection in the systemic mycoses, but cutaneous and subcutaneous infections can occur as part of the disseminated disease or by direct implantation of fungi by trauma.
Examples: Blastomyces dermatitiais, Cryptococcus neoformans, Histoplasma capsulatum.
Deep cutaneous & subcutaneous mycosis
Subcutaneous mycoses are caused by fungi that, after traumatic implantation, invade cutaneous and subcutaneous tissue.
 Cutaneous endocrine disorders are due to imbalances in hormones and generally are manifested as non-pruritic, bilaterally symmetrical alopecia with the remaining hair coat dull and dry, easily epilated hair that fails to regrow after clipping, and pigmentary changes.
 Uncomplicated endocrine disorders of the skin consist of hyperkeratosis of superficial epidermis and of hair follicles; epidermal and follicular infundibular epithelial atrophy, hyperplasia, or normalcy; follicular dilatation; increased numbers of catagen and/or telogen hair follicles; empty hair follicles; and increased epidermal pigmentation.
 Inflammation due to secondary seborrhea or pyoderma frequently complicates the diagnosis.
 Endocrine dermatoses are most common in dogs.
 The most common endocrine dermatosis in dogs
 Thyroid gland secretes two hormones: T4 and T3
 Major modulator of thyroid-hormone production is thyroid stimulating hormone (TSH)
 TSH is regulated by the antagonistic effects of thyroid hormone and hypothalamic TSH-releasing hormone.
 T3 and T4 stimulate metabolism and promote growth and development of almost all tissues, including skin.
Congenital hypothyroidism
Usually in large animals
Pathogenesis: maternal ingestion of diets deficient in iodine or containing goiterogenic substances
Death or weak neonates with goiter, hypotrichosis
(Cushing's Disease, Cushing's Syndrome)
 The second most common endocrine dermatosis in dogs.
 ACTH secretion is regulated by a positive feedback mechanism mediated via corticotropin-releasing hormone (CRH) and a negative feedback mechanism mediated via cortisol.
 Cortisol influences function of most body systems including skin:
Causes atrophy of hair follicles and sebaceous glands, resulting in alopecia.
Inhibits fibroblast activity initiating atrophy of collagen and fibroelastic tissue in the dermis resulting in thin skin (pendulous abdomen due to loss of support)
Rearrangement of molecular structure of collagen and elastic tissue, leads to dystrophic binding of calcium to altered protein matrix (calcinosis cutis)
Anti-inflammatory and immunosuppressive effects of cortisol excess result in secondary superficial pyoderma and systemic infections
Cortisol excess causes a collagen defect in the wall of blood vessels which predisposes to an abnormal hemostatic reaction leading to bruising and ecchymoses.
o Symmetric trunkal alopecia to diffuse alopecia
o Thin skin, often with comedones
o Mild to moderate hyperpigmentation
o Abdominal distention
o Hepatomegaly (glycogen storage)
o Ecchymoses
o Calcinosis cutis (focal firm plaques)
o Concurrent superficial pyoderma, seborrhea
o Pruritus, if present, it is due to bacterial infection or calcinosis cutis
o Polydipsia, polyuria, and polyphagia
o Prolonged anestrus or male infertility
o Microscopic changes, epidermal and follicular atrophy (telogen phase), sebaceous gland atrophy, calcinosis cutis.
 Changes
Age: over 6 years
Intolerance to cold
Infertility in females and lack of libido in males
Hair coat dry, dull, coarse, sparse
Alopecia (symmetrical or asymmetrical)
Adnexal atrophy, dermal edema (myxedema), hyperpigmentation, scaling
Secondary superficial pyoderma with mild to moderate pruritus
The most common sex hormone disorder (estrogen-secreting testicular or ovarian tumors)

 Changes:
Middle-aged to older intact male (usually unilateral cryptorchid)
Descended testicle is usually atrophied
Feminization (gynecomastia, pendulous prepuce) and attraction of other male dogs
Bilaterally symmetrical alopecia (perineum, posterior thighs, genital region)
Variable hyperpigmentation (often marked)
Variable seborrhea
 Diagnosis
Skin and testicular biopsies
Serum estrogen levels
Response to castration
Immunologic skin diseases are classified as either
hypersensitivity (allergic) or autoimmune
Hypersensitivity (allergy) is
mild to severe reaction that develops in response to normally harmless foreign compounds (e.g. antiserum, hormones, pollen, insect venoms).
Autoimmune diseases develop when
antibodies or T cells are reactive against self-antigens rather than against foreign antigens.
Type I reactions (immediate hypersensitivity)
 Mediated by active substances (e.g. histamine) released or formed de novo by mast cells and basophils following reaction between antigen and specific antibody (usually IgE) bound to receptors on the membrane of the mast cells or basophils.
 Could be systemic and/or local.
 Lesions: pruritic and circumscribed wheals with raised, erythematous borders.
 Inherited predisposition exists.
 Examples: atopic dermatitis, insect bite hypersensitivity, food allergy, drug eruption, anaphylaxis
Type II reactions (cytotoxic hypersensitivity)
 Cytotoxic reactions involving interaction of IgG or IgM with antigens bound on cellular membranes; complement fixation frequently occurs, leading to cellular damage.
 Cell damage is mediated by:
Antibody-dependent cell-mediated cytotoxicity
Antibody-dependent cell dysfunction
 Examples: pemphigus, pemphigoid, some drug eruptions.
Type III reactions (immune-complex (Arthus) hypersensitivity)
 Immune complexes (IgG or IgM + antigen) deposit in tissues and fix complement generating cytokines and other factors that attract neutrophils.
 Examples: purpura (infections with Streptococcus equi); systemic lupus erythematosus; drug eruptions
Type IV reactions (delayed hypersensitivity)
 Mediated by sensitized T cells that, after contacting a specific antigen, release cytokines attracting macrophages and/or recruit other lymphocytes that are cytotoxic.
 Examples: some food allergies, some drug eruptions, some aspects of flea-bite hypersensitivity.
Usually presented as
pruritic skin diseases with self-inflicted trauma.
Most cutaneous hypersensitivity reactions are mediated either by type I or type IV reactions or by a combination of one or more of the four reactions.
Hypersensitivity reactions are common in dogs and horses, less common in cats and uncommon in food animals.
(atopic dermatitis, allergic inhalant dermatitis)
 Average age of onset is from 1 to 3 years
 Accounts for 3% to l5% of skin disorders
 Type I hypersensitivity reaction
 Skin is the major target organ in dogs, cats, and horses
 Route of allergen exposure is suspected to be predominantly respiratory (at least in dogs)
 Inherited predisposition to develop immediate hypersensitivity reaction to a variety of antigens by excessive production of IgE which, when coupled to a specific antigen, trigger degranulation of dermal mast cells and circulating basophils.
 Lesions: erythema, urticaria, self-inflicted trauma (licking, rubbing due to pruritus), sometimes with secondary pyoderma or seborrhea.
 Diagnosis
There is no single test that will confirm a diagnosis of atopy.
History, gross, histopathology
Rule out food and flea-bite allergy.
Intradermal allergy testing is the most widely accepted method of identifying the atopic dog.
ELISA - determination of allergen specific IgE
Flea-bite allergic dermatitis
 The most common hypersensitivity dermatitis in dogs and cats (coastal and Great Lakes regions)
 Type I and type IV reactions to flea bites (saliva)
 Seasonal pruritic pustular dermatitis with secondary lesions of self-inflicted trauma (excoriation) and alopecia in the caudal regions
 Microscopically hyperplastic superficial perivascular dermatitis with edema, mast cells, basophils, lymphocytes, histiocytes, and eosinophils (sometimes intraepithelial).

 Diagnosis:
History, gross, histopathology
Demonstration of fleas - absence of fleas during physical exam does not eliminate FAD as a differential diagnosis since one flea bite every 5 to 7 days is sufficient to cause hypersensitivity reactions in susceptible animals.
The best diagnostic tests are provocative exposure and response to therapy
Culicoides hypersensitivity in horses -
similar to flea-bite hypersensitivity in dogs
Food hypersensitivity dermatitis
 Non seasonal pruritic disease in young dogs
 Type I and/or type IV reaction to food antigens
 Changes
Erythema, urticaria, self-inflicted trauma (licking, rubbing due to pruritus)
Microscopically, capillary dilatation, edema, mast cell degranulation, infiltrates of eosinophils, epidermal hyperplasia
 Diagnosis:
History, gross, histopathology
Rule out other allergies
Elimination diet trial
Allergic contact dermatitis
 Type IV hypersensitivity reaction to chemicals (various dyes, plant resins, soaps, detergents,…)
 Lesions:
Erythema, papules with or without vesicles; pruritus with self-inflicted trauma (exudation, crusts lichenification, hyperpigmentation, alopecia) affecting regions in contact with antigen.
Microscopically, spongiotic superficial perivascular dermatitis, epidermal hyperplasia with varying numbers of eosinophils
Hypersensitivity reactions to drugs (e.g.
Erythema multiforme
Hypersensitivity reactions to drugs are uncommon in dogs and cats, are rare in other domestic animals, and may result from any of the four types of hypersensitivity reactions
Group of vesicular/pustular diseases
Pathogenesis: acantholysis associated with binding of auto-antibodies to desmosomal proteins (type II reaction) and, subsequently, disruption of cell adhesion, resulting in formation of pustules.

 Pemphigus foliaceus (subcorneal or intragranular pustules with acantholytic cells)
The most common pemphigus
Occurs in dogs, cats, horses, and goats.
Lesions: localized (muzzle, periocular, pinnae, foot pads, around nails) or generalized vesicular to pustular dermatitis with scales, crusts, alopecia, and superficial erosions.

 Others: pemphigus erythematosus, pemphigus vulgaris, paraneoplastic pemphigus
Pemphigoid (Bullous pemphigoid)
 Develops in dogs and horses
 Pathogenesis: (i) deposition of anti-hemidesmosomal antibodies in the basement membrane (type II reaction); (ii) damaged epidermal-dermal junction; (iii) formation of subepidermal vesicles and bullae containing fibrin, neutrophils, or eosinophils; rupture of bullae and formation of erosions/ulcers
 Lesions: bullae and ulcers affecting oral cavity, mucocutaneous junctions, axillar and groin regions
Systemic lupus erythematosus (SLE)
 Multiorgan disease of dogs, cats, and horses
 Pathogenesis: Genetic predisposition to immune dysregulation, which includes defective T cell suppressor function and cytokine dysregulation. B cell hyperactivity results in formation of auto-antibodies to a variety of cells and to nucleic acids. Immune complexes formed by antigen-antibody binding are deposited in a variety of tissues (including skin), and result in type III hypersensitivity tissue damage.
 Lesions:
Immune-mediated pathologic processes in many organs including skin.
Basal cell degeneration/necrosis, depigmentation, interface infiltration of many lymphocytes and plasma cells resulting in erythema, scaling, erosion, ulceration, and crusting.
Discoid lupus erythematosus
 Relatively common in dogs
 Mild variant of SLE
 Pathogenesis: immune-mediated basal cell degeneration and necrosis, depigmentation, interface infiltration of many lymphocytes and plasma cells.
 Lesions: depigmentation, erythema, scaling, erosion, ulceration, and crusting affecting the nasal planum, nasal dorsum, pinnae, lips, periocular regions and oral mucosae.
 Autosomal dominant disease affecting Collies and Shetland sheepdogs
 Occurs in puppies and young dogs
 Suspected pathogenesis: vasculitis secondary to immune complex deposition (type III reaction) is the primary change with subsequent ischemic damage to epidermis (basal cell degeneration), adnexa, dermis and muscles resulting in atrophy.

 Lesions: alopecia, erythema, scales and crusts affecting the face, lips, external ears, distal extremities and/or the tip of the tail.
Diagnosis of autoimmune skin disorders
The diagnosis is based on distribution and appearance of gross and microscopic lesions. Other diagnostic tools include the demonstration of immunoglobulins (IgG, IgM, or IgA) and/or complement in intercellular areas (pemphigus vulgaris, pemphigus foliaceus, and erythematosus), in the basement membrane (pemphigus erythematosus, bullous pemphigoid, systemic lupus erythematosus, discoid lupus erythematosus), or in vessels (cutaneous vasculitis). The demonstration of antinuclear antibody titers is used for diagnosis of systemic lupus erythematosus.
Seborrheic Disease Complex
Seborrhea is a chronic disease complex secondary to abnormalities of cornification and/or function of sebaceous glands associated with a change from nonpathogenic resident bacteria to pathogenic, coagulase-positive staphylococci.

Dry form (seborrhea sicca), with dry skin and white-gray scales.

Greasy form (seborrhea oleosa), with scaling and excessive brown to yellow lipids that adhere to the skin and hair.

 Primary idiopathic seborrhea

 Secondary seborrhea (associated with chronic inflammation

 Sebaceous adenitis (immune-mediated)
Zinc Deficiency
Occurs in pigs and dogs.

Lesions: scaling and crusting with marked diffuse parakeratosis

- Inherited reduced ability to absorb Zn (Alaskan Malamute)

- Rapidly growing pups of large breeds