Skin Environmental - Pathology

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Chemical damage

Contact dermatitis

• Results due to exposure to chemicals (not immunologic reaction)
  • Acids, alkali, detergents, irritant plants etc.
• In cats and dogs lesions usually on skin of abdomen, feet, chest, eyelids, axillae
• In horses lesions on muzzle, lower limbs, under tack
• Grossly:
  • Erythematous pathes and papules
  • Occasionally vesicles
  • Lesions caused by self-trauma include ulcers and crusts
• Microscopically:
  • Hyperplastic, spongiotic dermatitis
  • Superficial perivascular inflammation
  • Necrosis may be caused by corrosive substances

Ergot poisoning

• Caused by ingestion of grains or grass contaminated by fungus Claviceps purpurae
• Affects especially cattle
• Toxic alkaloids damage capillary endothelium, peripheral arterial and venous constriction -> thrombosis and possible tissue ischaemia
• Clinical signs develop about a week after consumption
• Grossly:
  • Red and swollen extremities
  • Dry gangrene may develop on pinnae and tail

Fescue poisoning

• Caused by excessive consumption of Festuca arudinacea
• Clinical signs develop about two weeks after consumption
• Grossly:
  • Dry gangrene of extremities
  • Similar to ergot poisoning

Selenium poisoning

• Caused by ingestion of plants that have accummulated excessive amounts of selenium
• May affect any herbivore, possibly also pigs
• Acute poisoning:
  • Multiple organ systems are involved
• Chronic poisoning
  • Poor hair quality, partial alopecia
  • Horses - loss of mane and tail hair, deformed hooves that may be shed

Physical damage

Acral lick dermatitis

• Also called lick granuloma or neurodermatitis
• Mostly occurs in dogs due to constant licking or chewing
• Areas most affected are carpal, metacarpal, metatarsal, radial or tibial areas
• Usually a single lesion
• Grossly:
  • Circumscribed hairless areas that may ulcerate
• Microscopically:
  • Compact hyperkeratosis
  • Hyperplasia of follicular and epidermal epithelium and sebaceous glands
  • Collagenous fibres causing dermal thickening
  • Perivascular and periadnexal plasma cell accumulation
  • May be associated with mild snsory polyneuropathy

Callus

• Hypertrophy of epidermis, particularly at pressure points
• Usually affects giant breed dogs and pigs kept on hard floor
• May be followed by folliculitis, furunculosis and ulceration
• Microscopically:
  • Hyperkeratosis and acanthosis or epidermis and follicular epithelium
  • Comedones and follicular cysts may be present, potentially rupture and cause secondary pyoderma
  • Excessive keratin widening follicular openings

Feline psychogenic alopecia

• Occurs in cats
• Broken hairs cused by persistent licking -> partial alopecia
• Areas mostly affected: dorsal midline, perineal, genital, medial thigh, abdomen
• Microscopically:
  • Usually normal skin
  • Possibly increased telogen follicles

Injection site reaction

• May be caused by subcutaneous injections
• Granulomatous nodules form with central necrotic and foreign material
• Macrophages and multinucleated giant cells around the centre
• Surrounded by granulation tissue, perivascular lymphocytes that may form lymphoid follicles, eosinophils
• Cats may develop fibrosarcomas secondary to vaccination
• Dogs, especially poodles, may develop lymphoplasmacytic panniculitis and perivasculitis, vasculitis and follicular atrophy secondary to killed rabies vaccine

Intertrigo

• Also called skin fold dermatitis
• Develops due to irritation and bacteria in areas of skin friction and moisture (tears, saliva, glandular secretions, urine)
• Areas affected are commonly facial fold in brachycephalic breeds, lip fold, body fold, vulvular fold (obese females), tail fold (corkscrew tails)
• Cows with large, pendolous udder may become affected in area between thigh and udder
  • In severe cases, skin and subcutis may slough

Pyotraumatic dermatitis

• Also called acute moist dermatitis or 'hot spot'
• Common in dogs, especially self-inflicted due to pain and itching
• Usual causes: allergies, irritants, matted hair, parasites
• Lesions tend to be worse in hot and humid weather
• Grossly:
  • Hairless, red and moist lesion
  • Fluid exudate
  • Edges are circumscribed and red
• Microscopically:
  • Superficial erosive to ulcerative exudative dermatitis
  • May be deeper suppurative folliculitis

Radiation damage

• Cells sensitive to radiation include anagen hair follicles, germinal basal cells, melanocytes and endothelial cells
• Early changes:
  • Erythema, epidermal blisters and oedema, erosions and ulceration
  • Healed by scarring, hyperpigmentation with lower doses and hypopigmentation with higher doses
  • Temporary or permanent alopecia
• Chronic changes:
  • Scarring, altered pigmentation, alopecia
  • Epidermal and adnexal atrophy
  • Degeneration of vascular and elastic tissue
  • Fibrosis of dermal and subcutaneous tissue
  • Ulceration
  • In severe damage, squamous cell carcinoma may develop

Low temperature damage

• Prolonged cold can cause ice crystal formation and vascular injury resultic in damage to tissue due to increased intracellular salt concentration
• Slow chilling can cause vasoconstriction, cellular damage -> secondary vasodilation and increased permeability -> oedema
• Severe and persistent cold causes vasoconstriction, increase in blood viscosity and tissue anoxia
• Lesions may occur in wet or hypoglycaemic neonates or animals recently moved from warm to cold environment
• Areas affected are extremities
• Lesions consist of gangrene and necrotic tissue

High temperature damage

• May result from excessive heat, liquids, flames, friction, lightning, electricity
• Partial or full thickness burns (first, second and third degree burns)
• Full thickness burns:
  • Total destruction of skin and adnexa
  • Has to be repaired by grafting
  • Life threatening
• Partial thickness burns:
  • Some structures preserved -> regeneration may occur
  • Grossly:
    • Erythema (capillary dilation)
    • Oedema (increased permeability of capillaries)
    • Vesicles
  • Microscopically:
    • Coagulation necrosis of epidermis
    • Subepidermal vesiculation
    • Necrosis of adnexa
    • Degenerated subepidermal collagen
    • May involve large numbers of neutrophils if secondary ifection is present

Sunlight damage

• Transient erythema may develop into sunburn erythema (warmth, swelling, pain)
• Diffusion of inflammatory mediators (e.g. cytokines) from damaged keratinocytes and endothelial cells
• Photooxidation of existing melanin -> pigment darkening
• Melanogenesis
• Immune responses of skin are reduced by UV light

Solar dermatosis and neoplasia

• Caused by chronic sunlight damage
• Damaged tissue generates free radicals than may damage nucleis acids and proteins
• If damage repaired prior to mitosis - no lasting effect
• If mitosis occurs before repair, post-mitotic repair is prone to faults and DNA mutations may result in neoplasia

Solar dermatitis

• Particularly in white animals and where little or no hair is present
• Grossly:
  • Erythema, scaling and crusting
  • -> Wrinkled nand thickened skin
  • Squamous cell carcinoma or haemangiosarcoma/haemangioma may develop
• Microscopically:
  • Dyskeratotic cells
  • Intercellular oedema
  • Vacuolated keratinocytes
  • Followed by hyperkeratosis, parakeratosis and acanthosis
  • Endothelial swelling
  • Haemorrhage
  • Hyperplasia
  • Dermal fibrosis
  • Dogs may develop actinic comedones

Photoenhanced dermatoses

• Many immune-mediated cutaneous disease are made worse by sunlight
  • Lupus erythematosus
  • Dermatomyositis
  • Pemphigus erythematosus
• Vasculitis in extremities, especially white-haired horses
• Grossly:
  • Erythematous, well circumscribed crusted lesions or hyperkeratotic plaques
• Microscopically:
  • Vasculitis of superficial dermal vessels
  • Thrombi may be seen