Skin Environmental - Pathology
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Chemical damage
Contact Dermatitis
Ergot Poisoning
Fescue Poisoning
Selenium Poisoning
Physical damage
Acral Lick Dermatitis
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
Photosensitisation
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