Skin Environmental - Pathology

From WikiVet English
Jump to navigation Jump to search


WikiPathWikiPath Banner.png
()Map INTEGUMENTARY SYSTEM (Map)



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:
  • 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:

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:
  • Microscopically:

Photosensitisation

  • Primary
    • Ingestion of photodynamic substance from plants (Hypericum perforatum and Fagopyrum sagittatum - buckwheat) or fungal contaminants
    • Induced by drug administration - phenothiazines, tetracyclines, thiazides, sulphonamides
  • Abnormal porphyrin metabolism
    • Bovine congenital porphyria
    • Bovine erythropoeitic protoporphyria
  • Hepatogenous
    • Impaired excretion of phylloerythrin (chlorophyl metabolism product) due to hepatic disease
    • Biliary obstruction
    • Inherited defects
    • Hepatic injury due to toxic plants or fungal contaminants, chemicals or some infectious agents
  • Grossly:
    • In areas lacking hair or pigment
    • Erythema, oedema -> blisters, exudation, necrosis, sloughing or keratitis
  • Microscopically:
    • Subepidermal vesicles
    • Ulceration
    • Secondary infection

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