Lecture 29

Congenital Disorders

Ichythosis

Generalized scaling that arise from defects in the formation of stratum corneum

Clinical sign: lamellar hyperkeratosis (scales), lichenification and crusting

Pathogenesis involves mutation genes involved in keratin formation and lipid organisation

Epidermolysis Bullosa

Caused by mutations in the structural proteins like keratins, integrins, collagens

Clinical signs: blistering and ulceration of skin and mucous membrane

Congenital Hypotrichosis

Absence of hair follicle and/or abnormal follicular development → clinically see less hair

• Affects all domestic species

Actinic Diseases

These diseases are caused by UV exposure

Damage can be acute or chronic:

• Acute = direct endothelial damage leading to erythema

• Chronic = thickened inflamed skin

Photosensitisation Dermatitis

Photodynamic substances in skin are activated by UV-A or visible light

Type I = Exogenous origin of photodynamic agents (such as consumption)

Type II = Aberrant heme pigment synthesis (hereditary condition)

Type III = Abnormal build up of phylloerythrin due to damaged liver

• Causes include Lantana camara (lantana) or Tribulus terrestris and mycotoxins such as sporidesmin

The lesions are in areas of the body with nonpigmented skin and hair and concurrent exposure to sunlight (face, nose).

In sheep with heavy fleeces, lesions occur on the pinnae, eyelids, face, nose, and coronary band; sheep can also have extensive oedema of the head resulting in the name facial eczema

Infectious Diseases

Viral Diseases

Viruses can enter either locally or systemically through ciraemia

Contagious Ecthyma/ contagious pustular dermatitis (Orf or Scabby Mouth)

• This is a highly contagious zoonotic parapox virus

  • Can see ballooning degeneration and intracytoplasmic inclusion bodies

Vesciular diseases can include FMD (Foot and Mouth disease), Vesicular stomatitis, Vesicular exanthema, Swine vesicular disease → all of which lead to systemic infections

These are epitheliotropic viruses (therefore localise in the skin during viraemia) → ballooning degeneration → rupture and loss of cohesiveness → vesicle formation

Bacterial Skin Diseases

Pyoderma

Greasy Pig Disease

This is an exudative epidermatitis

Acute, rapidly spreading, exudative pyoderma of young pigs

Caused by Staphylococcus hyicus

Cutaneous lacerations and poor nutrition predispose the condition

Dermatophilosis

Caused by Dermatophilus congolensis

Proliferative, exudative dermatitis, producing raised, alopecic, and sometimes papillomatous lesions covered by a thick, keratinized crust on any area of the body

Within the hyperkeratotic skin and hair follicles there are branching filaments that form parallel rows of coccoid zoospores

Mycobacterial Granuloma

Feline leprosy ****caused by Mycobacterium lepraemurium

Fungal Diseases

Malassezia Dermatitis

Malassezia has been recognized as an opportunistic secondary pathogen

Excessive sebum production, moisture accumulation, and disruption of the normal barrier function may lead to yeast proliferation, inflammation and pruritus

Dermatophysis A highly contagious, zoonotic, superficial fungal infection

Known as ringworm but not caused by a worm but by fungus

Fungi tend to die in areas of inflammation but are viable at the periphery, thus giving rise to the peripheral red ring and the term “ringworm”

Young and immunocompromised are susceptible

Predisposed to overcrowding, high humidity and poor sanitation

Pathogenic genera include Epidermophyton, Microsporum and Trichophyton

Parasitic Diseases

Sarcoptic Mange

Infests humans, pigs, dogs, ruminants, horse and severe disease in wildlife

Zoonotic disease – caused by Sarcoptes scabei

Burrow tunnels into and under the stratum corneum

Lesions are due to

• Direct damage from burrowing

• Irritant effects from secretions and excreta

• Hypersensitivity reactions

Clinical signs: alopecia, thickened crusts, erythema, pruritic lesions, lichenification

Demodectic Mange

Normal inhabitants of hair follicle and adnexal glands

Immunocompromised and young animals are more susceptible

2 forms

• Localised - self limiting condition in young animals

• Generalised – in juveniles following localized form

Clinical signs: alopecia, erythema, hyperpigmentation and comedones

Endocrine Disorders

Typical clinical signs include:

• Bilaterally symmetrical alopecia → nonpuritic

• Hyperpigmentation

• Secondary pyoderma and scaling

Histological changes include:

• Hyperkeratosis

• Atrophic sebaceous glands

• Dilated atrophic follicles filled with keratin

Major diseases:

Hypothyroidism → can see myxedema

Hyperadrenocorticism → can see lots of comedones

• Can be endogenous or exogenous

Gonadal hormone imbalance → alopecia starts at the caudal end

Alopecia X → pathogenesis unclear but can see lots of alopecia and thin skin

Equine pituitary adenoma → causes hypertrichosis = hair retention

Immune Mediated Dermatoses

Atopic Dermatitis

This is a hypersensitivity dermatosis which is Type I

Genetically predisposed

• Onset before 3 years of age

Causes inflammatory and pruritic allergic skin disease

• Pruritis and lesions on forepaws and concave pinnae → can present with ear infection

Underlying pathogenesis includes epidermal barrier dysfunction

Perivascular and interstitial dermatitis – non- specific lesions

Urticaria

This is a hypersensitivity dermatosis which is Type I

This is common in dogs and horses

These are characterised by wheals which are focal areas of oedema

Can be variably pruritic but in most cases not really

Can be caused by insect bites, environmental agents etc.

This is a transient nature of clinical signs and goes away within 24-48 hours

Insect Hypersensitivity

This is a hypersensitivity dermatosis which is Type I but can also see Type IV for these issues

In horses this can be caused by culicoides

In dogs and cats this can be caused by flea-bite hypersensitivity

Most lesions caused by self mutilation

Flea Allergy Dermatitis

Dogs see alopecia and erythema in the caudal region

Cats can see erythmeatous plaques in the abdomen as well

Histologically you can see perivascular interstitial dermatitis, eosinophils and later mononuclear cells

There may also be small foci of epidermal micro abscesses

Cutaneous Adverse Food Reaction

This is a hypersensitivity dermatosis which is Type I

This is a response to food antigen leading to concurrent gastrointestinal signs

There is also skin lesions following marked self trauma

Pemphigus Complex

This is an autoimmune disease

This is when the body reacts against self antigens leading to an aberrant T or B cell response

• May have a hereditary components

Lesions can be localised around the face, ear and eyes or generalised such as in horses

• Starts as small vesicles → then bullas → then pustules → erosions and ulcerations

Pathogenesis

Autoantibodies are made against the desmoglein proteins of the keratinocytes → causes seperation and individualisation of the keratinocytes (=acantholytic cells) → disruption of the keratinocyte layer

Lupus Erythematosus

This is an autoimmune disease

This a spectrum of diseases ranging from mild skin diseases to a generalised systemic disease

Antibodies are created against nuclear antigens (the nucleus) → immune response which can cause organ damage

• May have a hereditary components

Discoid lupus erythematosus

Dogs presented with pigmentation of the nasal area, crusting and pustule formation

Can see lymphocytic interface dermatitis histologically

Nutritional Diseases

Protein deficiency → dull, dry, brittle hair coat

Fatty acid deficiency → diffuse scaling, loss of haircoat sheen and alopecia

Vitamin-responsive dermatoses → epithelial hyperkeratosis, squamous metaplasia of secretory epithelium

• Vitamin A is important for skin development

Mineral-responsive dermatoses → scaling and crusting dermatitis

• Zinc responsive dermatitis is seen in huskies and Alaskan malamutes

Misc Skin Disorders

Feline Eosinophilic Granuloma Complex

Can see plaques on the abdomen, eosinophilic granulomas formed around the face or ulcer formation around the lips

Histologically see ulcerated skin, necrotic collagen, eosinophilic and macrophagic infiltrates in the dermis layer

Equine Pastern Dermatitis/Greasy Heel

This is a cutaneous syndrome due to:

• Genetics

• Long hair coats

• Moisture

• Trauma

See the lesions in the hind limbs typically and around the hoof and pastern

There are 3 different presentations

• Mild form = mud fever → see inflammation and erythema and alopecia in the pastern region

• Exudative form = greasy heel → see exudative discharge

• Chronic proliferative form = grapes → proliferative lesions which look like grapes due to exuberant granulation tissue