Crust and Scale

Question 1

1. What is crust?
2. What is scale?

Answer 1

1. Dried exudate, cells, pus, scale adherent to the surface. May be covering areas of erosion / ulceration.
2. Accumulation of loose fragments of the cornified layer of the skin.

Question 2

Causes of erosion / ulceration.

Answer 2

Trauma - mechanical injuries e.g. acute moist dermatitis, skin fold pyoderma.
- thermal injuries.
- chemical injuries.
Radiation.
Neoplasia.
Infectious agents (viruses, fungi, protozoa).
- e.g. feline cowpox, herpes virus, calicivirus.

Question 3

1. Prevalence of immune-mediated skin disease?
2. Pathogenesis of immune-mediated skin disease?
3. Therapy for immune-mediated skin disease?
4. Prognosis of immune-mediated skin disease?

Answer 3

1. Uncommon to rare.
2. Drugs, neoplasia, systemic disease.
   Variety of immune mechanisms.
3. Immunosuppressive therapy. Look to manage underlying causes or triggers where possible.
4. May be poor.

Question 4

Pemphigus foliaceus.

Answer 4

More common immune-mediated skin disease.
Intercellular bridges (desmosomes) are the target of the immune system.
Disrupts layer of the skin and causes formation of pustules.
Pustules are transient and can often be seen as layers of crust where they have been rather than the pustules themselves.
Mainly affecting face, nose, in ears, sometimes down the back.
Associated with abnormal immune regulation or antigenic stimulation e.g. neoplasia (paraneoplastic pemphigus), infectious agents, drugs, autoimmune disorders, certain haplotypes, pregnancy, chronic skin disease.

Question 5

Clinical signs of pemphigus foliaceus.

Answer 5

2-7 years of age onset.
Disease chronic in 75%.
Skin lesions usually generalised.
- face and pinnae.
- footpads.
- trunk.
Pruritus

Question 6

1. Canine pemphigus foliaceus primary lesions.

Answer 6

1. Vesicles and pustules (often transient).
   May look like superficial pyoderma.
2. Trauma readily leads to crusting and erosions - circular.
   Scaling, alopecia.

Question 7

Canine pemphigus foliaceus diagnosis

Answer 7

Cytology of the pustule:
- numerous acantholytic keratinocytes – nucleated skin cells which are round in shape and free floating (should not be).
- neutrophils (eosinophils in some cases).
- no cocci.
Bacterial culture and susceptibility testing - should be sterile.
BUT - see substantial secondary bacterial infection w/ cocci on cytology, so treat first for microbial infection and then collect samples.
Skin biopsy for histopathology (and bacterial and fungal culture).
- punch or elliptical incision to encompass pustule.
- find intraepidermal and/or intrafollicular pustules with abundant acantholytic keratinocytes in upper layers of epidermis.
- may need several samples.
- beware the pustules are delicate and can traumatise readily.

Question 8

Feline pemphigus foliaceus.

Answer 8

Less known than with the dog.
Most common auto-immune skin condition in the cat.
Drug eruption has been documented as an underlying cause.
There are no breed, sex, or age predilections.
Lesions usuallu seen on head, esp. pinna, nasal planum.
Can see extension to the face, bridge of nose, muzzle, around eyes.
Tail and ventral abdomen incl. around the nipples.
Claw beds can have a thick caseous green purulent discharge - multiple digits and feet affected. Claws usually normal in appearance.
Transient pustules and vesicles.
- readily replaced by erosions and overlying crusts.

Question 9

Diagnosis of feline pemphigus foliaceus.

Answer 9

Fairly straightforward w/ involvement of claw beds of several feet. But this is not the only possible cause.
Other clinical signs may lead to confusion with dermatophytosis - fungal culture usually negative.
Often treated with ABX for paronychia - cocci bacteria are secondary - relief usually temporary.
Some cases wax and wane - which may suggest positive response to antimicrobial therapy - confusing response with natural course of disease.
Cytology from an undisturbed pustule will reveal numerous neutrophils (some eosinophils) w/ acantholytic keratinocytes.
Skin biopsy and histopathology.

Question 10

Presentation of pemphigus foliaceus in the horse.

Answer 10

Predominantly crusting from pustules.
Around the hooves and limbs, sometimes along the back.

Question 11

Tx of pemphigus foliaceus.

Answer 11

Glucocorticoids - Prednisolone / methylprednisolone / dexamethasone.
- 2mg/kg prednisolone per day until in remission.
- care with doses >2mg/kg.
- go to alternate day therapy as soon as safe to do so.
- slowly reduce dose to avoid relapse (every 2-3w).
Azathioprine.
- not recommended in cats!
Chlorambucil.
Ciclosporin.

Question 12

Canine discoid lupus erythematous.
- presentation, signs and diagnosis.

Answer 12

Affecting nose and face.
Photosensitive dermatosis that involves the nasal planum - exacerbated by UV light.
Clinical lesions - hypopigmentation, erythema, scaling, erosions and ulcerations.
– Loss of normal architecture.
Dx = Histology - lichenoid, lymphoplasmacytic interface pattern.

Question 13

Canine discoid lupus erythematous treatment.

Answer 13

Topical glucocorticoids.
Topical tacrolimus (Protopic) - slow to act – 6-8w.
Azathioprine.
Chlorambucil.
UV protection/avoiding higher UV periods of day.
Vitamin E - 400-800mg/day.
Essential fatty acids - n6 and n3 products.
Nicotinamide (niacinamide) and Tetracycline?
– immune-modulating effects.
Oral glucocorticoids.
Ciclosporin.
Nose flap plastic surgery?
Nose protectors?

Question 14

Equine pastern dermatitis / mud fever.
- Clinical features?
- Ddx?

Answer 14

More common on hind pasterns.
Cellulitis, ulceration, crusting, oedema.
Fissuring due to skin mobility.
Photosensitisation.
Granulation tissue may be excessive if healing delayed.
Lameness.
Ddx - immune-mediated = pemphigus foliaceus, vasculitis.

Question 15

Other causes of equine ulcerative pastern dermatitis.

Answer 15

Bacterial infection: Staphylococci, dermatophilosis.
Parasites: chorioptic mange / trombiculidiasis.
Dermatophytosis (ringworm).
Contact dermatitis (likely to affect all legs).
Photosensitisation (white socks).
Chronic progressive lymphoedema.
- described in draft breeds (Clydesdale, Shires, Belgian, Gypsy Vanner).
Keratinisation defects.

Question 16

Scales - what are they?

Answer 16

Loose fragments of keratin debris.
Most are dry, powdery or flaky.
Can see waxy, greasy scales in some disorders.
- can be associated with rancid odour.

Question 17

What causes excessive scales?

Answer 17

Major finding in disorders of the process of cornification.
Something has gone wrong in one of the steps:
- Bundling of the keratin to establish the corneocyte core.
- Replacement of the cell membrane with a thick cornified envelope.
- Formation of lipid lamellar bilayers.
- Desquamation (exfoliation). (desmosomes may have remained in place when they shouldn’t have).

Question 18

1. In stratum corneum, what are the corneocytes embedded in - what is this important for?
2. From where are epidermal lipids derived?
3. Composition of lipid-rich matrix?

Answer 18

1. lipid-rich matrix - important for normal exfoliation.
2. keratinocytes and sebaceous glands.
3. Phospholipids, sphingolipids, sterols, FREE FATTY ACIDS, omega-3.

Question 19

Mechanisms of scale formation.

Answer 19

Abnormalities in epidermal cell turnover.
Abnormalities in keratin synthesis and/or intra-epidermal lipid synthesis.
Abnormalities in surface keratinocyte cohesion.
Abnormalities in sweat or sebaceous gland function. e.g. anhidrosis - see hyperthermia and cutaneous changes e.g. alopecia and scaling due to loss of normal contribution to lipid layer in the skin.

Question 20

1. Prevalence of primary keratinisation disorders.
2. Prevalence of secondary or acquired keratinisation disorders - common causes.

Answer 20

1. Uncommon to rare and usually related to breed congenital disorders.
2. Most common in practice and scale formation is secondary to a defined underlying cause - e.g. atopic dermatitis, ectoparasite infection, microbial infections.

Question 21

Primary keratinisation defects seen in practice.

Answer 21

Sebaceous adenitis.
Idiopathic nasodigital hyperkeratosis.
Ichthyosis.
Zinc associated dermatosis.
Lethal acrodermatitis (English bull terrier).
Vitamin A responsive dermatosis.
Ear margin dermatosis.
Feline acne - blackheads on the chin – 2’ infection possible.

Question 22

Idiopathic nasodigital hyperkeratosis.

Answer 22

Can be an age-related change.
Brachycephalic breeds - not as much wear.

Question 23

Feline acne.

Answer 23

Just blackheads with some excess keratin w/ no inflammation or discomfort – leave alone.
Follicle flushing agents can be irritating.
Patient tolerance and stress of treatment.
More value in treating if the feline acne is causing more problems.

Question 24

Ichthyosis (fish scale).

Answer 24

Rare (golden retrievers, JRTs, American bulldogs).
Congenital / hereditary.
Primary defects in formation of stratum corneum production.
Decreased corneocyte desquamation (retention hyperkeratosis).
Adhered scaling.
Can be mild.
Can be more severe - can have a Malassezia overgrowth associated with this.
Manage rather than cure.

Question 25

Causes of secondary scale formation.

Answer 25

Inflammation caused by allergy, parasites, microbial infection.
Endocrine imbalances - w/ other signs of endocrine disease.
Nutritional factors:
- zinc responsive dermatoses.
- hepatocutaneous syndrome (AA abnormalities, liver disease).
- fatty acid deficiency / responsive dermatosis.
- vitamin A responsive dermatosis.
Environmental factors - rarely discomfort.

Question 26

1. Zinc responsive dermatoses types.
2. Zinc responsive dermatoses clinical signs.

Answer 26

1. I - adult dogs – husky, malamute, American Eskimo, Samoyed etc. –> unable to absorb zinc.
   II - young, growing dogs – large breeds –> diet low in zinc, high in phytate or calcium e.g. cereal or soy based.
2. Erythema and alopecia.
   Scaling and crusting.
   Can be pruritic.

Question 27

1. Presentation of zinc responsive dermatosis type I.
2. Diagnosis of zinc responsive dermatosis type I.

Answer 27

1. Lesions periorbital, dorsal nose, lateral muzzle, perioral, ventral mandible, pinnae, foot pads.
2. Clinical signs.
   Compatible histological findings from skin biopsy.
   Measuring zinc levels in blood or hair NOT diagnostic.

Question 28

Scaling in goats and alpacas.

Answer 28

Can be seen in various diseases incl. pyoderma, ectoparasites etc.
Rare primary disorders e.g. pygmy goat.
Owners often use zinc supplements but zinc deficiency is uncommon.
- no reliable diagnostic test – based on response to zinc supplements.
- alpacas w/ darker fleeces may be more likely to be affected.

Question 29

General principles of managing scaling disorders.

Answer 29

Address underlying cause and treat all secondary microbial infections.
Topical therapy for scaling:
- keratolytic activity causes damage to keratinocytes with subsequent shedding.
- Keratoplastic activity affects kinetics of basal cell turnover.
- Ingredients may include sulphur coal tar, bezoyl peroxide, selenium sulphide (Head and Shoulders), salicylic acid, a-hydroxyl acids, urea, glycerine, phytosphingosine.