Equine dermatology 2 Flashcards

1
Q

What are common causes of crusting and scaling?

A

Infectious

  • Dermatophilosis (Rain Scald)
  • Dermatophytosis (Ringworm)
  • Bacterial infection- Staphylococcus spp. –> follicullitis/furunculosis/pyoderma

Dermatosis of lower limb

  • Leucocytoclastic vasculitis
  • Pastern dermatitis

Photo dermatitis

Seborrhea

Localised keratinisation defects

  • Cannon keratosis
  • Linear keratosis

Immune-mediated

  • Pemphigus foliaceus – RARE
  • Coronary band dystrophy- RARE

Idiopathic

  • Multisystemic eosinophilic epitheliotrophic disease (MEED)- RARE
  • Generalised granulomatous disease (SARCOIDOSIS) – UNCOMMON
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2
Q

What is the disease profile of dermatophilosis?

A
  • Dermatophilus congolensis
  • G +ve facultative anaerobic actinomycete
  • Thought to exist in quiescent state (no clinical signs) in chronically infected animals until conditions are favourable for proliferation
    • Skin damage- other skin disease, insect bites, environmental trauma etc
    • Wet skin – sweating, rain, washing
  • ? Genetic susceptibility- some horses more prone
  • Contagious
  • Immunocompromised/malnourished animals
  • Short lived immunity so can get recurrent infections
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3
Q

What are the clinical signs of dermatophilosis?

A
  • Follicular/non follicular tufted papules–> rapidly coalesce–> exudative —> matted hair (= paintbrush lesions)
  • When plucked leave erosions/ulcerations- may bleed or be purulent
  • Commonly seen on
    • rump and top line- rainfall
    • Saddle area- trauma/ sweating under tack
    • Face and neck- trauma/sweating under tack
    • Pasterns, coronet, heels= mud fever/grease
    • heel/scratches – poorly drained pasture/muddy
  • Lesions may be painful e.g. Distal limb swelling, oedema, lameness
  • Can be on white skin
  • Rarely pruritic
  • Healing stage–>dry crusts, scaling and alopecia
  • Lesions smaller in summer
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4
Q

How is dermatophilosis diagnosed?

A
  • History
  • Clinical exam
  • Impression smears- cytology
    • G +ve branching, filamentous
    • Chain like coccus “railway tracks”
  • Culture- microaerophilic / high CO2
  • Skin biopsy
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5
Q

What are the DDx for dermatophilosis?

A
  • Staphylococcal follicullitis
  • Dermatophytosis
  • Pemphigus foliaceaus RARE
  • Photo dermatitis
  • Other causes of pastern dermatitis
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6
Q

How is dermatophilosis managed?

A
  • Prevent wetting e.g. stable horse
  • Remove rugs etc to prevent sweating
  • Keep tack and grooming kit clean/individual use
  • Most cases spontaneously regress within 1 month if kept dry
  • Remove crusts , dispose carefully
  • Topical treatment
    • Chlorhexidine shampoos
    • Silver sulphadiazine (Flammazine )cream
    • NOT steroids because this is a infection!!
  • Systemic treatment
    • if horse systemically ill however horse tends not be with this infection
    • If severe, generalised, chronic infection
    • Antibiotics appropriate for gram+ bacteria- penicillin/ TMPS
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7
Q

What is the disease profile for a staphylococcus infection?

A
  • Sporadic infection
  • G +ve Staphylococcus aureus
  • Common Spring and Summer- post clipping/ during coat change
  • Especially fine skinned horses- TB’s
  • PAINFUL (if you try and pull these scabs off it hurts)
  • Contact areas of tack, saddle patch, riders legs
  • Potentially contagious if shared tack, equipment
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8
Q

What are the clinical signs of a staphylococcus infection?

A
  • Lesion starts as focal papule
  • Hairs stick up against lie of the coat, can be glued by small crusts
  • Can progress to furunculosis – nodules, draining tracts, ulcers, crusts
  • Can get cellulitis, lymphatic engorgement (= runners)
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9
Q

How is a staphylococcal infection diagnosed and treated?

A

Diagnosis:

  • Clinical signs
  • Swab and culture and exudate
  • Remember Staphylococcus aureus is a commensal – look for pure growth on selective media

DDX

  • Pemphigus foliaceaus
  • Other bacterial infection- Strep/ dermatophilosis
  • Onchocerciasis – this is pruritic

Management

  • NSAIDS –> pain
  • Avoid contact with tack, rider, rugs other horses
  • Topical antiseptic shampoos – Chlorhexidine/ povidone iodine based
  • Systemic antibiotics
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10
Q

What is the clinical profile of dermatophytosis?

A
  • HIGHLY CONTAGIOUS and COMMON
  • Potentially ZOONOTIC
  • Transmitted via contact with infected animals/environment- tack, rugs, grooming kit, bedding, fencing, transport vehicles, people
  • 2 causes in horse
    • Trichophyton equinum and verrucosum
    • Microsporum gypseum and equinum
  • Incubation period 1-6 weeks
  • Young animals –> esp. susceptible
  • Some immunity with age/post infection – unusual for a healthy horse to get dermatophytosis a second time.
  • Spores very resistant , survive for long periods in environment
  • Disease is endemic in many livery/racing yards
  • NOTE:
    • Racehorses are NOT allowed on racecourses with active lesions
    • Horses may NOT be exported with lesions
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11
Q

What are the clinical signs of dermpatophytosis?

A
  • Common at sites of tack contact-
  • face, neck, dorsolateral thorax, girth ( legs- rarely)
  • multiple lesions
  • Initially change in angle of hairs –> small often circular patches
  • Amongst hairs- amounts of finely keratinised squames (=Cigarette ash!)
  • Fungus produces keratolytic enzymes –> weakening hairs –> easily broken / epilated
  • Focal areas coalesce –> extensive scaling and flaking
  • Healing occurs from the centre
  • most active fungal growths at margins of the lesion- imp for sampling
  • Variable pain
  • Variable pruritus
  • Difficult to tell which fungal spp. is involved just by clinical presentation
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12
Q

How is dermatophytosis diagnosed and managed?

A

Diagnosis

  • Hair plucks at periphery of lesions
  • Microscopy
  • Culture ( can take up to 30days) sabouraud’s medium + red phenol dye agar turns red if +ve
  • Microsporum spp. Add drop vit B to culture as tricky to grow
  • Woods lamp NOT useful in horse
  • Skin punch biopsy- fungal spores within hair follicles

Management

  • ID of species not critical for treatment
  • Most infections are self-limiting (5-10 weeks)
  • Wear gloves to tx as potentially ZOONOTIC

Two main principles:

  1. Treat active infection to decrease spore formation
  2. Eliminate infective spores from environment
  • Topical/ systemic drugs
  • Disinfectants – anti-fungal action
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13
Q

Discuss the disease profile of pastern dermatitis?

A

COMMON! Often winter! Often multifactorial! Chronic wetting of the skin! White legs but not exclusively!

  • INFECTIOUS – bacteria, fungus, virus, parasite

vs

  • NON-INFECTIOUS- trauma, immune mediated, neoplastic

DDX:

  • Dermatophilosis- crusts on top of pus, not that painful
  • Staphylococcal dermatitis – extremely painful
  • Pastern and cannon leukocytoclastic vasculitis-not painful
  • Other autoimmune disease eg. SLE , immune mediated necrotising vascultis
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14
Q

What are the clinical signs of pastern dermatitis?

A

Clinical signs:

Mild- alopecia, erythema, mild serum exudation

Progression to – papules, significant serum exudation -> crusts -> scabs

+/- pain on palpation

+/- lameness

+/- cellulitis

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15
Q

How is pastern dermatitis diagnosed?

A
  • Clinical signs
  • Coat brushings
  • Skin scrapes
  • Swabs from exudate – culture/sensitivity
  • Skin biopsy – often poor return, may help in recurrent or refractory cases
  • Eliminate other causes e.g. Chorioptes spp.
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16
Q

How is pastern dermatitis treated?

A

Management/treatment

  • NOTE- often owners have tried various tx concoctions before you see the horse
  • No SINGLE tx
  • Some cases –> not totally resolvable
  • secondary infections –> bacteria / fungi –> complication

General Approach:

  1. Clean and clip area
  2. Debride crusts- e.g. Dermisol cream/Sudocream +clingfilm wrap+ stable bandage 12h overnight
  3. Next day- gently wash area with dilute Chlorhexidine , dry and clip more if needed
  4. If crusts still there repeat STEP 2
  5. It’s a fine balance between over wetting and needing to wash area
  6. apply topical treatment
  7. Dispose of crusts carefully /don’t re-use same towel to dry

Topical treatments:

Chlorhexidine- hibiscrub

Antiseptic, anti-fungal eg. Malaseb shampoo

Antibiotic creams eg. Flammazine cream

Combined antibiotic+steroid cream eg. Fuciderm, many “homemade mixtures”

Care with repeated use of topical steroid- could delay epithelisation / cause thinning of skin , BUT may help with pain/inflammation

Other treatments:

NSAIDS

17
Q

How can pastern dermatitis be prevented?

A
  • AVOID over wetting skin- use barrier creams for exercise eg. Petroleum jelly
  • CARE DO NOT to aggressively wash and scrub area
  • Clean, dry bedding, avoid prickly straw
  • Dry paddocks
18
Q

What is this?

A

Pastern leukocytoclastic vasculitis

  • Follows the blood vessels
  • Cause unknown ? Associated with bacterial infection

Clinical signs:

  • in almost all cases affects white limbs, often follows BV’s Lat and med limb
  • Firmly attached crusts on distal limbs

Diagnosis: skin biopsy

  • See vasculitis, karryorrhexis of neutrophils

Treatment:

  • Topical
  • Systemic steroids
  • eg, prednisolone/dexamethasone
  • Avoid sun
19
Q

What is the disease profile of photo dermatitis?

A

SUNBURN:

  • Primary direct damage to the epidermis by UV light
  • Commonly unpigmented, pink skin eg. palomino, cream horses
  • Areas maximally exposed to the sun, nose, muzzle – erythema, scaling, necrosis
  • Prevent using suncream
20
Q

Discuss the disease profile of photosensitisation?

A

Occurs following normal light exposure

Indirectly caused by photodynamic agents in skin due to

  • Ingestion of plants containing photodynamic agents –>direct absorption into blood eg. UK Hypericum perforatum – St. Johns Wort
  • failure of the liver to de-toxify phlloerythrin (by- product of chlorophyll digestion) hepatotoxic plants eg. Senecio jacobea= Ragwort
21
Q

How can you diagnose and manage photosensitisation?

A
  • Check paddocks –> ID plants
  • Ragwort –> usually unpalatable when alive BUT when cut palatability ꜛ eg. In hay
  • Toxic effects –> not seen –> months after ingestion
  • Can affect multiple horses in a group
  • Not all horses have liver failure BUT its prudent to rule out

Clinical signs: erythema, oedema, pain, vesicles, serum exudation, skin necrosis, ulceration, sloughing, possible other signs of liver disease, secondary bacterial infection

Management : sun avoidance ( stable in day, turnout at night), UV masks, high factor sun screens, avoid grazing with toxic plants. use topical creams to remove crusts and soothe eg. Dermisol/aloe vera .

  • evidence of severe liver disease have guarded prognosis.
22
Q

What rare condition is seen here?

A

Pemphigus foliaceus – RARE

  • Antigen in horse not known
  • Lesions often start on face –> generalised over several months
  • Early lesions –> papules and crusts
  • Annular thick crusts, annular erosions with/without epidermal collarettes, annular alopecia, oozing, matted hair coat, scaling.

Diagnosis:

  • Skin biopsy – acantholysis, neutrophils, eosinophils
  • Direct smear of pustules/erosions- cytology
  • Immunohistochemistry
23
Q

How can pemphigus foliaceus be treated?

A

Treatment

  • Rarely can resolve spontaneously – foals
  • Aggressive treatment- immunosuppressive doses systemic steroids , prednisolone PO SID starting at 2-4mg/Kg or dexamethosone (issue as giving horses large doses of steroids could cause laminitis)
  • Immunomodulators- Azathioprine
  • Gold salts- aurothioglucose
  • Approx 50% cases relapse after prolonged treatment
24
Q

What are common causes of erosions and ulcers?

A
  • Saddle sores/tack rubs- most resolve, can leave leucoderma (change in skin pigment) leucotrichia (where hair grows back white)
  • Chemical irritants
  • Vasculitis
    • Can be caused by post infection eg. Streptococcus equi equi –> PURPURA HAEMORRHAGICA- urticaria, oedema of head, limbs, petichiation of mm, exudation, skin slough
    • Treatment : steroids, antibiotics, nursing
    • drug related
    • Photo-activated
    • Type III + Type I hypersensitivity

Other causes:

  • Chemical or thermal burns
  • Coital exanthema (EHV3)
  • Pemphigus vulgaris/ Bullous pemphigoid
  • Inherited defects- Cutaneous asthenia, epidermolysis bullosa, aplasia cutis
  • Ulcerative lymphangitis eg. Corynebacterium paratuberculosis
  • Glanders and Farcy- NOTIFIABLE (Burkholderia mallei)
  • Epizootic lymphangitis – NOTIFIABLE (Histoplasma farciminosum)
  • Vesicular stomatitis – NOTIFIABLE
25
Q

Discuss haircoat disorders in horses?

A
  • Hirsuitism- equine cushings disease (PPID)
  • Seasonal abnormal shedding
    • alopecia, face, shoulders, rump
      • skin is normal
  • horse otherwise healthy
    • pathogenesis unknown
    • Spontaneous recovery over several months
  • Anagen defluxation – disease (infectious, metabolic, fever) can dsrupt the hair cycle –> sudden hair loss, hair shaft breakage
  • Telogen defluxation- stress (pregnancy, fever, severe illness, surgery, anaesthesia) causes abrupt, premature cessation of growth of anagen hairs, within 1-3 months a large number of telogen hairs are shed
  • Both spontaneously resolve when inciting cause corrected
26
Q

Discuss coat colour changes in the horse?

A

Most coat colour changes go to white

Leukotrichia/Leukoderma:

  • acquired loss of coat colour
  • without loss of skin pigment e.g. Freeze brand
  • bandage rub
  • patches of white hair
  • non progressive

Vitiligo- gradual appearance of non-pigmented skin without other changes e.g. Pink peri-ocular areas of Arabs

Spotted Leukotrichia

  • Shire, TB, Arab
  • Non-inflammatory white haired spots on normal skin
  • Get increased number of static spots

Reticulated Leukotrichia

  • White hair patterns
  • Can be painful
  • Quarter horse , TB, SB
  • Cause unknown

All 4 conditions can be differentiated by clinical signs or histopathology of biopsies.

No treatment

27
Q

List DDx for alopecia?

A

Anomalous

  • congenital hypotrichiosis- Percheron
  • mane and tail follicular dysplasia
  • -asynchronous shedding

Metabolic:

  • telogen defluxation
  • PPID ( hypertrichiosis)

Neoplastic

  • Occult sarcoid
  • Lymphoma

Inflammatory/infectious:

  • Ectoparasite
  • Dermatophytosis
  • Dermatophilosis

Inflammatory/autoimmune:

  • culicoides hypersensivity
  • Atopic dermatitis
  • Alopecia Areata
  • -Cutaneous lupus erythematosus
  • MEED/ sarcoidosis
  • Drug eruptions

Toxic

  • contact dermatitis
  • -scalding (urine/faeces)
  • heavy metal- Selenium, arsenic, mercury

Traumatic:

  • scarring

Vascular:

  • ischaemic damage –> minaturisation of BVs
28
Q

What is seen here?

A

Linear keratosis

  • A little patch of hyperkeratosis that goes alopecic
  • Relatively common
  • All ages/breeds, TB and Quarter horses, rare in ponies

Clinical signs :

  • Initially small areas hyperkeratosis–> develop alopecia
  • Lesions develop in a linear direction
  • Neck, chest, quarters
  • No pain, pruritus

Diagnosis:

  • Clinical presentation
  • skin scrapes to eliminate other diseases
  • skin biopsy- regular/irregular hyperplasia
  • Hyperkeratosis
  • lymphocytic follicullitis
  • Management:
  • No treatment/ not required
  • Permanent/progressive