Dermatology Flashcards

1
Q

Bulla

A

> 1cm fluid filled, elevated lesion in/beneath epidermis

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2
Q

Crust

A

Dried exudate

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3
Q

Erosion

A

Partial loss of epidermis

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4
Q

Erythema

A

Reddening

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5
Q

Macule

A

> 1cm circumscribed, flush with skin surface, area of colour change

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6
Q

Nodule

A

> 5mm circumscribed, elevated, solid lesion

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7
Q

Papule

A

<5mm circumscribed, elevated lesion

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8
Q

Plaque

A

> 1cm elevated, flat lesion

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9
Q

Scale

A

Flaky skin (keratinocytes)

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10
Q

Ulcer

A

Total loss of epidermis

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11
Q

Vesicle

A

<1cm fluid filled, elevated lesion in/beneath epidermis

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12
Q

Wheal

A

Oedematous, circumscribed lesion (transient, e.g. ‘hives’)

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13
Q

Diagnostic tools for equine skin disease

A

Tape strips

Skin biopsies

Samples for culture

Skin scrape

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14
Q

Tape strips

A

Press cellophane tape to skin

Place tape on slide and examine

Useful for parasitic skin disease
- Oxyuris eggs
- Lice
- Occasionally mites

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15
Q

Skin biopsies

A

Discontinue anti-inflammatories 2-3 weeks before sampling

Target active, primary lesions

Try to include some adjacent normal skin

Care if sampling coronary band - can affect hoof growth, take ‘shave’ – not full thickness, or sample lesions elsewhere

Rinse with sterile saline, don’t scrub

Don’t crush the sample

Place in formalin for histopathologic analysis

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16
Q

Taking skin samples for culture

A

Do not scrub

Target pustules/underneath scabs

Swab in transport medium

Preferably before starting antibiotics

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17
Q

Skin scrapes

A

Edge of scalpel blade + liquid paraffin

Scrape until small amount of ooze from skin

Look at material on slide

Can add more liquid paraffin

Useful (best) for mites

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18
Q

Parasitic skin disease

A

Pediculosis
Mites (mange)
Helminths
Habronemiasis
Onchocerciasis

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19
Q

Two species of louse affecting horses

A

Damalinia equi
- biting louse
- dorsolateral trunk

Haematopinus asini
- sucking louse
- mane/tail/fetlocks

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20
Q

Clinical signs of pediculosis

A

Pruritus (not always)

Scaling/alopecia (‘moth-eaten’ appearance)

Often asymptomatic and noticed incidentally

Can cause anaemia (Haematopinus) in very severe infestations

Any time of year, but more common Autumn to Spring (can’t reproduce >38°C)

Commonly young/old horses, or immunocompromised/stressed animals (but any age/signalment can be affected)

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21
Q

Diagnsosis of pediculosis

A

Usually diagnosed on appearance of lice with naked eye

Quite often come to the coat surface when horse is warm, or sedated for another procedure

Can use coat brushings, or identify louse eggs attached to hairs under microscope

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22
Q

Treatment/management of pediculosis

A

Transmitted by direct and indirect (tack, rugs, grooming equipment) contact
○ Can theoretically live up to three weeks off host, but usually < 1 week
○ Hot wash rugs etc. to manage yard situation

In contacts should be treated at same time as clinical cases

Topical pyrethrins (permethrin or cypermethrin) (e.g. Deosect, Switch) for either/both species of louse is most common/effective treatment
○ Treat twice at 14 day intervals to cover hatching eggs
○ Can also use 1% selenium sulphide shampoos at 14 day intervals
○ Louse powder is for buildings, not horses
○ Oral ivermectin for H. asini is described, but less efficacious for D. equi so not routinely used
○ Clean environment/decontaminate tack, rugs, etc.

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23
Q

Pathophysiology of mange

A

Physical irritation and hypersensitivity to mite saliva

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24
Q

Clinical signs of mange

A

Maculopapular eruptions
Thickened skin
Pruritus

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25
Q

Species of mite affecting horses

A

Chorioptes equi
Sarcoptes scabei
Psoroptes equi
Trombicula

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26
Q

Chorioptes equi

A

Leg mange

Very common

Consider in all feathered breeds

Chewing legs, stomping, kicking

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27
Q

Diagnosis of choriopric mange

A

Treat presumptively
Skin scrapes if you want to confirm

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28
Q

Treatment of chorioptic mange

A

Clip feathers, especially when using topicals

Topical fipronil spray

Injectable doramectin (Dectomax®)

Selenium shampoo washes (keratolytic)

Treat twice at 14 day intervals

Advise treat in contacts (even if asymptomatic)

Clean the stable/fomites (including disposing of all bedding)

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29
Q

Psoroptes equi

A

Body mange

Very contagious to other horses

Biting mites feeding on cellular debris and serum

Transmitted by direct contact with infected horses or fomites

Affect forelock/mane/tail, may then spread to trunk

May show signs of headshaking, alopecia, crusts, but pruritus may be variable

Diagnose with skin scrapes

Treat as for Chorioptes

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30
Q

Sarcoptes scabei

A

Zoonotic

Scabies/head mange

Highly contagious between horses and will affect humans

Burrow into epidermis, preferentially head/ears at first but spread over body

Deeper mite, so may be missed on skin scrape

Can survive for 3 weeks off host

Ivermectin at 14 day intervals for 2-3 repetitions

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31
Q

Trombicula

A

Chiggers/harvest mites

Neotrombicula and Eutrombicula mites that live on small rodents as the natural host

Papules/wheals have a central red ‘spot’ which is the mite larva

Affect face, muzzle, ventral abdomen/thorax, distal limbs

May cause discomfort to horse and can be treated with pyrethrins, may require steroids additionally

Self-limiting condition

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32
Q

Oxyuris equi

A

‘Pinworm’

Primary gastrointestinal parasite (adult lives in colon), but causes skin disease when eggs are deposited

Gravid female worms stick eggs to perianal skin

Eggs become infective in 4-5 days

The sticky substance holding the eggs dries up and flakes off, and the eggs persist in the environment

Causes itching, tail rubbing, self-trauma around rump

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33
Q

Diagnosis of Oxyuris equi

A

Tapestrips from perianal skin

NOT faecal worm egg counts

If suspicious treat anyway, don’t rely on tape strips

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34
Q

Treatment of Oxyuris equi

A

Evidence is lacking, and there’s no consensus between clinicians, which causes confusion

Suggest starting with ivermectin/moxidectin, but resistance is increasing

Pyrantel would be another sensible choice

Fenbendazole also licensed as effective but would not be my preference

Wash perianal skin to interrupt life cycle

Can apply petroleum jelly to prevent eggs sticking

Do NOT use anthelmintics around anus/rectally

Clean environment

35
Q

Habronemiasis

A

Uncommon in the UK.

H. muscae and H. microstoma (house fly intermediate host) and Drashcia megastoma (stable fly intermediate host)

Lesions occur when L3 larvae are deposited on a wound or moist areas of skin

Cause nodular skin disease or ‘summer sores’, may contain white granular material

May be pruritic, may self-traumatise

Common sites: periocular, penis/prepuce, lips, any site with a wound

Similar appearance to exuberant granulation tissue, sarcoids

Spring and summer, partially/completely regress in winter

36
Q

Treatment of Habronemiasis

A

Oral avermectins

May consider topical glucocorticoids +/- DMSO to relieve itching

37
Q

Onchocerciasis

A

Onchocerca cervicalis – microfilarial nematode

Vector borne (midges), worse in the summer

Adult worm can live for 10 years in nuchal ligament

Lesion distribution: eyes, muzzle, neck, chest, ventral abdomen

Alopecia, scale, self-trauma from scratching

Rare in UK

Moxidectin and ivermectin are effective, so less common with use of these anthelmintics.

38
Q

Diagnosis of onchocerciasis

A

Skin biopsies

39
Q

Treatment of onchocerciasis

A

Moxidectin/ivermectin

May require severeal monthly treatments

May have adverse reaction so can give concurrent NSAIDs or steroids

40
Q

Viral skin diseases in horses

A

Coital exanthema

Viral papilloma

41
Q

Viral papilloma

A

Papillomavirus caballi

Two main syndromes - warts or aural plaques

42
Q

Warts caused by Papilloma virus caballi

A

Young: 6mo – 4yrs

Muzzle, lips, nose, eyes

Spontaneously regress usually within 3-4 months

Investigate if persist for >2 years (or if warts spread to atypical areas of the body)

Underlying conditions? Consider altered immune status if there’s a failure to clear infection naturally

Intervention may actually increase lesion persistence so try to avoid unless necessary

Cryotherapy probably best as induces necrosis and possibly viral antigen

43
Q

Aural plaques caused by Papillomavirus caballi

A

> 1 year of age

Do not spontaneously regress

‘Cauliflower’ growths inside pinnae

Small, then coalesce

Treat if causing an issue

Imiquimod topically

May become sore and head shy

44
Q

Fungal skin conditions in horses

A

Dermatophytosis (ringworm)

45
Q

Dermatophytosis

A

‘Ringworm’

Trichphyton spp. (T. equinum, T. verrucosum) and Microsporum spp. (M. gypseum, M. equinum) are most common in horses

Zoonotic/transmissible

Hair and epidermis affected

Keratolytic enzymes from fungus weaken hair – epilate easily

Alopecic regions with surface scale

Predilection sites where tack etc. contact skin as skin damage allows for fungal infection to star

46
Q

Diagnosis of dermatophytosis

A

qPCR is now best method – results within 24 hours and detects multiple species

Fungal culture possible, but takes 2-3 weeks

Need to start treatment/barrier nurse in lieu of results

47
Q

Treatment of dermatophytosis

A

In healthy horses infection is self-limiting and will resolve in 5-10 weeks, but zoonotic/transmission potential too significant to allow this

Remove surface scale/bathe to remove debris before applying topical enilconazole washes

Ensure all fomites (tack, stable, trailer etc.) are disinfected and not shared between horses

48
Q

Bacterial skin conditions in horses

A

Staphylococcal pyoderma

Cellulitis

Dermatophilosis

49
Q

Staphylococcal pyoderma

A

S. aureus, S. pseudintermedia

Crusts, papules, pustules

May be very pruritic (variable)

Can also be very painful potentially

Often along dorsum related to tack/rugs

50
Q

Diagnosis of Staphylococcal pyoderma

A

Often treated with antimicrobials based on appearance

Culture to confirm, try to get samples from under intact crust

51
Q

Treatment of staphylococcal pyoderma

A

Systemic antimicrobials (e.g. TMPS, penicillin)

Topical silver sulphadiazine (Flamazine)

52
Q

Cellulitis

A

Bacterial infection of subcutaneous tissue/deep dermis

Commonly distal limb, but not necessarily

Very common, may present as an emergency

May be ‘fracture’ lame

Heat, pain, swelling

May be systemically unwell - pyrexic

Commonly Staphylococcus, also Streptococcus

Secondary to wounds/puncture injuries, injections, skin trauma?

If so, manage the primary cause if it is still presenting an issue

53
Q

Treatment of cellulitis

A

NSAIDs

Antimicrobials
§ systemic – TMPS usually a good first choice (orally), or penicillin (injectable)

Some cases may require corticosteroids (evidence poor)
§ Possibly some conflation with lymphangitis cases

Cold hosing

Walking in hand

Poor consensus between clinicians, treat systematically, if it’s not resolving reconsider the plan and ensure you’ve ruled out any underlying driving factors (e.g. foreign bodies etc)

54
Q

Dermatophilosis

A

Dermatophilus congolensis
○ Branching, gram +ve, facultative anaerobe
○ Use this to your advantage when treating – create an AEROBIC environment

‘rain scald’ (dorsum), ‘mud fever’ (limbs)

Crusting, forms tufts of hair attached to crusts (’paintbrush’)

Carrier animals perpetuate infection

Crusts are infective, so clean them up/dispose of them

55
Q

Diagnosis of Dermatophilosis

A

Send crusts to lab, minced with saline, examined on smear for branching filamentous organism with parallel rows of cocci

Treated presumptively usually

56
Q

Treatment of dermatophilosis

A

Soak and remove crusts

Pat dry

Topical antimicrobials
○ E.g. fucidic acid gel

If severe, systemic e.g. TMPS

57
Q

Pastern dermatitis

A

Usually described by client as ‘mud fever’, but there are lots of causes beyond Dermatophilus congolensis

Often multifactorial, is a syndrome not a single disease entity

Often treated symptomatically, and with those concurrent conditions in mind

58
Q

Treatment of pastern dermatitis

A

Manage the environment, prevent from getting wet

Barrier creams can be useful, but potential of creating an unhealthy skin environment with thick creams

Clip hair to treat skin with topical medications

May require antibacterial washes and topical antimicrobial/steroid creams to manage lesions when they flare up

59
Q

Inflammatory and immune mediated skin diseases in horses

A

Urticaria ‘hives’

Insect bite hypersensitivity (‘sweet itch’, IBH)

Atopy (food, environment)

Eosinophilic granuloma

Pemphigus foliaceus

Chronic progressive lymphoedema

Photosensitisation

60
Q

Urticaria (‘hives’)

A

Roughly circular raised wheals - may coalesce

Immunological and non-immunological causes

May be a one-off event, or may be chronic

Investigate causes if recurrent

61
Q

Immunologic urticaria

A

Insect bites, food allergies, drugs, environmental allergens

Type I (and III) immune reaction

Type I: characterised by mast cell degranulation, IgE mediated

Th2 helper and IgE response -> eosinophils and mast cells

62
Q

Non-immunologic urticaria

A

Heat/cold exposure

Dermatographism (after twitching the neck, use of whip etc will see focal urticaria)

Cholinergic (exercise/heat)

63
Q

Treatment of Urticaria

A

Steroids if severe
§ May need dexamethasone IV initially before moving onto oral prednisolone
§ Very severe cases may progress to respiratory tract obstruction

Antihistamines may be useful
§ Hydroxyzine might be useful initially, may cause drowsiness (ridden safety implications)
§ Chlorphenamine (Piriton) first generation and at useful doses likely to cause drowsiness (implications for ridden safety)

Cold hosing may provide some relief

64
Q

Insect bite hypersensitivity (Sweet itch, IBH)

A

Culicoides spp. hypersensitivity

Hypersensitivity to saliva, but also insect mouthparts etc.

Type I hypersensitivity response
○ characterised by Th2 helper and IgE response, with subsequent eosinophil and mast cell response

Type IV hypersensitivity also implicated
○ Delayed hypersensitivity reaction
○ T-cell and macrophage mediated

Association between being affected with asthma and IBH (and vice versa).

IBH is associated with airway hypersensitivity

Can be a serious welfare issue if not well controlled

May necessitate euthanasia in severe cases

Onset typically 3-4yrs/age (can be older)

65
Q

Clinical signs of Insect bite hypersensitivity (‘sweet itch’, IBH)

A

Intense pruritus

Alopecia, lichenification, excoriations from self-trauma

Lesion distribution:
§ Common: dorsal distribution. Mane and tailhead are classic, also withers, face, neck (Syndrome I – very common UK)
§ Ventral chest and abdomen, jaw, (Syndrome II – not common in UK)
Both (Syndrome III)

66
Q

Diagnosis of Insect bite hypersensitivity (‘sweet itch’, IBH)

A

Based on classical lesion appearance and distribution

If atypical/does not respond to management may wish to rule out other ectoparasites, other causes of dermatitis, lesions affecting the tail may occur with cases of pinworm etc.

To obtain definitive diagnosis may pursue intradermal allergy testing - Expensive and not usually necessary

67
Q

Management of Diagnosis of Insect bite hypersensitivity (‘sweet itch’, IBH)

A

Revolves around avoiding exposure to midges
§ Avoid standing water
§ Stable at dawn and dusk when midges are worse
§ Use topical insecticides
□ Pyrethrins (Deosect, Switch)
Permethrin or cypermethrin
□ Benzyl benzoate effective, but probably doesn’t persist as long
□ Citronella etc. from the tack shop are not sufficient/effective
§ Fly rugs
§ Stable with fans if severe (midges are weak fliers)
§ Move to coastal/exposure pasture

May need treatment with systemic/topical glucocorticoids to alleviate itch initially, but management changes are vital
§ Antihistamines unlikely to be helpful

Nicotinamide supplement (Cavalesse)
§ Poor evidence

IL-5 vaccination in occasional use (not licensed)
§ Switch Th2 response to Th1 response

68
Q

Atopy

A

Multiple allergies stack up to take them over the pruritic threshold

Allergen specific IgE to environmental allergens

Pruritus, or urticaria, eosinophilic granuloma, secondary pyoderma

Commonly see secondary pyoderma

Intradermal skin testing: direct management, not a diagnostic tool to label horse with ‘environmental allergies’

Stop treatments at least 14 days before testing

Manage with steroids when required

Control secondary bacterial dermatitis- Topical or systemic antimicrobials

Essential fatty acids

If struggling to control itch consider pentoxyphylline

69
Q

Atopy: food allergy

A

Trial novel diets, keep it simple, eliminate all supplements and additives

Need to try for minimum of 6 weeks before trying something new
○ Can then re-add challenge to see if it was the cause

70
Q

Atopy: environmental allergy

A

Intradermal skin testing is useful to direct management, it isn’t a diagnostic tool to confirm environmental allergies

Remember to take off of medications at least 14 days before testing

Only test relevant allergens!

Dermatitis and urticaria

71
Q

Treatment of environmental allergy atopy

A

Subcutaneous and sublingual allergen specific vaccinations

65-70% subcut vacc positive response and may achieve long term remission

Some respond better to sublingual than subcut and vice versa

Response takes several months but aiming for a longer term solution

72
Q

Eosinophilic granuloma

A

Can be associated with atopy, but not necessarily

Firm nodules associated with collagen degeneration

Usually feel like a pea under the skin

Usually small, <1cm, can be bigger

Usually along dorsum but may be elsewhere

Overlying skin/hair normal (unless trauma from tack)

Aetiology not understood - ?
Hypersensitivity reaction ?
○ Possible association with insect bites? But not well understood

Usually left untreated

Can surgically excise or use intralesional steroids if large/becoming traumatized

73
Q

Pemphigus foliaceus

A

Very uncommon, potentially life-threatening

Autoantibodies produced against keratinocyte proteins and disrupt intercellular adhesion -> space fills with fluid -> pustules/blisters

Crust and scale, eruptions

Coronary band may be only area affected initially

May have urticaria first, may become alopecic

Weight loss, pyrexia, some may be extremely painful

74
Q

Diagnosis of Pemphigus foliaceus

A

Often diagnosed late due to similar appearance to other conditions

Impression smears of intact pustules/crusts may be useful

Biopsy: must include intact crusts attached to skin/hair

Acantholytic cells and neutrophilic infiltration

75
Q

Treatment of Pemphigus foliaceus

A

High doses of steroids until no new lesions, then taper

Maintenance dose for life

Gold salts also reported as useful potentially

Azathioprine may be helpful especially if cannot use steroids

Generally treatment most successful in younger patients

76
Q

Chronic progressive lymphoedema

A

Progressive limb swelling, chronic severe skin disease

Heavy horses (Clydesdales, Shires, Friesians, Cobs etc.)

Genetic predisposition, altered lymphatic function and elastin metabolism

Significant welfare issue

Onset early age, but may not be noticed until much later

Skin lesions secondary to poor lymphatic circulation

Life long, progressive disease

May cause severe lameness

Presents often as pastern dermatitis

Secondary parasitic/bacterial infection very common

77
Q

Diagnosis of Chronic progressive lymphoedema

A

Presumptive
§ Advanced imaging techniques have been used in studies but not feasible
§ Biopsies not going to diagnose the problem due to depth of lymphatics from skin
§ May need diagnostics to rule out secondary/concurrent diseases

78
Q

Treatment of Chronic progressive lymphoedema

A

Manage secondary infections (bacterial and parasitic)

Keep feathers clipped

Bandaging (if carefully managed) may help

Prognosis fair if carefully managed, otherwise often a significant welfare issue

79
Q

Photosensitisation

A

Lesions caused by UV light exposure after skin is sensitised by photodynamic agent

Usually affecting white haired skin

80
Q

Four types of photosensitisation

A

Primary (type I): ingestion/absorbtion of photodynamic agent
§ Can be through skin contact with substance/plant

Hepatogenous (type II): liver cannot excrete phylloerythrin (from chlorophyll)

(Porphyria: abnormal pigment synthesis)

(Photosensitivity of unknown aetiology)

81
Q

Type I photosensitisation

A

Ingestion of St John’s wort the most common, also buckwheat, spring parsley

Some clovers cause contact photosensitivity and hepatic photosensitivity

82
Q

Type II photosensitisation

A

Any cause of liver disease – may not show any other clinical signs of hepatopathy

Cholestasis, mycotoxin ingestion, pyrrolizidine alkaloid toxicity (Ragwort)

83
Q

Commonly used medications for treating equine skin disease

A

Steroids (dexamethasone - injectable, or prednisolone - oral)

Topical steroids (hydrocortisone spray, betamethasone +fusidic acid gel)

Antihistamines (results often disappointing) (cetrizine, hydroxyzine, chlorpheniramine)

Shampoos and washes (keratolytics, antibacterial/fungal, moisturising)