Dermatology Flashcards
1
Q
Are pustules, vesicles, papules, wheals/hives, erythema and nodules primary or secondary lesions?
A
Primary
2
Q
Are scales, crusts, excoriations, fistulae, ulcers, necrosis, hyper or hypopigmentaion, lichenification, hyperhidrosis and scars primary or secondary lesions?
A
Secondary
3
Q
Lentigo describes macular patches of non-inflammatory hyperpigmentation. At which sites are these most commonly seen?
A
Mucocutaneous junctions
4
Q
Define lentigo, leukoderma, vitiligo and leukotrichia
A
Lentigo: macular patches of non-inflammatory hyperpigmentation.
Leukoderma: Depigmentation of areas of previous trauma or inflammation. Non-painful and no Tx required.
Vitiligo: Idiopathic acquired depigmentation with no known cause of trauma/inflammation. Can occur in any horse but Arabians over-represented, and more common in pregnant or post-partum mares. May regress spontaneously.
Leukotrichia: Acquired loss of pigment in hairs usually due to previous trauma or inflammation, including previous injections of dexamethasone or lignocaine. Reticulated leukotrichia may be inherited in QH, TB and SB. A painful form exists with painful crusts that may last months.
5
Q
Which hairs are unaffected by hirsuitism?
A
Mane, tail and feathers are not affected
6
Q
What is anogen or telogen defluxion and how are they differentiated?
A
Anogen defluxion: A disease or drug (eg high fever, systemic illness, malnutrition) interferes with anogen hair growth resulting in abnormalities of the hair or hair shaft and hair loss within days. On microscopy the hairs are dysplastic with a weak or narrow shaft and root ends that have no root sheath.
Telogen defluxion: If a stressful situation has halted anogen hair growth so you have sudden synchrony of many hairs in telogen phase, then 2-3 mo later a sudden shedding and wave of new growth. On microscopy these are uniform hairs with no shaft abnormalities and a non-pigmented root end lacking a root sheath. Differentiation is only with microscopy.
7
Q
What is primary seborrhea and what is the treatment?
A
Seborrhea is excessive scaling and crusting with or without greasiness. In cases of primary seborrhea there is increased skin turnover time and basal cell proliferation. On histo you see a significant orthokeratotic hyperkeratosis and the superficial dermis shows only a non-cornified epidermis, suggesting a keratinisation defect.
Tx: involves shampooing, initially daily for 1-2weeks then twice weekly for life. Dry seborrhea typically responds to sulphur based shampoos, the oily form may respond to degreasing agents such as tar-based products.
8
Q
What is the typical age of onset and location on the body of linear keratosis?
A
Age 1-5 yrs
Location neck, forelimb and lateral thorax typically.
9
Q
What is the genetic defect in HERDA and what is the clinical outcome?
A
Autosomal recessive missense mutation of the cyclophilin B gene which is important in the formation of collagen’s triple helicle molecule.
Affected horses are usually normal at birth but within a couple of days develop loose, hyperextensible skin and wounds that result in disfiguiring scars. It has been proposed that an influence of sunlight may be the reason why lesions are typically dorsally distributed.
10
Q
In addition to skin lesions, what other abnormalities are associated with HERDA
A
Abnormalities of the cornea, heart valves, tendons, ligaments, bones and great vessels may be seen.
11
Q
What is the genetic defect in Warmblood Fragile Foal Syndrome and the clinical outcome?
A
Autosomal recessive point mutation in equine pro-collagen-lysine 2-oxoglutarate 5-dioxygenase gene. The result is thin, fragile skin characterised by tearing and ulceration from minor trauma. Joint laxity may be severe.
12
Q
What is the clinical manifestation of Junctional epidermolysis Bullosa, what are the 2 types and which breeds are affected?
A
Results in blisters, erosions and ulceration of the skin and mucous membranes that quickly enlarge to include patchy skin loss over the whole body. Some foals may slough their hooves. The secondary sepsis is generally fatal. Type 1 affects French and Belgian drafts. Type 2 is similar and affects American Saddlebreds.
13
Q
What topical/environmental factors contribute to development of dermatophilosis and what are the microscopic features?
A
Requires moisture and damage to the skin for the release of the infective, motile flagellated zoospores of Dermatophilus congolensi (can remain viable in crusts for up to 42 mo). Poor nutrition may also be a predisposing factor but not always.
Diagonsis is based on mince preparations of crusts (in 1-2drops of saline) showing rail-road track appearance (fine-branching multiseptate hyphae with transverse and longitudinally arranged cocci).
14
Q
What is pigeon fever and what are the clinical features and most effective treatment options?
A
Deep abscessation (often of the pectorals but also ventral abdomen) secondary to Corynebacterium pseudotuberculosis (gram +ve facultative intracellular pleomorphic bacteria) infection. Clinical features are slowly developing abscesses that drain a thick creamy-green purulent discharge with lymphangitis and corded lymphatics that may form fluctuant nodules that abscessate and drain. May show gait stiffness and lameness. Tx: Once abscesses mature lance and drain them, and treat with systemic Abx (ideally doxycycline, fluoroquinolones or TMPS) for at least 30 days after complete clinical resolution.
15
Q
What is botryomycosis, what are the common organisms and clinical presentation/treatment options?
A
Granulomatous disease or pseudomycetoma most commonly associated with Staph aureus but also can be Pseudomonas, Proteus, E. coli and other non-inflammatory aerobic and anaerobic bacteria. Often secondary to a wound. A granulomatous infection results as the horse is able to contain but not clear the infection. May see tissue grains. Tx is surgical excision and long-term Abx treatment.
16
Q
What is the Splendore Hoeppli phenomenon?
A
In-vivo formation of intensely eosinophilic material around microorganisms or biologically inert material that is thought to protect the organism from antibiotics and phagocytosis.
17
Q
Which virus is associated with warts and aural plaques?
A
Equus caballus papillomavirus
18
Q
What is vesicular stomatitis and what are the typical clinical findings?
A
- Reportable
- Flu-like illness with excessive salivation may be the first sign
- Incubation period is 24-72hrs
- Oral vesicles up to 2cm that rupture leaving large painful erosions and ulcers
- Rarely lesions develop on the hooves, prepuce and teats, and may see crusting lesions on the muzzle, lips or ventral abdomen.
- Seasonal occurrence in summer and autumn, and possibly transmitted by biting insects although direct contact may also occur.
- Diagnosis based on antibodies to fluid samples from the animal or by viral isolation from swabs of lesions, blister fluid and tissue flaps. Confirmation with serology.
- Recovery generally occurs in 2 weeks.
19
Q
What are the clinical features of Horse Pox?
A
- Fever and anorexia
- Zoonotic
- Erythematous maculopapular eruptions and vesicles that develop into umbilicated pustules with a depressed centre and a raised erythematous border.
- Pustules rupture and a crust develops and the lesion heals, often with scarring.
- The oral version is characterised by lesions on the inner lips/buccal mucosa, and in severe case in the pharynx/larynx.
- Leg pox usually develops on the pastern and may be confused with greasy heal
- Diagnosis is via histo showing intracytoplasmic inclusion bodies and ballooning degeneration of the epidermis, intrapeidermal microvesicles, reticular degeneration, acantholysis, superficial and deep perivascular dermatitis and intra-epidermal microabscesses and pustules.
- Tx is symptomatic, recover in 2-4wk
- Occasionally fatal in yong horses, but lifelong immunity in those that survive.
20
Q
List the common organisms involved in Dermatophytosis and the clinical findings of the disease.
A
- Trychophyton equinum, Trychophyton mentagrophytes, Microsporum gypseum and Microsporum canis.
- Self limiting w/in 1-6mo or Tx with anti-fungals washes or accelerated hydrogen peroxide shampoo and application of 0.2% enilconazole as a leave in rinse.
- Immunocompromise, overcrowding, stress, increased moisture from sweating or excessive bathing with detergent shampoos may predispose.
- Incubation period is several weeks
- Fungi invade the hair follices and hair shaft, releasing allergenic enzymes resulting in hair shaft compromise and alopecia.
- Pruritus can be severe
- Diagnosis is based on direct examination of the hair shaft for microconidia and hyphae, as well as skin biopsy, PCR and fungal culture.
21
Q
Why is Woods lamp examination not useful in cases of equine Ringworm/Dermatophytosis?
A
Commonly implicated species don’t tend to fluoresce.
22
Q
What is the causative organism in Piedra and what is the appearance?
A
Fungal species: Piedraia sp or Trichosporon beigelii.
Nodules on the hair shaft resulting in breakage of the hairs at the site of infection.
23
Q
What is Sporotrichosis?
A
*Zoonotic mycosis
- Caused by Sporothrix schenckii
- Early lesions are papules that may exude a seropurulent material.
- Nodules are most common along the thigh or proximal foreleg and chest
- Subcutaneous nodules develop along the lymphatics, draining the affected area, resulting in cording and drainage of thick, brown exudate. In rare case it may become systemic
- Diagnosis is based on cytology or skin biopsy (cigar shaped yeast in macrophages and neutrophils on Giemsa stain)
Tx. Ethylene diamine dihydroiodide in feed 1-2mg/kgPO BID for 7-10d then 0.5-1mg/kg BID for 1mo past resolution of clinical signs. Sodium iodide has also been successful but can cause abortion in pregnant mares.
24
Q
What is mycetomata and what are the characteristic features?
A
Chronic fungal pyogranulomatous infection of the skin and sub-cut. Actinomycetes or other fungi implicated.
Lesions are characterised by tissue granules/grains being exudated from nodules that may be pigmented and are often ulcerated, associated with swellings and drainage tracts.
Complete surgical excision should be curative; additional topical treatment is indicated if complete excision is not possible.
25
What is Phaeohyphomycosis and how might this be differentiated from mycetomata?
Chronic, subcutaneous mucosa and occasionally systemic infection caused by pigmented opportunistic fungi that results in nodules of variable size that are typically cool, non-painful and non-pruritic.
Distinguished clinically from mycetomata by an absence of tissue grains. Tx is surgical excision and fluconazole +/- potassium iodide.
26
What is pythiosis and what makes this a dermatologic emergency?
- A fungal dermatoses caused by the aquatic fungus Pythiom insidiosum - infective zoospores gain entrance after prolonged exposure to contaminated water.
- Distal limbs most commonly affected as well as ventrum, chest, periocular and nasal areas.
- Early lesions are single or multiple minute areas of necrosis that progress rapidly to circular, ulcerative granulation-tissue like masses with serosanguinous discharge.
- Intensely pruritic (hallmark of the disease)
- Lameness, regional lymph node involvement, anaemia and hypoproteinaemia develop.
- If untreated it becomes systemic and horses die within 6mo
- Self trauma often results in haemorrhage from the lesions as well as a thick serusanguinous discharge that may resemble leeches.
- Tracts within the lesion will contain kunkers (another hallmark) which are gritty and white-yellow masses that can be expressed with pressure. The kunkers can be seen to branch (distinguishes them from granules in other fungal disease)
- Dx is by kunker examination (fungal hyphae, host exudate and protein) as well as serology, culture and biopsy.
- Tx: radical excision, 3+ doses of pythium immunotherapy and topical application of antifungal solutions. IVRP with 50mg amphotericin B or oral/IV iodides.
27
What are common pathogens/aetiologies in pastern dermatitis?
Dermatophilus congolensi
Staphylococcus aureus
Photosensitivity
Chorioptic mange
28
What are the clinical signs and treatment options with pastern dermatitis
- Chronic dermatitis and hair loss
- Lameness may be present
- Treatment is gentle cleaning with chlorhex (must dry thoroughly afterwards), topical application of antibiotics and systemic antibiotics in severe case. IVRP may be beneficial. Anti-inflammatories, including steroids in some cases may be warranted.
- Diagnosis may require biopsy with culture and sensitivity. Silver stain can be useful to rule out spirochetes.
29
Which are the two common types of lice in horses and what is their distribution?
```
Biting lice (Damalina sp, also known as Weneckiella equi, Bovicola equi) most prevalent on the dorsal trunk
Sucking lice (Haematopinus asini) found in the mane and tail and fetlock regions.
```
30
List common mites that affect horses
```
Sarcoptes scabei (head mange)
Chorioptes equi (leg mange)
Psoroptes equi (body mange)
Pyemotes tritici (straw itch mite)
Trombicula and Eutrombicula (chiggers)
```
31
What is the common disease progression with mite infestation?
S. scabei: early in disease they are predominantly around the head and neck (preference for ears) but spread to the whole body with time.
Pruritus, scaling, crusting, excoriations and lichenification are common. They are difficult to find on scrapings but usually respond to ivermectin 200ug/kg PO every 2 weeks for 3 treatments.
Chorioptes: host specific and more common in winter. Feed on epidermal debris on distal limbs and perineum. Lesions include papules, alopecia, erythema, scabs, crusting. May contribute to lymphoedema. Tx is topical eprinomectin solution as well as frontline.
Psoroptes are highly contagious and can infest the ear canal causing otitis externa.
Trombiculiasis is caused by an infestation of free-living mites that cause papules or wheals with a small red or orange dot centrally (the mite). Its a self limiting disease.
Pyometes are only occasional mites of horses, most often when hay is stored overhead. They produce a maculopapular crusted eruption on the head, neck and trunk that is only occasionally pruritic.
Dermanyssus gallinae are poultry mites that occasionaly parasitise horses - they feed at night and turn from grey to red in doing so. They cause pruritic papules and crusts of the head and legs. Skin scrapings and tape tests must be done at night.
Demodex mites are normal commensals so infection suggest immunocompromise.
32
What are the common features of onchocerca infection?
Adult nematode is in the nuchal ligament, and anti-parasiticides don't treat it here.
- Disease is caused by the microfilariae as they migrate
- Can cause dermatitis (initially dermatitis that progresses to scales, crusts, plaques and may become ulceration, oozing and lichenified).
- May be associated with ERU, sclerosing keratitis, vitilego of the bulbar conjunctiva and conjunctival nodules.
- May develop oedema and itching, +/- uveitis and umbilical oedema 1-10 days after treatment with ivermectin associated with antigen response to microfilarial death.
- Diagnosis is based on mince preparations in which you see the rapid motion of the microfilariae.
33
What is the lifecycle of Habronema and what is the clinical manifestation of cutaneous habronemiasis?
Adults live in the stomach, larvae passed in faeces; flies are the intermediate host and deposit larvae near the horse's mouth where they are swallowed to complete the life cycle. If deposited on skin or open wounds, cutaneous habronemiasis occurs.
- Ulcerative skin lesions with pruritus and sulphur granules in some cases.
- DDX are bacterial granuloma, fungal granulima, pythiosis, exuberant granulation tissue, eosinophilic keratitis, SCC and sarcoid
- Biopsy is diagnostic
- Nematode larvae are large with a spiny tail and usually amotile.
Tx: oral ivermectin to kill adults and disrupt the cycle; surgical excision of skin lesions may help as well as topical treatment and wound management. Protect the wound from flies.
If conjunctival, topical echothiophate drops TID may be useful.
34
What is the causative agent of Warbles?
Hypoderma bovis and Hypoderma lineatum
35
What are the cutaneous and non-cutaneous signs of iodine toxicity?
Cutaneous: dry seborrhea of the mane and tail and in some cases the hair coat.
Non-cutaneous: Cough, excessive lacrimation, salivation, nasal discharge and joint pain.
36
What are the common signs of selenium toxicity and what is the pathogenesis?
Se substitutes for sulphur in sulphur containing amino acids and alters keratinisation of the hoof and hair.
Hair coat becomes rough and there is dramatic loss of mane and tail hairs with generalised alopecia.
Lameness occurs due to cracks and separation of the coronary band (may slough in some horses)
37
What are the signs of arsenic toxicity?
Long hair coat, thinning of the mane and tail, severe dry seborrhea with weight loss.
38
What are the cutaneous and systemic signs of mercury toxicity?
Cutaneous: generalised alopecia and subsequent loss of mane and tail.
Systemic: GIT disorders, depression, anorexia and weight loss in addition to the above cutaneous signs.
39
What is the cause of urticaria?
Mast cell degranulation and release of active compounds including histamine, platelet activating factor and prostaglandins.
40
List different types of urticaria/wheals and the types of conditions they are more often associated with
- Papular wheals: biting insects
- Giant wheals: polycyclic urticaria (often drug reactions)
- Annular wheals (non-specific)
- Angioedema (much rarer manifestation of allergy)
41
What is the typical age of onset of insect bite hypersensitivity?
3-4yrs and progresses with age
42
True or false: There are both heritable and immunotolerance components to IBH?
True
43
What is the pathogenesis of atopic dermatitis?
Abnormalities of the skin barrier may predispose absorption of allergenic proteins which are then carried to the lymph nodes inducing IgE production. Allergen specific IgE binds to mast cells, basophils and langerhans cells and other cells within the skin and mucous membranes and further allergens are captured. Subsequent exposure results in amplification.
44
What features may make you suspicious of food hypersensitivity?
Pruritus limited to the base of the tail and anus, as well as non-seasonal urticaria. Can see concurrent skin lesions (flaking, lichenification etc)
Transdermal exposure can also trigger so house away from other horses' feed.
45
What type of reaction is a contact allergy?
Type IV hypersensitivity
46
What is the treatment approach to allergic skin disease?
- Eliminate allergen exposure
- Steroids may be necessary, at least initially
- Cetirizine and hydroxyzine hydrochloride may be useful as antihistamines (orally is preferred due to adverse reactions with IV administration)
- Pentoxifylline may be useful as an immunomodulator that is steroid sparing and has rheologic effects that may reduce the risk of laminitis with concurrent steroids
- ASIT to reduce the hypersensitivity reaction
- Fresh ground brown flax in feed may have an anti-inflammatory affect in the skin.
- Shampoos may improve comfort and rehydrate the skin and improve the epidermal barrier integrity
47
How is ASIT thought to work?
Mechanism unknown but thought to induce production of blocking antibodies by shifting the immune response to one dominated by IgE to one dominated by IgG. This alters the proportion of Type I and Type 2 T-helper cells and induces production of T-regulatory cells.
Approximately 60-85% of horses respond to this therapy but it can take from 1-24mo (average of 3-6mo) before effects are noted. In best case scenario it may result in remission of the allergy. Steroids, antihistamines and fatty acids may be used concurrently with no adverse effect.
48
What is the defect/abnormality associated with Pemphigus foliaceous?
Autoantibodies against desmolgein 1 and desmoglein 3 destroy the bonds that maintain cell-cell adhesion. The cells separate from one another leaving a space that fills with fluid, resulting in a blister or pustule close to the skin surface. These are fragile and often rupture quickly after being formed, resulting in oozing, crusting, and erosions of the skin. Some horses may develop acute, chronic or recurrent hives before progressing to fulminant PF.
49
What are the clinical signs of pemphigus foliaceous?
- Typical blister like or erosive lesions, sometimes localised to the face or coronary bands
- Systemic signs such as severe pain, fever, anorexia and lethargy in severe cases
- May have matted coat.
50
How is pemphigus foliaceous diagnosed?
- Biopsy of a blister and intact crust to the underlying skin surface - intragranular to subcorneal acantholysis, sometimes with a predominance of eosinophils in the inflammatory infiltrate.
- Impression smears of the contents of intact pustules or the underside of exudative crusts may help - may show rafts of deeply basophilic acantholytic cells and non-degenerate neutrophils
51
What is the treatment and prognosis for pemphigus folicaeous?
Tx: High doses of steroids: prednisolone 1-2.5mg/kg PO q12h until no new lesions develop (often 7-10d) then tapered over several weeks to a maintenance dose of 0.5-1mg/kg EOD indefinitely.
Chrysotherapy (gold salts) have been used with success
Aurothiomalate can be used weekly if no adverse effects (eosinophilic and cutaneous reactions).
Azathioprine may be used as a steroid sparing drug.
Prognosis: Spontaneous regression has occured in some cases of young horses but most require lifelong treatment. Approx 50% of those that initially respond to treatment relapse and become progressive less responsive to treatment with each relapse.
52
What is pemphigus vulgaris and what is the defect/abnormality associated with this condition?
Autoantibodies against desmoglein 3 has been associated with an immune reaction at the basement membrane.
Horses show vesicles, bullae and painful ulcers in the mouth and other mucocutaneous junctions. Lesions can also occur in the mane, tail and coronary bands.
53
What is bullous pemphigoid?
Autoimmune disease that occurs when antibody binds to the basement membrane zone and complement fixation occurs, resulting in production of anti-inflammatory mediators chemotactic for neutrophils and oesinophils which release proteolytic enzymes that disrupt the dermal-epidermal cohesion, resulting in subepidermal cleft and vesicle formation.
54
What is the typical lesion distribution with bullous pemphigoid? What is required for diagnosis
Crusts and ulcers are common with lesions extending throughout the gastrointestinal tract and in the axilla and groin region of the skin.
Diagnosis requires biopsy of an intact vesicle or bullae. Biopsy of a crusted or ulcerative lesion will be non-diagnostic. Acantholysis is not a feature.
55
What is the treatment for bullous pemphigoid and associated prognosis?
Treatment is as for pemphigus folicaceous: high dose corticosteroids, aurothiamolate if adverse effects don't develop, azathioprine etc. However the prognosis is generally poor/treatment is less successful.
56
What are the clinical features of systemic lupus erythematosus and what is the treatment efficacy?
A multisystemic autoimmune disease involving weight loss, bilaterally symmetric alopecia, seborrhea, orl ulceration, lympadenopathy, glomerulonephritis and fibrinous synovium. Concurrent IMHA may occur.
Diagnosis is based on biopsies showing interface dermatitis with linear deposition of IgG at the basement membrane zones of the epidermis and hair follicle. Treatment is high dose corticosteroids but the prognosis is poor.
57
What are the clinical features and diagnostic features of discoid lupus erythematosus?
Patchy erythema, crusting, alopecia and scaling on the face, ears and neck, or in some cases limited to the coronary bands and chestnuts/ergots.
Pain and lameness may feature and leukoderma or leukotrichia may feature.
Biopsy is required for diagnosis and shows interface dermatitis with focal hydropic degeneration of basal epidermal cells, pigmentary incontinence and focal thickening of the basement membrane. May be aggravated by sunlight.
Sunscreen and topical steroids may help, and systemic corticosteroids may be useful.
58
What are common features, predisposing conditions and systemic signs associated with immune mediated vasculitis?
Common features: Purpura, oedema and erythema of the skin; urticaria followed by pitting oedema of the distal limbs, head and ventral abdomen; tissue exudation and sloughing in severe cases.
Predisposing conditions: Often unknown, but common ones include EVA, EI, Strangles and C. pseudotuberculosis.
Systemic signs: Fever, depression, anorexia, weight loss, lameness.
59
Why are topical antibiotics often more effective than systemic with decubital ulcers?
Poor circulation and venous and capillary congestion often prevent therapeutic doses of antibiotics reaching the site, hence topical application is often more effective.
60
What are the different classifications of burns and which skin layers are involved in each?
First degree: most superficial layers of the epidermis but the germinal layer is spared so repair is rapid.
Second degree: can be superficial or deep; superficial involve the stratum corneum, stratum granulosum and a few cells of the basal layer; deep involves all layers of the epidermis. The only germinal spares are those within the ducts of sweat glands and hair follicles
Third degree: loss of epidermal and dermal layers so healing is by contraction and epitheliaslisation occurs from the wound margins.
Fourth degree: all skin and underlying muscle, bone and ligaments.
61
What is the pathophysiology behind tissue damage secondary to burns?
The local tissue damage results from protein coagulation and cellular death. Adjacent the burns arteries and venules constrict and capillary beds dilate. Capillary wall permeability increases in response to vasoactive amines. These vascular responses result in fluid, protein and inflammatory cells accumulating in the wound. Vascular sludging, thrombosis and dermal ischaemia occur, resulting in further tissue damage. Tissue ischaemia continues for 24-48hrs after injury, thought to be due to local release of thromboxane A2. A 4-fold loss in fluid occurs due to destruction of lipid layers in the skin. Neutrophil function and chemotaxis greatly decreases predisposing to infection.
62
What are the systemic effects of burn injuries?
Hypovolaemia, fluid and electrolyte derangement, pulmonary oedema, anaemia, increased basal metabolic rate, increased caloric needs and depressed cell-mediated and humoral immune responses.
63
What are the treatment approaches to burns?
- Cold therapy to stop tissue necrosis in the acute phase of superficial burns
- Full thickness burns can be managed with occlusive dressings, exposure techniques to encourage eschar production, continuous wet dressings (semiopen dressing - most practical for large burns in equids) and excision and grafting.
Systemic antibiotics are contraindicated in the absence of systemic infection. Topical treatment should include broad spectrum non-irritating water based creams such as silver sulphadiazine. Aloe vera may help by relieving pain, decreasing inflammation, stimulating cell growth and killing bacteria and fungi.
64
What is the mechanism behind frost bite / cold injury? And what are the areas most commonly affected?
Cold temperature inhibit cell metabolism and cause tissue dehydration, cell disruption by ice crystals, ischaemia and vascular damage.
Common sites are ear tips, glans penis, coronary bands and heels.
65
What are the four types of photosensitisation and the typical features of each?
Type 1: Primary photosensitisation occurs with plants such as Alsike clover. It's important to assess liver function in these horses as some clovers cause both primary and secondary. Lesions are often on the distal limbs and muzzle with contact/primary.
Type 2: Hepatogenous photosensitisation - as the liver becomes compromised it cannot excrete phylloerythrin, a photodynamic agent, so it accumulates. Can be secondary to primary liver disease and cholestasis or secondary to ingestion of toxic plants and mycotoxins.
Type 3: Photosensitisation from aberrant pigment synthesis (porphyria)
Type 4: Idiopathic
66
List differentials for photosensitisation.
- Sunburn
- Contact dermatitis
- Dermatophilosis
- Photoactivated vasculitis
- Pemphigus foliaceous
- Bacterial/Fungal infection.
67
What are the clinical features, predisposing factor, histologic findings and treatment of leucocytoclastic vasculitis?
Clinical features: Erythema and exudation, commonly of the lower limbs in mature horses (often non-pigmented skin), progresses to crusting and open sores or ulcerated areas. More painful than pruritic.
Predisposing factors: Photoaggravated so exposure to sunlight often features, as well as being associated with drug reactions and infection with Staphylococcal species.
Histologic findings: Leucocytoclastic skin lesions with perivascular inflammation, blood vessel degeneration and clots.
Treatment: Reduce exposure to sunlight/UV light. Bandaging, resolve infection if this is underlying, steroids may be useful.
68
What are sarcoids?
Cutaneous accumulations of transformed fibroblasts which are locally invasive, non-metastastic and rarely regress spontaneously.
69
Which virus have sarcoids been causally associated with?
Bovine papilloma virus type 1 and 2; potentially also type BR-UEL-4. Viral burden has been associated with sarcoid severity
70
What is the common distribution of occult sarcoids and what is a feature of this type with regard to progression?
Common around the mouth, eyes, neck and other relatively hairless areas. Have a tendency to sit dormant for long periods and then undergo spontaneous enlargement or conversion to a more aggressive type.
71
What is the common distribution for verrucous sarcoids and what is a feature of this type with regard to malignancy?
Predilection for the face, body, groin and sheath areas. This type can undergo malignant transformation.
72
What are the types, predilection sites and characteristics of nodular sarcoids?
Type A1: mass has no cutaneous involvement, located subcutaneously and are easily moveable.
Type A2: mass also has no cutaneous involvement but are locally invasive with a "bound down" character. These types are very common around the eye.
Type B: the skin overlying cannot be moved over the nodule and is frequently abnormally thin, hyperkeratotic or ulcerated. They tend to be more aggressive than Type A.
B1: lack deep tissue invasion
B2: are attached to deeper and surrounding structures.
Predilection sites for nodular sarcoids are groin, sheath or eyelid and they can quickly progress to more aggressive forms, particularly when traumatised.
73
What are the characteristic features and different types of fibroblastic sarcoids?
Well circumstribed fibrous nodules in the dermis covered by intact epidermis or an ulcerated surface that haemorrhages easily (most are the latter). Often aggressive and spread locally. They often resemble granulation tissue.
Type 1: pedunculated with or without a discernable root.
Type 2: Have a broad base (sessile) and frequently extend beneath the visible lesion a fair distance.
74
What does a mixed sarcoid usually represent?
Often represents progression of an occult or verrucous sarcoid to a more aggressive form
75
What is the progression of malignant sarcoids typically?
Track along or invade lymphatics or other vessels and invade underlying structures.
76
What are important things to consider with surgical intervention?
- Wide margin in an attempt to resect all affected tissue
- Have a backup plan in case biopsy exacerbates the lesion or you don't get it all (intralesional chemotherapeutics are a good option)
- Change surgical instruments between excision and closure to reduce seeding of virus to deeper tissue
- Re-growth is considered possible or even likely until the lesion has healed completely and is covered by normal epithelium without a sign of the tumour.
77
What are the histological features of sarcoids and what can they appear similar to histologically?
Fibroblastic proliferations of cells that form whorls or interlacing bundles often oriented perpendicular to the basement membrane. The epidermis when present is hyperplastic with characteristic elongated rete ridges.
Can be difficult to differentiate from Schwannomas.
78
What is the recurrence rate with sarcoids?
varies from 15-82%
79
Why is the recurrence rate less with laser excision?
Laser energy is absorbed by surrounding tissues hence tumour killing extends approximately 0.2mm beyond the wound margin.
80
List treatment options for sarcoids and their proposed MOA where appropriate.
- Cryotherapy: debulking first is advisable
- Intra-tumoural hyperthermia: heating to 38-45C boosts deliver of O2 to the lesion and improves the distribution of chemo agents if used in conjunction
- Intralesional platinum drugs (cisplatin, carboplatin): reported resolution rate of 96% in one study. Injected at 1mg cisplatin/cm3 in a hashed approach(debulk first if large tumour); repeat monthly as req. Beads release over 30days and should be placed at 1.5cm intervals.
- Electrochemotherapy: creates pores in the cell membrane enhancing uptake of cisplatin and increasing toxicity. GA required. Repeated 4weekly for 1-5tx.
- Mitomycin C: DNA crosslinking agent similar to cisplatin injected at 0.5-1mL/cm3 q8h until resolution.
- 5 fluorouracil and thioracil may be successful after 3-5tx. Results in preferential sloughing and necrosis of the sarcoid tissue.
- Bacillus calmette guerin: attenuated strain of mycobacterium bovis can be injected - thought to stimulate lymphocytes and increase natural killer cells. Success rates range from 83-100% for periocular sarcoids but much lower elsewhere on the body. Can result in anaphylaxis so pre-treatment with flunixin or corticosteroids is recommended
- Seeds of radon-222 or gold-198 and removable needles of radium-226, cobalt-60 or iridium-192 have been used and should be considered in recurrent or aggressive/surgically inaccessible sarcoids.
81
What are the commonly reported sites of cutaneous squamous cell carcinoma and which breed is predisposed?
- Periocular
- Conjunctiva
- Ocular adnexa
- External genitalia
Halflingers at increased risk of third eyelid SCC despite pigmented skin.
Draft breeds also seem to have increased incidence thought to be genetic
82
What treatment is recommended for SCC?
```
Surgical excision or debulking
- Topical treatment if complete excision is not possible
Tx can include:
- Cryosurgery
- Cisplatin
- Mytomycin C
- 5-fluorouracil
- Radiation therapy
Similar treatments to sarcoids.
```
83
What is the pulsed approach to treatment with 5-fluorouracil and mitomycin C?
Mitomycin C: every 6 hours for 7 days, stop for 7 days. Repeat cycle until tumour resolution.
5-Fluorouracil: treat for 3-4 days then stop until the following month, repeat monthly until resolution.
If application is to the penis apply every 2 weeks as the drug is retained in the prepuce for 10-14 days.
84
Why has piroxicam been advocated as an adjunctive treatment of skin tumours?
It is proposed to induce apoptosis and angiogenesis and stimulate the immune system through inhibition of PGE2 production in epithelial tumours
85
What is the proposed aetiology of development of melanoma?
Thought to be secondary to genetic mutation in the melanin metabolism molecular pathway.
86
What are the characteristics of benign melanocytic nevi?
Originating in the superficial dermis or at the dermo-epidermal junction. Involvement of the epithelium is common.
87
What are the histologic features of melanoma?
Nests of large pleomorphic epithelial cells which contain variable amounts of pigment mixed with melanophages. Mitotic cells, binucleate cells and euchromatic nuclei are occasionally seen.
88
What are the histologic features of malignant melanoma?
Pleomorphic epithelioid cells with vascular, lymphoid and or dermal invasion, variable pigmentation and a moderate to high number of mitotic figures.
89
What is the MOA of the oncept vaccine?
It contains the human DNA sequence the encodes tyrosinase which is usually found within melanocyte and is crucial to the melanocytes ability to produce melanin and survive. The idea is that the vaccine will result in destruction of the tyrosinase in the cancerous melanoma cells and ultimately the inability of the tumour to survive.
90
Mast cells tumours are benign cutaneous nodules seen mostly on the head and sometimes as diffuse swellings distal to the carpus/tarsus. Which breed is predisposed?
Arabians
91
Which breeds are predispoed to cutaneous lymphoma and what are the 2 types?
QH, TB, SB affected most frequently.
T-cell lymphoma is an epitheliotropic scaling disease widely disseminated throughout the skin. Carries a poor prognosis. Tx with prednisolone, PEG1-asparaginase once weekly and low dose cyclophsophamide or immunisation with autologous tumour cell vaccine may be useful.
T-cell rich B-cell lymphoma (non-epitheliotropic lymphoma) is a nodular disease. Carries a better prognosis. Can have one or many nodules. Steroids and intralesional cisplatin have been useful in some cases.
92
Pseudolymphoma presents as nodular to papular skin lesions secondary to chronic antigenic stimulation, often on the head and trunk. The lesions are firm, raised and haired. Differentiation from lymphoma is important as the prognosis is good with pseudolymphoma. How are they differentiated?
Histologically. Pseudolymphoma has lymphoid nodules and eosinophils as an important differentiation aid.
93
What is the typical signalment of horses with haemangioma?
Typically less than 1 year and possibly born with them
94
What are the typical clinical features of haemangioma?
Generally solitary tumours often on the distal limbs. Can be circumscribed, nodular, firm to fluctuant, blue-black in colour and can be dermal or subcutaneous, hyperkeratotic or verrucous.
95
What is an atheroma?
A cyst thought to develop from hair follicle retention in the false nostril that is present from birth and increases in size with time.
96
What are the typical features of panniculitis?
Inflammation of the subcutaneous fat.
- Deep seated nodules and plaques
- Singular or multiple and of varying size
- Can be hard and well defined or soft and ill-defined
- Initially lesions are not fixed to the overlying skin but with progression they become cystic and rupture onto the skin surface and drain a yellow-brown bloody oily material.
- May be febrile, depressed, anorexic.
Biopsy diagnostic.
Some respond to prednisolone others need lifelong treatment.
97
Multisystemic eosinophilic epitheliotropic disease is a rare disease characterised by nodules in numerous organs, ulcerative stomatitis, severe wasting, significant exfoliation and eosinophil infiltration of the skin. What are the characteristics of the skin lesions during the early phase and with progression?
Early lesions: scaling, crusting, exudation and fissuring at the coronary band. Oral ulcers are usually present at this stage.
With progression: generalised exfoliative dermatosis develops, may be pruritic.
98
What are the features of sarcoidosis and what are the different forms?
Localised form tends to be limited to the skin, most commonly in the lower limbs. Skin disease begins as scaling, crusting and alopecia on the face, limbs and/or trunk. May progress rapidly or slowly. May get peripheral lymphadenopathy.
Partially generalised and generalised form are characterised by extensive exfoliations, severe wasting and granulomatous inflammation in multiple organ systems.
Dx: biopsy of the skin shows a multifocal nodular to diffuse lymphogranulomatous dermatitis with multinucleate giant cells with or without vasculitis.
Tx: is high dose prednisolone or dex; pentoxyfilline and omega fatty acid supplementation.
Prognosis is good in the majority of horses but some will require lifelong low dose pred.
