Dermatology Flashcards
Are pustules, vesicles, papules, wheals/hives, erythema and nodules primary or secondary lesions?
Primary
Are scales, crusts, excoriations, fistulae, ulcers, necrosis, hyper or hypopigmentaion, lichenification, hyperhidrosis and scars primary or secondary lesions?
Secondary
Lentigo describes macular patches of non-inflammatory hyperpigmentation. At which sites are these most commonly seen?
Mucocutaneous junctions
Define lentigo, leukoderma, vitiligo and leukotrichia
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.
Which hairs are unaffected by hirsuitism?
Mane, tail and feathers are not affected
What is anogen or telogen defluxion and how are they differentiated?
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.
What is primary seborrhea and what is the treatment?
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.
What is the typical age of onset and location on the body of linear keratosis?
Age 1-5 yrs
Location neck, forelimb and lateral thorax typically.
What is the genetic defect in HERDA and what is the clinical outcome?
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.
In addition to skin lesions, what other abnormalities are associated with HERDA
Abnormalities of the cornea, heart valves, tendons, ligaments, bones and great vessels may be seen.
What is the genetic defect in Warmblood Fragile Foal Syndrome and the clinical outcome?
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.
What is the clinical manifestation of Junctional epidermolysis Bullosa, what are the 2 types and which breeds are affected?
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.
What topical/environmental factors contribute to development of dermatophilosis and what are the microscopic features?
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).
What is pigeon fever and what are the clinical features and most effective treatment options?
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.
What is botryomycosis, what are the common organisms and clinical presentation/treatment options?
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.
What is the Splendore Hoeppli phenomenon?
In-vivo formation of intensely eosinophilic material around microorganisms or biologically inert material that is thought to protect the organism from antibiotics and phagocytosis.
Which virus is associated with warts and aural plaques?
Equus caballus papillomavirus
What is vesicular stomatitis and what are the typical clinical findings?
- 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.
What are the clinical features of Horse Pox?
- 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.
List the common organisms involved in Dermatophytosis and the clinical findings of the disease.
- 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.
Why is Woods lamp examination not useful in cases of equine Ringworm/Dermatophytosis?
Commonly implicated species don’t tend to fluoresce.
What is the causative organism in Piedra and what is the appearance?
Fungal species: Piedraia sp or Trichosporon beigelii.
Nodules on the hair shaft resulting in breakage of the hairs at the site of infection.
What is Sporotrichosis?
*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.
What is mycetomata and what are the characteristic features?
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.
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.
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.
What are common pathogens/aetiologies in pastern dermatitis?
Dermatophilus congolensi
Staphylococcus aureus
Photosensitivity
Chorioptic mange
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.
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.
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)
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.
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.
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.
What is the causative agent of Warbles?
Hypoderma bovis and Hypoderma lineatum
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.
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)
What are the signs of arsenic toxicity?
Long hair coat, thinning of the mane and tail, severe dry seborrhea with weight loss.
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.
What is the cause of urticaria?
Mast cell degranulation and release of active compounds including histamine, platelet activating factor and prostaglandins.
