EIM 15-18 Haem/Endo/Skin Flashcards
The most common cause of thrombocytopenia in hospitalized horses
increased utilization or destruction of platelets secondary to a primary infectious, inflammatory, or neoplastic disease process.
Thrombocytopenia is also common in strangulating/ischemic gastrointestinal disorders.
An association between thrombocytopenia and a poor prognosis has been demonstrated in
hospitalized horses in general and in horses with colon torsion.
Thrombocytopenia occurs in cases of EIA due to ?
combined effect of immune-mediated destruction and decreased platelet production
A foal presents with ulcerative dermatitis, thrombocytopenia and neutropenia. Based on the most likely suspected diagnosis, what treatment would be indicated?
DEXAMETHASONE
Neonatal Alloimmune Thrombocytopenia. Immune-mediated destruction of platelets following ingestion of preformed antiplatelet antibodies with the colostrum has been reported in horse and mule foals and is suspected to be more common in the latter.
responsive to corticosteroid administration, suggesting an immune-mediated component.
The most common clinical sign of Glanzmann’s thrombasthenia is
epistaxis
Glanzmann’s thrombasthenia
Prolonged or recurrent epistaxis appears to be the most common clinical sign whereas the presence of petechiae or ecchymosis is more variable.
Definitive diagnosis: demonstration of reduced CD41/61 expression on the platelet surface using flow cytometry.
Glanzmann’s thrombasthenia is a quantitative deficiency or a qualitative defect of the platelet fibrinogen receptor (also referred to as GP IIb/ IIIa, αIIbβ3 integrin, or CD41/61). It is an autosomal recessive disorder, and the genetic defect has been localized to the gene encoding GP IIb (also referred to as αIIb).
Breeds: QH, TB, SB, WB, Peruvian Paso
NOTE: distinct from ‘Atypical Equine Thrombasthenia’ = Reduced fibrinogen binding, only occurs in TBs, normal number of CD41/61 expression
Von Willebrand’s Disease
Is rare in horses, only congenital
Diagnosis achieved by measuring plasma von Willebrand antigen levels using an ELISA
Hemophilia A in horses
Reported in Thoroughbreds, Standardbreds, Quarter Horses and an Arabian
Typically factor VIII deficiency, but also can occur with factor IX and X and to a lesser degree factor VII and prothrombin (F 2) deficiencies.
Transmitted via an X-linked recessive trait, colts affected
Iron deficiency anemia
is characterized by low serum ferritin concentration, decreased stainable iron stores in the bone marrow, decreased plasma transferrin saturation, normal or increased total iron binding capacity (TIBC), hypochromic erythrocytes (decreased MCHC), and microcytosis (decreased MCV)
hemangiosarcoma
Present as a disseminated malignancy involving the spleen, heart, lung, liver, and soft tissues of the trunk and extremities
hemangioma
Typically benign, solitary, deep, dermal tumors
What are two well documented causes of IMHA in horses?
NI - primary IMHA
penicillin
EIA
Reverse transcriptase and integrase are utilised by the virus to generate and integrate viral DNA into the host cell genome
Replication occurs in monocytes, dendritic cells, tissue macrophages, and endothelial cells
Fever and thrombocytopenia considered to be the most reliable clinical indicators
One of the ELISA kits detects gp45
Time from infection to seroconversion may take up to 180 days
“ELISA is a sensitive gal”
Babesia caballi
Carrier: can be cleared
Invasion site: erythrocyte
Severity: milder
Incubation period following infection by tick: 10-30days
cELISA target: Apical merozoite protein rhoptry (RAP) 1
TX: Imidocarb, quarantine, or euthanasia
Theileria equi
Carrier: lifelong
Invasion site: leukocyte
Severity: severe; colic, resp, neuro signs also possible
Incubation period following infection by tick: 12-19 days
cELISA target: Equi merozoite antigens (EMA) 1 and 2
TX: Imidocarb, quarantine, or euthanasia
Red Maple Leaf toxicity
Wilted/dried leaves of silver and sugar maple also potentially toxic
Signs of haemolysis predominate before mid-September, whereas signs of methaemoglobinaemia predominate after mid-September
Oxidising agents include gallic acid, and pyrogallol (formed from the metabolism of gallic acid and gallotenins by Klebsiella pneumoniae and Enterobacter clocae in the ileum
Factors associated with mortality include lack of pyrexia on admission and corticosteroid administration
Immune Mediated Vasculitis
Deposition of complexes of antigen and immunoglobulins in the walls of the capillaries and other small blood vessels leads to a type III hypersensitivity reaction
Microscopically, lesions are characterised by a leukocytoclastic vasculitis
Secondary complications such as laminitis and thrombophlebitis are not uncommon
Anaplasmosis
Obligate intracellular bacterium infecting neutrophils
Transmitted by Ixodes ticks
Worldwide distribution
Incubation period of ~10 days
Signs vary from subclinical to high fever (100 – 106.9 F)
how can you diagnose IMHA
Coomb’s test
Presence of autoagglutination
Osmotic fragility testing of RBC’s
Reported causes of equine hypothyroidism are
Iodine deficiency
Iodine excess
Neoplasia
Hypothyroidism in adults is rare and usually non life threatening
In equine primary hypothyroidism, what will be increased/decreased?
Horses with primary hypothyroidism have decreased T4 and T3 concentrations and increased TSH concentrations
The major cause of neonatal hypothyroidism in foals is
nutritional, resulting in congenital goiter (thyroid enlargement at birth). Possibly due to Iodine deficiency in utero (inadequate intake by the dam) OR Iodine excess in utero (excessive intake by the dam)
CHD: congenital hypothyroidism and dysmaturity
First recognized 1970s
Prolonged gestation + signs of dysmaturity
-Musculoskeletal abnormalities (weakness, delayed ossification carpal and tarsal bones, OCD, prognathia)
-Thyroid enlargement rare (different to neonatal hypothyroidism)
–Still have thyroid gland hyperplasia on biopsy though
Etiology unknown
-Nitrates? Combo with low iodine forage
Typically disease of western Canada and north-western USA
Usually die a few days after birth, or suffer many complications
CS: Neonatal Hypothyroidism
Enlarged thyroid or normal thyroid size
Stillbirths, prematurity
Weakness, lethargy, depression, weak suckle
Long haircoat, rough hair coat, silky if premature/dysmature
Respiratory insufficiency and distress
Incoordination
Cold intolerance and hypothermia
Physeal dysgenesis, defective ossification
Carpal and tarsal bone collapse, hypoplastic carpal bones
Common digital extensor tendon rupture
Forelimb contracture
Prognathism, delayed incisor eruption
Growth retardation and death
Or born apparently normal but develop skeletal lesions weeks later
diseases that may have low TH levels but not truly hypothyroid
Nonthyroidal illness syndrome (e.g. septic / SIRS horses)
Obesity, laminitis, insulin resistance, EMS
Infertility, agalactia
Poor performance
Rhabdomyolysis
Dermatopathies, alopecia
Anhidrosis
TH therapy to euthyroid horses may be harmful, inhibiting the HPTA, and suppressing endogenous TH synthesis and secretion.
Thyroid Tumors
Thyroid adenoma -Age related phenomenon, > 16yo -Benign, usually unilateral -Not associated with thyroid dysfunction Thyroid adenocarcinoma -Malignant, euthyroid, hypothyroid, and hyperthyroid Thyroid medullary carcinoma -Parafollicular cell (C-cells) tumor Multiple endocrine neoplasia (MEN)
Adrenal insufficiency (AI) - reduced capacity of the adrenal gland to secrete adrenocortical steroids in sufficient amounts to meet physiologic needs, thus resulting in clinical and laboratory disturbances – typically occurs in acutely ill horses/foals. At which level of the HPAA does this usually occur in horses/foals?
Steroid deficiency of the adrenal cortex
inadequate production of cortisol in relation to an increased demand during periods of severe illness and stress, and it is characterized by high ACTH/cortisol ratios.
Pheochromcytoma
Tumors that arise from the chromaffin cells of the adrenal medulla
Rare in horses, most non-functional (thus undiagnosed)
In horses, these tumors have low incidence of malignancy, usually unilateral
Median age 17yo (13 – 38), poor prognosis
If functional – acute onset CS
Diagnosis - measurement of blood catecholamines / metabolites in urine
acute onset CS seen with functional phaeochromcytomas in horses
COLIC: abdominal pain from large hematomas/hemoperitoneum or gastrointestinal distention secondary to ileus Anxiety Tachycardia, tachypnea Profuse sweating Muscle tremors, ataxia Hyperthermia Dry and pale mucous membranes, increased capillary refill time Mydriasis Abortion has been documented.
Hematologic abnormalities of functional pheochromocytomas
A: hemoconcentration (due to splenic contraction)
B: stress leukogram
C: hyperglycemia
D: hyperlactatemia
E: Electrolyte changes - hyponatremia, hypochloremia, hyperkalemia, hypocalcemia, hypophosphatemia
pathogenesis of ppid: which of the three neuroendocrine dopaminergic tracts are most critical in regulating cell proliferation and hormone production and release in the pars intermedia?
Periventricular dopaminergic neurons
The periventricular neurons originate in the periventricular nucleus, adjacent to the third ventricle, and project through the infundibular stalk, terminating in the pars intermedia. In the pars intermedia, the periventricular neurons directly innervate melanotropes, where they release dopamine that interacts with dopaminergic D2-type receptors on melanotropes
proposed mechanisms of equine anhidrosis
Poor sweat gland response to β2-adrenergic stimulation
Deficiency in β2-adrenoceptor agonists
Inflammation
what is the most consistent early lab finding in horses with vitamin d intoxication?
hyper-phosphatemia
What drugs should you chose to lower calcium?
furosemide - inhibits the Na+/K+/2Cl− cotransporter in the distal nephron, increasing urinary excretion of calcium
glucocorticoids
Thiazide diuretics are contraindicated because they stimulate calcium reabsorption
what is the main cause of hypophosphatemia in critically ill patients?
Redistribution (intracellular shift of PO4)
What is the pathophysiologic mechanism behind muscle fasiculation/tetany of hypocalcemia?
fast Na+ channels open with small changes in membrane potential
extracellular Ca2+ binds to Na+ channels to reduce Na+ entry, increasing depolarization threshold (mechanism by which Ca2+ antagonizes the effects of hyperkalemia)
Which clotting factor is Ca2+
IV
Which clotting factor is Ca2+ a co-factor for?
II, VII, IX, X, XI, XII, XIII
2, 7, 9, 10, 11, 12, 13
How does oxalate affect dietary calcium absorption?
decreases it
What are the clinical signs associated with chronic dietary phosphorus excess?
A) Clinical signs of calcium deficiency - lameness, abnormal cartilage and bone development, fracture, osteodystrophis fibrosa (nutritional secondary hyperparathyroidism)
B) Weight loss, weakness, depraved appetite (pica), lameness, DOD
The target organ for PTH is
the kidney
promotes 1,25(OH)2D3 synthesis
Blood concentration of 1,25(OH)2D are regulated by
Increased by:
low PO4
low PTH
Decreased by: high PO4 high Ca high 1,25(OH)2D high FGF23
Calcitonin
Inhibits osteoclast function
Post-prandial increases in serum levels mediated by gastrin
Secreted in response to hypercalcemia
Secreted by parafollicular (C cells) of thyroid
Decreases plasma Ca2+ and PO4 concentrations
Important for protection against extreme hypercalcemia not really day-to-day
Most important – prevents bone resorption during lactation
The diagnosis of food allergy is most accurately made by
eliminating the causative feed from the diet of affected horses through a food elimination trial. A complete dietary history is essential, and all components of the diet (concentrate, forage, and supplements) should be considered.
A practical approach to a food elimination trial is to begin by eliminating any supplements and concentrates from the diet for 4 to 6 weeks. The offending substance is identified by reintroducing one dietary item at a time each week and observing the horse for recurrence of clinical signs, usually within 24 to 72 hours.
Note: Food allergy in horses can occur not just by ingestion, but also inhalation and contact.
True contact allergies in horses are what type of hypersensitivity reaction:
Type IV
Potential allergens are usually small molecules that penetrate the skin, bind to dermal collagen or carrier proteins, and are taken up by antigen-presenting cells (Langerhans cells) in the dermis.
On re-exposure, an inflammatory response occurs that results in skin disease.
Development of allergic contact reactions can takes months to years; a horse may suddenly develop clinical signs of a hypersensitivity reaction to a substance to which it has been exposed for years without prior incident.
ASIT
Theory of hyposensitization is to redirect the immune response to an allergen, shifting the IgE dominated to IgG dominated response
Pemphigus foliaceus
autoimmune disease of the skin
autoantibodies against desmoglein-1&3 (DSG1,3) destroy the bonds that maintain cell-to-cell adhesion.
YOUNGER horses are more likely to respond to therapy, less likely to have relapses, have potential for spontaneous regression
Systemic signs = fever, depression, lethargy, anorexia, weight loss
definitive dx = histologic examination of a skin biopsy specimen
Treatment options = CCS / chrysotherapy (aurothiomalate) / azathioprine
acute death can occur
systemic lupus erythematous
Rare; Dx on skin biopsy
Tx: immunosuppressive doses of glucocorticoids
CS: Weight loss, bilaterally symmetric alopecia, seborrhea, oral ulceration, and lymphadenopathy
Some horses have concurrent Coombs test-positive hemolytic anemia
Poor prognosis
discoid lupus erythematous
Rare; Dx on skin biopsy
Tx: immunosuppressive doses of glucocorticoids
CS: Areas of patchy erythema, crusting alopecia, and scaling on the face, ears, and neck. + / - coronary band lesions +/- chestnuts/ergots
Aggravated by sunlight
Usually can be managed - prognosis not as bad as SLE
Which is the most practical therapy for large, full-thickness burns in horses:
Continuous wet dressings (semi-open technique)
What type of photosensitivity does St John’s Wart (Hypericum perforatum) cause when ingested?
Type 1: primary photosensitivity
photodynamic agent is ingested, systemically administered (certain drugs) or absorbed through the skin
What type of photosensitivity does phylloerythrin cause when ingested?
Type 2: hepatogenous photosensitivity (phylloerythrin > 8.0 μg/dL)
Which is the most common toxic cause of hepatogenous photosensitization?
Pyrrolizidine alkaloids
E.g. Crotalaria spp., Amsinckia spp. (fiddleneck), Senecio spp. (tansy ragwort, groundsels), common heliotrope, Patterson curse
Sarcoids
Are the most common neoplasm in horses worldwide
Consist of cutaneous accumulations of transformed fibroblasts
Can stay dormant for extended periods of time before spontaneously enlarging or converting to more aggressive types
STACHYBOTRYOTOXICOSIS
Mycotoxicosis caused by toxins of the fungus Stachybotrys atra
This fungus grows on hay and straw and produces toxins referred to as macrocytic trichothecenes
These toxins cause bone marrow suppression, profound neutropenia, thrombocytopenia, and necrotic-ulcerative lesions of the skin and mucous membranes
Lesions commonly begin at mucocutaneous junction as focal areas of necrosis and ulceration. Petechiae, ulcers, large areas of necrosis, catarrhal rhinitis, and laryngitis follow
Skin lesions as early as 24 h after toxin ingestion. Systemic signs incl lethargy, anorexia, weight loss, hyperactivity, proprioceptive deficits, colic, muscular stiffness, and 2nd degree AV block
Affected animals develop haemorrhagic diathesis, haemorrhagic enteritis, septicaemia, and die
Dx based on hx, csx, finding toxin in feed. If toxicosis recognised early in course of dz, withdrawal of affected feed has resulted in resolution.
Animals with extensive lesions and chronic exposure = poor px
Lice
Highly host-specific, obligate parasites that spend entire life cycle (20-40 days) on host
In ideal environvment, can live 2 to 3 weeks off host, however less than 7 d more typical
Transmission by direct or indirect contact
Biting lice – Damilinia equi - feed on epidermal debris and prefer dorsolateral trunk
Sucking lice – Haematopinus asini - feed on blood and tissue fluid, most commonly infest mane, tail and fetlock region
When managing lice infestation, goal is to treat all animals on the premises
Ivermectin 0.2 mg/kg PO q 2 weeks for three txs – gen effective for sucking lice
Biting lice – topical eprinomectin (Eprinex) 0.5 mg/kg SIW for 4 tx
Both biting and sucking respond to insecticidal or 1% selenium sulphide shampoos – kill adult lice, but hatchling nits will require a second shampooing in 2 weeks. Two applications of insecticidal sprays or powders containing pyrethrins and pyrethroids at 14-day intervals also efficacious
Presence of lice in the nearby env should be addressed by cleaning and decontaminating all tack and grooming supplies and decontaminating the stabling area using a commercial flea premise spray
Chorioptes Equi
Spend entire 3 week lifecycle on host, but can live off the horse for 70 days
Tends to be more common in winter months
Feed on epidermal debris at preferred sites, which incl distal limbs and perineum
Infested horses exhibit intense pruritis with chewing, licking, stomping of the feet, and rubbing of the tail and perineal area
Skin lesions incl papules, alopecia, erythema, scabs and crusting o the pasterns, fetlocks, or perineum
Dx can sometimes be made by deep skin scraping - burrow deep
Draft breed horses or other horses w feathered fetlocks are predisposed to C equi where they may contribute to the lesions of chronic progressive lymphedema (CPL)
Incl in list of ddx for pastern dermatitis
If dx, treat all horses on property
Tx w topical eprinomectin solution (Eprinex) at the manufacturer’s recommended therapeutic dose for cattle of 500 ug/kg bwt weekly once for four administrations is recommended – administer along back line, from withers to proximal tail
Resistance to ivermectin and moxidectin may be developing
ONCHOCERCIASIS
Lesions of onchocerca cervicalis infection begin as simple thinning of the hair coat, oft around the eyes, muzzle, neck, chest and ventral abdomen
As dx progresses, lesions vary from focal to generalised areas of alopecia, scales, crusts and plaques and may become severely excoriated, ulcerated, oozing and lichenified
Ocular diseases associated with O cervicalis include ERU, sclerosing keratitis, vitiligo of the bulbar conjunctiva, and conjunctival nodules
Nematode lives in the ligamentum nuchae and produces microfilariae that migrate through the skin and are ingested by the intermediate host, the Culicoides species
Microfilarial populations vary seasonally and are highest in the spring and summer, which are also peak season for the Culicoides vector
Csx of onchocerciasis believed to be caused by an idiosyncratic hypersensitivity rxn to one or more microfilarial antigens because many horses that have circulating microfilariae do not have lesions
Important disease of horses worldwide, no breed or gender predilection, usu horses 4 years of age and older
Dx most reliably made with a mince preparation or via histologic examination of skin from a biopsy specimen
Mince prep req 4-mm or 6-mm punch specimen – mince and incubate room temp 30 – 60 min – look under microscope for rapid motion of microfilariae
Skin biopsies: perivascular eosinophilic dermatitis
Tx w either ivermectin or moxidectin at standard dosage effective against microfilariae – may require two monthly treatments before csx resolve
~25% horses w severe disease have adverse rxn, such as ventral midline oedema or pruritis, which occurs 1 – 10 d after tx – tis rxn believed to be caused by dead and dying microfilariae
None of the currently available anthelmintics kills adult parasites in the ligamentum nuchae, and affected individulas require periodic retreatment w ivermec when csx recur
The more recent use of deqorming by FECs appears to have increased the incidence of Onchocerca-related dermatitis
Habronemiasis: house fly is the intermediate host for what species?
Habronema muscae
Draschia megastoma
Habronemiasis: stable fly is the intermediate host for what species?
Habronema majus
Habronemiasis
Adult nematodes live in stomach and produce larvae, which are passed in the faeces and ingested by maggots of the previously mentioned intermediate hosts
The intermediate host deposits infective larvae near horse’s mouth – which the horse then swallows to complete the cycle
Cutaneous habronemiasis occurs when the intermediate host deposits infective larvae on skin, open wounds, or chronically moist areas
Horses with cutaneous habronemiasis have ulcerative nodules in the spring and summer that partially or completely regress in the winter
Pin worms
A diagnosis of pinworm is based on clinical signs and identification of pinworm eggs on cellophane tape preparations
Eggs develop to the infective stage within a 2- to 3- day period. At this time the cement substance cracks and dries and then detaches from the skin as it flakes. The flakes contain are large number of eggs that adhere to walls, buckets, and other objects in the environment
Adult pinworms are found in the colon
The female worm deposits eggs around the anus
In ideal conditions, pinworm eggs can survive in the environment for up to 1 month
Reports of resistance to ivermectin and pyrantel dewormers - can use FBZ
Selenium concentrated plants often grow
in the Great Plains and Rocky Mountain areas of the US
Selenium Toxicity
At toxic levels, selenium is substituted for sulphur in sulphur-containing amino acids and alters keratinisation of the hoof and hair
Selenium in excess of 1-4 ppm from blood, 11-45 ppm for hair, and 8-20 ppm for hoof indicate chronic toxicity
The hair coat becomes rough, and there is a dramatic loss of mane and tail hairs
Generalised alopecia may also be visible
Lameness can be severe as the coronary band and hoof develop cracks and separate, and some hooves eventually slough
TX of Selenium Toxicity
Horses should be moved from the selenium source as quickly as possible, but recovery often prolonged and prognosis for severely affected animals poor.
A high-protein diet rich in sulfa-containing amino acids and 2 to 3 mg PO SID of DL-methionine may be beneficial.
CHRONIC ARSENIC TOXICITY
Clinical signs of chronic arsenic toxicity include a long hair coat, thinning of the mane and tail, and severe dry seborrhea. Horses may also develop poor body condition and weight loss.
Once upon a time, heaps of wankers though that it was a good idea to use arsenic to improve hair coat and body condition. This practice probably still exists in Oklahoma.
Definitive diagnosis is by measurement of arsenic levels in the kidney or liver (>10 ppm)
Reported treatments for chronic arsenic toxicity include sodium thiosulphate and dimercaprol
Atopic Dermatitis
Second most common form of skin allergy in horse
Inherited hyperreactivity to environmental allergens that produce skin disease, and less, commonly, respiratory disease
The skin barrier of atopic horses is different to that of normal horses, likely allowing absorption of allergenic proteins, which are then carried to the lymph node
Cytokines involved include IL-4, IL-5, IL-6, IL-13, and IL-31
Characterized by uniform hairs with no shaft abnormalities and a nonpigmented root end lacking a root sheath
Telogen Defluxion
Characterized by dysplastic hairs; the hair shaft may be weak or narrow, and the root end contains a root sheath
Anagen Defluxion
Hair loss occurs within days of the insult or drug – high fever, systemic illness, or malnutrition.
Anagen Defluxion
Sudden shedding of hair and a new wave of growth occurs 2-3 months after a stressful situation.
Telogen Defluxion
what is an important ddx to rule out for primary seborrhea?
Pemphigus foliaceus
all other ddx’s are idiopathic and untreatable
HERDA
Hereditary Equine Regional Dermal Asthenia
- cutting horses
- autosomal recessive
- is caused by a missense mutation of the peptidyl-prolyl cis-trans isomerase B gene, which encodes cyclophilin B and is important in the formation of collagen’s triple helical molecule
Warmblood Fragile Foal Syndrome
is autosomal recessive
most commonly causes lesions on pressure points
is caused by a point mutation in the equine pro-collagen-lysine, 2-oxoglutarate 5-dioxygenase 1 (lysyl hydroxylase1) gene
DERMATOPHILUS CONGOLENSIS TREATMENTS
A) sedating the horse, soaking and removing the crusts
C) shampooing the area with chlorhexidine
D) keeping the horse dry
E) applying topical antibiotics
G) PPG IM for 5-7 days
H) TMS PO for 5-7 days
Common cause of superficial pyoderma
staphs
The incubations period for VS is
24-72 hours
the most common fungal disease in the horse
Dermatophytosis - Trichophyton equinum, T. mentagrophytes, Microsporum
gypseum, and M. canis
superficial fungal disease of horses that causes nodules on the hair shaft – black or white filamentous nodules consisting of tightly packed hyphae on the mane and tail
piedra
Fungal dz causing hard subcutaneous nodules develop along the lymphatics
Sporotrichosis
a zoonotic mycosis caused by Sporothrix schenckii
Mycetomata
Single or multiple nodules of varying size can occur almost anywhere on the body of the horse – often pigmented and ulcerated and may discharge tissue grains
chronic pyogranulomatous infections of the skin and subcutaneous tissues caused by actinomycetes (actinomycetoma) or fungi (eumycotic mycetoma)
Typical location for culicoides hypersensitivity
mane
tail
ventral abdomen
face
Which is the typical location for pruritus due to Black flies?
ears
How long should topical and systemic antimicrobials be discontinued before sampling for skin fungal and bacteriologic culture?
at least 36 hours
Blue-black circumbscribed nodules or dark hyperkeratotic/verrucous lesions
hemangioma
Subcutaneous nodules which ulcerate and drain honey-colored material
glanders
Severe seborrhea, ulcer, nonhealing wounds, hypertrichosis
arsenic poisoning
Swelling of coronary band, necrosis of feet, sloughing of ears/tail/feet
ergotism
Lymphedema, panniculitis, alopecia, leukoderma, scaling of face/neck/trunk
SLE
Vitiligo of Arabian horses
also called Arabian fading syndrome or pinky syndrome
waxing and waning, symmetric leukoderma with lesions 1mm-3cm in size on the muzzle, face, lips, and periocular areas
May also occur at the mucocutaneous junctions of the genital and anal area. The skin may repigment within 1-2 years (rare). Considered heritable; limited success with topical glucocorticoids or vitamin-mineral supplementation.
sarcoid development
A) Often occurs in areas that have experienced trauma
B) Have been associated with BPV-1 and 2 and potentially BR-UEL-4
C) Genetically susceptibility is thought to play a role in which horses exposed to BPV develop sarcoids
D) Biting flies may be route of transmission
How are fibroblastic sarcoids different from pythiosis?
Sarcoids are generally neither painful nor pruritic and grow more slowly
Do sarcoids metastasize?
Malignant/malevolent sarcoids are locally malignant but don’t metastasize to other areas
Sarcoid Treatment
A) 0.5-1 cm margin of normal tissue is recommended for surgical excision
B) new scalpel blades, instruments, and gloves should minimize tumor spread after excision
C) CO2 laser treatment may have some benefit over conventional surgical excision
D) With cisplatin adjunctive treatment, 96.4% resolution rate after 4 years in 573 horses
E) Intratumoral hyperthermia can be combined with chemotherapy to boost the delivery of oxygen to the lesion, improves the distribution of chemotherapy inside the tumor and significantly increases the uptake of the chemotherapeutic agent
What breed is genetically susceptible to ocular SCC?
Halflingers - 5.5X more likely if they are R/R than R/N or N/N
there is a commercially available genetic test
___ has been implicated as a positive etiologic agent in equine SCC
EcPV2
equine papillomavirus
Mast Cell Tumors
A) Arabians are predisposed
B) Tumors are usually single and located on head or lower extremity
C) Radiographs show soft tissue mineralization
D) surgical excision is usually curative
E) Tumors respond well to triamcinolone treatment
Which form of cutaneous lymphoma has a poorer prognosis?
epitheliotropic lymphoma has a worse prognosis than non-epitheliotropic
Pseudolymphoma
excellent prognosis - often spontaneously regresses
Panniculitis
Show deep-seated nodules and plaques. Lesions may be single or multiple and vary in size. They may be hard and well defined or soft and ill defined. Initially, lesions are not fixed to the overlying skin, but as the disease progresses, nodules become cystic and rupture onto the skin surface. The ulcerating nodules drain a yellow to brown to bloody oily material. Pain varies. Healed lesions may leave depressed scars. Affected animals may be febrile, depressed, lethargic, and anorectic
Equine Axillary Nodular Necrosis
The condition has no known age, gender, or breed predilection. Clinically, single or multiple nodules develop unilaterally in the axillae. The nodules are painless, nonpruritic, haired, well-circumscribed firm masses that vary in size from 0.5 to 4.0 cm or greater in diameter. Multiple lesions tend to be arranged in a row
Eosinophilic granuloma
Probably the most common nodular skin disease of the horse
Firm dermal nodules that are associated with degenerative collagen.
No breed, gender, or age predisposition has been identified for this disease. Nodules usually arise in the warmer months of the year.
Sites most commonly affected are the withers, back, and sides of the neck
Treatment of eosinophilic granuloma
surgical excision, intralesional corticosteroids, or systemic corticosteroids
MEEDs
Rare idiopathic disease
—nodules or masses in numerous organs, ulcerative stomatitis, severe wasting, significant exfoliation, and eosinophil infiltration of the skin
—hypoalbuminemia, hypoproteinemia, impaired small intestinal carbohydrate absorption, and increased GGT, ALP, and bile duct isoenzymes
Treatment of MEEDs
symptomatic and includes anthelmintics, antibiotics, azathioprine, and corticosteroids
Sarcoidosis
can occur as a localized, partially generalized, or generalized condition
The skin disease begins as scaling, crusting, and alopecia on the face, limbs, and/or trunk.
Clinical signs may progress rapidly or slowly. Peripheral lymphadenopathy may develop concurrently with weight loss, muscle wasting, anorexia, exercise intolerance, and fever
SeM-specific antibody titres > _____? are strongly suggestive of vasculitis secondary to strangles vaccination or exposure
(>1:12,800)
Anaplasma marginale causes ____ hemolysis
Extravascular
Extravascular hemolysis results in ____ colored urine
Normal
Copper and lepto result in ______
Intravascular hemolysis
Red urine
Anaplasma affects adults or calves more
Adults - less able to regenerate RBCs
