Exam 2 Flashcards

1
Q

Chronic Progressive Lymphedema

A
  • Disease of lymphatic drainage of skin
  • Breeds: Belgian, draught horses, Shire, Clydesdale, German breeds
  • 50-90% develop clinical signs
  • Initally: scratches-like, masked by feathering
  • Genetic component
  • Chronic and progressive
  • Starts at ~2 years, euth at ~>6 years
  • distal aspect limbs: lumpy skin/subcutis, back of pastern, recurrent secondary infections
  • palliative care (control infections, compressive bandages, exercise
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2
Q

Cannon Keratosis (Stud Crud)

A
  • Not related to urine splashing, not just males, not infectious
  • middle-aged or older
  • Genetic?
  • Esp. cranial aspect of rear cannon
  • lifelong
  • hairloss
  • Seborrhea: too much scale is being produced on surface of skin
  • Non-painful unless secondary infections
  • non fatal
  • Treat with anti-seborrhea shampoos
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3
Q

Parasites (4)

A
  • Lice: on skin
  • Mites: in skin
  • Onchocerciasis
  • Summer sores
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4
Q

Summer sores

A
  • Open, non-healing wounds
  • Esp.: around eyes, on lips, external genetalia, fetlocks, coronary band
  • Parasite + reaction: individual horses
  • esp. bad in summer
  • debulking + ivermectin
  • Incidence decreases with routine systemic dewormers
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5
Q

Dermatophilus (Rain rot or Scald)

A
  • Caused by Dermatophilus congolensis
  • Painless swelling: hair loss
  • Dorsum
  • Trasmissible bacterium
  • Characteristic appearance: thick crusts easily epilated, raw skin beneath
  • Wet climates: rain sheets
  • Anti-microbial shampoos
  • Zoonotic
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6
Q

Dermatophytosis (Ringworm)

A
  • Fungal infection (multiple)
  • Esp. young and/or malnourished horses
  • Higher incidence in fall/winter in temp climates
  • Decrease of UV light exposure when stabled
  • Zoonotic
  • Raised, circular swellings initially, then hair loss and crusting
  • Dilute bleach
  • Antifungal shampoos
  • Tack as fomites
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7
Q

Eosinophilic Grnauloma

A
  • Collagenolytic granuloma or nodular necrobiosis
  • Common!
  • Painless blemish
  • Fly bite sequel: hypersensitivity or allergic response
  • Chest and back esp.
  • Spring/summer
  • May contain mineral (nodular necrobiosis)
  • Remove surgically if nuisance
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8
Q

Aural Plaques (Ear Fungus)

A
  • Thick skin plaques
  • Bilateral
  • Concave aspect of pinna
  • Viral, not fungal: Papilloma virus
  • Fly-transmitted: black flies
  • More active in summer
  • Blemish
  • Sensitive ears
  • Older horses
  • Do not resolve
  • Various treatments: imiquimod, blood rot
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9
Q

Equine Papilloma Viruses

A
  • Esp. grass warts
  • Common: 6 mo.-4 yr
  • Papillomavirus
  • Muzzle + lips
  • Genital
  • May be generalized
  • Genital form, leads to SCC
  • Spread: contact, insects
  • Resolve in 3 months
  • Persistent=immunosuppressed
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10
Q

Fistulous Withers

A
  • Swelling of withers: Supraspinous bursa
  • Draining tracts, fever, and pain
  • Cause: trauma, ill-fitting saddles, overwork, overloading/poorly balanced loads
  • Infections: Actinomyces bovis, Onchocerca cervicalis, Brucella abortis!
  • Treatment: surgery, antibiotics
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11
Q

Anhidrosis

A
  • Loss of ability to sweat: overstimulation of sweat glands by stress hormones in summer months
  • Esp. warm humid areas
  • Risk of heat stroke
  • Sweating areas reduced to: jaw, neck, base of ears, between pelvic limbs, under saddle
  • No age, sex, breed, color predisposition
  • Esp. performance horses
  • Diagnosis by series of dilutions of terbutaline
  • Chronic: poor dry hair coat + lethargy during hot times of year
  • Control: removal of severe climatic stress, limit exercise to cool parts of day, shade, movement of air, misters, cold-water hosing, recovery may occur after move to temperate climate
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12
Q

Hirsutism

A
  • Long, non-shedding hair coat
  • Older horses
  • Associated with PPID (Equine Cushing’s Disease)
  • Treat the underlying disease
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13
Q

Photosensitization

A
  • Dermatitis of ALL unpigmented skin
  • Secondary to hepatic injury: metabolit of chlorophyll enters skin due to impaired biliary excretion
  • PA-containing plants (Pyrrolizidine alkaloids)
  • Weight loss, jaundice, behavioral change if severe
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14
Q

HERDA

A

Hereditary Equine Regional Dermal Asthenia

  • Asthenia=weak
  • ‘Hyperelastosis cutes’
  • Quarter horses: Some cutting horse bloodlines, normal at birth, develops at 2-4 years
  • Hyperextensible skin + scars
  • Esp back of affected horses
  • Homozygous recessive trait: do not breed carriers
  • Genetic test for cyclophilin B mutation
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15
Q

Linear Keratosis

A
  • Esp. QH, TB, Standardbreds
  • Unknown cause, genetic?
  • Birth-5 years
  • Vertical bands: Alopecia + increased keratin, esp. neck, shoulder, thorax
  • Asymptomatic blemish
  • lifelong
  • No treatment: may be mild progression
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16
Q

Disease of Pigmentation

A

Albinism
-Overo lethal white (non-functioning coon)
-Lavender foal syndrome (weakness, neuro signs)
Leukotrichia
-white hairs
-Retriculated = tiger-striping (>1 year old)
-other forms of pigment loss
Vitiligo
-autoimmunity to melanin

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17
Q

Sweet Itch

A
  • form of hypersensitivity to midges
  • active during summer
  • horses kept in marshy areas
  • esp in tail head, but can see it up to the mane
  • Shave skin, inject allergens, where there is redness there is an inflammatory response
  • seen in WY
  • pretty common
  • Treat with steroids
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18
Q

What are the 3 main types of cancer in horses?

A
  1. Squamous Cell Carcinoma
  2. Melanoma
  3. Sarcoids
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19
Q

What is cancer?

A

genes involved in promoting/inhibiting growth in in normal cells are being knocked out

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20
Q

What is metastasis?

A

can travel to another place, if can do that, is cancer

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21
Q

Characteristics of benign tumors

A
  • slow growth
  • usually encapsulated
  • smooth surface
  • local compression
  • cells differentiated
  • cells uniform and resemble each other
  • blood vessels in tumor well formed
  • minor or no necrosis
  • NEVER metastisize
  • DNA content usually normal
  • karyotype usually normal
  • normal mitotic figures
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22
Q

Benign tumors are not fatal unless….

A
  • bleed out
  • compression of vital organ
  • growth in confined space
  • hormone production
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23
Q

Characteristics of malignant tumors

A
  • metastasis
  • local invasion
  • irregular surface
  • little or no capsule
  • may be large with rapid growth
  • often death if untreated
  • less well differentiated than benign neoplasm
  • may not resemble tissue of origin
  • loss of anchorage dependence
  • loss of contact inhibition
  • pleomorphism
  • increased mitotic activity
  • vessels numerous/poorly formed
  • necrosis and hemorrhage
  • DNA content increased
  • additional chromosomes present
  • karyotypic abnormalitites
  • nuclei large hyeprchromatic
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24
Q

Common tumors of horses

A
  • sarcoid
  • viral papillomas/aural plaques
  • SCC
  • melanoma/malignant melanoma
  • thyroid adenoma
  • pituitary adenoma in pars intermedia
  • lipoma
  • ovarian tumors (=granulosa cell tumor)
  • mast cell tumor
  • lymphoma (leukemia)
  • teratoma of undescended testicles
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25
Q

Sarcoid

A

-occur typically anywhere flies tend to land or there’s been a cut

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26
Q

Papilloma-Equine warts

A
  • Mucocutaneous transitions
  • EcPV-1 (muzzle and lips)
  • EcPV-2 (genital areas, associated with genital SCC, like HPV-16, integrated into cell genome)
  • young horses (<3y)
  • hardy viruses
  • immunity: disappearance 1-6mo after appearance
  • chemical or freezing to remove
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27
Q

Aural Plaques

A
  • in ears
  • concave aspect, pinna
  • esp. summer/fall
  • papilloma virus on EM (not isolated)
  • often bilateral
  • non-painful
  • bother owner more than horse
  • no reported treatments
  • do not regress
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28
Q

Common squamous cell carcinomas

A
Occular:
-3rd eyelid, conjunctiva, cornea, eyelid
-UV light/pale skin
Penile/Preputial
-Smegma (EcPV-2)
-often aggressive in young horses
Face
-UV light/pale skin
Perineal
-UV light/pale skin, vulva/clitoral
Stomach
-often aggressive
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29
Q

Treatment of SCC

A
Surgical:
-early small lesions
-least successful on large, long standing lesions
Other:
-more advanced lesions
-cryotherapy
-cytotoxic chemicals
-Immunomodulation (BCG)
-Radiation: considered best, expensive, specialty clinics
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30
Q

Melanoma

A
  • virtually in all gray horses: >6-8y, some families worse than others
  • black tarry discharge
  • esp. tail perineum but can be anywhere
  • some become malignant
  • surgery vs. other approaches
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31
Q

Lymphoma

A
  • incidence: 1.3-2.8% of all tumors
  • no viral association
  • typically 4-10y old
  • most commom: multicentric: LNs and internal organs
  • generally diagnosed late in clinical course
  • common subtype: T-cell rich, B-cell lymphoma
  • chemotherapy and radiation therapy
  • palliative glucocorticoid use more common
  • most commonly internal
  • leukemia unusual
  • no effective treatment
  • when skin involved: often indolent, cutaneous nodules, T-cell rich, B cell lymphoma
  • may be stallion-like behavior
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32
Q

Thyroid adenoma

A
  • Common in older horses: 30% for horses >10y, 75% in horses >20y
  • unilateral or bilateral
  • biopsy or needle aspirate to confirm
  • no need for treatment unless: compression of adjacent structures, growing, hyperthyroidism
  • other thyroid masses: goiter, cystic hyperplasia, adenocarcinoma of thyroid follicles or C cells
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33
Q

Granulosa cell tumor

A
Common
-male/female hormones secreted
-aggressive/stallion-like behavior
-markedly prolonged estrus
-unilateral
-slow growing
-do not metastasize
Dx
-palpation
-ultrasound
-testosterone + inhibin
-anti-mullarian hormone
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34
Q

Pituitary adenoma, pars intermedia

A
  • pituitary pars intermedia dysfunction (PPID)
  • melanocyte-stimulating hormone (MSH) production
  • typically >18y
  • long hair coat
  • pressure on hypothalamus (body temp, appetite, cyclic shedding)
  • Polyuria/polydipsia (PU/PD)
  • poor muscle tone and weakness
  • somnolence
  • abnormal distribution of adipose tissue
  • swelling of periorbital fossa, laminitis
  • increased infections
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35
Q

Lipoma

A
  • common in older horses
  • intra-abdominal
  • long stalk=strangulation of SI
  • cause of colic
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36
Q

What is the urinary tract?

A
  • collect and removes fluid wastes from body
  • when animal dehydrated urine is more concentrated to preserve fluids
  • when animal well hydrated urine is more dilute
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37
Q

Structures of urinary tract

A

Kidneys, ureters, bladder, urethra

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38
Q

Equine urine usually looks…

A

Normally cloudy: abundant calcium carbonate crystals, mucus

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39
Q

Pollakiuria

A

Peeing too often, but normal total volume

  • estrus
  • calculi
  • cystitis
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40
Q

Polyuria

A

Peeing too much urine

  • many primary diseases of kidney
  • pituitary pars intermedia dysfunction
  • diabetes mellitus and diabetes insipidus
  • behavioral problems
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41
Q

Suspect urinary problems when…

A

weight loss + abnormal urination

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42
Q

Diagnosis of urinary tract problems

A
  • rectal palpation
  • urinalysis
  • blood work: blood urine nitrogen (BUN), creatinine, anemia, lowered chloride and sodium
  • Ultrasound: morphology, presence of stones
  • endoscopy
  • kidney biopsy
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43
Q

Acute renal failure

A
  • Kidneys stop working due to toxicity or severe dehydration
  • toxins:
  • some antibiotics
  • overuse of NSAIDs
  • heavy metals
  • plants
  • products of muscle breakdown or erythrolysis
  • Diagnosis: elevated BUN and creatinine
  • Treatment: IV fluids, dopamine (dilates blood vessels), furosemid (diuretic)
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44
Q

Where does acute renal failure cause problems?

A

In large intestine

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45
Q

Chronic kidney failure

A
  • loss of 20-30% nephrons
  • after damage occurred: chronic renal infection, post-intoxication
  • symptoms: loss of appetite, weight loss, decline in performance, dilute urine
  • cannot be cured: avoid NSAIDs, low protein diet, sodium bicarbonate, anemia, avoid dehydration
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46
Q

Pyelonephritis

A
  • ascending bacterial infection of kidneys from bladder (fever, high WBC count in circulation)
  • relatively rare in horses
  • treatment: antibiotics, control kidney failure
  • complications: formation of stones in urinary tract
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47
Q

Urolithiasis

A
  • most commonly in bladder
  • sequel to cystitis
  • also: kidney, ureter, urethra
  • symptoms:
  • straining during urination
  • inability of horse to urinate full stream
  • colic
  • blood in urine
  • esp. mares, particularly geldings
  • treatment: removal of stones: surgery, lithotripsy (shock waves), antibiotics
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48
Q

Uroliths in other locations

A
  • kidney or ureter or urethra
  • secondary to: passage of kidney stone or bladder stone
  • rarely performed surgery
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49
Q

Cystitis

A
  • inflammation of bladder: due to trauma, secondary to lumbar spinal cord disease, opportunistic bacterial infection
  • symptoms: frequent urination, straining, urine leakage
  • treatment: depends on underlying problem
  • complications: risk for pyelonephritis or kidney failure
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50
Q

Psychogenic polyuria/plydipsia (PU/PD)

A
  • drinks too much water due to boredom: upsets electrolyte imbalance, dilute urine
  • Diagnosis: no sign of kidney failure, inability to concentrate urine
  • treatment: 40ml/kg/day water intake
  • change environment
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51
Q

Ruptured bladder in foals

A
  • at/shortly after birth
  • depressed within week of birth: urinary toxins in blood
  • both foals and fillies
  • life threatening: urine in abdomen, toxemia
  • requires surgery to close
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52
Q

Patent urachus in foals

A
  • when urachus fails to close, or leaks after birth
  • risk of: urine scald of skin, ascending infection of urinary tract
  • most close on their own
  • may need caustic chemical to seal urachus
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53
Q

Renal neoplasia

A
  • generally rare: prevalence <2%
  • most primary
  • others secondary (esp. lymphoma)
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54
Q

Pituitary Pars Intermedia Dysfunction (PPID)

A
  • true Cushing’s disease
  • common, in some part esthetic
  • older animals
  • predisposed to insulin resistance
  • hypertrophy/hyperplasia in pituitary gland, with increased ACTH (increased cortisol released from adrenal glands)
  • abnormal fat deposits
  • long curly hair that wont shed (hirsutism)
  • bulging supraorbital fat pads
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55
Q

Treatment of PPID

A
  • body clip in summer months
  • regular dental + hoof care
  • Pergolide mesylate or cyproheptadine or combination
  • increased risk of infections
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56
Q

What is hirsutism?

A

long curly hair that wont shed

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57
Q

Most common PPID infections

A
  • sole abscesses
  • dermatitis
  • dental and gum disease
  • enteric parasitism
  • respiratory infections
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58
Q

Equine Metabolic Syndrome (what it looks like)

A
  • aka: ‘peripheral Cushing’s, easy keeprs, insulin-resistant’
  • humans: insulin-resistant (similar to pre-diabetics), obesity = increased risk for secondary diabetes mellitus +coronary artery disease
  • Horses: esp. ponies (genetic component), cresty neck and thick sheath, insulin resistance, obesity = increased risk of laminitis
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59
Q

Equine Metabolic Syndrome

A
  • typically 5-15 years
  • common esp. in ponies
  • insulin insensitivity: glucose intolerance, increase insulin, increased leptin, pro-inflammatory state, hyperinsulinemia affects ~22-29% of susceptible equine population
  • overfeeding nonstructural carbohydrates
  • obese horse with cresty neck + predisposition to laminitis
  • weight reduction + exercise
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60
Q

Distinguishing EMS from PPID

A
EMS:
-onset earlier
-laminitis
-test: increased fasting insulin
-few progress to diabetes
-control: weight loss
PPID
-onset in middle/old age
-laminitis
-hisutism
-excessive sweating
-PU/PD
-skeletal muscle atrophy
-test: low dose dex suppression test, increased ACTH
-control: counteracting effect of ACTH
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61
Q

Sick euthyroid syndrome

A
  • ‘eu’ because thyroids healthy: low circulating thyroid secondary to other illness
  • ‘hyperthyroidism’: true hypothyroidism RARE in horses
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62
Q

Thyroid adenoma

A
  • common in older horses
  • generally asymptomatic
  • diagnosed by palpation or biopsy
  • may be bilateral
  • thyroid carcinomas-rare
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63
Q

Goiter with musculoskeletal disease

A
  • western USA + Canada
  • musculoskeletal + goiter (mandibular prognathia, flexural deformation)
  • avoid: adequate iodine
  • affected foals: good odds if not severe and survive 1st week of life
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64
Q

Pheochromocytoma

A
  • tumor of adrenal medulla
  • increased epinephephrine and norephinephrine
  • anxiety, sweating, increased heart/respiratory rates
  • generally untreatable
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65
Q

Ovarian Diseases

A
  • granulosa cell tumor
  • relatively common
  • benign
  • hormone producing: persistent estrus, anestrus, masculinization
  • confirmation by hormone tests
  • can be bred after removal of affected ovary-usually 1 year later
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66
Q

Anhidrosis

A
  • loss of ability to sweat
  • factors: familial trait, semi-tropical/tropical climates, TBs and warmbloods, born west/midwest the moved to warm climates
  • onset: sudden vs. gradual, esp. in summer
  • prevalence: 10% at farm level, 2% at animal level
  • risk of hyperthermia (heat stroke)
  • confirmation: intradermal sweat test
  • move to cooler climate
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67
Q

Big Head-Bran Disease

A
  • secondary hyperparathyroidism
  • associated with high phosphate diets with low calcium hay
  • esp. foals and lactating mares
  • PTH hormone productio + increased activity of vitamin D
  • end result: poorly mineralized bone with fibroplasia = ‘big head’
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68
Q

Management of big head

A
Avoid:
-care with high phosphate diets
Manage:
-calcium supplementation
-restricted exercise
-NSAID for pain
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69
Q

What is the immune system responsible for?

A

protecting the horses body against the constant influx of pathogens from its environment

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70
Q

What are external influences on the immune system?

A

weaken the function of the immune system

-stress: transportation, performance, change of routine, pain, fear

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71
Q

What are the physical barriers of the immune system?

A

-skin and mucous membranes

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72
Q

What is the internal protection of the horse?

A

-when the physical barriers are breached, immune system is activated

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73
Q

Organs of the immune system

A
  • spleen: active immune cells’ information modulated form the vagus nerve
  • bone marrow: in neonate, thymus is active in construction of immune system
  • lymph nodes: multiply and produce antibodies
  • autonomous nervous system: informs anatomical sites of the immune system
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74
Q

Cell Mediated Immunity in the Equine

A
  • non specific
  • leukocytes respond to a threat by degranulation (releasing substances to help destroy the threat) and phagocytosis
  • body cells participating in this part die off and are pus
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75
Q

Humoral Branch of the Immune System

A
  • must be previously exposed for this part to work
  • previous exposure primes lymphocytes and complement system
  • involve plasma cells and antibodies that are capable of colonal expansion (can multiply and produce more antibodies to fight threat)
  • complement system functions to break down/remove damaged cells
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76
Q

What happens (steps) when immune system starts working?

A
  • immune system reacts violently

- inflammation that causes swelling

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77
Q

Some examples of when the immune system reacts

A

lameness, injuries, colic!

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78
Q

Drugs to use for inflammation and swelling

A

Bute, banamine, previcox

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79
Q

Shock organ in the horse is the…

A

lungs

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80
Q

What is involved in shock? specific aspects

A
  • vagus nerve system
  • inflammatory cells form the immune system
  • humoral factors like TNFalpha
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81
Q

Pigeon Fever (Corynebacterium pseudotuberculosis) from Dr. Weiss

A
  • lives in dry hot dusty soil and manure (as in feed lots)
  • infection through open wounds, biting flies, inhalation
  • as bacteria stays in abscesses they create, they are difficult to reach with antibiotic therapy
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82
Q

Clinical presentation of Pigeon fever (Dr. Weiss)

A
  • one or more abscesses on chest/face
  • febrile/anorexic horses might have mutliple abscesses
  • may get ulcerative lymphagitis along extremities
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83
Q

Important things to know about Pigeon Fever (Dr. Weiss)

A
  • ruminants suffer same disease, can only infect eachother if have same strain
  • infected individuals need to be isolated
  • difficult to eradicate
  • treatment is similar to strangles, anti-inflammatories, warm poultices on abscesses so they can drain, antibiotics only in select cases
  • prevention includes fly control, remove manure, husbandry
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84
Q

Autoimmune diseases

A
  • COPD
  • Hives
  • all kinds of allergies
  • some conditions are genetically anchored, others caused by influence of environment on immune system
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85
Q

Laboratory support of autoimmune diseases (tests)

A
  • allergen testing
  • intradermal skin testing
  • IgE measurements of blood in horses
  • IgE measurements do not work for food allergies
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86
Q

Why do we vaccinate? (Dr. Weiss)

A

protect horses against catastrophic contagious diseases by preparing the immune system

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87
Q

What will the horse’s immune system make from vaccination?

A

antibodies for protection

-these immunoglobulins are circulating in blood stream or waiting in the tissue

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88
Q

Core vaccines

A
  • tetanus
  • WEE/EEE
  • west nile
  • rabies
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89
Q

What is immunology?

A

study of the immune system

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90
Q

What 3 areas of study (-ology) work together to help avoid situations where the immune system needs to be activated?

A

epidemiology, serology, immunology

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91
Q

What is the conformation of the brood mare reproductive tract?

A
  • vulvar labia presents a barrier for contamination
  • no retrograde urine contamination
  • cervix is a barrier to keep infections out
  • uterine body, pooling of fluid is not possible and bacteria can’t cause infection
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92
Q

What is a healthy environment of the uterus?

A

low pH=acidic

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93
Q

Where does the placenta evolve from?

A

chorion-a thin membrane that lines the egg shell on the inside

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94
Q

What kind of placenta does a horse have?

A

diffuse-epitheliochorial placenta

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95
Q

What position is used to check that the entire placenta has been expelled?

A

lazy “F” position

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96
Q

When should you avoid vaccinating a pregnant mare?

A

in the first trimester to avoid any complications

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97
Q

If ____ is in good working order, an infection can be avoided?

A

the local immune system

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98
Q

Hematogenous infection

A

mare is systemically sick and the bacteria/virus infect the uterus, placenta, and fetus causing inflammation and infection

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99
Q

Ascending infection

A

Noxious agents enter mare’s repro system through cervix, causes inflammation and disrupts oxygen and nutrient supply for foal by destroying the villi of the chorioallantois membrane (placental membrane)

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100
Q

Unidentified infection

A

cause for infection cannot be determined

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101
Q

What are the most common noxious agents in infections of brood mares?

A

EIS, EHV1, EVA, CEM

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102
Q

Is a retained placenta life threatening?

A

yes

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103
Q

In situations of infections causing stillbirth, what can be seen and why?

A

dystocia or premature placental separation from the retention of parts of the placenta

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104
Q

What is a red bag?

A

premature placental separation

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105
Q

If a retained placenta is addressed promptly after birth, what can you do?

A
  • remaining membranes can be removed with copious lavage
  • manually picking off placenta
  • anti-infammatories and antibiotics
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106
Q

If retained placenta is not addressed, what happens?

A
  • toxins released into mare’s blood stream
  • sepsis, laminitis, schock
  • chronic infection/inflammation in mare’s endometrium
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107
Q

What should the mare produce before birth and what is in this?

A

Colostrum

  • nutrients
  • calcium
  • antibodies
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108
Q

What is agalactia?

A

when the mare does not produce any milk at all

-treatment can include keeping mare away from foal, pain killers, and fluids

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109
Q

What is mastitis?

A

painful inflammatory process in the udder tissue

-needs treatment immediately with anti-inflammatories, pain killers, antibiotics

110
Q

What is glocoma?

A

too much fluid being produced in the eye or not enough fluid being drained

111
Q

What is a carract?

A

clouded lens

112
Q

What is tonometry?

A

measuring intraocular pressure

113
Q

What do you do to examine the eyes?

A
  • menace reflex
  • obstacle course
  • ability to constrict pupil
  • direct and indirect ophthalmoscopy
  • tonometry
  • fluorescein (dye): corneal ulcers, blocked NL duct
114
Q

About equine vision and ocular anatomy

A
  • largest globe of any land mammal
  • complete bony orbit
  • visual field of 350 degrees
  • strong eyelid muscles
  • copora nigra on dorsal margin of iris
  • recognizes color
115
Q

Eyes in foals

A
  • dimished coneal sensitivity
  • low tear production
  • reduced menace reflect until 7-1- days (increased reisk of corneal trauma)
  • various congenital ocular abnormalities: most common cataract
  • some inherited, some associated with multiple ocular anomalies
  • most idiopathic in utero
116
Q

Vulnerable complex structures of the eye

A
  • esp. large cornea, slow to heal
  • after trauma: uveitis, cataract=sequestered antigens unleashed
  • retinal detachment
  • intraocular hemorrhage
  • scars distort eyelids
117
Q

Trauma in eye

A

common due to:

  • prominent eyes
  • outdoor
  • curious
  • flies + sarcoid
  • fungal complications (cornea), steroid risk
  • corneal healing: no blood supply, ulcers with perforation
118
Q

Blocked nasolacrimal (tear) duct

A
  • weepy eye (nuisance)
  • conjuctivitis sequel
  • treatment: flush NL duct
  • some permanent
119
Q

Conjunctivitis +Keratitis

A
Inflamed conjunctival sac: 
-bacterial or allergies
-trauma
-dust
Most uncomplicated:
-good response to abs
-protect from flies
Complications:
-keratitis (keratoconjunctivitis)
-blocked NL duct
120
Q

Keratoconjunctivitis

A
  • inflamed cornea
  • normally avascular
  • deep ulcers slow to heal
  • superficial ulcers: most traumatic, risk of 2nd infection (bacterial, fungal), perforation risk, iris adhesions
  • antibiotic ointments + atropine + NSAIDs
121
Q

Melting ulcers (keratoconjunctivitis)

A
  • loss of overlying epithelium
  • collagenase production
  • risk of perforation in <24h
  • fungi esp.
  • horses at high risk of anterior uveitis
  • esp. with abuse of topical ointments with corticosteroids or long-time use of antibiotics
  • veterinary emergency
122
Q

Treatment of Keratoconjunctivitis

A
  • topical or subconjuctival broad-spectrum antibiotics (melting ulcers-antifungal medications)
  • atropine (pain)
  • also: antibiotic-soaked collagen lenses or contact lenses
  • anti-proteinases
  • systemic antibiotics
  • surgery:
  • lamellar keratectomy
  • conjuctival graft to promote healing
123
Q

Treatment of Keratoconjunctivitis

A
  • topical or subconjuctival broad-spectrum antibiotics (melting ulcers-antifungal medications)
  • atropine (pain)
  • also: antibiotic-soaked collagen lenses or contact lenses
  • anti-proteinases
  • systemic antibiotics
  • surgery:
  • lamellar keratectomy
  • conjuctival graft to promote healing
124
Q

Cataract

A
  • opaque lens
  • importance of severity and site
  • some congenital: may be genetic
  • sequel to: trauma, recurrent uveitis
  • leave alone or surgery: phacoemulsification + lens implant
125
Q

Recurrent (periodic) uveitis

A
  • moon blindness
  • common cause of blindness in horses in USA
  • uveitis = inflammation of grape (blood vascular layer)
  • probably related to exposure to bacterial antigens
126
Q

Uveitis definition

A
uvea = vascular (middle) layer of eye
uveitis = inflammation of this layer
127
Q

Recurrent Uveitis

A
  • other causes: esp trauma
  • Leptospira is one tirgger
  • major autoimmune component
  • genetics: appaloosa
  • one or both eyes
  • waxes and wanes
  • hard to control
128
Q

Recurrent Uveitis Complications and treatment

A
Blindness due to complications:
-persistent uveitis
-glaucoma
-mature cataracts
-retinal detachment
-hemorrhage
-atrophy
Anti-inflammatory + mydriatics
Experimental:
-antibiotics
-vaccination
-vitrectomy + gentamycin
-sustained-release cyclosporine
129
Q

Common cancers in and around eye

A
  • SCC
  • Sarcoid
  • Papilloma
  • Lymphosarcome
  • Melanoma
130
Q

Cancer Eye (SCC)

A
  • Esp. UV exposure
  • common in WY
  • eyelids
  • haw
  • slow to metastasize, locally destructive
  • draught, appaloosa, paints
  • 11 years
  • surgical removal
131
Q

Sarcoid

A
  • Variable: 5 clinical types, not always obviously sarcoids
  • BPV-1,2,5
  • Surgery vs. other:
  • immunotherapy
  • chemotherapy
  • freezing or heating
  • irradiation in situ
  • photodynamic therapy
132
Q

What is CVID?

A

Common Variable Immunodeficiency

  • dysfunction of the immune system
  • specifically B-cell branch or the humoral response is inept at protecting horse from pathogens
  • have deficient quantities or no bB cells
133
Q

What gene is involved in CVID?

A

PAX5 gene

134
Q

Clinical Signs of CVID

A
  • prolonged/recurring bacterial infections
  • bacterial meningitis
  • peritonitis
  • lyme disease
  • depression/ill thrift
135
Q

Treatment/Prevention Options for CVID

A
  • treat infections as they come

- reduce environmental risk

136
Q

What is the generic cause of CVID?

A

epigenetic cause

137
Q

Is there a cure for CVID?

A

no

138
Q

When are most deaths of foals?

A

60-70% first month of life

139
Q

How to predict a healthy foal

A
  • pre-partum fetal examination
  • ultrasound
  • fetal heart rate, aortic diameter
  • maximal fetal fluid depts
  • uter-placental contact, thickness
  • fetal activity
  • score of 0-2 for each
  • cumulative score
140
Q

Foal Immunity at Birth

A
  • ensure mom is clean
  • stall disinfected and bedded with fresh straw
  • no immunoglobulin transfer across placenta
  • at birth: immunocompetent, low concentrations of immunoglobulins detectable
  • regular traffic of bacteria into system circulation
  • primary immune response to envt antigens not detectable til 2 wks
  • dependence on maternal immunity
141
Q

Checking a foal is not compromised

A
  • sits up sternally shortly after birth
  • responsive
  • 60 breaths at birth
142
Q

Protection from Mare’s milk

A
  • ~5 liters colostrum in first 18 hours
  • antibodies: abosorbed <24 hours, confined to intestine lumen >24hr
  • other components:
  • energy
  • protein
  • hormones
  • minerals
  • trophic factors enhancing immune competency
143
Q

1,2,3 rule for foals

A
  • stand in 1 hours
  • nurse in 2 hour
  • placenta passed in 3 hours
  • pull blood at 24h to check IgG
144
Q

Well Mare check

A
  • nutritional condition
  • womb and mammary infections
  • evidence of trauma and fistulas
  • placenta
145
Q

Well Foal check

A
  • common congenital defects: hernia, cleft palate, cataract

- IgG in blood

146
Q

Vaccination of foals

A
  • ensure mare vaccinated properly: protects foal in first 6m of life
  • traditionally >6 months
  • vaccinate for: tetanus, influenza, EHV-1 -4, strangles, rabies, WEE/EEE, WNV
147
Q

Fractured ribs/contusions of foals

A
  • common: ~10% of necropsied neonatal foals
  • primary cause of death:
  • hemothorax
  • pneumothorax
  • damaged heart
  • death within wk of birth
  • contributing to death: failure to nurse or rise
148
Q

Trauma of foals

A
  • most important single cause of death 0-12m
  • musculoskeletal injury
  • typically on grass
  • ribs: especially foaling
  • long bones
  • skull
149
Q

Septicemia

A
  • sleepy foal: recumbant +_ diarrhea
  • multiple agents, generally environmental or commensal bacteria
  • survival rate ~50% with intensive care
  • a special case: Actinobacillus
  • high mortality
  • often present within 1 day of birth
  • in WY, not uncommon
150
Q

Neonatal Maladjustment Syndrome (dummy foal)

A
  • fetal asphyxia esp. at foaling
  • most common CNS disorder of neonatal foals
  • neurological damage
  • mild to severe
  • altered consciousness, inability to suckle, lack of affinity for mare, tongue protrusion, star-gazing, localized/generalized seizures
  • difficulty breathing
  • FPT compilcation
  • nursing + patience vs. euth
151
Q

The Pregnane Hypothesis

A
  • normal birth
  • increased prenanes in blood
  • abnormally quiet sleepy neonatal foal
  • madigan foal squeeze procedure
152
Q

Meconium impaction

A
  • most common cause of colic in neonate
  • typically passed several hours after birth
  • tarry feces
  • if not passed or pain, enema
153
Q

Patent Urachus

A
  • passage of urine via umbilical stump
  • cautery (mild)
  • surgery (if persistent)
154
Q

Navel Ill

A
  • typically swelling/pain
  • sometimes internal to foal (inner side belly wall)
  • ultrasound
  • antibiotic treatment, generally good response
  • sx if non-responsive
155
Q

Hernia

A
  • suspected genetic component

- present at birth: resolve naturally, wait til >3m for repair of small hernias

156
Q

Ruptured Bladder

A
  • typically at birth
  • colts esp.
  • straining to urinate, little/no urine
  • colic
  • swollen abdomen
  • belly tap and/or contrast material
  • surgery esp. when caught early
157
Q

Diarrhea in foals

A
  • meconium retention
  • 70% of foals have diarrhea episode
  • rotavirus: common in many areas
  • not common in WY
  • most common cause of outbreaks
  • often ~3m
  • death more likely in young foals, but rare
  • dehydration + shock
  • short duration, 3 days
  • vaccinate mares!
158
Q

Gastro-Duodenal Ulcer Disease (GDUD)

A
  • important in older nursing and early weanlings
  • ulcers in: glandular stomach, upper SI
  • pain, salivation, teeth grinding, colic, reflux
  • no recognized agent: presumed to be secondary to other stresses
159
Q

Developmental Orthopedic Diseases

A
Osteochondrosis
-excessive cartilage
-arthritis risk
Angular limb deformities:
-valgus/varus deformation
-conservative vs. sx
Contracted tendons:
-physical therapy
Inflamed growth plates:
-physitis/epiphysitis
-role of diet
-NSAIDs
160
Q

What is the major factor affecting physical performance of a perfomance horse? (Weiss)

A

oxygen consumption

161
Q

What happens when the physiological parameters involved oxygen consumption of performance horses increases dramatically during exercise? (Weiss)

A
  • emptying of splenic reserve causes doubling of amount of erythrocytes in blood
  • seven fold increase in heart rate
  • increase in respiratory frequency
  • tidal volume doubles
162
Q

What does training of performance horses cause? (Weiss)

A
  • lowering of heart rate
  • increase in hematocrit
  • increase in oxygen affinity of hemoglobin
163
Q

What else can alter oxygen consumption in performance horses? (Weiss)

A

-feeding regimes

164
Q

Oxygen consumption in performance horses is influenced by which energy source that is used to obtain a sufficient energy density in the feed? (Weiss)

A

fat and sugar can be used to replace starch

165
Q

What other important physiological function do we need to worry about during long trailer hauls? (Weiss)

A
  • water intake

- fresh air/breathing for horse

166
Q

What other important physiological function do we need to worry about during long trailer hauls? (Weiss)

A
  • water intake

- fresh air/breathing for horse

167
Q

What is the reason many professional horse owners bring their own food? (Weiss)

A
  • used to that food

- don’t want to pick up diseases

168
Q

How much does your horse drink on an average day?

A

10-15 gallons

169
Q

What can happen from over-exercising performance horses? (Weiss)

A
  • anaerobic muscle work due to improper conditioning regime and routine
  • exhaustion of the pH buffer in the blood and tissue of lungs
  • overheating internally
  • severe stress and lowering of immune system
  • dehydration due to electrolyte depletion
170
Q

What structures are stressed when horses jump? (Weiss)

A

tendons, gut, hamstring, stifle, neck, spine

171
Q

What is a soundness exam?

A

when you are purchasing a horse, exam to make sure they are sound (mainly externally)

172
Q

What do you do in an outbreak of strangles?

A
  • isolate horses with swollen nodes
  • no antibiotics! poultice swollen nodes, drain
  • monitor other horses
  • multiple PCR tests to establish horses free of infection
  • vaccination choices
173
Q

When to use antibiotics during a strangles outbreak?

A
  • catch early

- swollen lymph nodes don’t look like they will burst

174
Q

What can happen when you vaccinate a horse during a strangles outbreak?

A
  • purpura hemorrhagica

- cause immune-mediated reactions

175
Q

Managing infectious outbreaks:
First thing you do is __
Second thing you do is___

A
  1. isolate horse

2. monitor other horses

176
Q

If multiple cases during an outbreak, what do you do?

A

Create 3 groups:

red: infected/presumed infected
amber: at risk-direct/indirect contact with infected
green: no clinical signs, no direct/indirect contact with infected horses

177
Q

How to manage an infected group of horses during an outbreak

A
  • separate building or pasture
  • ideally 25m from other horses
  • safe disposal of bedding, uneaten feed, water
  • appropriate disinfectant for boots and outer wear
178
Q

What should you avoid on the road to prevent a disease?

A
  • bring own buckets, water, feed
  • avoid nose-to-nose contact of your horse with others
  • wash hands after touching other horses
  • disinfect boots; clean outerwear
179
Q

What should you do at home to prevent a disease?

A
  • 3 wks of isolation for new horses

- record who comes in and who leaves

180
Q

When do you know a disease outbreak is over (Strangles)?

A

Infected horses:
-3 neg nasopharangeal washes/swabs over 3 wk period
-endoscopic testing of guttural pouch
Uninfected horses:
-temps daily
-serological tests
-persistently infected guttural pouch infection: treat

181
Q

Strangles treatment (take home)

A
  • understand best practices

- where to find information

182
Q

Strangles control (take home)

A
  • benefits of quarantine
  • benefits of good isolation
  • introduced by carriers or actively infected animals
  • detecting PI animals
  • organism hardy
183
Q

Zn phosphide poisoning Treatment

A
  • supportive, no antidote

- generally ineffective

184
Q

Zn phosphide poisoning control

A
  • awareness of poisons, insecticides, herbicides
  • don’t make assumptions
  • persistence in environment
  • ‘inaccessible’ in burrows
185
Q

Stomatitis

A
  • inflammation of the tissue of the mouth
  • plant fragments in feed, coarse feed
  • foreign body
  • vesicular stomatitis
  • phenylbutazone
  • blister beetle, in WY but still somewhat rare
186
Q

Why is dental disease important?

A
  • 3rd most common problem in adult horses involves teeth
  • ~25% of horses have dental abnormalities
  • 80% prevalence of dental lesions in horses at necropsy
187
Q

What is diastema?

A

gap between teeth, food can get lodged

188
Q

What can result from a fractured tooth?

A

root abscess

189
Q

Brachydont

A
  • short crowned
  • most crown above gumline
  • all fully erupted before maturity
  • long enough to survive lifetime
  • humans
190
Q

Hypsodont

A
  • long crowned
  • most crown below gumline
  • erupt slowly during animal’s lifetime
191
Q

What is the 3:1:4:3 dental formula?

A

3 incisors
1 canince
4 premolars
3 molars

192
Q

What is the 3:1:4:3 dental formula?

A

3 incisors
1 canince
4 premolars
3 molars

193
Q

Teeth Facts

A
  • deciduous and permanent teeth:
  • permanent teeth in by ~5y
  • grass abrasive
  • complex surface of teeth used for aging
  • removal of permanent teeth a difficult procedure
194
Q

Morphology of teeth (more teeth facts)

A
  • ‘wolf’ teeth: 1st premolar, commonly perceived source of bit problems, usually maxillary
  • each set of 6 cheek teeth operate a unit, importance of gaps between teeth
  • no ‘neck’ as in human or canine teeth
  • no true tooth ‘root’
  • multiple ‘pulp horns’ in cheek teeth with maturity
  • dentin formed in teeth over entire lifetime
  • apical foramina constrict at >5y
195
Q

Maxillary cheek tooth (layers)

A

3 layers:

  • enamel
  • dentin
  • cementum
196
Q

What happens when a pulp cavity is exposed?

A
  • nerves are exposed
  • can cause infection
  • can repair and plug it
197
Q

What is the pulp canal and periodontal attachment?

A

pulp canal=vascular/connective tissue

periodontal attachment=anchors tooth to tooth socket/jaw

198
Q

Changes in teeth with time

A

Young horses: high enamel, low dentin
-hard, brittle teeth
-readily floated, may shatter when cut with shears
Older horses: increased proportion of dentin
-less brittle
-more difficult to float
Changes in pulp cavity:
-decreased blood supply
-decreased dentin-forming cells
‘Smooth mouth’ when occlusal surface formed largely by cementum
-spaces develop between equine permanent incisors but development is delayed by the medial pressure of outmost incisors

199
Q

What is ‘smooth mouth’?

A

teeth worn to ‘roots’ with occlusive covering of cementum

200
Q

Assessing Teeth

A
  • watch horse eat, food dropped
  • palpate cheeks
  • discomfort in TMJ
  • head tossing/bit discomfort: possible problems with wolf teeth
  • balance of incisors
  • oral speculum to see/feel molars
  • radiographs if problems detected
201
Q

Assessing Teeth

A
  • watch horse eat, food dropped
  • palpate cheeks
  • discomfort in TMJ
  • head tossing/bit discomfort: possible problems with wolf teeth
  • balance of incisors
  • oral speculum to see/feel molars
  • radiographs if problems detected
202
Q

Suspect dental problems when…

A
  • change in behavior (dropping food, head tilting, excessive salivation)
  • quidding: rolling hay into balls, dropping them
  • loss of weight/condition
  • halitosis (bad breath)
  • refusing foods
  • eating slowly
  • packing food into cheeks
  • food/hay in feces
  • swellings under jaw, side of face, above eyes
  • chewing on bit
203
Q

Gaps between cheek teeth

A
  • diastema (singular), diastemata (plural)
  • creation of food pockets
  • devolpmental vs. senile diastemata
  • food pockets lead to periodontitis leads to osteomyelitis in advanced cases
204
Q

Periodontal disease

A
  • occurs in ~60% of horses 15-20yo
  • sequel to diastemata and displaced teeth
  • organic dental plaque + bacteria leads to mineralized plaque leads to dental calculus
  • development of deep periodontal pockets with gingivitis
  • eventually, infection of pulp, apical infection, and death of tooth
205
Q

Check teeth enamel overgrowth

A
  • enamel ‘points’
  • can affect horses on predominantely roughage diet
  • buccal (Cheek) side of upper cheek teeth
  • lingual (tongue) side of lower cheek teeth
206
Q

Pulpitis and other miseries

A
  • inflammation in confined dental chamber

- higher pressure leads to collapse of vascular supply leads to death of tooth

207
Q

‘apical’ infections

A

=tooth root infection

  • cheek teeth
  • rare in incisors or canine teeth
  • front maxillary teeth: maxillary bone swelling with sinus tracts
  • back maxillary teeth: maxillary sinusitis
  • getting in from 3 routes: blood-borne > fracture > periodontal
208
Q

Overjet/Overbite

A
  • maxillary teeth project rostral to mandibular teeth
  • reduced wear of central incisors
  • often concurrent poor alignment of cheek teeth
209
Q

Removing teeth (when?)

A

-limited effectiveness of salvaging diseased teeth in horses
Esp:
-periodontal disease
-infundibular caries of maxillary cheek teeth
-bacterial infection of pulp
Also:
-retained deciduous incisor/premolar
-loose tooth
-fractured crown
-supernumerary, displaced, misaligned tooth
-impacted tooth
-non-vital tooth because jaw fractured
-overgrowth tooth causing severe, soft-tissue drama
-dental tumors

210
Q

Easier teeth to remove (incisors and wolf teeth)

A
  • more likely to be done intra-orally
  • if straightforward, removal under sedation possible
  • failure to shed deciduous incisor: malalignment of permanent incisor
  • supernumerary incisors: mostly cosmetic, harder to remove
  • fractured mandible with loose teeth
211
Q

Harder teeth to remove (canines and wolf teeth)

A
Canines:
-uncommon
-bit injuries; pulpitis
-harder to remove, anesthesia
Wolf teeth:
-first premolar
-historically, overdone procedure
212
Q

Most challenging to remove: cheek teeth

A
Intra-oral:
-current recommendation
-sedated horse
-analgesia
-local nerve block
-rigid halter or head stand
-restrained in stocks
Extra-oral:
-retropulsion into oral cavity
-buccotomy with removal of alveolar bone (higher rates of complications)
213
Q

Specialist tools and patience

A
  • up to ~1hr with 100s of gentle oscillations

- molar separators + molar extractor + elevator with fulcrum

214
Q

Complications for cheek teeth extracted per os

A
In all cases:
-avoiding step mouth
-float 2x annually
~7%:
-fracture with apical portion persisting
-damage to adjacent teeth
-fracture of jaw
-sequestrum of adjacent bone
-impaction of feed in alveolus
-fistulas/sinusitis
215
Q

Retropulsion removal of teeth

A

-common but professionally discouraged
-strongly recommended: weaken periodontal ligament first
-high rate of complications: ~40% require second surgery, further back the tooth, more likely a problem
Problems:
-sequestra of bone/teeth fragments
-damage to adjacent teeth
- nerve damage
-major bone damage
-damage to nasolacrimal duct, parotid salivary duct, or palatine artery

216
Q

What are stem cells?

A

Pluripotenet Cells
-bone, cartilage, soft tissue
Cell Homing
Two sources: bone marrow, adipose tissue

217
Q

Application of stem cells

A
  • musculoskeletal injuries: tendonitis/desmitis, degenerative joint disease
  • wound treatment
218
Q

Does stem cell therapy work?

A
  • not a cure
  • accelerates healing
  • just a tool
  • reduced chances of reoccurence
219
Q

What is microchipping in horses?

A

highly reliable and biocompatible form of horse identification

220
Q

Is microchipping of horses safe?

A

yes, no risk of chip migration

221
Q

With who is microchipping of horses mandatory?

A
  • not mandatory by US govt

- mandatory for: USEF and USHJA, Jockey Club

222
Q

What is the ISO standard number for microchipping? USA country code for a microchip?

A

ISO standard: 11784/11785

USA code: 840

223
Q

Brucellosis in Horses

A
Brucella abortus:
-B. suis occasionally involved
-endemic in GYA elk and bison
-transmission to cattle
-zoonotic
'Fistulous withers' and 'poll evil':
-bursitis between shoulder blades or atlantal bursa
224
Q

Diseases outside GYA

A
  • non-endemic areas: almost always other bacteria
  • endemic area:
  • state vet
  • serological testing
  • attempted culture
  • curettage + lavage + antibiotics + vaccination
225
Q

Equine Viral Arteritis

A
-arterivirus
Present but rare in USA:
-seroprevalence of 1-2%
-at least 6 outbreaks
-carrier stallions (STD)
-esp. v young and v old debilitated and immunosuppressed
-most infections inapparent
-multiple strains: most low pathogenicity
Three presentations:
-flu-like illness
-abortion
-pneumonia
-USDA uniform methods and rules for EVA
-MLV vaccine, USDA controlled
226
Q

Pigeon Fever (‘dryland distemper’, ‘wyoming strangles’)

A
  • Corynebacterium pseudotuberculosis
  • esp. SW USA, recurrently in WY and CO during summers
  • fly transmitted
  • esp. young adult horese
  • abscesses in pectoral area and ventral midline
  • generally recovery within 2wks of rupture and discharge
  • complications: internal abscesses, laminitis
  • lesions resemble TB
  • don’t use antibiotics
227
Q

Big-Head

A
  • Aka: nutritonal secondary hyperparathyroidism, bran disease, miller disease, osteitis fibrosa, swollen face disease, and equine osteoporosis
  • low in calcium and/or high in phosphorus
228
Q

Hendra Virus

A
-related to measles and CD
Originates in fruit bat:
-Melbourne-Papua New Guinea
-Asymptomatic infectins
-Bat to horse transmission?
-ARDS in horses
-zoonotic
229
Q

Hendra virus in horses

A
  • incubation: 6-18 days, shed virus during asymptomatic period
  • depression, pyrexia, dyspnea, tachycardia
  • nasal discharge
  • sudden death 1-3 days after onset
230
Q

Hendra virus in people

A
  • incubation period 4-18 days, may be up to 1 yr
  • flu-like disease: fever, myalgia, headaches, vertigo
  • pneumonitis, rapid progression to respiratory failure
  • meningoencephalitis
231
Q

Equine Piroplasmosis

A
  • protozoan
  • tropical/subtropical, formerly USA, recent periodic incursions into US (associated with illegal horse importation, needle-sharing, pre-race blood-doping)
  • multiple tick species incl. US endemic ticks
  • long-lived infection in horse (years), reservoirs: asymptomatic horses and competent tick vectors
  • mechanical transmission possible
  • no vaccine, no 100% treatment
232
Q

Anemia in horses

A

-blood parasite
-acute vs. chronic
Most typically, acute disease:
-fever
-weakness
-labored/rapid respiration
-anemia
-thrombocytopenia
-jaundice
-systemic inflammatory response

233
Q

Dourine-Equine Trypanosomiasis

A
  • equine version of human ‘sleeping sickness’
  • STD
  • horses only
  • in S. America and elsewhere (USA/Canada, europe)
  • chronic blood-borne parasite: Trypanosoma equiperdum
234
Q

Clinical Signs of Dourine

A

Acute STD:
-Mares: vaginal discharge
-Stallions: edema of external genetalia
Chronic Disease: CNS
-treatement not recommended, induces carrier state
-risk from imported semen from endemic areas

235
Q

What is the average life span of a horse?

A

27 years

236
Q

1st, 2nd, 3rd reasons why horses die

A
  1. digestive
  2. endocrine
  3. musculoskeletal
237
Q

Digestive problems in older horses

A
Various forms of colic
-GI impaction or rupture
-gastric ulcers and neoplasia
-colonic impaction
-intestinal displacement/volvulus, other strangulating lesions
Intestinal inflammation:
-enteritis, typhlitis, colitis
Intestinal neoplasia
Liver failure
Worn teeth and periodontitis
238
Q

Dental problems in old horses

A
  • Senile diastemata: food impaction, periodontal disease
  • pulpal exposure
  • decreased occlusal surface + reduced enamel ridges, less grinding efficiency, ‘smooth mouth’
  • loss of cheek teeth
  • loss of enamel folds
239
Q

Common causes of less efficient teeth of old horses

A
  • decreased surface area + decreased enamel ridges
  • decreased GIT ability to digest protein and fiber
  • decreased excessive incisor wear
  • periodontitis in ~80% of horses >20y
  • loss of reserve crown leads to poorly anchored tooth leads to displacement/tooth loss
240
Q

Dealing with less efficient teeth of old horses

A
  • pelleted/extruded dies ~14%
  • reducing fiber length of hay
  • ‘smooth mouth’: moistened pellets or cubes in liquid consistency
  • antibiotic oral gels for chronic periodontitis
  • regular dental examination
241
Q

Musculoskeletal disease of older horses

A

Lameness

  • laminitis, esp. chronic
  • osteoarthritis/DJD
  • esp. lower limbs, metacarpus/metatarsus, fetlock, tarsus/carpus
242
Q

Pituitary pars intermedia dysfunction (Equine cushings) (older horses)

A

focal/multifocal hyperplasia of fars intermidia (PI) leads to diffuse hyperplasia of PI leads to adenomatous hyperplasia of PI leads to microadenomas leads to adenoma

243
Q

Respiratory system of older horses

A
  • equine asthma
  • pneumona, esp. as sequel to choke, infectious
  • guttural pouch empyema
  • sinusitis
244
Q

Central Nervous System/Eyes of older horses

A
Age-related neurodegenration:
-white matter and neuronal vacuolation
-vascular degeneration +/- iron deposition
-'wear and tear' pigment
-abnormal axons ('spheroids')
-'neuraxonal dystrophy'
-no true alzheimer's disease
Degenerative myelopathy
-EPM
-Uveitis
245
Q

Urogenital disease of older horses

A
  • interstitial nephritis
  • bladder tumors
  • Penile SCC
  • ovarian carcinoma
246
Q

Cardiovascular system of older horses

A
  • cardiac valvular disease
  • myocardial necrosis
  • verminous arteritis
  • tumors of cardiovascular system
  • aortic-iliac thrombosis
  • Hemoabdomen (vascular tears)
247
Q

Biggest type of neoplasia in older horses

A

pituitary adenoma

248
Q

What is the most common malignant neoplasm of old horses?

A

squamous cell carcinoma

249
Q

Euthanasia in older horses

A
Safety issues: falling and thrashing
1. Barbiturates (ace)
-safe disposal of carcass (wildlife hazard)
2. Gunshot or penetrating captive bolt
-experience + care regarding ricochet
3. Adjunctive only: potassium chloride
Unacceptable:
-choral hydrate
-neuromuscular blocking agents
250
Q

What does a soundness exam mean to a veterinarian?

A

to examine something closely
-horse-racing term, referring to requirement that horses be checked for health and soundess by veterinarian before being allowed to race

251
Q

Which diseases are typically missed on a soundness exam?

A
  • strangles
  • gastric cancer
  • parasites
  • internal cancer
252
Q

What is typically found on a soundness exam?

A

Lameness

-designed to find out will horse meet requirements of what buyer wants it to be used for

253
Q

Overview of Soundness Exam

A
  • buyer initiates prepurchase exam (one vet should not represent both parties)
  • purpose: to discover pre-existing/potential problems (not gurantee of soundness, helpful to know intended use of horse)
  • roles of parties should be defined
  • major source of litigation, due to: lack of understanding of prepurchase exam process, buyer’s excessive expectation of secure investment
254
Q

Veterinarian’s responsibilities of a soundness exam

A
  • experience with breed
  • understanding of intended use
  • away of breed or use requirements
  • thorough, orderly examination
  • generates report for buyer
  • accurately assesses buyer’s expectations
  • define limitations of prepurchase exam
255
Q

What does a veterinarian need to know/do prior to a soundess exam?

A
  • no contact with horse or seller in previous medical or personal role
  • be aware of state and international disease testing (review with buyer, EIA test)
  • offer drug testing
256
Q

Buyer’s responsibilities during a soundness exam

A
  • buyer owns the information but should maintain confidentiality
  • buyer can request previous medical records
  • may request trial period
  • help verify specific rule requirements
257
Q

Prepurchase exam: history

A
  • questionnaire to seller: info is legally buying
  • questionnaire to buyer: expectations, potential use, previous experience
  • note modifying conditions:
  • intended to compete at higher level
  • coming off lay-off period
  • some infirmities may be acceptable to experienced rider
  • financial investment
  • pleasure horse
258
Q

Prepurchase exam: environment

A
  • habits/vices matter
  • environtment: bedding, stall appearance
  • animal’s demeanor
259
Q

Prepurchase exam

A
At rest:
-heart rate
-respiratory rate
-body temp
-what is normal?
Re-evaluate after exercise (did murmur appear/disappear)
260
Q

Prepurchase exam: microchip

A
  • verify placement (nuchal ligament)

- verify ID #

261
Q

Prepurchase exam: head

A
Teeth:
-hypsodont
-speculum, thorough exam
-dentistry required?
-verify teeth mirror age
Eyes:
-darkened room
-ophthalmoscope
-ulcers, cataracts, others
-periodic ophthalmia
Ears:
-sarcoid, melanoma, papilloma
262
Q

Prepurchase Exam: musculoskeletal

A
  • musculatrue: face, neck, back, symmetry, atrophy, pain, spasm
  • palpate spine and pelvis for misalignment
  • evidence of scar tissue for previous surgeries
  • EPM, rare in WY-raised horses, but not impossible
  • palpate all 4 legs: tendons, muscles, heat or swelling
  • observe: uneven wear on toes
  • test hooves
  • observe horse in motion
263
Q

Prepurchase exam: musculoskeletal, exam in motion

A
  • level footfall
  • gait abnormalities
  • range of motion
  • mobility of neck, back and pelvis
  • head movement
  • flexibility and fluidity
  • muscle use
  • tail carriage
264
Q

Prepurchase exam: reproductive

A
Mares:
-perineal conformation
-udder symmetry
Stallions:
-both testicles descended
Geldings:
-castration remnants
Generally not:
-pregnancy examination
-uterine swab and biopsy
265
Q

Generally not done during prepurchase exam:

A
  • Echocardiography
  • rectal palpation
  • x-rays
266
Q

Is glanders present in the US?

A

no, eradicated in the US

267
Q

Is glanders a reportable disease?

A

glanders

268
Q

Is glanders zoonotic?

A

yes

269
Q

Is there treatment/vaccine for glanders?

A

high fatality in horses/humans

  • treatment is experimental
  • no vaccine
270
Q

Where can you go to find information about drugs for horses?

A
  • Compendium of Veterinary Products
  • FDA website
  • USDA