ANS 442 Exam 3 Notes

• Combined Immunodeficiency (CID) Syndrome


  Failure of immune system, begins at 3-4 months as immunity from colostrum wears off, foals die by 4 to 6 months
• CID Syndrome


  • Primary seen in Arabs (possibly 25% of Arabs carriers)
  • Autosomal recessive gene (both parents carriers)
  • No practical treatment
• Neonatal Isoerythrolysis (NI)


  Similar to Rh factor incompatibility in humans, RBCs of foal destroyed by antibodies in colostrum
• NI


  1. Mare's immune system exposed to foal's blood and forms antibodies against it

  2. Foal becomes anemic 12-36 hr after birth

  3. Foal may die within a few days
• NI


  • Rare, mare's immune system usually not exposed to RBCs of foal
  • Test mares serum or colostrum, prior to foaling
  • If problem, prevent foal from nursing for 3d, tube non-reactive colostrum and feed milk replacer
  • Blood transfer - don't use blood reactive to antibodies in colostrum
  • Concern in thoroughbreds, doesn't happen to first foals but foals after
• Hemophilia


  Lack of blood coagulation upon injury (bleeders)
• Hemophilia


  • Sex linked recessive trait, transmitted from mare to half of sons, half of daughters would carry gene but not bleeders
  • Essentially lethal - nearly any injury results in death
• Lethal Whites


  Lethal when dominant homozygotes present
• Lethal Whites


  1. Occurs when 2 dominant whites mates (Ww x Wx) (WW lethal) (Ww white) (ww pigmented)

  2. Fetus dies early in utero
• Lethal Dominant Roan


  Due to gene that causes roan color pattern, color lethal in utero when dominant homozygote
• Lethal Dominant Roan


  • Can only occur from mating two roan horses, 75% fertility rate (⅔ foals roan), homozygous roan stallions have been identified
• White Foal Syndrome (ileocolonic aganglionosis)


  Causes digestive system defects, failure to form certain types of nerves to GI tract, milk builds up - colic
• White Foal Syndrome


  When two "frame - coat color frames body" overo (jagged white) paints mated (not always), mechanism not clearly understood
• Atresia coli


  Part of white foal syndrome, foals may appear healthy and normal for 8-24 hr, get increasingly severe colic and die
• Anal Atresia


  No anal orifice, surgery seldom successful
• Hydrocephalus (water head)


  Accumulation of cerebrospinal fluid (prior to birth) caused head to enlarge, can cause dystocia, lethal - probably a dominant mutation
• Hydrocephalus


  • Commonly reported defect with unknown origin, abnormalities in spinal column
• Umbilical hernia


  Relatively common, possibly inherited, usually not serious but potential problem
• Cryptorchidism


  Failure of testicular descent, believed to be inherited trait, recommended crypto not be used for breeding; fertility could be limited
• Wobbles


  Incoordination, partially in hind quarters, rare in older horses, degeneration of spinal column (cervical vertebrae 3 and 4)
• Epitheliogenesis imperfecta


  Foals often aborted, stillborn, or born with missing skin on rump, neck, extremities and mouth
• Epitheliogenesis imperfecta


  • Autosomal recessive (both parents must be carriers), seen in Saddlebred, QH and Belgians
• Hoofcare: Trimming and Shoeing


  Could shoe when trying to fix a hoof problem, walking on hard surfaces, traction for racehorses, wearing shoes would be good on pavement, but barefoot is good when on sand or grass
• Hoofcare Supplies


  • Hoof pick
  • Hoof knife
  • Hoof nippers
  • Hoof rasp
• Unsoundness (US)


  Defect interferes with usefulness of horse, can be congenital or acquired
• Types of Unsoundness


  • Working: legs, respiratory (heaves), cardiovascular system (heart murmurs), eyes
  • Breeding: problem with reproduction tract (ie. tipped vulva)
• Blemishes


  Looks bad but doesn't affect serviceability
• Factors that can play a role in blemishes and unsoundness


  • Age: young and old tend to have most problems
  • Conformation: predispose horse to injury
  • Training techniques: speed, turns, stops
  • Type of training surface: too hard, soft
• Blindness


  Cloudy eyes, hesitant movements, pupil dilation
• Periodic ophthalmia (moon blindness)


  Streptococcal infections cause antigens to irritate eyes, may lead to total blindness (US), not permanent
• Night Blindness


  Vitamin A deficiency (TUS)
• Overshot jaw (parrot mouth) or undershot jaw (monkey mouth)


  Genetic (US)
• Fistulous withers


  Bruise, pressure from collar or saddle, takes a long time to heal (TUS), may be related to poll evil, affects bursa which may lead to permanent lameness
• Bucked shins (dorsal metacarpal disease)


  Sore shins, young horses worked at high speed, 30-60 days rest (TUS)
• Bowed tendon


  Excess strain causes damage usually to superficial digital flexor tendon, over exertion and fatigue, conformation (sloping pasterns), shoeing, training surface (deep sand), wrapping tendons too tight (US)
• Carpal fractures


  Hyperextension of knee (poor conformation), painful, probably see synovitis or capsulitis in joint (US/TUS), inflammation in knees is a warning sign
• Ringbone


  New bone growth in 1st and 2nd phalanges, caused by trauma, concussion (US)
• Sidebone


  Calcification of lateral cartilages of hoof, lame during calcification (TUS), then only blemish (B)
• Splint


  2nd and 4th metacarpal/metatarsal bones, bone remodeling due to increased concussion (TUS/B), time needed to heal usually, however, when there is a fracture of the splint bone, surgery may be needed to remove the done
• Sesamoiditis


  Degenerative condition of sesamoid, inflammation and possible fractures, caused by over-use (TUS), warning sign is heat and inflammation