FA Med Exam 3

  1. What factors could affect feet and leg disorders?
    obesity, BCS, flooring, envronmental conditions (moisture, friction, mud), nutrition
  2. How many digits do ruminants have?
    • 4 (2 dew claws + 2 claws)
    • MT 2, 3, 4, 5
  3. What are the three basic features of the claw?
    Hoof (keratin); corium (dermal soft tissue); third phalanx (bone P3)
  4. How quickly does sole and wall grow, and what is the normal length?
    • sole: 4mm/month
    • wall: 5-6mm/month, ~75mm normally
  5. What trace minerals are important for internal hoof growth?
    Cu, Zn, biotin
  6. What are weight bearing surfaces on the claw?
    • front: medial
    • rear: lateral
    • More weight on the front half
  7. What is the blood supply to the claw?
    • dorsal: dorsal metatarsal a. -> axial proper digital a. -> terminal arch
    • plantar: terminal arch & marginal a.
  8. What is the digital cushion, and what is it for?
    • At heel, corium is impregnated with fat, fibrous and elastic tissue
    • Increases circulation by pushing blood out of foot
  9. What are arteriovenous anastomoses?
    • Vascular connections in the corium
    • There are smooth muscles at arterial end; if they constrict -> increased blood flow thru dermis
    • This is important for temp regulation, laminitis and systemic toxins (paralysis of smooth muscles and opening of AVAs aka shunting)
  10. How can you anesthetize the digit?
    • Bier block: inject 2% lidocaine (~20 cc for adult) in vein below the tourniquet
    • Dorsal common digital vein (dorsum)
    • Lateral digital vein (near dewclaws)
  11. How does infection spread from the coffin joint, and what does it cause?
    • axially: footrot
    • abaxially: vertical fissure aka sand crack
  12. Where are septic extensions likely to happen?
    The area of the coffin joint flexor pouch, navicular bone + bursa, DDF tendon + sheath
  13. Where are the cruciate ligaments?
    • connect P1-P1 proximally
    • connect P2-P3 distally
    • Preserve the proximal during claw amputation
  14. Where are the tendon extensor sheaths?
    • Forelimb: Common digital extensor
    • Hindlimb: Long digital extensor
    • Extensor sheaths extend to mid P2
  15. Where are the tendon flexor sheaths?
    • 6-8 cm proximal to proximal sesamoid bones to just above coronary band
    • Usually entered during digit amputation
    • Signs of infection: swelling up leg from the digit; very lame!
  16. All lameness cases can result from what aspect of farm mis-management?
  17. What are the "hooks"?
    tuber coxae
  18. What are the "pins"?
    tuber ischium
  19. What problems does an overgrown claw cause?
    • Backward rotation of P3 -> pinch corium between P3 and sole
    • Heel erosion also makes this worse
  20. What is the purpose of hoof trimming?
    • Restore normal shape
    • Improve gait
    • Decrease lameness
    • Do once a year at end of lactation
  21. How do you trim a hoof?
    • 0. Wear gloves
    • 1. shorten toe using visual approach by starting at point where wall starts to point medially
    • 2. draw line to heel
    • 3. pare sole and trim wall as needed, stop when reach soft sole
    • 4. Keep nippers parallel to sole surface so don’t gauge sole or wall
  22. What are some causes of infectious diseases of the foot?
    • FMDV
    • BVD
    • Malignant catarrhal fever
    • Salmonella can occasionally cause dry gangrene of extremities from fetlock distally in calves (also tail, ears) (Salmonella dublin); more commonly in young calves see polyarthritis
    • VSV
    • Bluetongue virus
  23. What is cattle footrot?
    • Caused by F. necrophorum (suppurative necrosis from leukocidal exotoxin) and Prevotella melaninogenica (tissue invasion via proteases including collagenases). T. pyogenes facilitates anaerobe growth
    • CS are seen in interdigital space; fetid, foul, anaerobic odor; severe lameness
    • Resistant strains cause “super foot rot” or “super foul”
  24. What is sheep footrot?
    • Caused by F. nerophorum and Dichelobacter nodosus (obligate anaerobe that has proteases)
    • Considered to be a highly contagious disease!
    • Many strains (~20) so vaccination is difficult!
    • Milder forms are called “foot scald” or “benign foot rot”
  25. What is the pathogenesis of sheep footrot?
    Trauma can help initiate infection, e.g. maceration of skin from constant wet, feces, urine, mud etc.
  26. How is footrot tx?
    • Systemic or local abx will allow rapid (2-3 d) recovery except if bone/joint involvement
    • Local wound debridement
    • If deep structures involved wrap them (coffin joint/ tendon sheath/ navicular bursa/ bone) = poor prognosis
  27. How is cattle footrot prevented?
    • Isolate
    • Reduce environmental contamination
    • Keep high traffic areas clean, dry, no sharp stones, stubble
    • Fence off low wet areas
    • Use Fusobacterium vaccines with management improvements
    • Footbaths, if practical (two baths 10' long x 6" deep, change q150-300 cow passages)
  28. How is sheep footrot prevented?
    • Regular foot trimming
    • Footbaths 1x/wk
    • Isolate/cull
    • Check herd additions
    • Vaccination (complete boosters at least 4 weeks before anticipated exposure)
    • Avoid confinement in wet, muddy areas
  29. What is non-papillomatous interdigital dermatitis?
    • aka heel horn erosions aka slurry heel
    • Organism colonizes the epidermis, but does not extend into dermis (in comparison to footrot)
    • Has a gray, fetid, serous exudate
    • Lameness but less severe than footrot
    • Associated with poor hygiene
  30. How is non-papillomatous interdigital dermatitis prevented?
    • Vaccination of cattle with D. nodusus vaccines is not successful
    • Improve farm hygiene
  31. How is non-papillomatous interdigital dermatitis tx?
    • Clean, debride
    • Tetracyclines/Nuflor/Beta lactams
  32. What is a heel horn erosion (“slurry heel”)?
    • Does not usually cause lameness
    • Sequelae to chronic non-papillomatous interdigital dermatitis
    • Interdigital epidermal D. nodosus infection in cattle looks like a "V" diagonally across heel
    • Can lead to sole ulcers, sole abscesses, white line disease, complete heel loss
  33. How are heel horn erosions prevented?
    • Clean environment
    • Footbaths
    • Stalls of sufficient length so cattle can stand up without back feet in gutter
  34. What is papillomatous dermatitis?
    • Contagious, superficial dermatitis of cattle
    • Usually just above heels on rear feet
    • Sometimes front feet, dorsal area of interdigital space
    • More lame than expect!
    • Can be erosive or proliferative
  35. What is the etiology and pathogenesis of papillomatous dermatitis?
    • Suspect spirochete: Treponema
    • Multifactorial: environment, host, management
    • Rough, wet, unsanitary flooring, accumulation of feces/urine
    • Transmission between cattle and fomites: inadequately disinfected hoof-trimming instruments, livestock trailers, and farm equipment
  36. How is papillomatous dermatitis prevented?
    • Disinfect hoof trimming equipment (knives, hoof testers, etc.)
    • Footbaths with lincomycin or oxytetracycline, copper sulfate, or zinc sulfate
    • More effective in low prevalence (<10%); if high prevalence us individual topical first to reduce prevalence
    • Stall, corral, and alley hygiene
    • Want cow to spend 10 - 14 hr/day resting in clean dry area; no overcrowding
    • Closed herd
  37. How is papillomatous dermatitis dx?
    • Full-thickness 4-6 mm punch
    • See plaque of eroded acanthotic epidermis with parakeratotic papillomatous proliferation profusely colonized by spirochete-dominant bacterial flora
    • Invasion of stratum spinosum by spirochetes
    • Infiltration of neutrophils, plasma cells, lymphocytes, and eosinophils in dermis
  38. How is papillomatous dermatitis tx?
    • Topical abx (2-4 L ag sprayer)
    • Oxytetracycline
    • 25g Terramycin-343/L water
    • Incorporate oxytet powder in footwraps
    • Lincomycin
    • 8g Lincomix/L deionized or distilled water
    • Repeat q45-60 d
    • Systemic abx like PPG or ceftiofur
  39. What is corkscrew claw?
    • Abaxial wall (typically on lateral hind claws) grows beneath P3, displaces sole dorsally
    • Twisted, corkscrew appearance
    • Usually bilateral; older than 3 yr
    • Bony abnormalities because P3 abnormally narrow and long
  40. What is the tx and prevention of corkscrew claw?
    • Tx: claw trimming q3 mos, although cannot reverse process
    • Prevention: do not keep progeny from affected animals (maybe heritable)
  41. What are scissor claws, and how are they tx?
    • Overgrowth & overlapping claws assoc w/chronic laminitis
    • Hard to distinguish from slipper foot
    • Therapeutic trimming to treat
  42. What are slipper claws, and how are they tx?
    • Both claws long, overgrown, like slippers
    • Long claw with a flat dorsal wal
    • Assoc w/chronic laminitis
    • Tx by trimming to restore normal foot shape
  43. What is a sole ulcer?
    • Circumscribed zone of hemorrhage/necrosis at the sole-bulb junction of weight bearing digits
    • Incidence increase with high concentrates and protein
    • Danger if infection spreads!! e.g. to navicular bursa, deep flexor tendon sheath, and coffin joint
    • Tx is hoof trimming or wood block normal digit (and make sure to check the other leg!) + systemic abx (don't use chemical cautery)
  44. Why does a sole ulcer form in a preferential location?
    Flexor tuberosity causes excess compression of corium and leads to hemorrhage on caudal plantar aspect of P3
  45. What is the pathogenesis of a sole ulcer?
    • Subclinical laminitis -> softer sole horn -> more vulnerable to trauma
    • Ischemic necrosis of corium -> discolored, poor-quality horn with hemorrhage -> keratogenic layer subsequently has impaired activity -> further local hemorrhage and necrosis
    • So if you ever see yellowed or bleeding keratin, subclinical laminitis (maybe from diet) is possible
  46. What is white line disease?
    • Disintegration of the sole-wall junction (from soft horn) -> penetration with debris
    • Trapped pus spreads under sole/wall -> horn separated from keratogenic layer by pus -> pus discharges at coronary band; may penetrate navicular bursa, coffin joint
    • Spread of infection to navicular bursa -> heel swelling, worsening lameness, and if infection spreads -> poor px
  47. How is white line disease tx and prevented?
    • Systemic abx if advanced, wrap claws separately
    • Prevent by catching subclinical laminitis; minimize wet, unhygienic conditions; trim claws regularly; foot baths with astringents; removal of rough, coarse road ways
  48. What is a sand crack (vertical fissure)?
    • Lesion starts as fine fissures across perioplic corium and coronary band -> corium below the fissure gets damaged -> extension of fissure distally to bearing surface on hoof wall
    • Natural resolution is rare!
  49. What is the etiology and pathogenesis of sand cracks?
    • Trauma, dehydration, laminitis, trace element deficiency
    • Cu and Zn can affect skin and hair when deficient because both are essential for production and growth of good-quality claw horn
    • Maybe anatomy since P3 extensor process underlies area where see some sand cracks
  50. What is the tx and prevention of a sand crack?
    • Most = no treatment
    • If infected, pare out, flush, bandage
    • Antibiotics if deep/active infection
    • Maintain adequate trace element status in animals
  51. What is a hardship groove?
    • aka horizontal grooves and fissures
    • Groove in hoof wall; parallels coronary band
    • Indicates nutritional stress or sudden nutritional change
    • E.g. weaning (“weaning” groove), transportation, market, dehorning, vaccination
  52. How is a hardship groove tx and prevented?
    • Remove distal section if thimble to reduce movement during locomotion
    • Prevention = reduce stress
  53. How is traumatic exungulation tx?
    • Bier block (consider limb perfusion)
    • Clean with water/saline jet
    • If horn attached, clean all around without removing wall (protects germinal layers)
    • Abx (topical or systemic)
    • Wood block & wrap
  54. What is a sole abscess?
    • Pus between sensitive laminae and sole
    • CS are severe pain, 3-legged lame, ddx is a fracture
    • Complicated sole abscesses is associated with swelling above coronary band
  55. What is an interdigital fibroma?
    • Epidermal and dermal tissues show 4x normal thickness
    • Tissue proliferates, can become infected or necrosed which causes lameness
    • May spread to vital structures
    • Stretches distal interphalangeal (cruciate) ligament
  56. How can an interdigital fibroma be tx and prevented?
    • Sx to remove, avoid cruciate ligaments
    • Topical abx + wire claws together, wrap
    • May be heritable, don't breed
  57. What is the pathogenesis of laminitis?
    • Rapidly fermentable feed
    • -> rumenal lactic acidosis
    • -> rumen bacteria die off
    • -> endotoxins released
    • -> tissue swelling causes shunting away from corium
    • -> corium cells die and hoof horn cells stop making horn
  58. What can cause laminitis?
    • Systemic toxemias in metritis, mastitis causing elevations in histamine
    • Rapid weight gains
    • Small claw size (mechanical stresses on claw)
    • Grain overload
    • SARA (sub acute rumen acidosis) - most common cause in cattle - so change food gradually
  59. What are some herd tip-offs for laminitis?
    • > 10% cows over 4 yrs have abnormal claw growth
    • >10% culling rate for “feet and legs” excluding infectious foot diseases
    • >50% of all lameness <60 days post calving (higher [] food at calving)
    • >25% of any lactation group with sole hemorrhage
  60. What are the CS of SARA?
    • Reduced feed intake and rumenation
    • Mild diarrhea & foamy feces
    • Undigested grain in manure
    • Hoof/lameness issues usually 3-6 months later
    • Reduced milk fat: <3% because low pH suppresses fiber digestion and end products of fiber digestion used for milk fat
  61. How can SARA be dx?
    • Monitor rumen pH (puncture site on left side, at top of the patella about 15 to 20 cm behind the last rib; clip and prep site using a standard three scrub surgical prep)
    • 4-8 hrs after TMR, or 2-4 hrs after concentrate
    • Test the highest risk cows (i.e., within 60 days of calving), ~12 per group
  62. What is normal pH, and what does abnormal pH tell you?
    • Normal: >5.8
    • Marginal: 5.6-5.8
    • Abnormal: < 5.5
    • SARA present if 3 or more have pH < 5.5
  63. How can SARA be prevented?
    • Avoid overmixing or overprocessing TMR
    • Avoid excessive intake of CHOs
    • Avoid inadequate buffering (make sure there is adequate cud chewing!)
    • Avoid inadequate ruminal adaptation
  64. How can heifer-cow management affect laminitis?
    • House 1st calf heifers separately.
    • Allow heifers time (8 wk ideal) to adjust to post-calving environment
    • If mixing cows and heifers, move heifers in groups of 4 to 5 (stick together)
  65. What can cause increased muscle tone?
    • Seizures
    • Tetanus
    • Spastic paresis
    • Inherited periodic spasticity
    • Myopathic disorders:
    • Malignant hyperthermia
    • Caprine myotonia congenita
  66. What can cause decreased muscle tone?
    • Denervation
    • Botulism
    • Electrolyte imbalances (hypoK from Predef and hypoCa)
  67. What are the abnormalities of muscle rhabdomyolysis?
    • Increased CK, AST, LDH
    • Caused by infection, toxins, nutrition, ischemia, anesthesia compartment syndrome hypoperfusion
  68. What values do you expect for CK depending on etiology?
    • Increases if muscle injury, ~2-4 hrs half-life
    • Strenuous exercise = hundreds
    • Fatiguing exercise = low thousands (< 5000 IU/L)
    • Recumbency levels = typically < 3000 IU/L
    • Rhabdomyolysis = typically in the high 10s, 100s of thousands (lab needs to dilute sample)
  69. What values do you expect for AST/SGOT depending on etiology?
    • High: skeletal, cardiac muscle, liver, RBCs;
    • Increases more slowly than CK; peaks 12 to 24 hrs after injury and is more stable than CK so the t1/2 is measured in days
    • If increased CK + AST = recent active myonecrosis
    • If CK persistently elevated = muscle damage ongoing
    • If reduced CK & elevated AST = muscle damage not ongoing
  70. What is spastic paresis?
    • aka elso heel
    • seen in beef calves 2wks-7months of age and Pygmy goats
    • CS are straight hocks (can’t flex hock) from continuous gastrocnemius tension
    • Can be uni- or bilateral
  71. What is the pathophysiology of spastic paresis?
    Hyperactivity of gamma efferents
  72. How is spastic paresis tx?
    • Can try tibial neurectomy or gastrocnemius tenectomy
    • Better to just castrate!
  73. What is inherited periodic spasticity?
    • Episodic involuntary spasms affecting rear limbs, epaxial thoracolumbar muscles in dairy cattle
    • CS of crampiness, stretches, periodic spasticity, muscle trembling and backward extension of rear limbs after rising
  74. What is the etiology of inherited periodic spasticity?
    • Possibly a disorder of myotactic reflex or postural reflex mechanisms
    • Often associated with musculoskeletal pain (sore foot; other lameness)
  75. How is inherited periodic spasticity tx?
    • Treat any underlying lameness
    • Banamine, phenylbutazone (remember withdrawl), other NSAIDS
  76. What is fainting goat syndrome?
    • Autosomal dominant with incomplete penetrance from mutation in skeletal muscle Cl-channel
    • See signs by 6 weeks
    • Clinical signs are stiffness after rest, marked general rigidity after visual, tactile, or auditory stimulation, and are nonprogressive
    • Diagnosis is by EMG
  77. What is clostridial myositis?
    • Usually rapidly fatal
    • Infectious, not contagious
    • CS of Fever, tachypnea, tachycardia, anorexia, depression, lameness with swelling, pain, and crepitus at site of infection (from anaerobic gas production)
    • Cl. septicum causes malignant edema
    • Cl. chauvoei causes blackleg (if you're a chauvinist, you look at legs)
    • Cl. novyi (Type B) causes black disease (infectious necrotic hepatitis)
    • Cl. sordellii
    • Cl. perfringens
  78. What causes Bighead, Tetanus, and Redwater?
    • Cl. novyi Type A
    • Cl. tetani
    • Cl. hemolyticum
  79. How is clostridial myositis dx?
    • Clinical signs
    • Fluid aspirates for culture and FA
  80. What is the pathophysiology of clostridial myositis?
    • Found ubiquitously in the environment, feces, GI tract
    • Portal of entry = alimentary tract mucosa where spores become latent in liver & muscle tissue -> disease if tissue devitalized providing anaerobic environment (e.g. liver biopsy or liver flukes) OR external wound contamination
  81. What are the toxins in clostridial myositis?
    • Act locally and systemically to create widespread organ dysfunction
    • α - lecithinase
    • β - deoxyribonuclease
    • γ - hyaluronidase
    • δ - hemolysin
  82. What does an animal who died of clostridial myositis look like on necropsy?
    • Putrefaction with legs extended stiffly
    • Frothy, bloody discharge from the anus and nostrils
    • Foul odor (rancid butter) and congested lungs (edema)
    • Swelling, crepitus in affected muscles
  83. How is clostridial myositis tx?
    • Abx, fasciotomy, supportive care
    • Drug of choice is high dose IV K- or Na-penicillin or could use PPG (less expensive)
    • In outbreaks vaccinate or revaccinate herd
  84. What is the vaccine strategy for clostridial diseases?
    • Vaccinate young stock
    • If < 6 mos of age when they get initial series (i.e., primary and booster), booster again prior to one year
    • Revaccinate annually
  85. How can clostridial diseases be prevented?
    • Vaccinate
    • Remove carcasses (or all spores infect soil)
  86. What is sarcocystosis, and what is the transmission?
    • Find cysts in heart, esophagus and skeletal muscle (incidental at necropsy)
    • 2 host cycle where definitive host is carnivores and intermediate host is a ruminant
    • In cattle: S. cruzi (dog), S. hirsuta (cat), S. hominis (primates)
  87. How is sarcocystosis tx and prevented?
    • Amprolium or ionophore antibiotics before the 2nd stage of parasitemia
    • To control, prevent gross contamination of feed with feces!
  88. What is gossypol toxicity?
    • A phenolic pigment that binds protein and iron
    • Unbound or free gossypol is toxic
    • Clinical signs are ill thrift, weakness, decreased milk production, lack of spermatogenesis in bulls, death from liver (more with Pima var.)and heart failure
    • Naturally acts as an insecticide
  89. What [gossypol] is toxic?
    • Monogastrics, young calves <4mos should not > 100ppm = 0.01%
    • Mature ruminants tolerate 20 g of gossypol/hd/d = 5–6# cottonseed/hd/d
    • Rule of thumb: Don’t feed >7# cottonseed/hd/d
  90. What is toxic myopathy due to ionophores?
    • Mechanism: lipid-soluble complexes with cations to facilitate transport across lipid membranes
    • Use: growth promotants and coccidiostat and to prevent ketosis
    • Toxicity: causes rhabdomyolysis and cardiomyopathy. CS of anorexia, pica, diarrhea, hind limb ataxia, dyspnea, weakness, tachypnea
    • Necropsy: myocardial necrosis; pulmonary edema; pleural and peritoneal effusions; bloody pericardial effusion
  91. What are ionophores?
    • Monovalent: monensin (Na+), salinomycin and narasin (K+)
    • Divalent: lasalocid (Ca++ and Mg++)
  92. What is traumatic myopathy?
    • aka compartment syndrome
    • Decreased perfusion to down muscles causes mild elevations in CK from recumbency (probably <3000), unless there is actual muscle cell necrosis
  93. How is traumatic myopathy tx and prevented?
    • Txt: fix underlying cause, fluid therapy, NSAIDs, nursing care, good footing and bedding, flotation
    • Prevent: Careful positioning, draw down front leg forward, support upper limb, light anesthesia, IVF, positive inotropes
  94. What is nutritional myodegeneration (NMD) aka WMD?
    • Myodegeneration of cardiac & skeletal muscle
    • Young, rapid growing calves, lambs, kids
    • Selenium-deficient diets of dams in gestation
  95. How is WMD prevented?
    Correct Se and VitE deficiencies, esp Se def
  96. What are antioxidants, and why are they important?
    • Selenoproteins: glutathione peroxidases, deiodinase [converts T4 to T3], selenoprotein-P
    • VitE:
    • If antioxidant mechanisms overwhelmed, see membrane damage -> increased Ca -> damage to mitochondria -> impaired energy metabolism -> muscle hypercontraction, cell necrosis, hyalinization
  97. What is the common hx of animals that get WMD?
    • Young animals born in confinement and turned out early spring to exercise
    • Yearling cattle housed all winter, fed high grain diet with high moisture content and then suddenly turned out in the spring
  98. How do you dx WMD?
    • Chem: AST, CK, LDH
    • CK: very high 10’s, 100’s of 1000s
    • U/A: myoglobinuria often in yearlings
    • Blood Se (in ppm): 0.01-0.04 (deficient, should supplement), 0.05-0.06 (marginal, supplement often beneficial), >0.07 (normal). Can also measure blood Se by measuring RBC glutathione peroxidase
    • Liver selenium: normal = 0.25-0.5 ppm in cattle
  99. What are the CS of WMD?
    • Cardiac (acute-peracute): myocardial decompensation; tachypnea; resp distress; frothy nasal discharge; sudden death in <24 hrs usually 2-4 mos of age
    • Skeletal (slower onset): weakness, stiffness, recumbency, difficulty rising; stands briefly; lays down; swollen, firm, painful muscles; dysphagia; weak suckle if tongue affected
    • Cardiac form affects LV and septum in calves; both ventricles in lambs
  100. What do white bands on muscle necropsy mean?
    Bands of coagulation necrosis, fibrosis and calcification esp seen in WMD
  101. How do you tx WMD?
    • Cardiac involvement: tx rarely attempted
    • Skeletal muscle involvement: responds better but still guarded prognosis. Expect improvement in 3-5 days to stand or walk, but complications of pneumonia
    • Give Se: 0.055-0.067 mg/kg SC or IM (BO-SE, MU-SE)
    • Give VitE: Injectable (300 IU/ml as d-alpha-tocopherol, lasts ~ 3 weeks), oral (Emcelle, give daily)
    • Supportive therapy: abx, monitor fluid and electrolyte status
  102. How is WMD prevented?
    • Inject Se at birth (do not use Bo-Se in pregnant ewes, nor Mu-Se in third trimester theoretically)
    • Supplement with slow release oral formula once monthly (will often regurg)
    • Monitor herd q60-90 days, unless supplementing can monitor q6-12months
  103. What can cause Se deficiency?
    • Active growth plants that are high in linolenic acid (PUFAs have hydroperoxides that make toxic free radicals)
    • Acid soils, soil from volcanic rock, soil with high sulfur content are def in Se (blocks Se uptake by plants & absorption in GI tract)
    • Legumes accumulate less Se than grasses
    • Extended storage of grain has decreased Vit E
    • Calves fed milk replacers with fish oil, linseed oil, soybean or corn oil (all have increased PUFAs)
  104. What is exertional myopathy, and how is it dx?
    • Exercise intolerance, collapse with exercise
    • See elevated CK and can clinically look like WMD
    • Autosomal recessive inheritance
    • Diagnosis based on muscle biopsy and staining for phosphorylase on frozen sections, as well as presence of normal vitamin E/Se status
  105. What is myofiber hyperplasia?
    • congenital myopathy for double muscling in Belgian Blue, Piedmontese, South Devon
    • Increase in muscle Type 2B & reduced Type 1 and 2A
    • Dystocia and oral anomalies (tongue hypertrophy) are common
  106. What is ventral serratus rupture aka “flying scapula”?
    • Major component of sling for thorax between forelimbs
    • May occur with WMD
  107. What is peroneus tertius rupture aka cranial tibial, and how is it tx?
    • Peroneus tertius: distal femur to proximal metatarsal bone
    • Associated with trauma/struggling
    • Hock extended while stifle flexed
    • Tx: rest/support; ruptures in muscle belly more likely to recover than tendon/ or origin/insertion
  108. What is a pelvic adductor rupture, what is the tx and px?
    • Obturator, gracilis, pectineus muscles are ruptured
    • Caused at parturition or poor footing
    • Flotation or deep bedding with good footing to treat
    • Prognosis guarded
  109. What is a gastrocnemius rupture, and what is the tx and px?
    • Rupture at muscle-tendon junction common
    • Happens after lumbosacral epidural with lidocaine
    • See hock flexed while stifle extended
    • Treat with Thomas splint
    • Prognosis is poor
  110. What is normal synovial fluid?
    • Synovial cells: A=phagocytic; B=secretory (make hyaluronic acid)
    • Synovial fluid: plasma ultrafiltrate; should not clot
    • Cell composition: mononuclear cells ~ 90% of the total, MPN leukocytes ~10%, protein ~ 1.5 g/dL (but variable)
    • Viscosity: normal 2 cm stretch between two fingers (reduced viscosity from dilution, synovitis, or hyaluronic acid degradation)
  111. What is a mucin clot test?
    • To see if synovial fluid normal
    • 3 drops into 3 mL of 2% acetic acid (EDTA may interfere)
    • Shake gently
    • Normal = a tight, ropey clot
    • Abnormal = loose clot w/particles floating
  112. How do you collect synovial fluid?
    • Use RTT tube for culture
    • Use RTT & EDTA tube for cell count & general cytologic exam
    • Use Na-fluoride tube for glucose (to prevent bacteria from eating all the glucose)
  113. What characteristics does septic synovial fluid have?
    Very turbid, makes a clot, 50K-100K WBCs (90-95%), >4g/dL protein, flakes in mucin clot test
  114. How can infectious arthritis be dx?
    • Total nucleated cell count >25,000/ul OR PMN count > 20,000/ul or >80% polymorphonuclear cells
    • AND TP>4.5 g/dL
  115. What are the routes of infection causing infectious arthritis?
    • Foreign body (puncture)
    • Hematogenous
    • Calf with umbilical infection, septicemia
    • Extension of cellulitis from adjacent structure (eg. severe footrot)
  116. What bacteria can be seen in adult septic arthritis, and how do you dx?
    • T. pyogenes is most common adult bovine, also Strep, Staph
    • Don't culture - waste of money
    • Use indirect evidence like cell counts, gram stain, protein, ultrasound appearance
  117. What are the CS and dx of neonatal polyarthritis?
    • CS: Reluctance to bear weight, stiffness, joint effusion
    • Scleral injection, uveitis, hypopion, petechiae also if septic
    • Dx: PE, rads, synovial fluid cytology and culture, CBC, blood culture
  118. What aspect of arthritis symptoms might help narrow down the etiology?
    Physeal involvement not typical in mycoplasma polyarthritis
  119. What does neonatal polyarthritis look like on rads?
    • Lytic lesions (in physes too)
    • Physeal involvement not typical in mycoplasma polyarthritis
    • Radiographic changes in bone delayed up to 14-21 days after infection
  120. What are the common origins of hematogenous spread that causes neonatal polyarthritis?
    umbilicus, intestine (enteritis), pneumonia
  121. How can neonatal polyarthritis be prevented?
    high quality colostrum (FPT increases risk of sepsis)
  122. What bacteria cause neonatal polyarthritis?
    • Most common: enterics (E. coli; Salmonella)
    • Also Mycoplasma, will see concurrent otitis media, conjunctivitis, pneumonia
    • Less commonly Strep, Staph, T. pyogenes (older calves more likely)
  123. What is the txt and px for neonatal polyarthritis?
    • Joint lavage/arthrotomy
    • Long term broad spectrum antibiotics
    • If mycoplasma use chloraphenicol, macrolides, tetracyclines NOT beta lactams
    • Prognosis:favorable (early aggressive therapy) and guarded (multiple joints affected, delayed therapy)
  124. What is idiopathic gonitis?
    • Age: cattle 6-18 months
    • CS: effusion of lateral femorotibial joint, absence of joint laxity, less lame than septic arthritis
    • Dx: synovial fluid has high cellularity and TP but no bacteria and minimal/no neutrophil toxicity (beware - septic joints often don't see bacteria either). Radiographs show ±subchondral bone cysts (lateral tibial plateau; femoral condyles)
    • Txt: box stall rest, intra-articular steroids, parenteral and intra-articular antibiotics, joint lavage, arthrotomy/arthroscopy and surgical curettage, placement of egress and ingress drains.
    • Px: regardless of txt, 2/3 return to productivity
  125. What is a hock hygroma?
    • Chronic cellulitis of epidermis and subcutis over lateral hock following repeated trauma, which causes a bursa to form on lateral aspect of hock
    • Signifies there's a housing or environmental problem because she can't aly down without banging herself all up
    • Can become infected and require drainage and antibiotics
  126. What is precarpal bursitis?
    • Formation of a SC bursa over carpus that rarely involves carpal joint
    • Txt: sterile drain & wrap, can inject 10-20 cc renographin (makes scar tissue) & pressure wrap x 2 weeks with q5 d bandage changes, can insert drains (less cosmetic; not for show animals), or can sx remove
  127. What is subtendinous (calcanean) bursitis?
    • Septic bursitis of hock or bursa under SDF tendon ±osteomyelitis of calcaneus
    • Txt: drain via lateral incision followed by curetting/drain placement + antibiotics
    • Superficial flexor tendon should not be involved unless severe necrotic changes present
    • Px: guarded with osteomyelitis
  128. What does Mycoplasma cause, and how is it transmitted?
    • Diseases: mastitis, reproductive disease, respiratory disease, keratoconjunctivitis, otitis media
    • CS: facial and vestibular nerve deficits with bilateral or unilateral ear droop, ptosis, epiphora, head tilt and recumbency
    • Transmission: calves fed mycoplasma-contaminated colostrum or milk
  129. What causes mycoplasma arthritis in goats, and what are the CS?
    • Etiology: Mycoplasma mycoides ssp. mycoides (large colony type)
    • Pathophys: Stress -> shedding from chronic carriers, goat ear mites (Psoroptes cuniculi and Raillietia spp) may be a reservoir for M. mycoides ssp. mycoides
    • CS: Adults have fever, mastitis, pleuropneumonia and arthritis
    • CS: Kids have arthritis, septicemia, meningitis for 1-3 days then become BAR
    • Typical scenario: polyarthritis and pneumonia in kids concurrently with mastitis in does
    • Dx: PCR joint fluid (don't culture)
    • Txt: don't tx! Will cause chronic shedder, and no abx work very well
    • Px: Highest morbidity and mortality in young stock
    • Prevention: Isolate & perform milk cultures on herd additions; if doe dry at purchase, maintain isolation until culture at kidding and @ 2 and 4 weeks fresh or swab and culture ear wax (in dry does); if outbreak, heat treat colostrum
  130. What kind of virus is CAEV, and what cells are targeted?
    • Lentivirus
    • Targets monocytes and macrophages which localize in synovium, MG, CNS, lung (non-neutralizing antibodies produced and immune complexes cause chronic inflammation)
  131. How is CAEV transmitted?
    • Primarily colostrum and milk
    • Also in utero/ horizontal
    • Virus-infected cells in estrual mucus, preputial swabs, lochia post kidding, semen aspirated from tail of epididymis
    • So important to segregating infected/noninfected herdmates!
  132. What are the CS of CAEV?
    • Leukoencephalomyelitis:
    • 2-6 mos kids
    • Rear leg paresis or paralysis
    • Eat normally, alert, afebrile
    • Discomfort secondary to urine retention
    • Polysynovitis-arthritis:
    • Mostly in mature adults >2-3 years
    • Insidious onset
    • Carpus commonly affected
    • Chronic joint enlargement & weight loss
    • “Hard Bags”: mammary gland involvement
    • Decreased milk production; hungry kids; firm udder; milk looks normal
    • “Hard Lungs”: chronic interstitial viral pneumonia results in progressive respiratory distress/weight loss with or without evidence of polysynovitis/arthritis
    • Similar to ovine progressive pneumonia (OPPV) virus
  133. How is CAEV dx?
    • Joint fluid analysis:
    • Normal or increased volume
    • Brown-to-red tinged
    • Decreased protein
    • Increased cells (1000 to 20,000 cells/ul with 90% mononuclear cells
    • Contrasts with neutrophil increase typical of bacterial joint infection
    • CSF (on kids with leukoencephalomyelitis):
    • Increased CSF mononuclear cells
    • Official USDA tests:
    • AGID test using OPPV as antigen
    • Competitive ELISA (cELISA) – more sensitive
    • Test for maternal CAEV antibodies in kids up to 4 mos
  134. How is CAEV tx and prevented?
    • Tx: none, keep pet goats comfortable with NSAIDs, glucosamine, nursing care
    • Prevention:
    • Block transmission by contaminated milk or colostrum (use duct tape)
    • Isolate seropositive goats
    • Serologically monitor herd
    • Heat treat colostrum (too high = D), thoroughly mix! and watch temps!
  135. How does sacroiliac (sub)luxation occur?
    • Parturition, dystocia
    • Riding injury during breeding/heat
    • Predisposing factors like relaxation of pelvic ligaments (relaxin hormone)
  136. What are the CS and tx for sacroiliac (sub)luxation?
    • CS: subluxation = mild ataxia, rear limb weakness; luxation = severe posterior paresis, recumbency
    • Txt: rest, good footing, analgesics, NSAIDs, flotation therapy
  137. How does hip luxation occur?
    • Dystocia with sciatic (or ‘obturator’) paralysis
    • Slipping/falling due to weakness
    • Electrolyte weakness leads to struggle to get up -> splits
    • Neonates that are forcefully extracted if posterior presentation
    • Cranial dorsal is most common!
    • Caudal ventral is possible, determine by palpating femoral head per rectum through obturator foramen
  138. How is hip luxation tx, and what is the px?
    • 1) Limb is circumducted with maximal abduction (disperses blood/fluid)
    • 2) Attach a pulley and apply traction caudally while attempting to rotate the hock outward to forces femoral head medially back into acetabulum
    • 3) Apply hobbles and rest for at least 24 hours
    • Px: Younger animals, <12 hours duration, still standing, <400 kg, cranial luxation all correlated with better px
  139. What can cause flexural deformities in calves, and how is it tx?
    • Cause: Arthrogryposis, lupin ingestion by dam
    • Tx: choose cases carefully; conservative = splinting, support bandages, NSAIDs, toe extension shoes; invasive = sx to cut SDF / DDF tendons
  140. How much Cu is required for FA, and which animals are most susceptible?
    • Primary: if Cu in diet < minimum requirements (4-10 ppm in cattle, 5 ppm in sheep).
    • Young animals/fetus more susceptible than adult
    • Cattle more susceptible than sheep
    • Secondary: reduced availability of Cu due to high dietary Mo, S, Ca, Zn, Fe
    • Therefore keep Cu:Mo ratio more than 2:1, but 5:1 ideal for sheep and 6-10:1 ideal in grazing cattle
  141. What are the CS of Cu deficiency?
    • Enzootic ataxia/swayback, ill thrift, decreased immunity, anemia, reproductive inefficiency
    • Osteoporosis secondary to depressed osteoblastic activity -> spontaneous fractures and widened growth plates/metaphysis
    • Lysyl oxidase synthesizes collagen in connective tissue to mineralize bone; also aortic rupture reported in Cu deficient pigs
    • Achromotrichia because tyrosinase (Cu-dependent) converts L-tyrosine to melanin so you see diluted coat color
    • Diarrhea results from villous atrophy
  142. How is Cu deficiency dx, what are the expected results, and what can cause a false elevation?
    • Liver better than serum (serum decreases only when liver is depleted, and serum is slow to rise post supplementation)
    • Liver biopsy (or from necropsy) best! Ongoing basis
    • Sample at least 5 animals (want 25-100 ppm)
    • Before or after biopsy administer _______?
    • Ceruloplasmin is an acute phase protein, so serum Cu can be falsely elevated with inflammation
  143. How is Cu deficiency tx and prevented?
    • Some injectable forms (inj site abscesses) so oral supplementation preferred
    • Intraruminal boluses, top dressing of pastures, and or via addition of copper to salt mixes or a total mixed ration
    • Control competing dietary factors! Dietary Mo, S, Zn, Ca, Fe
    • Mineral mixes containing copper sulfate 0.25 – 0.5% in sheep, 0.2% in cattle
  144. What is physitis?
    • Age: 5-12 mos old; variable lameness
    • Etiology: overloading poorly formed metaphyseal bone and subsequent loss of structural integrity, microfracture, pain, and callus formation
    • CS: Enlarged, abnormal shaped distal physes (widened irregular physes; lipping)
    • Dx: CS, rads
    • Tx: Evaluate/adjust trace element status, pay attention to Cu, Zn, Ca, Ph
  145. What is osteochondrosis and OCD?
    • Osteochondrosis: abnormal physeal or epiphyseal cartilage growth
    • Osteochondrosis dissecans (OCD): a portion of articular cartilage splits off in an area of dysplastic subarticular cartilage and forms a flap
    • Caused by: rapid growth, nutrition, genetics, copper deficiency
    • CS: Joint effusion, mild to moderate lameness. Commonly in stifle, hock, shoulder
    • Dx: Rads, CBC, joint taps (aseptic)
    • Txt: Evaluate nutrition, correct macro/micronutrient deficiencies, rest
  146. What is osteodystrophy (rickets)?
    • Animals: young, rapidly growing animals
    • Etiology: P or VitD deficiency, inadequate exposure to direct sunlight, Ca def and excess dietary P causing nutritional secondary hyperparathyroidism; Mg, Zn, Mn, VitA deficiency
    • CS: bowlegged, stiffness, reluctance to move, lameness, joint enlargement, arching of the back, enlarged costochondral junctions
    • Dx: Thin cortices, bowing long bones, enlarged and widened physeal plates, irregular radiolucent band at meta- epiphyseal junction, physeal “lipping” (cattle with Cu deficiency may have physeal lipping). Need to determine ratio of bone ash:organic matter (bone ash is primarily CaP, normal = 3:2, rickets = 1:2 to 1:3)
    • Tx: Supplement with Ca2PO4 (23% Ca, 18.5% P), limestone plus a P source, injectable VitD
    • Prevention: balanced diet
    • Px: fair to good if ambulatory
  147. What is spider lamb syndrome?
    • aka ovine hereditary chondrodysplasia
    • Etiology: semilethal AR disease in Suffolk, Suffolk crossbred, and Hampshire sheep (lambs must be ss to show CS)
    • CS: angular limb deformities (“knock-kneed”, carpus valgus), kyphosis, scoliosis, concavity of sternum, crooked roman nose), failure to thrive
    • 2 syndromes: abnormal at birth (stillborn or die within days of birth, or die from scours and pneumonia by 1 month); develop abnormal signs 3-8 weeks (one or more limbs affected, decreased growth rate after 4-8 wks, eventually progresses til lamb can’t walk)
    • Dx: rads (widened irregular growth plates w/retained islands of cartilage, esp look at olecranon lateral and flexed); stillborn lambs may not exhibit radiographic changes.
    • Prevention: destroy carrier rams (can use carrier ewes to get market lambs or to progeny test rams)
    • Breeding stock classification: white - no known spider progeny, gray - sire or dam or sibling has produced a spider lamb but this individual has not, black - individual has produced a spider lamb
  148. When would you use a flotation tank?
    • Downer cow with no metabolic or skeletal reasons (i.e., fracture) for being down, and that the cow is alert (i.e., not sick with mastitis, metritis, or other metabolic disease).
    • To determine which limbs weight bearing or not (once standing in tank)
    • To facilitate faster recovery following development of recumbency (ie, get them up sooner than later!)
  149. What does tibial paralysis look like?
    • Characteristic knuckling of fetlock; slight dropped hock
    • Often secondary to calving paralysis (sciatic paralysis)
    • Txt is support wrap...maybe distal limb cast for 2-4 weeks (often more economical than leg wraps)
  150. What causes infectious bovine rhinotracheitis?
    • BHV1.1
    • aka rednose
  151. What diseases does BHV1 cause?
    • IBR (BHV1.1): resp, conjuctiva, ocular
    • Repro (BHV1.2): infectious pustulovulvovaginitis/balanposthitis, abortion
  152. What causes bovine herpes mammallitis?
  153. What causes fatal meningoencephalitis?
  154. What are the characteristics of IBR infection?
    • Caused by: BHV1.1
    • Pathogenesis: aerosol, fomites, genital secretions (semen, fetal fluids, tissues)
    • CS: abortions (late), conjuctiva, deep corneal vascularization, corneal edema (peripheral along limbus, so not pink eye)
    • Dx: paired serology, PCR
    • Prevention: vaccination (at 6mo with MLV, annually re-vx)
  155. Where are plant awn eye problems usually seen?
    conjunctival fornix, nasolacrimal duct, under 3rd eyelid
  156. What are the CS of plant awns in eyes?
    • Photophobia
    • Epiphora
    • Blepharospasm
    • **Limbic corneal ulceration**
    • Pinkeye secondarily
  157. How do you tx plant awn in the eye?
    • None, but good idea to recheck
    • Triple abx eye ointment
    • Parenteral antibiotics post removal may help prevent pinkeye but often heal spontaneously
    • Inspect under 3rd eyelid
  158. What are the characteristics of thelaziasis infection?
    • aka eyeworms
    • Caused by: Thelazia gulosa (cattle), T. skrjabini (cattle and horses), T. lacrymalis (horses), T. californiensis (dogs, sheep, and other wild mammals)
    • Life cycle: L3 larvae regurgitated from face fly crop during feeding; larvae develop over 3-6 weeks; adult worms can ulcerate eyes
    • Dx: direct observation
    • Txt: remove worms, levamisole, doramectin (Dectomax)
  159. What are the characteristics of entropion?
    • Most common eye disease in neonatal lambs
    • Congenital (primary): usually lower eyelid and bilateral
    • Acquired (secondary): upper or lower eyelid
    • CS: rubbing of the eye, ocular and nasal discharge, photophobia, epiphora, blepharospasm, corneal ulceration over lower (or upper if upper lid) half of cornea
    • Txt: inject penicillin (1-2 cc) into lower lid, skin staples to evert the lid, place 2-3 vertical mattress sutures
  160. What are 5 common sites of predilection for bovine lymphosarcoma?
    uterus, abomasum, epidural space, right atrium, retrobulbar LNs
  161. What are the characteristics of bovine cancer eye (ocular squamous cell carcinoma, OSCC)
    • In 10% of Herefords
    • Median age: 7.4 yrs
    • Cattle with nonpigmented periocular tissues most susceptible (~75% of affected cattle lack pigmentation)
    • UV exposure is risk factor
  162. What are the OSCC prescursors?
    • Plaque: dense white keratinized non malignant tissue located on the corneoscleral limbus or lid margin
    • Papilloma: cornified wart-like tissue usually from eyelid
    • Acanthoma: keratinized tumor shaped like a horn; the keratin can be removed from the surface of the tumor leaving a small invasive, malignant mass growing off corneal surface
  163. What is exenteration?
    Involves removal of the eye, adnexa, and part of the bony orbit
  164. What are three zoonotic proliferative cattle lesions?
    pseudocowpox, orf, bovine papular stomatitis
  165. How can you tell if a growth is malignant or metastatic?
    • Malignant = smelly
    • Metastatic = look for enlargement of submandibular, parotid, prescapular lymph nodes
  166. How do you tx OSCC?
    • Medical: hyperthermia (anesthetize and proptose eye with retrobulbar block, apply electrode probe across tumor, sensor keeps tissue between electrodes at 52°C, then rotate 90° and repeat) or cryotherapy (freeze and thaw x3, for tumors <0.5cm)
    • Surgery: 3rd eyelid removal, excise, exenteration (standing or under GA)
  167. What is infectious bovine keratoconjunctivitis?
    • aka pink eye
    • Caused by: Moraxella bovis (g- rod) and Moraxella bovoculi (g- cocci), has pili to adhere and cytotoxin
    • Peaks: July - Sept
    • Transmission: carrier cattle (eyes, vagina, nose), foxtails, flies, concurrent infx, DVMs
    • CS: corneal edema that starts centrally; central corneal ulcer
    • Dx: corneal swab culture
    • Txt: LA-200 and Draxxin are approved, conj inj penicillin, patch eye for comfort
    • Prevention: disinfect materials btw cows, fly control, foxtail control, vaccine (must be 4 wks before = June...and Cu/Se supp), ear tags
  168. What is infectious keratoconjunctivitis in sheep/goats?
    • Caused by: Mycoplasma (esp M. conjuctivae), Chlamydophila pecorum...M. ovis (g- cocci) is less important and can be found in healthy sheep and goats
    • CS: Conjunctival hyperemia, photophobia, blepharospasm, epiphora, becomes mucopurulent
    • Dx: corneal ulcer culture (Mycoplasma); conjunctival scrape, cytology or paired serology (Chlamydophila); culture or PCR (M. ovis)
    • Txt: self-limiting in a few weeks, tetracycline
  169. What causes microphthalmos?
    • Cattle: in utero BVD infection
    • Short horn cattle: large lids/3rd eyelid/entropion
    • Jersey calves: autosomal recessive disorder
    • Herefords: autosomal recessive encephalopathy, had skull malformation (doming)
    • Lambs: from seleniferous pastures
    • Piglets: VitA deficiency in sows
Card Set
FA Med Exam 3