CattleII- Neuro Dz

  1. Routes of entry of meningitis are usually through... (2)
    gut (ingestion) or navel (neonates)
  2. What are the most common agents of meningitis in calves? (2)
    Salmonella dublin, E. coli (NOT ETEC)
  3. Describe the pathophysiology of meningitis in neonates.
    poor passive antibody transfer--> bacteria cross bloodstream b/c poor immune system function--> bacteria distribute to multiple sites (CNS, eye, joints)--> inflammation of meninges
  4. Describe the diagnosis of meningitis.
    CSF: cells >100, neutrophils, +pandy
  5. What are the treatments for neonatal meningitis? (3)
    Banamine, aspirin, antibiotics (SMZ-TMP, florfenicol, cefotaxime)
  6. How can neonatal meningitis be prevented? (3)
    ensure adequate colostrum, clean environment for calving, clean calf hutches
  7. What are the most common potentiating factors of hypoglycemia of calves?
    usually seen in the first 48hr of life or as a complication of scours
  8. Clinical signs of hypoglycemia. (4)
    normal to subnormal temperature, depression, later convulsions and stupor
  9. What is the treatment for neonatal hypoglycemia? (3)
    bolus glucose, re-warm animal (if temp is low), if septic give antibiotics
  10. What are clinical syndromes of hypomagnesemia? (3)
    • 2-3month old calves: whole milk tetany
    • adults cows: early spring on pasture- grass tetatny
    • lambs being transported: low Mg and Ca- transport tetany
  11. Clinical signs of hypomagnesemia. (8)
    restlessness, irritability, spastic gait, frequent urination, bellowing, hyperesthia, convulsions, death
  12. Describe the pathogenesis of whole milk tetany.
    • young ruminants absorb Mg in the SI, which reduces as they age
    • milk is a poor source of Mg, so around 2-4m they are prone to deficiency (decreased absorption couple with low amount in milk)
  13. Describe the pathogenesis of grass tetany.
    • adult ruminants absorb Mg from rumen, rectum, colon
    • in early spring, cold ground slows plant uptake of Mg so diets become deficient
  14. How can you evaluate Mg levels when attempting to diagnose tetany? (3)
    blood Mg below 1.5, CSF Mg below 1, vitreous humor PM
  15. What is the treatment for tetany? (3)
    Mg and Ca salts IV, MgO PO, MgSO4 SQ
  16. What are congenital causes of cerebellar hypoplasia? (2)
    BVDv, heritable in holsteins
  17. What defects may be apparent with BVD infection in utero? (3)
    cerebellar hypoplasia (intention tremors, wide based stance), cataracts, micro-ophthalamia
  18. What is the difference b/w type I and II hydrocephalus?
    • I: domed forehead, open fontanelles
    • II: closed fontanelles
  19. Clinical signs of hydrocephalus. (4)
    [spectrum] none, won't suckle, domed head, depression/ somnolence
  20. Cerebellar abiotrophy is a heritable problem in ___________, which is characterized by...
    Holsteins; normal at birth, after 3 months--> ataxia, hypermetric gait, tremors, good appetite, normal TPR, progressive signs
  21. Why would covering the animal's eyes with a blindfold makes the signs of cerebellar abiotrophy more pronounced?
    because there is so much visual compensation
  22. What is Weaver Syndrome?
    Bovine Progressive Degenerative Myeloencephalopathy- almost clinically identical to cerebellar abiotrophy, except it occurs in Brown Swiss cows (heritable)
  23. Neurologic disorders of the neonate. (9)
    • cerebellar hypoplasia
    • hydrocephalus/ hydrancephaly
    • mannosidosis
    • cerebellar abiotrophy/ Weaver syndrome
    • meningitis
    • hypoglycemia
    • hypoMg
    • vit A deficiency
    • enterotoxemia C
  24. Neurologic disorders of 3 months- 2 years old. (9)
    Histophilus somnus, Listeriosis, Pseudorabies, IBR encephalitis, poliencephalomalacia, bonkers, nervous coccidiosis, hypoderma, hypoMg
  25. Reportable neurologic disease of which Ohio is certified free.
  26. Polioencephalomalacia is _____________, which is associated with ___________.
    cerebral cortical necrosis; thiamine deficiency (Vit B1)
  27. B vitamins are usually a product of ___________.
    ruminal fermentation
  28. What are possible mechanisms of polioencephalomalacia? (3)
    • disruption of rumen microflora--> no more production of B vitamins (low roughage diet, diets high in sulfates/ molasses)
    • Clostridium sporogenes and Bacillus--> produce thiaminase in the rumen
    • impaired glucose metabolism--> resulting in cerebral edema
  29. Clinical signs of polioencephalomalacia. (7)
    • initially, isolation, disorientation
    • depression, head pressing
    • bruxism
    • blindness (absent menace, striabismus)
    • convulsions
  30. How is polioencephalomalacia diagnosed?
    • measure transketolase in RBC (board's question)
    • response to treatment (thiamine hydrochloride (IM/IV)
  31. What is the treatment of polioencephalomalacia? (3)
    • thiamine IV or IM
    • mannitol, furosemide to reduce brain edema
  32. Histophilus somnus causes...
    thrombotic meningoencephalitis sleeper syndrome
  33. Clinical signs of Histophilus-associated CNS disease are seen only with the ___________ form of disease.
    respiratory (as opposed to repro tract form)
  34. Describe the pathogenesis of Histophilus TME.
    Histophilus colonized lung after viral insult (opportunist)--> endothelial damage to vessels--> cytotoxin--> microthrombi formation--> thrombi create ischemic injury to cerebral cortex
  35. What is the characteristic stance of Histophilus TME?
    soles planted normally on the ground, but fetlocks are buckled forward "rocking forward on fetlocks"
  36. How is Histophilus TME diagnosed?
    • clinical signs: respiratory disease, knuckling fetlocks, down/ stuporous
    • CSF: neutrophils, +pandy (inc globulin protein)
  37. Gross pathology associated with Histophilus TME. (3)
    ischemic infarcts throughout cerebral cortex and spinal cord, synovitis, pneumonia
  38. What is the treatment for Histophilus TME?
    • [MUST INITIATE TXT BEFORE THEY GO DOWN, otherwise useless]
    • penicillin, cephalosporin, oxytet, tilmicosin, florfenicol
  39. Describe the effectiveness of Histophilus vaccines.
    they work better in the prevention of TME than they do to prevent respiratory disease
  40. What is the one disease that causes monocytic CSF infiltration, rather than neutrophilic?
  41. What is the usual source of infection with listeriosis?
    corn silage
  42. Describe the pathogenesis of listeriosis.
    ingestion of Listeria monocytogenes--> abrasions in mouth--> bacteria access trigeminal n. by lacerations in oral mucosa--> migrate up nerve to brainstem (takes ~7 days)--> unilateral brain infection, lateralizing signs
  43. Clinical signs of listeriosis reflect damage to which cranial nerves?
    V, VII, VIII, IX, and XII
  44. Clinical signs of listeriosis. (6)
    problems with mastication/ glutition, salivation, ptosis of eyelid, ear droop, lip droop, unidirectional circling--> ALL UNILATERAL
  45. How is listeriosis diagnosed?
    • CSF: lymphocytes, elevated protein
    • clinical signs
  46. What is the treatment for listeriosis?
    oxytet, florfenicol, fluids, correct acid-base (excess salivation--> loss of bicarb), supportive (can't drink, eat, blink)
  47. Clinical signs of nervous coccidiosis. (5)
    intestinal signs (diarrhea +/- blood, ill thrift), muscle tremors, convulsions, opisthotonos (backwards arching of the head), nystagmus
  48. How is nervous coccidiosis diagnosed?
    fecal float
  49. What is the treatment of nervous coccidiosis? (5)
    [very poor prognosis btw] tranquilizers, anti-convulsants, amprolium, albon, decoquinate
  50. Pathogenesis of tetanus.
    Clostridium tetani spores contaminate wound site (common in uterus in adults)--> toxin taken into nerve cells--> toxin migrates backwards to spinal cord--> interneurons in spinal cord continuously stimulated--> tetanic spasms of muscles
  51. Clinical signs of tetanus. (7)
    stiff, stilted gait, pump handle tail, prolapse of 3rd eyelid, hyperesthia with muscle spasms, death due to respiratory failure
  52. Treatment of tetanus. (4)
    • antitoxin
    • debride wound site
    • penicillin
    • sedatives to control hyperesthia- Diazepam, Ace
  53. How can you prevent tetanus?
    vaccination with tetanus toxoid early in life (CDT vaccine)
  54. What 3 nasopharyngeal bacteria are commonly implicated in otitis media/interna?
    Mannheimia, Pasteurella, Mycoplasma
  55. Clinical signs of otitis media. (6)
    circling in one direction, loss of equilibrium, unable to rise, ear droop, febrile, +/- exudation from ear canal
  56. Describe the diagnosis of otitis media. (3)
    normal CSF, presence of exudate from external ear canal, clinical signs
  57. Treatments for otitis media. (5)
    (antibiotics commonly used in BRD) florfenicol, ceftiofur, tilmicosin, banamine, antihistamine
  58. What causes sinusitis?
    dehorning--> exudation into frontal sinuses--> direct pressure on brain
  59. Clinical signs of sinusitis. (5)
    abnormal head carriage (nose carried high), head pressing, squinting, depression, distortion of frontal bones
  60. Diagnostic features of sinusitis. (2)
    dull percussion over frontal sinus, normal CSF (unless erosion of cranial vault)
  61. Treatment for sinusitis. (3)
    open dehorn sites, trephine frontal sinus, flush daily [relieve pressure, remove exudate]
  62. Etiology of pseudorabies.
    herpesvirus (natural host is pig- cattle are dead end host)
  63. What are characteristics of pseudorabies infection in cattle.
    aka Aujeszky's disease or Mad itch; short incubation period (90hr)
  64. Clinical signs of pseudorabies. (8)
    intense localized pruritus leading to self-mutilation, fever, +/- aggressive behavior, paralysis, muscular twitching, convulsions, staggering
  65. Describe the pathogenesis of pseudorabies.
    neurotropic virus attaches to peripheral nerves, migrating up to the spinal cord
  66. How is pseudorabies diagnosed?
    submit spinal cord (from an area innervating the dermatomes) to state diagnostic lab
  67. 3 distinct pathogeneses of botulism.
    • [all caused by C. botulinum] preformed toxin ingestion, toxicoinfectious botulism, wound contamination 
    • toxin elaborated in GI, absorbed and carried to peripheral nerve ending
  68. Clinical signs of botulism in cattle? (5)
    progressive weakness of muscles, drooping head, tongue paralysis, increasing respiratory difficulty--> death
  69. Botulism sorta looks like __________ but doesn't have to occur around _________.
    milk fever; parturition
  70. Treatment of botulism. (3)
    ultrahigh doses of penicillin, artificial ventilation, botulism antitoxin
  71. BLADS is heritable in ___________ and is characterized by...
    Holsteins; leukocytes lack ability to adhere to vessel walls (can't leave circulation)
  72. Clinical signs of BLADS. (4)
    recurring infections, gingivitis, periodontal diseases, elevating leukocyte counts inappropriate for type of infection
  73. How do you diagnose BLADS?
    • BLAD testing (ImmGen)- genomic DNA isolated from milk
    • WBC counts >100,000cells/μL
  74. What is alpha-mannosidosis?
    heritable CNS storage defect of angus, murray grey cattle, resulting in accumulation of mannose in neurons, macs, and RE cells
  75. What are clinical signs of alpha-mannosidosis?
    1wk-1year old; rear limb ataxia, tremors, aggression [accentuated by excitement]
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CattleII- Neuro Dz
vetmed CattleII