Livestock Neuro Flashcards

1
Q

Common disease with Cortical signs

A
  • PEM
  • Salt poisoning/water deprivation
  • lead poisoning
  • Vit A deficiency
  • rabies
  • enterotoxemia type D (sheep)
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2
Q

Clinical signs - where is the lesion

  • ataxia
  • CP deficits
  • altered mentation (aggression, depression)
  • CN deficits
  • Opisthotonus
A

Cortical!

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3
Q

PEM!

  1. Full name
  2. Who gets it?
  3. What does it do?
  4. Main cause?
  5. CS?
  6. What can the eye signs tell us about the lesion location?
  7. Dx?
  8. Tx?
  9. Px
  10. Prevention
A
  1. Polioencehalomalacia
  2. Small ruminants > cattle > camelid
  3. Necrosis of cortical gray matter
  4. Decreased thiamine production due to rapid addition or inc in a high conc diet, grain overload/engorgement (thiamine is important in main metabolic pathway for glucose metabolism in brain)
  5. Cortical neuro signs & Cortical blindness (lack of menace, normal PLR, dorsomedial stabismus)
  6. Eye and optic nerve lesions = ipsilateral blindness; optic tracts and lateral geniculate lesions = contralateral blindness with normal PLR
  7. Response to thiamine can help increase suspicion of PEM… Histopath confirms
  8. Thiamine, Dexamethasone, supportive
  9. Depends on duration
  10. Supplement with thiamine, adapt to high grain diets,m prevent free choice grain access, limit dietary sulfur
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4
Q

Salt poisoning!

  1. Etiology
  2. Dx
  3. Tx
  4. Prevention
A
  1. high salt intake, water deprivation, followed by rapid water intake (cerebral edema!)
  2. Hx and clinical signs, clin path (serum or CSF Na >160), feed analysis, necropsy/histopath
  3. Slowly decrease serum Na levels, steroids, thiamin, supportive (poor prognosis)
  4. Management (waterers, correct mixing, etc)
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5
Q

Lead Poisoning! Toxic to cells!

  1. Occurrence
  2. Dx
  3. Tx
  4. Prevention
A
  1. Most common intoxicant of cattle (calves&raquo_space;»> cattle > others)
  2. Hx, clinical signs, rads - reticulum and CrV rumen, blood or urine Pb levels, basophilic stippling on RBCs
  3. Remove source, Ca EDTA chelation, Thiamine, Steroids, Cathartics, Supportive, Rumenotomy
  4. Clean the lead from the environment
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6
Q

Rabies!

  1. Incubation period
  2. Which form is most common in cattle?
  3. Recumbency seen within _____ days
  4. Death within ____ days
  5. Should you always have rabies in your list of ddx for neuro cases?
  6. Dx
  7. Tx
  8. Prevention
A
  1. 3-6 months
  2. PARALYTIC form (flaccid)
  3. 3-5 days
  4. 10 days
  5. Yep
  6. hx, clinical signs, post mortem (negri bodies)
  7. no tx - quarantine prev vaccinated or slaughter immediately
  8. Vaccinate
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7
Q

Pseudorabies!
aka Mad Itch
- who gets this?
- is the US free of this?

A

swine

Nope, still in feral pigs

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8
Q

TSE!

  1. Two main ones? Who does each affect?
  2. What kind of disease is this?
  3. How is it transmitted?
  4. Is scrapie heritiable?
A
  1. Bovine spongiform encephalopathy (Mad Cow) –> cows; Scrapie –> sheep and goats only
  2. Prion - abnormal form of normal protein
  3. BSE - feeding rendered animal proteins from infected animals or spontaneous mutation; Scrapie: classical - horizontal and vertical, atypical - spontaneous mutation
  4. No, requires susceptible genotype AND exposure - Genetic susceptibility testing has only been developed for sheep
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9
Q

TSE! part 2

  1. CS of BSE
  2. CS of Scrapie
  3. Dx of BSE
  4. Dx of Scrapie
  5. Is there any tx?
  6. Prevention
A
  1. Long incubation period (4-6 years). In dairy cows, anxiety or apprehension about entering the milking parlor is a common sign. Cattle also exhibit behavioral changes and can be apprehensive or belligerent
  2. Behavioral changes and pruritis are big signs
  3. No current antemortem testing available –> histopath of spongiform lesions
  4. Third eyelid or rectal mucosal biopsy test by western blot or IHC to ID scrapie prions in lymphatic tissues
  5. No tx, progressive to death
  6. no feeding of ruminant derived protein, genetic testing for resistance (classical scrapie in sheep), notifiable dz
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10
Q

Common disease with brainstem lesions

A

Listeriosis
TEME
Parelaphostrongylus tenuis

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11
Q

LIsteriosis!

  1. What causes it?
  2. Where is it found?
  3. CS of Neuro form
  4. Dx
  5. Tx
  6. Prevention/Control
  7. Zoonosis?
A
  1. L. monocytogenes, Gram + bacteria
  2. Grows in improperly stored silage or forages w/pH >5.4; also found in soil and GIT
  3. Fever!!! (early), anorexia, depression, ataxia, head pressing; CN V-XII deficits, particularly V ad VII, *** neuro form does not cause abortion
  4. hx (access to silage), CS, monocytosis in CSF, necropsy, brain tissue culture
  5. Abx - long term, supportive
  6. Remove the source
  7. Zoonotic
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12
Q
TEME!  
1. Full name 
2. Organism
3. Where does infection begin? 
4. Clinical signs? 
5. Dx? 
Tx? Vaccine? Px?
A
  1. Thromboembolic Meningoencephalitis
  2. Histophilus somni - Gram negative
  3. Respiratory disease. Endothelial cells –> cell death –> initiation of clotting cascade –> THROMBOSIS. Activation of immune system
  4. FEVER and asymmetrical neuro signs
  5. Dx = CSF analysis, CBC (septicemia) –> necropsy
    Tx = Abx
    Vaccine = there is one but it has questionable efficacy
    Px = fair if caught early
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13
Q

BVDV

  1. CNS lesions occur if infected between ___-_____ days of gestation
  2. Clinical signs?
  3. Dx?
  4. Tx?
  5. Px?
A
  1. 90-170 days
  2. CEREBELLAR HYPOPLASIA…. also hydrancephaly, hydrocephalus, hypomyelinogenesis
  3. Dx = clinical signs that are present at birth
  4. Px = not compatible with life
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14
Q

Where’s the lesion….

Weakness, ataxia (rear limbs > front limbs), exaggerated reflexes, quadriplegia, respiratory or cardiac arrest

A

Cervical spine

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15
Q

Where’s the lesion….

Weakness in front legs and ataxia in rear legs. Exaggerated reflexes in the rear legs

A

Thoracic spine

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16
Q

Where’s the lesion…

Normal front legs, ataxia and weakness in rear legs, +/- exaggerated reflexes, abnormal urination and defecation control

A

Lumbar spine

17
Q

Where’s the lesion….

Normal front legs, weakness in rear legs, flaccid tail and anal tone, abnormal urination and defecation

A

Sacral spine

18
Q

What is the common cause of spinal injury? What are the sites of occurrence?

A

Trauma, abnormal bone mineralization, lymphosarcoma

Sites: C2-C4, T10-13, L3-6

19
Q

What is the most common cause of spinal abscesses?

A

Most occur secondary to a pre-existing vertebral body abscess

  • FPT neonates
  • vegetative endocarditis
  • septic injection sites
20
Q

Tick Paralysis! aka Peripheral neuropathy

  1. Pathogenesis 2. Clinical signs
  2. Ddx?
  3. Tx?
  4. Px?
A
  1. Female, dermacentor ticks –> salivary neurotoxin –> blocks ACh release at NMJ
  2. Ascending flaccid paralysis
  3. Botulism, WNV, meningeal worm
  4. Shear animal and locate tick - remove injectable ivermectin
  5. Px worsens with increased duration of recumbency
21
Q

“Sweeney”

Atrophy of shoulder mm, subluxation of shoulder

A

Suprascapular n

22
Q

Inability to extend affected forelimb

A

Radial n

23
Q

Difficulty rising, unable to flex stifle

A

Femoral n

24
Q

Component of calving paralysis, knuckling over at the fetlock

A

Sciatic n

25
Q

Component of calving paralysis, splay-legged

A

Obturator n

26
Q

How can we treat calving paralysis?

A

Steroids, NSAIDs, Support (floating, slinging), Hobbles (if obturator n damage)