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CLIN SCI- NEUROLOGY > Large Animal Neurology > Flashcards

Large Animal Neurology Flashcards

1
Q

are brain diseases more common in livestock or horses

A

livestock

horses more common to have spinal cord disease

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2
Q

What might be a cause of Horner’s disease in horse

A

neck trauma- iatrogenic caused by injections

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3
Q

the extent of joint movement

A

dysmetria

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4
Q

What are challenging maneuvers used in an equine neurological examine

A

1) Head up and walk
2) Circling
3) Tail pull
4) backing
5) over a curb
6) Hill
7) blindfold

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5
Q

How might you describe ataxia in a horse

A

1) Truncal sway
2) Proprioceptive deficits
3) Inconsistent foot placement
4) Irregular irregularities
5) Interference
6) Excessive lifting of feet and uncontrolled placement
7) Does not seem to know where feet are placed

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6
Q

too little joint movement
-stiff / tin soldier

A

hypometria

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7
Q

too much joint movement
-floating: lifting thoracic limbs too high

A

hypermetria

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8
Q

What are signs of paresis in a horse

A

1) Toe dragging
2) Knuckling (on hills)
3) Stumbling
4) Inability to resist tail pull

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9
Q

The ataxia score in horses is on a scale of

A

1 to 5
0: No neurological deficits
1: Neurologic deficits just detected at normal gait but worsened by backing, turning, loin pressure, or neck extension
2) Neurologic deficits easily detected at the walk and exaggerated by backing, turning, loin pressure, or neck extension
3) Neurological deficits prominent at the walk with a tendency to buckle or fall with backing, turning, loin pressure, or neck extension, postural deficits noted at rest
4) Stumbling, tripping, and falling spontaneously at a normal gait
5) Horse recumbent

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10
Q

Grade this horse on ataxia scale:
No neurological deficits

A

Grade 0

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11
Q

Grade this horse on ataxia scale:
Neurologic deficits just detected at normal gait but worsened by backing, turning, loin pressure, or neck extension

A

Grade 1

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12
Q

Grade this horse on ataxia scale:
Neurologic deficits easily detected at the walk and exaggerated by backing, turning, loin pressure, or neck extension

A

Grade 2

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13
Q

Grade this horse on ataxia scale:
Neurological deficits prominent at the walk with a tendency to buckle or fall with backing, turning, loin pressure, or neck extension, postural deficits noted at rest

A
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14
Q

Grade this horse on ataxia scale:
Stumbling, tripping, and falling spontaneously at a normal gait

A

Grade 4

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15
Q

Grade this horse on ataxia scale:
Horse recumbent

A

Grade 5

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16
Q

What will you see in a horse with peripheral nerve damage / LMN

A

weakness predominates
postural deficits and ataxia (mild)

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17
Q

What will you see in a horse with spinal cord damage

A

1) Paresis
2) Ataxia
3) dysmetria
4) spasticity

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18
Q

What will you see in a horse with cerebellum damage

A

Ataxia
Intention tremors

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19
Q

What will you see in a horse with damage to the vestibular system

A

Ataxia
Head tilt
Postural deficits pronounced

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20
Q

What will you see in a horse with damage to brainstem

A

Ataxia
Weakness
Dysmetria
Dysphagia
anisocoria
dilated pupils possible

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21
Q

What will you see in a horse with damage to the cerebral cortex

A

Postural deficits
Seizures
altered mentation
blindness

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22
Q

You might see horner’s syndrome in horses with damage to the

A

C1-C5
C6-T2

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23
Q

Damage to what spinal cord segment might you see a horse with urinary incontience, fecal retention, hypalgesia tail and perianal
normal thoracic and pelvic

A

S3-S5

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24
Q

What might see you with damage to the coccygeal spinal segement in a horse

A

decreased tail tone
hypalgesia caudal tolesion
normal thoracic and pelvic

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25
Q

What might you see with damage to S3-S5 in a horse

A

1) Urinary incontinence
2) Fecal retention
3) Hypalgesia tail and perianal
*Normal thoracic and pelvic

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26
Q

What might you see with damage to T3-L3 in a horse

A

1) Proprioceptive deficits (rear)
2) Normal gait in front
3) Rear limb weakness
4) Spasticity, pelvic limbs

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27
Q

What might you see with damage to C6-T2 in the horse

A

1) Proprioceptive deficits, worse in front than in rear
2) Weakness
3) Thoracic limb muscle atrophy
4) +/- Horner’s syndrome

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28
Q

What might you see in damage to C1-C5 in the horse

A

1) Spastic gait, worse in rear limbs
2) Proprioceptive deficits
3) Weakness
4) +/- Horner’s syndrome

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29
Q

What is the main reason for cranial nerve disease in a horse

A

Guttural pouch disease (often affects CN 7 and/or 8)

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30
Q

What are the main causes of spinal cord disease in the horse **

A

1) Cervical Vertebral Compressive Myelopathy
2) Equine Protozoal Myeloencephalitis
3) Eqine Degenerative Myelopathy/ Equine Neuronal Dystrophy
4) Trauma
5) Neoplasia

** Wobbler, EDM, and EPM is the most common **

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31
Q

What will you see with radial nerve paralysis in the horse

A

non-weightbearing
dropped elbow
inability to advance the limb

Causes: humeral fracture, trauma, post anesthesia

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32
Q

What will you see with femoral nerve paralysis in the horse

A

1) Nonweight bearing
2) Flexion of stifle, hock, fetlock
3) Loss of sensation medially

Causes: trauma, post anesthesia, dystocia

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33
Q

T/F: there is no vaccine for equine protozoal myeloencephalitis

A

True

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34
Q

What are the 5 core vaccines for horses

A

1) Rabies
2) Tetanus
3) EEEV
4) WEEV
5) West Nile Virus

Risk based: Equine Herpes Virus 1/4 (1- doesnt do a lot against neurologic or abortion)

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35
Q

What are common cortical diseases in livestock

A

1) Polioencephalomalacia (PEM)
2) Salt toxicity / water deprivation
3) Lead poisoning
4) Vitamin A deficiency
5) Rabies
6) Transmissible Spongiform Encephalopathies

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36
Q

necrosis of the grey matter

A

polioencephalomalacia (PEM)

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37
Q

What is a main cause of polioencephalomalacia in livestock

A

thiamine (vitamin B1) metabolism dysregulation

decrease ATP-dependent Na/K and H20 transport across cell membranes leading to neuronal dysfunction and ultimately swelling and laminar cotrical necrosis

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38
Q

What is the pathogenesis of polioencephalomalacia in cattle

A

main cause
thiamine (vitamin B1) metabolism dysregulation

decrease ATP-dependent Na/K and H20 transport across cell membranes leading to neuronal dysfunction and ultimately swelling and laminar cortical necrosis

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39
Q

What are the clinical signs of polioencephalomalacia in livestock

A

1) Ataxia
2) Proprioceptive deficits
3) Altered mentation (aggression; lethargy)
4) cranial nerve deficits
5) Seizures, coma, death
6) Anorexia
7) Diarrhea
8) muscle tremors
9) head pressing, star gazing
10) Opisthotonus
11) Eye signs

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40
Q

What livestock is polioencephalomalacia most common in

A

small ruminants > cattle > camelids

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41
Q

cortical blindness *

A

an animal that is blind has an absent menance but a functional pupilary light reflex

*if they have this then cortex damage is likely

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42
Q

How do you diagnose polioencephalomalacia

A

history and clinical signs and response to treatment

Necropsy: edema, laminar necrosis, may fluoresce under UV light, findings also with Pb and Na toxicity

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43
Q
A
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44
Q

What is the prognosis of polioencephalomalacia

A

good prognosis- patient will likely respond well to thiamine treatment

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44
Q

How might livestock animals get salt toxicity or water deprivation

A
  • High salt intake
    -H20 deprivation followed by rapid H20 intake
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44
Q

Salt toxicity/ water deprivation pathophysiology

A

1) Na+ accumulates in neurons and CSF
2) Hyperosmolarity leads to reduced energy dependent Na+ transport and inefficient cell Na+ removal
3) Thirst receptors trigger H20 consumption
4) Water in the extracellular fluid then shifts intracellularly
5) CNS edema; increased intracranial pressure
6) Acute encephalopathy

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45
Q

What is the pathophysiology of lead toxicity

A

1) Entry through GI or respiratory systems
2) Sequestered in bone matrix
3) Pb is toxic to cells, especially in neurons and RBS
4) Pb inhibits enzymes at Cu, Zn, Fe binding sites
5) inhibits heme synthesis and decreases RBC life
6) Capillary dusfunction
7) CNS hemorrhage and edema

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46
Q

What is a major differential for cattle with rabies

A

Aujeszky’s

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47
Q

a prion disease- protease resistance
induced conformational changes
disrupts normal cellular functions
found in all cell memebranes, especially neurons

A

Scrapie- Bovine Spongiform Encephalopathy

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48
Q

What is the only way to diagnose bovine spongiform encephalopathy in cattle

A

post mortem

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49
Q

How is bovine spongiform encephalopathy transmitted

A

1) feeding rendered animal proteins from infected animals
2) spontaneous mutation

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50
Q

How is scrapie transmitted

A

1) Horizontal and vertal - not inutero but in the placenta
not heritable
requires susceptible genotype and exposure

2) atypical: spontaneous mutation

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51
Q

How do the clinical signs of BSE differ from scrapie

A

Both: behavior changes, abnormal gait

BSE: Ptyalism, reluctance to be milk, fasciculations, proprioceptive deficits, licking

Scrapie: Pruritus, biting, licking, grinding teeth, more aware, weight loss, cannibslism

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52
Q

What symptom is signficant in sheeps with scrapie

A

Pruritus

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53
Q

How do you diagnose bovine spongiform encephalopathy

A

*No antemortem test
1) Histopathology for lesions
2) Western Blot

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54
Q

How do you diagnose scrapie

A

1) 3rd eyelid or rectal mucosal biopsy
2) Histopathology specific brain region
3) Genetic risk factor (all breeds are susceptible

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55
Q

gram + bacteria that grows in forages with pH >5.4 (improperly fermented silage)
also found in soil and GI

A

Listeria monocytogenes

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56
Q

What are the clinical signs of Listeria monocytogenes

A

Neurologic form:
-Fever (early), anorexia, lethargy, ataxia, head pressing
-CN V-XII deficits
Septicemic form
Abortion form

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57
Q

What cranial nerve deficits can be seen with Listerioisis

A

CN V-XII deficits

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58
Q

gram negative bacteria that causes thromboembolic meningoencephalitis

A

Histophilus somni

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59
Q

Histophilus somni causes

A

thromboembolic meningoencephalitis
-fever
-asymmetric signs frequent
-oculuar: retinal hemorrhages, hyphema, hypopyon
-respiratory, polyarthritis reproduction

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60
Q

What is the meningeal worm that affects sheeps, goats, and camelid

A

Paraelaphostrongylus tenuis

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61
Q

What is the pathogenesis of Paraelaphostrongylus tenuis

A

1) Adults in subarachnoid space and cerebrospinal venous sinuses of deer

2) Ova: released into blood and escapes via lungs

3) Slugs and snails (intermediate host)

4) Aberrant hot ingest organisms and within 2 weeks larvae migrate from GI to spinal cord and brainstem

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62
Q

How do you diagnose Paraelaphostrongylus tenuis

A

1) Endemic area or white tailed deer exposure
2) Posterior paresis
3) Ataxia
4) Proprioceptive deficits
5) CSF eosinophilia and increased protein
6) Necropsy

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63
Q

How do you treat Paraelaphostrongylus tenuis

A

1) Fenbendazole- treat larvae in CNS (ivermectin only affect circulating larvae)
2) Supportive care

Prognosis is fair to poor
Prevention is to prevent exposure to deer and use guinea fowl to eat intermediae hosts

Monthly ivermectin injections

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64
Q

Why shouldnt you use ivermectins to treat current Paraelaphostrongylus tenuis infestations?

A

Ivermectins only affect the circulating larvae

*Use fenbendazole to treat larvae in the CNS

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65
Q

What are the clinical signs of cerebellar disease in livestock?

A

1) Proprioceptive deficits
2) Intention tremor
3) Opisthotonus
4) Strabismus
5) Mystagmus
6) Hypermetria

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66
Q

What are some examples of cerebellar disease in large animals

A

1) Cerebellar hypoplasia
2) Staggers- grasses
3) Storage diseases

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67
Q

What CNS lesions can occur due to bovine viral diarrhea virus

A

1) Cerebellar hypoplasia - clinical signs at birth
2) Hydrancephaly
3) Hydrocephalus
4) Hypomyelinogenesis

*Days 90-170 of gestation

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68
Q

When are CNS lesions present in BVDV infections?

A

Days 90-170 of gestation

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69
Q

How might a cow get cerebellar hypoplasia from BVDV

A

natural infeciton during days 90-170 of gestation or vaccination with a modified live vaccine

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70
Q

How might spinal injuries occur in livestock

A

1) Trauma *
2) Abscess *
3) Abnormal bone mineralization
4) Lymphosarcoma

Common sites:
C2-C4; T10-T13; L3-L6

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71
Q

What are common peripheral neuropathies in livestock

A

Suprascapular n
Radial n
Femoral n
Sciatic n (Calving)
Peroneal n
Tibial n
Obturator n (calving)

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72
Q

What nerves are common peripheral neuropathies associated with calving paralysis? *

A

1) Sciatic Nerve
AND
2) Obturator Nerve

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73
Q

How do you treat calving paralysis in cows

A

1) Corticosteroids; NSAIDs
2) Support, floating, slinging
3) Hobbles (obturator nerve)

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74
Q

How do you determine if a horse has neurologic disease

A

1) Abnormal Behavior: Altered mentation, seizures, coma, circling, head pressing

2) Loss of function: Unable to swallow, muscle atrophy, inability to void urine

3) Abnormal gait:

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75
Q

How do you evaluate the hypoglossal nerve in the horse?

A

tongue tone

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76
Q

How do evaluate accessory nerve in the horse

A

cranial neck muscle symmetry

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77
Q

How do you evaluate the vagus nerve in the horse

A

“Slap” test for laryngeal abduction

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78
Q

How do you evaluate the glossopharyngeal nerve in the horse

A

test the ability to swallow

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79
Q

How do you evaluate the vestibulocochlear nerve in the horse

A

1) Head tilt/turn
2) circling/leaning
3) response to environmental sounds

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80
Q

How do you evaluate the facial nerve in the horse

A

1) facial symmetry
2) rostral tongue sensation

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81
Q

How do you evaluate the abducens nerve in the horse

A

1) eye position- retraction
2) lateral movement

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82
Q

How do you evaluate the trigeminal nerve in the horse

A

1) Cutaneous sensation
2) Tone of mastication muscles
3) Ability to Chew

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83
Q

How do you evaluate the trochlear nerve in the horse

A

Eye position
ventrolateral

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84
Q

How do you evaluate the oculomotor nerve in the horse

A

1) Pupillary light reflex
2) Eye position
3) medial movement

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85
Q

How do you evaluate the optic nerve in the horse

A

1) Menace response
2) Pupillary light reflex
3) Dazzle reflex

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86
Q

How do you test the olfactory nerve in the horse

A

detection of hidden treat

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87
Q

What cranial nerves are affected by the guttural pouch disease

A

5, 7, 8, 9, 10

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88
Q

What is a common way for a horse to get facial nerve dysfunction

A

trauama from tight halter

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89
Q

What should you do if you see deficits of cranial nerves 5, 7, 8, 9, or 10

A

inspect the guttural pouch on that side

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90
Q

What are the most common guttoral pouch diseases that can lead to cranial nerve deficits

A

1) Strep equi equi- retropharayngeal abscess leading to emphyema
2) Guttoral pouch mycosis
3) Temporohyoid Osteoarthropathy -styohyoid junction is enlarged

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91
Q

What do you see with cervical vertebral compressive myelopathy or Wobblers

A

all 4 limbs
1) Symmetrical ataxia
2) Dysmetria
3) Paresis
*normal mentation, intact peripheral nerve function

caused by focal spinal cord compression

92
Q

CVCM affects primarily

A

young, large breed, fast growing, male horses

93
Q

What is the most common cause of non-infectious spinal cord disease in the horse

A

CVCM (Wobblers)

94
Q

What else do you see with CVCM

A

developmental orthopedic disease- multifactorial etiology, sometimes horses have OCD lesions elsewhere

95
Q

How might older horses have CVCM

A

secondary to degenerative joint disease affecting articular process joints and possibly intervertebral disk space

96
Q

How do you diagnose CVCM in horses

A

Survey Radiographs to see if there is good spacing for the spinal cord but do not give spinal cord information
final diagnosis is by CT myelography

97
Q

How do you treat CVCM in horses

A

1) Dietary caloric restriction in growing horses only (<1-2 years of age)
2) Cervical vertebral interbody fusion surgery: 65-70% of horses improve and return to atheletic use

98
Q

What kind of horses is dietary caloric restriction only helpful in for the treatment of CVCM

A

growing horses only that are <1-2 years of age

99
Q

What causes EPM?

A

1) Sarcocystis neurona
2) Neospora hughesi
*Range of disease defined by range of opossum

100
Q

Sarcocystis neurona has been found to cause

A

EPM

101
Q

Neospora hughesi has been found to cause

A

EPM

102
Q

Is EPM focal or multifocal

A

Multifocal progressive disease

103
Q

What is the lifecycle of Sarcocystis neurona

A

1) Definitive host, opossum, where replicates
2) Horse ingests sporocyst (aberrant host)

104
Q

What are the clinical signs of EPM

A

Variable- can involve the brain or the spinal cord

Spinal cord: asymmetry, muscle atrophy, ataxia, dysmetria, paresis

Brainstem:
CN VII, VIII
Seizures
Lethargy

105
Q

can EPM cause symmetrical disease? **

A

yes, occasionally therefore it is a main differential for CVCM

but it is primarily asymmetrical disease

106
Q

How do you diagnose EPM

A

It can be very challenging because there are variable clinical signs and there is a high seroprevalence
1) Surface antigen on serum and CSF of SAG2, 4/3 ELISA
2) Confirm intrathecal antibody production via serum:csf titer ratio

107
Q

Serum:CSF titer ratio to confirm intrathecal antibody production is important in EPM diagnosis but how might there be antibodies in the CSF *

A

1) Antibody production in the CNS
2) Leakage over an intact BBB
3) Leakage over a diseased BBB
4) Iatrogenic contamination during CSF collection

108
Q

How do you treat EPM

A

1) Ponazuril- Marquis: disrupts the apicoplast organelle which is a chloroplast related organelle important in energy metabolism and cell division
28 day treatment with 63% efficacy

2) Sulfadiazine/pyrimethamine (ReBalance)
3) Diclazuril

109
Q

Ponazuril is used to treat

A

EPM

110
Q

What is the mechanism of action of Ponazuril

A

disrupts the apicoplast organelle which is a chloroplast related organelle important in energy metabolism and cell division
28 day treatment with 63% efficacy

111
Q

EDM/eNAD is a

A

diffuse neurodegenerative disease caused by genetic and environmental factors with a predisposition to vitamin E deficiency

leads to symmetric ataxia and proprioceptive deficits

onset of 1-12 months of age then stabilizing within days to months

occasionally occurs in late-onset in older horses

112
Q

What causes equine degenerative myelopathy *

A

diffuse neurodegenerative disease caused by genetic and environmental factors with a

predisposition to vitamin E deficiency

113
Q

What are the clinical signs of EDM/eNAD

A

symmetric ataxia
proprioceptive deficits
decreased menace, lethargy, behavior change

114
Q

How do diagnose EDM/ eNAD

A

1) Suggestive by excluding CVCM, EPM, or EHM
2) EDM confirmation in the bloodline
3) Low serum vitamin E <2ug/mL
4) Deficient dietary vitamin E
5) Post-mortem confirmation

115
Q

How do you treat EDM/eNAD

A

1) Vitamin E supplementation

*Prognosis is poor, unlikely improvement of clinically affected animals is seen after supplementation

supplementation of breeding stock and young horses can reduce incidence and severity of the signs

116
Q

What are the common peripheral neuropathies in horses

A

1) Radial nerve/ Brachial plexus
2) Suprascapular n
3) Fmeoral n
4) Obturator n
5) Sciatic n

Affected motor nerve leads to hypotonic/atonic effector muscle and muscle atrophy

117
Q

What is Sweeney

A

Suprascapular nerve paralysis due to trauma to nerve at point of the shoulder

muscle atrophy of the supraspinatus, infraspinatus, and triceps leading to a very prominent scapular spine

abnormal gait with shoulder exo-rotation

used to see in old time with horses pulling carts and tack fixed in incorrect area

118
Q

What 2 things will you see with a horse with Sweeney

A

1) muscle atrophy of the supraspinatus, infraspinatus, and triceps leading to a very prominent scapular spine

2) Abnormal gait with shoulder exo-rotation

119
Q

What causes Sweeney

A

Trauma to the suprascapular nerve at the point of the shoulder

120
Q

What muscles become atrophied with Sweeney

A

1) Supraspinatus
2) Infraspinatus
3) Triceps

121
Q

What diseases are CORE for horses *

A

1) Rabies
2) Tetanus
3) Eastern Equine Encephalomyelitis
4) Western Equine Encephalomyelitis
5) West Nile Virus Encephalomyelitis

122
Q

Rabies virus remains infectious in a carcass for

A

<24 hours

123
Q

What animals serve as a reservoir for rabies

A

Bat
Skunk
Racoon
Fox

124
Q

What occurs in the Centripetal stage of rabies

A

virus travels in the peripheral nerves to the CNS at ~1cm/day

125
Q

What occurs during the central stage of rabies

A

the CSF contains virus

126
Q

What occurs during the centrifugal stage of rabies

A

the saliva contains the virus

127
Q

How do you diagnose rabies

A

post-mortem diagnosis: IFAT on brain tissue or presence of Negri bodies

128
Q

What are the clinical signs of rabies in horses

A

1) Ataxia and paresis (43%)
2) Lameness (29%)
3) Recumbency (14%)
4) Pharyngeal paralysis (10%)
5) Colic (10%)

129
Q

Horses with rabies develop a fatal encephalopathy within

A

5-7 days

130
Q

Tetanolysin causes _______ while tetanospasmin is a ______

A

tissue destruction

neurotoxin- travels through lymphatics to NMJ and then to CNS. Blocks GABA and glycine of the Renshaw cells

131
Q

tetanospasmin blocks ______ and _____ of the _________

A

blocks GABA and glycine of the renshaw cells of the spinal cord

132
Q

What are the clinical signs of tetanus in horse

A

Develop within 5-10 days of infection
1) Increased sensitivity/anxiety
2) Altered facial expression: Risus sardonicus, protrusion of 3rd eyelid, spasms of the masseter (Lockjaw)
3) Colic
4) Drooling- swallowing is impaired

133
Q

What altered facial expression in the horse do you see with tetanis

A

1) Risus sardonicus
2) Protrusion of the rd eyelid
3) Spasms of the masseter: Lockjaw

134
Q

How do you diagnose tetanus in horse

A

1) Clinical signs
2) Vaccination status

135
Q

How do you treat tetanus in horses

A

1) Protection from loud noises and light
2) Antibiotics
3) Tranquilizers
4) Tetanus toxoid
5) Tetanus antitoxin

prevent with tetanus toxoid

136
Q

What is the reservoir host for west nile virus

A

birds

137
Q

What is the reservoir host for eastern equine encephalitis virus

A

birds

138
Q

What is the reservoir host for venezuelian equine encephalitis virus

A

rodents

139
Q

What is significant about VEEV

A

there is a rodent reservoir host and horses serve as a secondary amplifying host

140
Q

T/F: both humans and horses are dead-end hosts and cannot spread West Nile Virus to others in their area because they do not develop significant viremia

A

True

141
Q

Why is west nile virus a reportable disease in horses

A

Because horses are more susceptible to west nile virus so when there are more cases of horses then cases in humans increase

142
Q

What are the clinical signs of encephalomyelitis in horses

A

Inapparent infections with fever about 2 days after infection
10% of cases develop signs
Incubation 9-11 days
Clinical 5 days after infection

Signs: Changes in mentation, cranial nerve deficits (blindness, head tilt, dysphagia), muscle twitching, recumbency, death 2-3 days later

143
Q

How do you treat equine encephalitides

A

1) supportive care
2) anti-inflammatories
3) Interferon
4) IgG

144
Q

How do you diagnose Encephalitides in horses

A

IgM capture ELISA:

IgM elevated for 4-6 weeks
and it allows for differentiation of vaccine from the disease

145
Q

How do you control for Encephalitides in horses

A

mosquito control (EEEV, WNV)
vaccination (WNV)
surveillance

146
Q

What is the prognosis for West Nile Virus in horses

A

30% can recrudesce within 2 weeks
10# of recovered animals retain long-term complications

80% mortality when recumbent

147
Q

What is the pathogenesis of EHV-1

A

1) Primary infection at the respiratory epithelium
2) Viremia
3) Infection of endothelial cells- thrombosis, vascular cuffing, and hemorrhage
4) Spinal cord grey and white matter - infrequently brainstem

148
Q

What are the clinical signs of EHV-1

A

severity varies
1) asymmetric ataxia, dysmetria, paresis
2) Dog sitting- discrepancy between thoracic and pelvic limb signs
3) loss of tail tone
4) bladder incontinence
Recovery depends on extent of damage

149
Q

Does EHV-1 cause symmetrical or asymmetrical ataxia

A

asymmetric ataxia,
dysmetria,
paresis

150
Q

What are the risk factors of EHV-1

A

1) outbreak of fever and respiratory disease
2) following return from event
3) fall-winter-spring
4) tall breeds

151
Q

What results in a horse to dog sit *

A

EHV-1 : ascending myelopathy -results in a significant discrepancy between thoracic and pelvic limb signs

results in dog-sitting, loss of tail tone and urinary incontinence (UMN bladder)

152
Q

What posture do you see with EHM

A

ascending myelopathy -results in a significant discrepancy between thoracic and pelvic limb signs

results in dog-sitting, loss of tail tone and urinary incontinence (UMN bladder)

153
Q

What is the mechanism of polioencephalomalacia

A

1) Decreased thiamine production- diet
2) Increased thiaminase activty
3) increased thiamine analogs
4) Dietary deficiency of thiamine
5) Increased sulfur diet or water (not thiamine responsive)

154
Q

Thiamine is an important cofactor of

A

Transketolase
Pyruvate DH

155
Q

What do you see with cortical diseases in livestock

A

Absent menace (CN II- blindness) - utilizes cortex
Functional pupillary light reflex ( CN II and III): utilizes the brainstem through the colliculi

156
Q

Livestock with polioencephalomalacia have dorsomedia strabismus. What is happening *

A

Trochlear Nerve is impacted
not a true paralysis but due to cerebral edema

157
Q

How do you prevent polioencephalomalacia

A

1) Supplement with thiamine
2) Adapt to high grain diets
3) Prevent free choice grain
4) Limit dietary sulfur

158
Q

How do you treat polioencephalomalacia

A

1) Thiamine: Vitamin B1 (NOT Vit B complex)
2) Dexamethasone
3) NSAIDs if pregnant
4) Supportive care

159
Q

How do you diagnose salt toxicity / water deprivation in livestock

A

1) History and clinical signs
2) Clinical Pathology:
-Serum/CSF Na+ >160mmol/L
-CSF/serum Na+ >1
-CSF osmolality >300 mOsm/L
-Feed analysis
-Necropsy /Histopathology

160
Q

How do you treat salt toxicity / water deprivation

A

1) Slow decrease of serum sodium: 0.3-1.0 mEq/K Na+ /hr
2) Corticosteroids
3) Thiamin
4) Supportive care

*Prognosis is poor

161
Q

How do you diagnose lead toxicity in livestock

A

History and clinical signs, looking around pasture
1) Radiographs: reticulum and cranioventral rumen
2) Blood or urine Pb (Pre and post EDTA if chronic)
3) Basophilic stippling on red blood cells

162
Q

what changes to RBCs will you see with lead toxicity

A

basophilic stippling

163
Q

How do you treat lead toxicity

A

1) Remove source
2) Ca EDTA chelation
3) Thiamine *
4) Corticosteroids
5) Cathartics
6) Supportive care
7) Rumectomy to remove lead, only if you know there are large pieces, likely unhelpful

Prognosis is variable

164
Q

What are the ethical concerns regarding lead in livestock*

A

Lead can be found in milk, meat bones
No acceptable levels states
Not tested for or reportable in the USA

owners need to be made aware

Half life in blood is 48-2507 (average=90 days)

recommendation: not use for food or milk

165
Q

What is the incubation period of rabies in cattle

A

3-6 months

166
Q

What are the clinical signs of rabies in cattle

A

1) Dumb form- lethargy
2) Paralytic form: flaccid paralysis (most common in cattle)
3) Furious form: hyperexcitable, fear, rage

Others: vocalization, pruritus, ataxia, lameness, dysphagia

recumbency 3-5 days and death within 10 days

167
Q

What is the most common form of rabies in cattle

A

Paralytic form: flaccid paralysis

168
Q

What is the post exposure management to rabies in livestock

A

Based on State Health department
vaccinated livestock: revaccinate and observe for 45 days

unvaccinated livestock: slaughter immediately or quarantine for 6 months

169
Q

what are the two prion diseases of livestock

A

1) Scrapie
2) Bovine Spongiform Encephalopathy

170
Q

Is scrapies a heritable disease

A

NO but the susceptibility to it is

it requires susceptible genotype and exposure to the prion

171
Q

What are the clinical signs of BSE?

A

Cows over 5-6 years of age
-Behavior changes
-Ptyalism
-Reluctance to be milked
-Fasciculations
-Proprioceptive deficits
-Abnormal gait
-Licking

172
Q

What are the clinical signs of scrapie

A

Goats 2-4 years old

-Behavioral changes
-pruritus
-biting, licking, grinding teeth
-more aware goats
-weight loss
-abnormal gait /ataxia
-cannibalism

173
Q

Unlike BSE, is the diagnosis of scrapie possible antemortem

A

Yes- take a biopsy of the 3rd eyelid or rectal mucosal biopsy

variable between sheep and goats

you can also do histopath of specific brain region

174
Q

What sites can you biopsy for scrapies diagnosis

A

Lymphoid follicles in
1) rectal mucosa *
2) third eyelid *
3) tonsillectomy
4) Lymphoid biopsy

175
Q

How do you treat BSE and scrapie

A

There is no treatment

*It is progressive to death

176
Q

How do you control for BSE and scrapie

A

1) No feeding of ruminant derived protein
2) Prevention through genetic testing for resistance- only for classical scrapie in sheep
3) REPORTABLE DISEASE

177
Q

Genetic testing for prion diseases is only capable in *

A

classical scrapie in sheep

(atypical and goat scrapie are under investigation)

178
Q

The neurologic form of listeria likely occurs from ________ while the septicemic and abortion form likely occur from ______

A

Neuro: aersol exposure of conjunctiva or respiratory tract

Abortion/Septicemic: ingestion of infected soil or feed

179
Q

What cranial nerve deficits do you see with listeriosis

A

CN V- XII

180
Q

How do you diagnose listeriosis

A

1) History: access to silage
2) Clinical signs- fever, anorexia, lethargy, ataxia, head pressing
3) CSF: increased mononuclear cells, cloudy, increased protein
4) CSF culture
5) Necropsy, histopathology- microabscesses
6) IHC of brain
7) Brain tissue culture (difficult)

181
Q

How do you treat listeriosis

A

1) Long-term antibiotics (IV tetracycline after 5 days change to long acting), Penicillin, or chloramphenicol
2) Supportive care
3) Consider flock/herd treatment
4) Prognosis is good if caught early
5) Remove from source and prevent contamination

182
Q

What does the CSF of listeriosis show

A

monocytosis or lymphocytosis
cloudy
increased protein

183
Q

What is the risk of listeria *

A

ZOONOTIC

Listeria can be transmitted in the milk and milk products
therefore pasteurize milk for human or animal consumption
carriers can shed bacteria for extended periods of time

184
Q

What causes thromboembolic meningoencephalitis in livestock

A

histophilus somni

(gram - bacteria)

185
Q

What is the septicemic manifestation of histophilus somni

A

thromboembolic meningoencephalitis

-fever
-asymmetric signs frequent- brainstem and any CNs
-ocular: retinal hemorrhages, hyphema, hypopyon
-respiratory, polyarthritis, reproduction, ears, udder

186
Q

What are the clinical signs of thromboembolic meningoencephalitis

A

-fever
-asymmetric signs frequent- brainstem and any CNs
-ocular: retinal hemorrhages, hyphema, hypopyon
-respiratory, polyarthritis, reproduction, ears, udder

187
Q

What is the pathophysiology of thromboembolic meningoencephalitis

A

1) Respiratory disease
2) Septicemia
3) Formation of microthrombi and micronecrosis
4) Endothelial cells undergo cell death and expose subendothelial collagen initiating the clotting cascade and leading to thromboses
5) Activation of immune system and inflammatory processes

188
Q

How do you diagnose thromboembolic meningoencephalitis

A

1) History and clinical signs (respiratory disease)
2) CSF: increased protein and neutrophils, hemorrhage, and xanthochromia (yellow staining)
3) CBC- septicemia
4) Necropsy with histopathology and culture
-Suppurative meningitis
-Necrotic meningoencephalitis

189
Q

How do you treat thromboembolic meningoencephalitis

A

1) Antibiotics (oxytetracycline)
2) Prognosis is fair is caugt early
3) Prevention through vaccination although effiacy is questionable (might make signs worse)

190
Q

What is the meningeal worm that infects sheeps, goats, and camelids

A

Parelaphostrongylus tenuis

191
Q

What is the lifecycle of Parelaphostrongylus tenuis

A

1) adults live in the subarachnoid space and cerebrospinal venous sinuses of white tailed deer
2) Ova is released into the blood, escape via the lungs
3) Slugs and snails act as intermediate hosts
4) Aberrant hosts ingests organisms
5) within 2 weeks larvae migrate from GI to spinal cord and brainstem

192
Q

How do you diagnose Parelaphostrongylus tenuis

A

1) Endemic area- deer exposure
2) Posterior paresis
3) Ataxia
4) Proprioceptive deficits
5) CSF eosinophilia and increased protein
6) Necropsy

193
Q

Can you use ivermectins to treat Parelaphostrongylus tenuis

A

only kills circulating larvae (injections only)

use fenbendazole to treat larvae in the CNS and the treatment of this disease

194
Q

How do you diagnose bovine viral diarrhea virus

A

1) Clinical signs and testing for antibodies
2) Virus neutralization: antibodies present in precolostral blood if they have cerebellar hypoplasia
3) Usually not persistently infected - infected critical time (30-125 days)
*not compatible with life

195
Q

In damage to the cervical spine, hyperreflexia is present in the limbs. Which limbs is it greater in?

A

Pelvic > Thoracic

196
Q

damage to what spinal cord segment results in cattle dog sitting

A

thoracic spine
-if sternal: pelvic limbs extended and not tucked under

197
Q

In livestock, what ticks commonly cause tick paralysis

A

Dermacentor ticks- neurotoxin present in saliva of some
only takes 1
blocks acetylcholine release at NMJ

198
Q

What are the clinical signs of tick paralysis in cattle

A

-Ascending flaccid paralysis
-Increasing stumbling and weakness
-Increasing recumbency
-Respiratory failure and death
-anorexia
-Can have >1 aniaml affected

199
Q

What are differentials for tick paralysis in livestock

A

1) Parelaphostrongylus tenuis
2) Heat stress
3) Botulism
4) Rabies
5) Trauma, tumor, etc

*Ascending flaccid paralysis
-Increasing stumbling and weakness
-Increasing recumbency
-Respiratory failure and death

200
Q

How do you diagnose tick paralysis in livestock

A

1) tick search (shear)

201
Q

What is used to treat tick paralysis in livestock

A

1) tick search (shear)
2) Injectable ivermectin *
3) Supportive care
*Can take 2-3 days to recover even when caught early

*Prognosis worsens with increased duration and recumbency

202
Q

What will you see in cattle with radial nerve injury

A

-Dropped elbow
-Leg held in flexion with flexed carpus, pastern, and fetlock
-Dorsum of foot the ground

203
Q

What do you see in cattle with femoral nerve injury

A

-Hyperextension of the hip
-Babies: forced traction if born in posterior presentation
-Inability to fix stifle or flexion

204
Q

In cattle, the sciatic nerve is most commonly damaged due to

A

1) Forced extraction over oversized fetus
2) Improperly placed IM injections

205
Q

What are clinical signs of sciatic nerve damage in cattle

A

-Dropped and extended stifle
-Knuckling of fetlock
-Atrophy of hamstrings and muscles distal to stifle

If peroneal branch is injured:
-Hyperextension of hock
-Knuckling of fetlock and hock
-Cutaneous analgesia of cranial lateral limb distal to stifle

206
Q

What will you see if the peroneal branch of the sciatic is injured

A

-Hyperextension of hock
-Knuckling of fetlock and pastern
-Cutaneous analgesia of cranial lateral limb distal to stifle

207
Q

The peroneal nerve often gets damaged when animals _________________

A

recumbent or paretic animals because it very superficial

208
Q

The peroneal nerve is responsible for

A

Flexes muscles of hock
and extends the muscles of the digits

Therefore: damage to the peroneal nerve (commonly when animals are recumbent for long times) would result in:

-Hyperextension of hock
-Knuckling of fetlock and pastern
-Cutaneous analgesia of cranial lateral limb distal to stifle

209
Q

What would occur if the tibial nerve of the sciatic is injured

A

-Flexion of hock
-No dragging of toe
-Pelvic asymmetry
-Atrophy of gastronemius
-Cutaneous analgesia of caudal medial leg

210
Q

What are common ways for the tibial nerve to be damage in livestock

A

1) Improver IM injections
2) Dog bite wounds in sheeps and goats

211
Q

What supplies motor innervation to the adductor muscles

A

Obturator nerve

damage to this caused abduction of the limb (splayed leg)

212
Q

What is a common reason for cattle to damage the obturator nerve

A

pelvic trauma associated with dystocia

(well protected in small ruminants)

213
Q

How do you treat obturator nerve paralysis

A

hobbling of the legs (tie to two legs together) so that the animal cant splay their leg and they can walk

214
Q

What nerves are associated with calving paralysis

A

both the sciatic and obturator nerve

-inability to bear weight (sciatic and tibial n)
-knuckling of fetlock (peroneal)

215
Q

One of your clients calls you to evaluate a cow that has gradually been developing abnormal behavior. Over the past 2 weeks, the cow has appeared more anxious and restless. More concerning is that the owner saw the cow having difficulty walking and she fell down in the hind end. She was able to get up, but the owner is concerned there is progressive neurologic disease. You evaluate the cow and find her to be very sensitive to touch and sound. You also notice the cow is in poor body condition (weight loss) and indeed has trouble walking and especially seems uncoordinated and weak in the hind limbs. What is your next step?

A

Contact the state veterinarian

216
Q

Can tetanus be effectively vaccinated against in horses

A

Yes

217
Q

Can Equine Herpes Myeloencephalopathy be effectively vaccinated against in horses

A

NO

218
Q

Can CVCM be effectively vaccinated against in horses

A

NO

219
Q

Can rabies be effectively vaccinated against in horses

A

YES

220
Q

Can West Nile Encephalitis be effectively vaccinated against in horses

A

Yes

221
Q

Can Eastern and Western Encephalitis be effectively vaccinated against in horses

A

Yes

222
Q

Can Equine Protozoal Myeloencephalitis be effectively vaccinated against in horses

A

NO

223
Q

What is the best first line diagnostic test for West Nile Virus Encephalitis

A

Serum IgM capture ELISA

224
Q

What is the best first line diagnostic test for Equine Herpes Myeloencephalopathy

A

PCR on nasal swabs

225
Q

What is the best first line diagnostic test for CVCM

A

Neck radiographs

226
Q

What is the best first line diagnostic test for EPM

A

CSF and serum antibody testing

227
Q

What is the best first line diagnostic test for CN VII and VIII deficits in horses

A

upper airway endoscopy

228
Q

You are concerned a valuable 1-year-old steer has developed polioencephalomalacia. The calf is not able to eat or drink effectively. You collect samples for diagnostic testing and start treatment. You are not concerned for lead toxicity based on environmental and nutritional evaluation. What treatments do you include?

A

-Transfaunation
-Oxytetracycline IV
-Dexamethasone
-Procain Penicillin IM
-Vitamin B1
-Fluid admin IV or oral

229
Q

You are presented with a 9 year old pet goat that suddenly developed neurological signs this morning. You examine him in the afternoon and the main findings are that the goat is circling to the right and has a head tilt to the right. There is no significant weakness. Which differential diagnoses do you consider?

A

-lead toxicity
-thiamine deficiency
-sulfur toxicity
-listeriosis
-salt toxicity

230
Q
A

CLIN SCI- NEUROLOGY (3 decks)

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