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NAVLE - Equine > Equine Neurologic Diseases > Flashcards

Equine Neurologic Diseases Flashcards

1
Q

What are the 6 grades of ataxia in horses?

A
  • 0 = normal
  • 1 = normal at rest, requires manipulative tests to see deficits
  • 2 = mild abnormalities at normal gaits, more pronounces deficits with manipulative tests
  • 3 = obvious deficits at all gaits
  • 4 = obvious deficits at all gaits, trips or falls easily
  • 5 = recumbent, unable to rise
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2
Q

When is West Nile virus most prevalent in the US? Why?

A

later summer or fall –> mosquito vectors

  • affects equines, avians, and humans
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3
Q

What is the pathogenesis of West Nile virus like?

A
  • maintained in wild birds
  • transmitted to horses and humans (aberrant hosts) by mosquito vectors
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4
Q

What clinical sign is highly suggestive of West Nile virus infection? What other signs are seen?

A

head, neck, and muzzle muscle fasciculations

  • ataxia
  • hind end paresis
  • recumbency
  • lethargy, depression
  • rarely febrile, most infections are not detected or asymptomatic
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5
Q

How is West Nile virus infection diagnosed? Treated?

A

IgM ELISA serology

supportive care

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6
Q

What is prognosis of cases of West Nile virus like? What signs specifically carry a poor prognosis?

A
  • horses with hx of vaccination have less severe signs and better prognosis
  • most horses with mild signs recover, but neurologic deficits may be lifelong

caudal paresis or recumbency

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7
Q

What are 4 methods of preventing West Nile Virus infection?

A
  1. eliminate standing water
  2. control mosquito larvae
  3. insect repellent
  4. annual or biannual vaccination
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8
Q

How is equine encephalitis (EEE, WEE, VEE) maintained in the environment? Which is zoonotic?

A

maintained in wildlife and spread to horses via mosquito vectors

VEE - through horses with high viral loads
(horses are dead-end hosts of EEE and WEE)

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9
Q

What clinical sign is characteristic of equine encephalitis (EEE, WEE, VEE)? What other signs are seen?

A

somnolence (sleeping sickness)

  • depression, anorexia
  • fever
  • head pressing
  • blindness
  • circling, ataxia, recumbency
  • coma, seizures
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10
Q

How is equine encephalitis (EEE, WEE, VEE) diagnosed? Treated?

A

CSF tap - mononuclear pleocytosis and increased protein (+ serology)

supportive care

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11
Q

What is prognosis of equine encephalitis (EEE, WEE, VEE) like?

A

poor - high mortality (WEE > EEE, VEE), recovered horses often have lifelong neurologic defecits

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12
Q

What are 3 major ways of preventing equine encephalitis (EEE, WEE, VEE)?

A
  1. EEE+ WEE core vaccines
  2. reduce mosquitoes
  3. eliminate standing water
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13
Q

What equine herpesvirus causes neurologic disease? Where are outbreaks more commonly found?

A

EHV-1 –> causes respiratory disease and mutates to wild-type that causes equine herpes myeloencephalitis

western US

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14
Q

What horses are more likely to be exposed to equine herpesvirus (myeloencephalitis)?

A

those that show or travel with frequent exposure to other horses

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15
Q

What is the pathogenesis of equine herpes myeloencephalitis?

A
  • respiratory EHV-1 mutates into wild-type or neurogenic form
  • causes vasculitis in the CNS
  • readily contagious
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16
Q

What are 2 sets of clinical signs indicative of equine herpes myeloencephalitis? What other signs may be seen?

A
  1. ataxia and paresis, especially in the hind end (dog sitting!)
  2. urinary incontinence and loss of tail tone
  • fever, lethargy, depression
  • concurrent respiratory signs (rare)
  • abortion in pregnant mares
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17
Q

How is equine herpes myeloencephalitis diagnosed? Treated?

A

nasal swab PCR

supportive care + antivirals

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18
Q

What is prognosis of equine herpes myeloencephalitis?

A

fair depending on severity; recovery is prolonged

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19
Q

How is equine herpes myeloencephalitis prevented? What is not proven to work?

A

biosecurity and quarantining new horses

EHV vaccines

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20
Q

What is the pathogenesis of equine protozoal myeloencephalitis (EPM)?

A
  • opossums are the DH of Sarcocystis neurona and pass feces infected with sporocysts into the horse’s environment
  • the horse ingests the sporocysts and become infected
  • sporocysts develop and mature and access the CNS to cause multifocal, asymmetrical damage
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21
Q

What new species has recently been found to cause some cases of EPM?

A

Neospora hughesi –> transmission is poorly understood

(Sarcocystis neurona more common)

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22
Q

What is the classic sign of EPM? What are some other signs?

A

chronic unilateral hind end muscle atrophy

  • shifting leg
  • vague asymmetrical lameness, weakness, and mild ataxia
  • rarely severely systemic –> horses are usually BAR
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23
Q

What is a common diagnostic for EPM? What is most accurate?

A

serology titers - difficult to distinguish between exposure and true disease (exposure is common, disease is rare)

CSF titers

24
Q

What is the best treatment for EPM? What are other options?

A

ponazuril (Marquis) for up to 6 months

pyrimethamine and sulfadiazine –> folate inhibitors

25
What is prognosis of EPM like? How can it be prevented?
treatment usually improves clinical signs, but relapse and incomplete recovery are common safe storage of feed and opossum control
26
What is unique about horses and tetanus?
horses are one of the most sensitive animals to the neurotoxin of C. tetani
27
What is the pathogenesis of tetanus? What is the incubation period?
Clostridium tetani enters through a wound (esp anaerobic) and proliferates to release a neurotoxin that travels to the CNS 1-3 weeks
28
What are 4 classic clinical signs seen in horses with tetanus? What else is commonly seen?
1. stiff, spastic gait 2. easily startled + extreme noise and light hyperesthesia 3. inability to open mouth - lockjaw 4. third eyelid prolapse initially vague and commonly mistaken for lameness or colic before signs progress, raised head and tail, recumbency
29
How is tetanus diagnosed? Treated?
clinical signs, especially with history of a wound Penicillin + tetanus antitoxin + supportive care
30
What is prognosis like in horses with tetanus? How can it be prevented?
guarded to fair if treatment is initiated early, poor with severe signs - annual tetanus toxoid vaccination - prophylactic tetanus antitoxin in unvaccinated horses with a wound
31
What is the pathogenesis of rabies?
bite from infected wildlife --> several week to month incubation --> virus reaches CNS
32
What clinical signs are indicative of rabies in horses?
progresses rapidly over a few days, clinical course rarely up to 2 weeks - self-mutilation - lethargy, anorexia - colic, dysphagia
33
What are the 3 forms of rabies?
1. FURIOUS (cerebral) - odd or aggressive behavior, self-mutilation, vocalization 2. DUMB (brainstem) - somnolence, dementia, dysphagia, ataxia 3. PARALYTIC (spinal cord) - progressive ascending paralysis
34
How is rabies diagnosed? What is prognosis like? How can infection be prevented?
negri bodies + fluorescent antibody on brain tissue on necropsy --> REPORTABLE fatal and zoonotic core annual or biannual vaccine
35
Where is the prevalence of botulism highest in horses? What are 3 common risk factors?
mid-Atlantic, Eastern USA 1. silage or ryelage as feed 2. poorly stored forage 3. round hay bales
36
What is the pathogenesis of botulism?
ingestion of Clostridium botulinum or preformed toxin +/- infection of wounds or castration sites --> toxin blocks acetylcholine vesicle release at neuromuscular junction preventing electrical signals
37
What clinical signs are indicative of botulism in horses? When do they begin?
- symmetrical flaccid paralysis - gradually progressive weakness - respiratory paralysis = death - ileus, colic - mydriasis - poor tongue tone, dysphagia 1 day to 2 weeks post-ingestion
38
How is botulism in horses treated? What is prognosis like? How can it be prevented?
botulinum antitoxin + supportive care guarded to poor vaccination + proper feed storage
39
What is the pathogenesis of cauda equina (polyneuritis equi)?
granulomatous perinueritis of peripheral nerves and cranial nerves thought to be caused by a immune-mediated event that may be triggered by other bacterial or viral infections
40
What clinical signs are indicative of cauda equina?
- urinary/fecal incontinence - flaccid tail - ataxia is rare since lesions are mostly peripheral
41
What 5 cranial nerves are commonly affected by cauda equina?
1. CN III - depressed PLR 2. CN V - masseter atrophy 3. CN VII - tongue weakness 4. CN VIII - head tilt 5. CN IX/X - difficulty swallowing
42
How is cauda equina diagnosed? Treated?
necropsy supportive care --> poor long-term prognosis
43
What is the pathogenesis of equine degenerative myeloencephalopathy (DEM)? What horses are most commonly affected?
vitamin E deficiency and genetic component cause severe neuroaxonal dystrophy young horses <1 y/o
44
What clinical signs are indicative of equine degenerative myeloencephalopathy (DEM)?
- dull, quiet - *symmetrical ataxia of all legs*
45
How is equine degenerative myeloencephalopathy (DEM) diagnosed? Treated?
- rule out other causes of spinal ataxia - history of vitamin E deficiency vitamin E supplementation (rarely successful)
46
What is the pathogenesis of equine motor neuron disease (EMND)? What horses are most commonly affected?
chronic vitamin E deficiency causes peripheral motor neuron cell death adult horses
47
What clinical signs are indicative of equine motor neuron disease (EMND)? What is not seen?
- weakness - low head carriage and high tail carriage - *muscle atrophy* and fasciculations - weight and muscle loss with good appetite ataxia
48
How is equine motor neuron disease (EMND) diagnosed? Treated?
biopsy + history of vitamin E deficiency vitamin E supplementation --> rarely successful
49
What horses are most commonly affected by cervical vertebral malformation (Wobblers, cervical stenotic myelopathy)?
large, fast-growing breeds --> Warmbloods, Thoroughbreds
50
What is the pathogenesis of equine cervical vertebral malformation? What are the 2 types?
compressive lesion from C3 to C7, either fixed or dynamic - TYPE 1 = congenital malformation --> young horses, often noticed when beginning of training - TYPE 2 = osteoarthritic --> older horses
51
What other differentials should be considered in horses with cervical vertebral malformations?
- trauma - neoplasia - space-occupying lesion
52
What clinical signs are indicative of cervical vertebral malformation in horses? What is not seen?
- ataxia, usually worse in hindlimbs due to innervation being superficial in the spinal cord - poor performance - vague lameness cranial nerve or brainstem signs
53
How is equine cervical vertebral malformation diagnosed? Treated?
radiography + myelogram "basket" surgery (ventral cervical vertebral stabilization) improves signs but usually only grade 1 affected horses return to performance
54
What is the pathogenesis of sleep deprivation (pseudo-narcolepsy) in horses? What are the 2 ultimate causes?
horse is unable to complete full REM sleep --> unable to lay down 1. behavioral - high energy or anxiety in housing situation 2. pain/lameness - reluctance to lay down and get up safely
55
What clinical signs are indicative of sleep deprivation (pseudo-narcolepsy) in horses?
- appears to fall asleep while standing - knuckle forward onto front fetlocks or carpi - rocking backwards with head low in a sleeping posture - horse may be found with wounds, most frequently chronic abrasions at dorsal fetlocks young foals (ponies, miniatures) may have episodes, but commonly resolve with age
56
What are rare triggers of narcoleptic-type episodes in horses?
- saddling - grooming vaso-vagal response causes collapse
57
What is treatment like for horses with sleep deprivation (pseudo-narcolepsy)?
fix reasons for poor sleep and prevent secondary injuries - high energy/anxiety - pain/lameness

NAVLE - Equine (22 decks)

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