Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is West Nile virus infection diagnosed? Treated?

A

IgM ELISA serology

supportive care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

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

supportive care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is equine herpes myeloencephalitis diagnosed? Treated?

A

nasal swab PCR

supportive care + antivirals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is prognosis of equine herpes myeloencephalitis?

A

fair depending on severity; recovery is prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

biosecurity and quarantining new horses

EHV vaccines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What is prognosis of EPM like? How can it be prevented?

A

treatment usually improves clinical signs, but relapse and incomplete recovery are common

safe storage of feed and opossum control

26
Q

What is unique about horses and tetanus?

A

horses are one of the most sensitive animals to the neurotoxin of C. tetani

27
Q

What is the pathogenesis of tetanus? What is the incubation period?

A

Clostridium tetani enters through a wound (esp anaerobic) and proliferates to release a neurotoxin that travels to the CNS

1-3 weeks

28
Q

What are 4 classic clinical signs seen in horses with tetanus? What else is commonly seen?

A
  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
Q

How is tetanus diagnosed? Treated?

A

clinical signs, especially with history of a wound

Penicillin + tetanus antitoxin + supportive care

30
Q

What is prognosis like in horses with tetanus? How can it be prevented?

A

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
Q

What is the pathogenesis of rabies?

A

bite from infected wildlife –> several week to month incubation –> virus reaches CNS

32
Q

What clinical signs are indicative of rabies in horses?

A

progresses rapidly over a few days, clinical course rarely up to 2 weeks

  • self-mutilation
  • lethargy, anorexia
  • colic, dysphagia
33
Q

What are the 3 forms of rabies?

A
  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
Q

How is rabies diagnosed? What is prognosis like? How can infection be prevented?

A

negri bodies + fluorescent antibody on brain tissue on necropsy –> REPORTABLE

fatal and zoonotic

core annual or biannual vaccine

35
Q

Where is the prevalence of botulism highest in horses? What are 3 common risk factors?

A

mid-Atlantic, Eastern USA

  1. silage or ryelage as feed
  2. poorly stored forage
  3. round hay bales
36
Q

What is the pathogenesis of botulism?

A

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
Q

What clinical signs are indicative of botulism in horses? When do they begin?

A
  • symmetrical flaccid paralysis
  • gradually progressive weakness
  • respiratory paralysis = death
  • ileus, colic
  • mydriasis
  • poor tongue tone, dysphagia

1 day to 2 weeks post-ingestion

38
Q

How is botulism in horses treated? What is prognosis like? How can it be prevented?

A

botulinum antitoxin + supportive care

guarded to poor

vaccination + proper feed storage

39
Q

What is the pathogenesis of cauda equina (polyneuritis equi)?

A

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
Q

What clinical signs are indicative of cauda equina?

A
  • urinary/fecal incontinence
  • flaccid tail
  • ataxia is rare since lesions are mostly peripheral
41
Q

What 5 cranial nerves are commonly affected by cauda equina?

A
  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
Q

How is cauda equina diagnosed? Treated?

A

necropsy

supportive care –> poor long-term prognosis

43
Q

What is the pathogenesis of equine degenerative myeloencephalopathy (DEM)? What horses are most commonly affected?

A

vitamin E deficiency and genetic component cause severe neuroaxonal dystrophy

young horses <1 y/o

44
Q

What clinical signs are indicative of equine degenerative myeloencephalopathy (DEM)?

A
  • dull, quiet
  • symmetrical ataxia of all legs
45
Q

How is equine degenerative myeloencephalopathy (DEM) diagnosed? Treated?

A
  • rule out other causes of spinal ataxia
  • history of vitamin E deficiency

vitamin E supplementation (rarely successful)

46
Q

What is the pathogenesis of equine motor neuron disease (EMND)? What horses are most commonly affected?

A

chronic vitamin E deficiency causes peripheral motor neuron cell death

adult horses

47
Q

What clinical signs are indicative of equine motor neuron disease (EMND)? What is not seen?

A
  • weakness
  • low head carriage and high tail carriage
  • muscle atrophy and fasciculations
  • weight and muscle loss with good appetite

ataxia

48
Q

How is equine motor neuron disease (EMND) diagnosed? Treated?

A

biopsy + history of vitamin E deficiency

vitamin E supplementation –> rarely successful

49
Q

What horses are most commonly affected by cervical vertebral malformation (Wobblers, cervical stenotic myelopathy)?

A

large, fast-growing breeds –> Warmbloods, Thoroughbreds

50
Q

What is the pathogenesis of equine cervical vertebral malformation? What are the 2 types?

A

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
Q

What other differentials should be considered in horses with cervical vertebral malformations?

A
  • trauma
  • neoplasia
  • space-occupying lesion
52
Q

What clinical signs are indicative of cervical vertebral malformation in horses? What is not seen?

A
  • ataxia, usually worse in hindlimbs due to innervation being superficial in the spinal cord
  • poor performance
  • vague lameness

cranial nerve or brainstem signs

53
Q

How is equine cervical vertebral malformation diagnosed? Treated?

A

radiography + myelogram

“basket” surgery (ventral cervical vertebral stabilization) improves signs but usually only grade 1 affected horses return to performance

54
Q

What is the pathogenesis of sleep deprivation (pseudo-narcolepsy) in horses? What are the 2 ultimate causes?

A

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
Q

What clinical signs are indicative of sleep deprivation (pseudo-narcolepsy) in horses?

A
  • 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
Q

What are rare triggers of narcoleptic-type episodes in horses?

A
  • saddling
  • grooming

vaso-vagal response causes collapse

57
Q

What is treatment like for horses with sleep deprivation (pseudo-narcolepsy)?

A

fix reasons for poor sleep and prevent secondary injuries

  • high energy/anxiety
  • pain/lameness

NAVLE - Equine (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions