Equine Neurologic Diseases Flashcards
What are the 6 grades of ataxia in horses?
- 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
When is West Nile virus most prevalent in the US? Why?
later summer or fall –> mosquito vectors
- affects equines, avians, and humans
What is the pathogenesis of West Nile virus like?
- maintained in wild birds
- transmitted to horses and humans (aberrant hosts) by mosquito vectors
What clinical sign is highly suggestive of West Nile virus infection? What other signs are seen?
head, neck, and muzzle muscle fasciculations
- ataxia
- hind end paresis
- recumbency
- lethargy, depression
- rarely febrile, most infections are not detected or asymptomatic
How is West Nile virus infection diagnosed? Treated?
IgM ELISA serology
supportive care
What is prognosis of cases of West Nile virus like? What signs specifically carry a poor prognosis?
- 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
What are 4 methods of preventing West Nile Virus infection?
- eliminate standing water
- control mosquito larvae
- insect repellent
- annual or biannual vaccination
How is equine encephalitis (EEE, WEE, VEE) maintained in the environment? Which is zoonotic?
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)
What clinical sign is characteristic of equine encephalitis (EEE, WEE, VEE)? What other signs are seen?
somnolence (sleeping sickness)
- depression, anorexia
- fever
- head pressing
- blindness
- circling, ataxia, recumbency
- coma, seizures
How is equine encephalitis (EEE, WEE, VEE) diagnosed? Treated?
CSF tap - mononuclear pleocytosis and increased protein (+ serology)
supportive care
What is prognosis of equine encephalitis (EEE, WEE, VEE) like?
poor - high mortality (WEE > EEE, VEE), recovered horses often have lifelong neurologic defecits
What are 3 major ways of preventing equine encephalitis (EEE, WEE, VEE)?
- EEE+ WEE core vaccines
- reduce mosquitoes
- eliminate standing water
What equine herpesvirus causes neurologic disease? Where are outbreaks more commonly found?
EHV-1 –> causes respiratory disease and mutates to wild-type that causes equine herpes myeloencephalitis
western US
What horses are more likely to be exposed to equine herpesvirus (myeloencephalitis)?
those that show or travel with frequent exposure to other horses
What is the pathogenesis of equine herpes myeloencephalitis?
- respiratory EHV-1 mutates into wild-type or neurogenic form
- causes vasculitis in the CNS
- readily contagious
What are 2 sets of clinical signs indicative of equine herpes myeloencephalitis? What other signs may be seen?
- ataxia and paresis, especially in the hind end (dog sitting!)
- urinary incontinence and loss of tail tone
- fever, lethargy, depression
- concurrent respiratory signs (rare)
- abortion in pregnant mares
How is equine herpes myeloencephalitis diagnosed? Treated?
nasal swab PCR
supportive care + antivirals
What is prognosis of equine herpes myeloencephalitis?
fair depending on severity; recovery is prolonged
How is equine herpes myeloencephalitis prevented? What is not proven to work?
biosecurity and quarantining new horses
EHV vaccines
What is the pathogenesis of equine protozoal myeloencephalitis (EPM)?
- 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
What new species has recently been found to cause some cases of EPM?
Neospora hughesi –> transmission is poorly understood
(Sarcocystis neurona more common)
What is the classic sign of EPM? What are some other signs?
chronic unilateral hind end muscle atrophy
- shifting leg
- vague asymmetrical lameness, weakness, and mild ataxia
- rarely severely systemic –> horses are usually BAR
What is a common diagnostic for EPM? What is most accurate?
serology titers - difficult to distinguish between exposure and true disease (exposure is common, disease is rare)
CSF titers
What is the best treatment for EPM? What are other options?
ponazuril (Marquis) for up to 6 months
pyrimethamine and sulfadiazine –> folate inhibitors
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
What is unique about horses and tetanus?
horses are one of the most sensitive animals to the neurotoxin of C. tetani
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
What are 4 classic clinical signs seen in horses with tetanus? What else is commonly seen?
- stiff, spastic gait
- easily startled + extreme noise and light hyperesthesia
- inability to open mouth - lockjaw
- third eyelid prolapse
initially vague and commonly mistaken for lameness or colic before signs progress, raised head and tail, recumbency
How is tetanus diagnosed? Treated?
clinical signs, especially with history of a wound
Penicillin + tetanus antitoxin + supportive care
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
What is the pathogenesis of rabies?
bite from infected wildlife –> several week to month incubation –> virus reaches CNS
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
What are the 3 forms of rabies?
- FURIOUS (cerebral) - odd or aggressive behavior, self-mutilation, vocalization
- DUMB (brainstem) - somnolence, dementia, dysphagia, ataxia
- PARALYTIC (spinal cord) - progressive ascending paralysis
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
Where is the prevalence of botulism highest in horses? What are 3 common risk factors?
mid-Atlantic, Eastern USA
- silage or ryelage as feed
- poorly stored forage
- round hay bales
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
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
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
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
What clinical signs are indicative of cauda equina?
- urinary/fecal incontinence
- flaccid tail
- ataxia is rare since lesions are mostly peripheral
What 5 cranial nerves are commonly affected by cauda equina?
- CN III - depressed PLR
- CN V - masseter atrophy
- CN VII - tongue weakness
- CN VIII - head tilt
- CN IX/X - difficulty swallowing
How is cauda equina diagnosed? Treated?
necropsy
supportive care –> poor long-term prognosis
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
What clinical signs are indicative of equine degenerative myeloencephalopathy (DEM)?
- dull, quiet
- symmetrical ataxia of all legs
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)
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
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
How is equine motor neuron disease (EMND) diagnosed? Treated?
biopsy + history of vitamin E deficiency
vitamin E supplementation –> rarely successful
What horses are most commonly affected by cervical vertebral malformation (Wobblers, cervical stenotic myelopathy)?
large, fast-growing breeds –> Warmbloods, Thoroughbreds
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
What other differentials should be considered in horses with cervical vertebral malformations?
- trauma
- neoplasia
- space-occupying lesion
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
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
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
- behavioral - high energy or anxiety in housing situation
- pain/lameness - reluctance to lay down and get up safely
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
What are rare triggers of narcoleptic-type episodes in horses?
- saddling
- grooming
vaso-vagal response causes collapse
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
