Equine Neurologic Diseases Flashcards
What are causes of Equine Encephalomyelitis
Western equine Encephalitis virus
Eastern Equine Encephalitis Virus
Venezuelan Equine Encephalitis virus
How is EEE/WEE/VEE transmitted, and what is the reservoir?
mosquitoes- there is no direct form of transmisison.
EEE/WEE reservoir = birds
VEE= rodents
Can humans contract EEE?
yes there were 38 human infections
Clincial Signs associated with Equine encephalomyelitis
similar for all 3 viruses (EEE>VEE>WEE)
initial onset of fever, anorexia, and depression.
Rapid progression to central neurologic signs: ataxia, decreased vision, wandering, drowsiness, photophobia, head pressing, paralysis “ sleeping sickness”
Young animals are more suscecptible to disease
Diagnosis of Equine encephalomyelitis
Suggestive based on the time of year (vector season)
CSF tap - non specific
IgM antibody capture ELISA >1:400 indicative of infection vs. vacciantion
PCR and IHC
Treatment for Equine encephalomyelitis
Supportive care: hydration/nutrition, Neuro stall/sling, Urination/defecation
Antiinflammatories
NSAIDs- yes
Steroids are contraindicated
What are recommended prevention measures for EEE/WEE/VEE
mosquito control
Vacciantion: Core vaccination for all Equines
Booster anually or semi-annual in areas with persistent mosquito populations
What are the reservoir hosts for West Nile Virus
Birds are the reservoir hosts
Many mosquito species can spread disease
Clinical Signs associated with West Nile Virus
Extremely varied: most common: ataxia or weakness, altered mentation, recumbency
Muscle fasciculations (muzzle twitching is common)
Recrudescence of signs can occur
Mortality ~30%, chronic neurologic deficits common
Diagnosis of West Nile Encephalitis
Suggestive based on time of year (vector season) and clinical signs in an animal without a history of recent vaccination.
PCR and IHC, VI
Treatment of West Nile encephalitis
Supportive care: hydration/nutrition, Neuro stall/sling, urination/defecation
Antiinflammatories:
NSAIDs - yes
Steroids are controversial
Prevention methods for West Nile Virus
Mosquito control
Vacciantion- considered a core vaccination.
Fairly efficacious Vx
Clinical Signs associated with Rabies
“The great Imitator”
Can initially present as a lameness, colic, fever of unknown origin, pharyngeal paralysis (choke), hyperesthesia, ataxia, recumbency, any neurologic sign, abnormal vocalization
what are the 3 forms of rabies
furious- aggressive behavior
Dumb- depression
Paralytic - recumbent
What are methods of diagnosis for Rabies
No antemortem definitive diagnostics exist
Necropsy: direct or indirect FA test
Treatment methods for Rabies
None! always fatal
Prevention methods for Rabies
Core vaccination!
Single vaccination
In foals from vaccinated mares, you would have to adminsiter 2 vaccines to overcome the maternal antibodies
Anual booster
How do you intervene with post-exposure of vaccinated animals with rabies
immediately revaccinate and quarantine for 45 days
How do you proceed in cases of post-exposure of unvaccinated animals with Rabies
Contact public health officials
Options vary based on location: euthanize, 6 month isolation/quarantine
What are the 2 most common Brainstem/CN Neurologic Differentials
Guttural pouch mycosis
otitis media
How is EHM transmitted
Transmitted via respiratory (aerosol, droplet), direct contact or fomites
What equine neurologic condition is associated with leukocyte viremia?
Equine Herpesvirus-1 Myeloencephalopathy (EHM)
What is the cause of clincial signs in EHM?
Endothelial cell damage -> inflammatory cascade and thrombosis -> ischemic injury
Clinical signs associated with EHM?
transient fever with clinical signs 6-10 days after infection
Acute onset of ataxia and tetraparesis that may progress to recumbency
urinary incontinence, bladder distension, weak tail/anal tone
How is EHM diagnosed
CSF with xanthochromia with increased protein and normal cell count is very suggestive- almost pathognomonic
PCR of whole blood and nasal secretions for definitive diagnosis
What necropsy findings will you have with EHM?
Vasculitis, and thrombosis of spinal cord and brain
Treatment associated with EHM
ISOLATION is essential
Supportive care: fluids, nutritional support, Evacuation of bladder and rectum
Anti-inflammatories
Antivirals: acyclovir, valcyclovir in valuable animals (some benefit in decreasing clinical signs but extremely expensive)
heparin- potentially prevent thrombi production
Methods of prevention for EHM
quarantine or separate housing for horses that are leaving the farm more frequently: shows, races, fairs, trail rides etc.
In the case of an outbreak: REPORTABLE!!!!!
Quarinitine of premises and isolation of all clinical animals 2 weeks past all clinical signs.
T/F Rhino/flu vaccine is effective at preventing EHM
False: It is NOT effective at preventing the neurologic form
What causes EPM?
Sarcocystis neurona migration
Clinical signs associated with EPM
Clinical signs are highly variable.
Can infect any part of the CNS, so almost any neurologic sign is possible
Spinal cord is more commonly affected than the brain
Primary clincial signs: limb weakness and ataxia
How is EPM diagnosed?
CSF antibody titers: ratio of CSF-serum most commonly used: very predictive of EPM If less than or equal to 100
What is the indicated treatment in EPM cases?
Ponazuril or Diclazuril oral
supportive care: NSAIDs, Vitamin E, corn oil
how can you prevent EPM?
Protect feed and water source from opossum feces (do not feed on the ground), separate water sources)
Avoid stress and steroid use.
What is the etiology associated with tetanus?
Clostridium tetani
What causes the clinical signs associated with Tetanus
Tetanospasm binds irreversibly to presynaptic inhibitory neurons -> muscle rigidity and spasms
What clinical signs are associated with Tetanus?
Early stages: sudden spastic paralysis
Later stages: continuous muscle spasms and rigidity, head and neck lockjaw with 3rd eyelid prolapse, Sawhorse stance, tail elevation
How is tetanus diagnosed?
Lack of identification of wounds in many cases- due to delayed progression
clincial signs in the absence of recent vaccination is the most common historical findings
What treatment methods are associated with tetanus?
administration of tetanus antitoxin if unvaccinated or vaccine status unknown, debride wounds, penicillin, supportive care (l\sedation, muscle relaxants, quiet stall)
high mortality rate, Prolonged recovery (regenerate neurons)
How do you prevent tetanus?
it is considered a core vaccine!
Booster following injury
What is the causative agent of botulism
Clostridium botulinum
What is the MOA of Clostridium botulinum?
Prevents Ach release at the neuromuscular junction and leads to flaccid paralysis
Clinical signs associated with Botulism
Flaccid paralysis
Foals: initially less active, rest with head on the ground, drag hooves when walking, progress to down and unable to rise
Adult: dysphagia, tongue weakness, muscle tremors, abnormal gait, progress to ataxia and recumbency
Death from paralysis of respiratory muscles 48- 72hrs.
how is botulism diagnosed/
PCR and elisa of serum or feed is common
Treatment methods for Botulism
Early administration of antitoxin (prior to recumbency)
supportive care
Recovery of dysphagia 1-2 weeks, 4 weeks for limb strength
Prevention and control for Botulism
Vaccination: commercial toxins for “at risk barns:”
3 dose initial series, with annual revaccination
