Equine - encephalitis Flashcards

1
Q

What is the structure of alphavirues (EEEV/WEEV/VEE)

A
  • 11 kb (+) ssRNA
  • enveloped with glycoproteins
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2
Q

What are equine alphaviruses?

A
  • characterized by CNS dysfunction and moderate to high mortality in horses
  • Viruses genetically and antigenically distinct
  • considerable antigenic diversity
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3
Q

What is EEEV?

A
  • Occurs in:
    • Eastern Canada, States East of the Mississippi River
    • AR, MN, SD, TX, MI, LA, MT,
    • Caribbean islands
  • Clinical disease can occur in horses, humans, alpacas, llamas, cattle, swine, cats and dogs
  • Enzootic in birds along east coat
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4
Q

What is the mortality rate of EEEV in humans?

A

30-70%

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5
Q

can humans/horses transmit EEEV?

A

no dead-end-hosts

low level viremias insufficient vector transmission

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6
Q

What is WEEV?

A
  • Occurs in:
    • western canada
    • States west of the mississippi river
    • Mexico and South america
  • Associated with increased rainfall in early spring followed by warm temperatures
  • Infrequent in US but circulates in wildlife
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7
Q

Human mortality rate of WEEV

A

3-7%

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8
Q

What is VEEV

A
  • Occurs in South and Central America
  • Not diagnosed in US for >40 years
  • REPORTABLE
  • associated with jungle/swampy areas
  • all mammalian hosts capable of developing high-titer viremia for up to 5 days
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9
Q

What makes VEEV different for EEEV/WEEV?

A
  • enzootic in rodents (not birds)
  • Horses and humans are NOT dead-end hosts - Amplify VEEV
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10
Q

What is the human mortality rate of VEEV

A
  • 10-35%
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11
Q

What is the structure of Flaviviruses?

A
  • 10kb (+) ssRNA
  • Enveloped proteins
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12
Q

What is WNV?

A
  • Similar to EEEV/WEEV
    • more widespread
  • horses and humans dead end hosts
  • birds are reservoirs
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13
Q

What is the human mortality rate of WNV

A

3-5%

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14
Q

What are the clinical findings of Equine Arboviral Encephalomyelitis Viruses? (EEEV, WEEV, VEEV, WNV)

A
  • Clinical signs similar and nonspecific
    • depression, reduced activity, fever, decreased appetite
  • Infections may be subclinical
  • Progression and severity of disease is different between viruses
    • More: EEEV and VEEV
    • Less: WEEV and WNV
  • Neurologic signs typically occur 9-11 dpi
    • may have shorter incubation with EEEV/VEEV (5dpi)
    • “sleeping sickness”
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15
Q

What are neurologic signs that are more common with EEEV and VEEV?

A
  • Altered mentation, blindness, restlessness, hypersensitivity, head pressing, circling, dysphagia, irregular ataxic gait, paresis and paralysis, seizures and death
  • symmetric ataxia affecting all limbs, progresses to quadriparesis
  • Many progress to recumbency 12-18 hrs after onset of neurological signs
  • death within 2-3 days of clinical onset (EEEV)
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16
Q

What are the WNV clinical signs?

A
  • Variable
  • May present as neurologic abnormalities, colic, lameness, anorexia, fever, depression
  • Neurologic abnormalities may vary
    • >90% Spinal cord disease
      • asymmetric, multifocal or diffuse ataxia and paresis
      • forelimb, hindlimb, unilaterally or a single limb
    • 40-60% behavioral changes, mental aberrations
      • hyperesthesia with fractious reactions to aural, visual, and tactile stimuli
    • 60-90% Fine and course tremors of face and neck
    • Urinary dysfunction (infrequent)
17
Q

What clinical findings can be found in all viral encephalomyelitis? (WEEV/ WNV/ EEEV/ VEEV)

A
  • Cranial nerve deficits
    • weakness or paralysis of the face and tongue
      • dysphagia, quidding, esophageal choke, nystagmus
  • facial edema due to lowered head, depression
  • Trauma due to seizures, neurologic dysfunction
  • secondary morbidities due to recumbency
18
Q

What gross lesions are common with EEEV/VEEV

A

widespread and prominent congestion of the meninges

19
Q

What gross lesions are common with WEEV/WNV

A

small multifocal areas of discoloration and hemorrhage throughout the brain and spinal cord

20
Q

What are the microscopic lesions of equine encephalitis viruses

A
  • Meningoencephalitis
    • varying amounts of vasculitis, necrosis, hemorrhage, inflammatory cell infiltrate (neutrophils and mononuclear cells)
    • often multifocal
21
Q

How is equine viral encephalitis diagnosed?

A
  • Viremia typically resolved by the time of neurologic sings
  • Serologic tests
    • IgM capture ELISA
    • neutralizing Ab titers; IgG paired samples
  • CSF analysis (increased WBC and proteins) PCR
  • Postmortem: IHC, PCR, Virus isolation
    • Test for rabies in ALL horses with encephalitis
22
Q

How is equine viral encephalitis treated?

A
  • Control pain and inflammation
  • Prevent injuries and trauma
  • Supportive care
23
Q

What is the prognosis for equine viral encephalitis?

A
  • Poor prognosis if persists to recumbancy
  • Mortality in hoses showing clinical signs:
    • EEEV 50-90
    • WEEV 20-50
    • VEEV 50-75
    • WNV 35-45
  • Can have residual neurologic deficits even after recovery
    • EEEV/VEEV/WEEV >>>>>WNV
24
Q

What vaccine exists for Equine viral ecephalitis?

A
  • AAEP - Core vaccine includes EEEV, WEEV, WNV
  • EEEV/WEEV
    • inactivated adjuvanted whole virus
  • WNV
    • Inactivated adjuvanted whole virus
    • Non-replicating adjuvanted vector vaccine
    • Inactivated adjuvanted vector vaccine
  • Initial series of 2 vaccinations 4-6 wks apart