neurology 1 pt 2 Flashcards

1
Q

viral diseases effecting the equine brain? importance?

A
  • Alphaviruses – EEE/WEE/VEE
  • Flavivirus - WNV
  • Lyssavirus – Rabies
  • All are reportable
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2
Q

New World Alphaviruses
- structure
- environmental sensitivities
- what viruses in this category?

A
  • Single strand, positive sense RNA, enveloped
  • Sensitive to drying & UV radiation
  • The viruses:
    > Eastern Equine Encephalitis virus (EEE)
    > Western Equine Encephalitis virus (WEE)
    > Venezuelan Equine Encephalitis virus (VEE)
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3
Q

EEE/WEE/VEE
- how do we diagnose / differentiate?

A
  • Viral species
    > Differentiated by Hemaglutination Inhibition (neutralizing
    specificity)
  • Fluorescent Antibody test
  • Complement Fixation test
  • ELISA!
  • PCR!
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4
Q

Eastern Equine Encephalitis
- importance
- geography
- age affected

A
  • Major concern
  • Primarily southeast USA
  • Occurs in Canada, northern states
  • Florida – most cases are unvaccinated or only initial vaccine dose administered
  • Usually < 3-years-old
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5
Q

EEE viral cycling, hosts

A

mosquitoes > birds > mosquitoes > birds….. cycle

  • but sometimes those mosquitoes bite horses or humans!
    <><><><>
    Sylvatic cycle
  • Passerine birds (eg. songbirds)
  • Ornithophilic mosquitos
    > Culiseta melanura
  • Non-avian transmission
    > Culex erraticus
  • “Dead end hosts” – horses, humans, other mammals (low viremia)
  • Snakes
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6
Q

EEE clinical syndrome categories, by signs

A
  • Inapparent infection, fever
  • Generalized febrile illness, anorexia, depression, tachycardia, diarrhea
  • Encephalomyelitis – esp young horses; usually assoc. with second febrile crisis. Death in 2-3 days.
    > (rapidly progressive, high mortality rate)
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7
Q

EEE pathogenesis

A
  • Access to body, replicate in lymph nodes, spread – hematogenous & neuronal
  • Large strain variation as to virulence
  • Reservoir hosts – usually subclinical infection
  • Many horses & humans – subclinical infection
  • Incubation period 2-3d up to 3 weeks
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8
Q

EEE – Clinical Signs

A

Obtunded, stupor
Ataxia
Paralysis
Incoordination
Circling
Staggering
Recumbency
Anorexia
Irregular gait
Teeth grinding
Head pressing
Hyper-excitable
Seizures
Death
<><><><>
Not all infected animals develop signs of disease; a horse may be infected with the virus, develop antibodies to it, and eliminate the virus without showing any obvious signs of illness.

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9
Q

EEE clinical course
- how does it compare to WEE, VEE

A
  • 2 – 14 days
  • EEE – most die or euthanized
  • WEE, VEE – may survive
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10
Q

EEE DDx

A
  • Alphavirus
  • WNV
  • Rabies
  • EHV-1
  • EPM
  • Wobbler Syndrome
  • Leukoencephalomalacia
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11
Q

EEE diagnostic tests

A
  • Complete blood count
  • Serum biochemistry profile
  • CSF!!
    > Increase protein level
    > Increased nucleated cell count (mononuclear)
  • Viral testing serology – live animal with fever
  • IgM - >1:400 suggests recent infection
  • Necropsy – brain tissue
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12
Q

EEE pathologic findings

A
  • Necrotizing encephalitis w neuronal dysfunction
  • Neuronal necrosis, neurophagia
  • Marked perivascular cuffing (mono & neuts)
  • Focal & diffuse microglial proliferation
  • Gray matter lesions > white matter lesions
  • Most marked: cerebral cortex, thalamus, hypothalamus.
  • Spinal cord – mildly affected (cervical > lumbar)
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13
Q

EEE treatments

A
  • None
  • Empiric/supportive
    > Corticosteroids
    > Diuretic (Mannitol)
    > Sedation – detomidine
  • Humans – alpha-interferon
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14
Q

EEE control

A
  • Vaccination!!!
    > Adequate initial series
    > Annual or biannual boosters
  • Mosquito control
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15
Q

WEE
- traditional geography
- other strains?
- outbreaks?

A
  • “West of the Mississippi River”
  • Does occur east of the Mississippi River
  • Other strain: Highland J virus – less pathogenic
  • Limited sporadic outbreaks in horses
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16
Q

VEE
- types?
- outbreaks?

A
  • Exotic disease
  • At least 6 different types
    > Epidemic forms – IAB, IC, IE
    > Endemic forms:
    => ID– Central America
    => IF– Brazil
    => II – Florida
    => III – VI elsewhere
  • Large outbreaks in horses & humans (always occurs at
    same time)
17
Q

West Nile Virus
- virus family
- what is causes, in who?
- hosts?

A
  • Family – Flaviviridae
  • Genus – Flavivirus
  • Positive-sense, single stranded RNA
  • Encephalitis – horses, humans, other mammals
  • Bird – mosquito cycling, other
  • Horses & humans – “dead end” hosts
  • May infect >300 species of birds
18
Q

‘sentinels’ for West nile virus

A
  • May infect >300 species of birds
  • House sparrow – amplifying host
  • Corvids (eg. Crows) – high mortality > tips us off that something is wrong
19
Q

WNV
- seasonality
- signalment?

A
  • Seasonality – July → October
  • No breed or sex predilection
20
Q

WNV signs
- what is unique?
- prognosis?

A
  • Usually acute onset, rapid progression
  • Brain & spinal cord
  • Behavioral/mentation change
  • Muscle fasciculations > We don’t see this with other similar diseases! good for differentials!
    <><><><>
  • Non-specific – fever, inappetance, depression
  • Colic, lameness
  • Progression of brain & spinal cord signs
    <><><><>
    Prognosis
  • 30% mortality (die or euthanized)
  • Survivors – 90% may become normal
21
Q

WNV
- Dx
- prevention

A

Diagnosis
- Geographic area
- Vaccination status
- Ancillary testing
> IgM capture-ELISA
> CSF
<><><><>
Prevention
- Vaccination – many types of vaccines
- Mosquito control

22
Q

Rabies
- type of virus?
- who gets it?
- transmission
- stains

A
  • Family Lyssavirus
  • Genus Rhabdovirus
  • Negative strand RNA virus
  • Disease of mammals
  • Passed by animals with clinical signs (or near)
  • Strains: Fox, bat, raccoon
23
Q

rabies clinical signs, forms, clinical course

A
  • Any signs that are acute, severe, rapidly progressive intracranial disease.
  • Plus – autonomic instability, dysphagia, paresis, paresthesia, hydrophobia
    <><><><>
    Forms:
  • Dumb: mentally depressed
  • Furious: hyperexcitable, fearful, enraged
  • Paralytic: flaccid paraparesis, tetraparesis, tetraplegia
    <><><><>
  • Shifting lameness
  • Ataxia
  • Colic
  • Decreased to absent reflexes
  • Progressive CNS signs
    <><><><>
    Clinical course – 1-8 days; may die acutely
24
Q

rabies incubation

A
  • Few days to 6 months
  • Depends on where bitten
25
Q

rabies frequency of clinical signs in horses

A

Cases: 21
- Recumbency 21
- Hyperesthesia 17
- Tail & anal paralysis 12
- Ataxia, paraplegia 11
- Fever 11
- Lameness 5
- Pharyngeal paralysis 2
- Colic 2

26
Q

rabies necropsy signs

A
  • Non-suppurative meningoencephalomyelitis
  • Histology
  • Changes most severe in dorsal root ganglia & most CNS regions
27
Q

Rabies - Diagnosis

A
  • Fluorescent antibody test (DFA)
    IFA
  • Histology: Negri bodies (may not be seen if early in disease)
  • Cell culture
  • Mouse inoculation
28
Q

rabies prevention

A

vaccine!!!