Unit 4 - Equine CNS Flashcards

(79 cards)

1
Q

What are the infectious causes of cortical neurologic disease?

A
EEE/WEE/VEE
Rabies
WNV
Bacterial meningitis
Brain abscesses
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2
Q

What are the etiologic agents of equine encephalomyelitis?

A

Western Equine Encephalitis virus
Eastern Equine Encephalitis virus
Venezuelan Equine Encephalitis virus

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3
Q

What is equine encephalomyelitis transmitted by?

A

Mosquitos

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4
Q

Which of the etiologic agents of equine encephalomyelitis is has no bird involvment and is an FAD?

A

VEE

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5
Q

What are the reservoir for EEE and WEE?

A

Birds

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6
Q

What are the dead end hosts for EEE and WEE?

A

Horses and humans

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7
Q

T/F: Horses are not a dead end host for VEE.

A

True

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8
Q

Where is EEE found geographically?

A

Easter, southern, and midwestern states

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9
Q

Where is WEE found geographically?

A

It is widely disseminated across the US and Canada

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10
Q

Where is VEE found geographically?

A

Central and South America

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11
Q

Rate the equine encephalomyelitis viruses from most to least severe.

A

EEE&raquo_space; VEE > WEE

Mortality rates follow this trend too

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12
Q

What clinical signs are associated with equine encephalomyelitis?

A

Initial onset of fever, anorexia, and depression
Rapid progression to central neurologic signs
Peracute cases may be found dead

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13
Q

The neurologic form of equine encephalomyelitis is also called what?

A

Sleeping sickness

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14
Q

What neurologic signs are associated with equine encephalomyelitis?

A

Ataxia, decreased vision, wandering, drowsiness, photophobia, head pressing, and paralysis

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15
Q

What age group of animals are most susceptible to equine encephalomyelitis?

A

Young animals < 5years

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16
Q

What is the best antemortem diagnostic for equine encephalomyelitis?

A

IgM capture ELISA (>1:400 indicative)

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17
Q

Aside from IgM capture ELISA, how is equine encephalomyelitis diagnosed?

A
Suggestive based on the time of year and location in animal without history of a recent vaccination
CSF tap
PCR and IHC
VI
Paired serum if survival is long enough
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18
Q

How is equine encephalomyelitis treated?

A

Supportive care - hydration/nutrition, neuro stall/sling, urination/defecation
Anti-inflammatoris - NSAIDs preferred

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19
Q

How is equine encephalomyelitis prevented and controlled?

A

Mosquito control

Vaccination

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20
Q

What are the reservoir hosts for West Nile Virus (WNV)?

A

Birds

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21
Q

What spreads WNV?

A

Mosquitos

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22
Q

What clinical sign is somewhat unique to WNV that should move it to the top of your list if they are exhibiting it?

A

Muscle fasciculations - muzzle twitching

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23
Q

What are the most common clinical signs associated with WNV?

A

Weakness or ataxia

Altered mentation, recumbency

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24
Q

T/F: WNV can be fatal in horses and chronic neurologic deficits are common

A

True

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25
How is WNV diagnosed?
``` Suggestive based on time of year and clinical signs in an animal without a history of recent vaccination CSF tap IgM antibody capture ELISA PCR, IHC, VI Paired serum ```
26
What will the CSF tap show in patients with WNV?
Non-specific lymphocytic pleocytosis and elevated TP, possibly mononuclear pleocytosis
27
How is WNV treated?
Supportive care - hydration/nutrition, neuro stall/sling, urination/defecation Anti-inflammatoris - NSAIDs preferred
28
How is WNV prevented and controlled?
Mosquito control | Vaccination
29
What is the etiologic agent of rabies?
Rabies virus - neurotropic rhabdovirus
30
What species is rabies most commonly associated with in the midwest?
skunks and raccoons
31
What is the most common form of transmission of rabies in the US?
Bite of the infected animal
32
What is the range for the incubation period for rabies?
It ranges from 2-9 weeks depending on the location of bite
33
Rabies is considered the great imitator. Why?
It can initially present as a lameness, colic fever of unknown origin, pharyngeal paralysis, hyperesthesia, ataxia, recumbency, any neurologic sign, abnormal vocalization
34
What are the three main forms of rabies?
Furious - infects brain Dumb - infects brain stem Paralytic - infects spine
35
T/F: Rabies is always fatal
True
36
How is rabies diagnosed?
Clinical signs Direct or indirect FA test at necropsy Negri bodies
37
How is rabies treated?
It isnt
38
How is rabies prevented?
Vaccination Re-vaccinate post-exposure and quarantine for 45 days Contact public health officials if not vaccinate and exposed
39
What are the infectious causes of brainstem/CN neurologic disease?
Guttural pouch mycosis | Otitis media
40
T/F: There are no infectious causes of cerebellar neurologic disease.
True
41
What are the infectious causes of spinal and peripheral nerve neurologic disease?
``` EHM EPM Tetanus Spinal abscesses Verminous meningoencephalomyelitis ```
42
How is EHV-1 myeloencephalopathy transmitted?
Respiratory, direct contact, or fomites
43
EHV-1 myeloencephalopathy is a ______ associated viremia. ______ cell damage causes an inflammatory cascade and _____ causing ______ injury.
Leukocyte Endothelial Thrombosis Ischemic
44
What age group of horses are more commonly affected by EHM?
Older horses
45
What clinical signs are associated with EHM?
Transient fever Acute onset of ataxia and tetraparesis that may progress to recumbency Urinary incontinence, bladder distension, weak tail/anal tone
46
When does the onset of EHM clinical signs occur?
6-10 days after infection
47
What is the average mortality rate of EHM?
50%
48
How is EHM diagnosed?
``` Tentative based on CS and history CSF PCR 4 fold increase in titers Necropsy ```
49
What will a CSF tap show in a patient with EHM?
Xanthochromia with increased protein and normal cell count
50
How is EHM treated?
``` Immediate isolation Supportive care - fluids and nutritional support Anti-inflammatories Antivirals +/- Heparin ```
51
How is EHM prevented and controled?
Prevent introduction of new virus strains
52
What is the protocol for EHM prevention/control in case of outbreaks?
CONTACT THE STATE VET - reportable Quarantine the premesis and isolation of all clinical animals 2 weeks past all clinical signs Twice daily temperature monitoring
53
What is the etiologic agent of equine protozoal myeloencephalitis (EPM)?
Sarcocystis neurona
54
What is the definitive host of Sarcocystis neurona?
Opossum
55
How is Sarcocystis neurona transmitted?
Ingestion of feed or water contaminated with opossum feces
56
What clinical signs are associated with EPM?
They vary greatly - can infect any part of the CNS so almost any neurologic sign is possible (spinal cord >> brain, asymmetric > symmetric) Limb weakness and ataxia
57
How is EPM diagnosed?
Serology CSF antibody titers PCR on CSG Necropsy - may find protozoa but absence doesn't rule it out
58
How is EPM treated?
Anti-protozoal medications (28 days) | Supportive care - NSAIDs, Vitamin E, corn oil
59
How is EPM prevented and controlled?
Protect feed and water sources from opossum feces Avoid stress and steroid use +/- preventative utilization of ponazuril or diclazuril
60
What is the etiologic agent of tetanus?
Clostridium tetani
61
How can horses become infected with tetanus?
Via spore formation in the environment or contamination of wounds with spores from environment
62
What is the pathogenesis of tetanus infection?
Tetanospasmin binds irreversibly to presynaptic inhibitory neurons resulting in muscle rigidity and spasms
63
Tetanus clinical signs can develop up to ___ months after wound inoculation.
2
64
What clinical signs are associated with the early stages of tetanus?
Startling by loud noises leads to sudden spastic paralysis
65
What clinical signs are associated with later stages of tetanus?
Continuous muscle spasms and rigidity Head and neck - lockjaw, 3rd eyelid prolapse Sawhorse stance Tail elevation
66
How is tetanus diagnosed?
Lack of ID of wounds in many cases | Clinical signs in the absence of recent vaccination
67
How is tetanus treated?
Administration of antitoxin if unvaccinated or status unknown Debride wounds Penicillin Supportive care
68
T/F: There is a low mortality rate associated with tetanus, but a prolonged recovery time.
False - high mortality rate
69
How is tetanus prevented and controlled?
Vaccination, booster vax following injury
70
What are the infectious causes of motor unit/peripheral nerve neurologic disease?
Botulism
71
What is the etiologic agent of Botulism?
Clostridium botulinum
72
T/F: Botulism is contagious.
False - tis not
73
What are the 3 routes of infection of botulism?
Ingestion, wounds, ingestion of performed toxin
74
What clinical signs (general) are associated with botulism?
Flaccid paralysis and death from paralysis of respiratory muscles within 48-72 hours
75
What clinical signs are associated with foals that have botulism?
Initially less active, rest with head on the ground Drag hooves when walking Progress to down and unable to rise
76
What clinical signs are associated with Botulism in adults?
Dysphagia, tongue weakness, muscle tremors, abnormal great, progress to ataxia and recumbency
77
How is botulism diagnosed?
Detection of toxin in serum or feed - PCR or ELISA
78
How is botulism treated?
Early administration of antitoxin | Supportive care
79
How is botulism prevented and controlled?
Vaccination in endemic areas