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Equine Medicine > Unit 2 - Neuro 3 > Flashcards

Unit 2 - Neuro 3 Flashcards

1
Q

What causes Eastern and Western Equine Encephalomyelitis?

A

Alphavirusus - togaviridae

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2
Q

What sylvantic hosts do EEE and WEE survive in during the winter months?

A

birds, small mammals, and reptiles

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3
Q

What is the main vector for WEE and EEE?

A

mosquitos

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4
Q

What else can transmit WEE?

A

ticks, assassin bug, and cliff swallow bug

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5
Q

How else can EEE be transmitted?

A

via nasal secretions

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6
Q

What is the peak season for transmission of EEE and WEE?

A

June to November

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7
Q

What is the mortality rate for WEE?

A

25-50%

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8
Q

What is the mortality rate for EEE?

A

50-70%

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9
Q

What are the initial clinical signs of WEE and EEE?

A

Mild fever, stiffness

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10
Q

What are the clinical signs 1-3 weeks post infection of WEE and EEE?

A

Mild fever, obtundation

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11
Q

What clinical signs are associate with further progression of WEE and EEE infection?

A

Cerebrothalmic signs, compulsive walking, altered behavior, hyperesthesia, recumbency, death

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12
Q

What cranial nerves does obtundation affect?

A

CN 7, 8, 9, 10, and 12

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13
Q

How is EEE and WEE diagnosed?

A

Time of year + clinical signs, capture IgM ELISA, CSF, and post mortem

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14
Q

What is the gold standard antemortem test for EEE and WEE?

A

Capture IgM ELISA

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15
Q

How is EEE and WEE treated?

A

Non-specific supportive care (hydration, nutrition, ensuring urination and defecation), NSAIDs, and +/- steroids (controversial)

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16
Q

How is EEE and WEE prevented?

A

appropriate vaccination (2 vaccine series with 6 mo and 1 year boosters) and mosquito control

17
Q

What is the etiologic agent of West Nile Viurs?

A

Flavivirus

18
Q

What is the reservoir host for WNV?

A

birds and wild vertebrates

19
Q

How does the WNV access the CNS?

A

It enters the CNS via hematogenous and transneural access via a disrupted BBB

20
Q

What is the peak season for WNV transmission?

A

July to October

21
Q

What are the clinical signs of WNV?

A

Weakness, ataxia, altered mentation, fever, muscle fasciculations, CN deficits, recumbency, paralysis of 1 or more limbs, and narcolepsy-like behavior

22
Q

What is the antemortem gold standard diagnosis for WNV?

A

IgM capture ELISA

23
Q

What will WNV look like at necropsy?

A

polioencephalomalacia

24
Q

How is WNV treated?

A

Non-specific supportive care (hydration, nutrition, ensuring urination and defecation), NSAIDs, and +/- steroids (controversial)

25
Q

How is WNV prevented?

A

appropriate vaccination (2 vaccine series with 4 mo and 1 year boosters) and mosquito control

26
Q

What are the initial clinical signs of tetanus?

A

stiff neck, trismus, rigid facial expression, and prolapse of nictitans membrane (3rd eyelid)

27
Q

What are the clinical signs 1-2 days post tetanus infection?

A

Generalized spasticity, sawhorse stance, elevated tail head, tonic muscle spasms, pharyngeal, laryngeal spasp, and dramatic fluctuations in HR

28
Q

How is tetanus diagnosed?

A

history, clinical signs, can gram stain wound, can submit wound exudate for toxin assay

29
Q

How is tetanus treated?

A

Clean and debride wound if present, treat infection, imuscle relaxation, neutralization of circulating toxin, ensure hydration, nutrition needs are met

30
Q

What is the prognsis for tetanus?

A

75% mortality rate in horses

Poor prognosis if recumbent

Usually stabilize in 2-7 days and then slowly improve

31
Q

How is tetanus prevented?

A

Initial 2 vaccines 3-6 weeks apart then yearly boosters. Re-booster before surgery, at the time of surgery

32
Q

What are the clinical signs of Botulism?

A

Tongue weakness, dysphagia, lethargy, muscle weakness, weak facial muscles, stilted hypometric gait, difficulty standing, and mydriasis, decreased PLR

33
Q

How is botulism diagnosed?

A

Clinical signs and you can test GI contents, feed, wound exudate etc. for toxin

34
Q

How do you differentiate between Botulism and Nigropallidal encephalomalacia infection?

A

Horses with botulism can’t swallow, but horses with NE can

35
Q

How is Botulism treated?

A

Early administration of anti-toxin - it has minimal efficacy in recumbent horses, clinical signs may progress for 12-24 hours post administration

Prophylactic antimicrobials in case of aspiration pneumonia

Fluid and nutritional therapy

36
Q

What is the prognosis for botulism if not recumbent?

A

7-14 days for resolution of dysphagia and 1 month for resolution of full limb strength

37
Q

What is the prognosis for botulism if recumbent?

A

poor

38
Q

How is botulism prevented?

A

BoNT/B vaccine in endemic areas (3 part series administered 4 weeks apart and then once yearly)

Equine Medicine (27 decks)

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