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Infectious Disease > Equine Neurologic Diseases > Flashcards

Equine Neurologic Diseases Flashcards

1
Q

What are causes of Equine Encephalomyelitis

A

Western equine Encephalitis virus
Eastern Equine Encephalitis Virus
Venezuelan Equine Encephalitis virus

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2
Q

How is EEE/WEE/VEE transmitted, and what is the reservoir?

A

mosquitoes- there is no direct form of transmisison.

EEE/WEE reservoir = birds
VEE= rodents

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3
Q

Can humans contract EEE?

A

yes there were 38 human infections

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4
Q

Clincial Signs associated with Equine encephalomyelitis

A

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

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5
Q

Diagnosis of Equine encephalomyelitis

A

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

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6
Q

Treatment for Equine encephalomyelitis

A

Supportive care: hydration/nutrition, Neuro stall/sling, Urination/defecation
Antiinflammatories
NSAIDs- yes
Steroids are contraindicated

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7
Q

What are recommended prevention measures for EEE/WEE/VEE

A

mosquito control
Vacciantion: Core vaccination for all Equines

Booster anually or semi-annual in areas with persistent mosquito populations

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8
Q

What are the reservoir hosts for West Nile Virus

A

Birds are the reservoir hosts

Many mosquito species can spread disease

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9
Q

Clinical Signs associated with West Nile Virus

A

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

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10
Q

Diagnosis of West Nile Encephalitis

A

Suggestive based on time of year (vector season) and clinical signs in an animal without a history of recent vaccination.

PCR and IHC, VI

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11
Q

Treatment of West Nile encephalitis

A

Supportive care: hydration/nutrition, Neuro stall/sling, urination/defecation
Antiinflammatories:
NSAIDs - yes
Steroids are controversial

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12
Q

Prevention methods for West Nile Virus

A

Mosquito control

Vacciantion- considered a core vaccination.
Fairly efficacious Vx

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13
Q

Clinical Signs associated with Rabies

A

“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

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14
Q

what are the 3 forms of rabies

A

furious- aggressive behavior
Dumb- depression
Paralytic - recumbent

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15
Q

What are methods of diagnosis for Rabies

A

No antemortem definitive diagnostics exist

Necropsy: direct or indirect FA test

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16
Q

Treatment methods for Rabies

A

None! always fatal

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17
Q

Prevention methods for Rabies

A

Core vaccination!

Single vaccination
In foals from vaccinated mares, you would have to adminsiter 2 vaccines to overcome the maternal antibodies
Anual booster

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18
Q

How do you intervene with post-exposure of vaccinated animals with rabies

A

immediately revaccinate and quarantine for 45 days

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19
Q

How do you proceed in cases of post-exposure of unvaccinated animals with Rabies

A

Contact public health officials

Options vary based on location: euthanize, 6 month isolation/quarantine

20
Q

What are the 2 most common Brainstem/CN Neurologic Differentials

A

Guttural pouch mycosis

otitis media

21
Q

How is EHM transmitted

A

Transmitted via respiratory (aerosol, droplet), direct contact or fomites

22
Q

What equine neurologic condition is associated with leukocyte viremia?

A

Equine Herpesvirus-1 Myeloencephalopathy (EHM)

23
Q

What is the cause of clincial signs in EHM?

A

Endothelial cell damage -> inflammatory cascade and thrombosis -> ischemic injury

24
Q

Clinical signs associated with EHM?

A

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

25
Q

How is EHM diagnosed

A

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

26
Q

What necropsy findings will you have with EHM?

A

Vasculitis, and thrombosis of spinal cord and brain

27
Q

Treatment associated with EHM

A

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

28
Q

Methods of prevention for EHM

A

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.

29
Q

T/F Rhino/flu vaccine is effective at preventing EHM

A

False: It is NOT effective at preventing the neurologic form

30
Q

What causes EPM?

A

Sarcocystis neurona migration

31
Q

Clinical signs associated with EPM

A

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

32
Q

How is EPM diagnosed?

A

CSF antibody titers: ratio of CSF-serum most commonly used: very predictive of EPM If less than or equal to 100

33
Q

What is the indicated treatment in EPM cases?

A

Ponazuril or Diclazuril oral

supportive care: NSAIDs, Vitamin E, corn oil

34
Q

how can you prevent EPM?

A

Protect feed and water source from opossum feces (do not feed on the ground), separate water sources)

Avoid stress and steroid use.

35
Q

What is the etiology associated with tetanus?

A

Clostridium tetani

36
Q

What causes the clinical signs associated with Tetanus

A

Tetanospasm binds irreversibly to presynaptic inhibitory neurons -> muscle rigidity and spasms

37
Q

What clinical signs are associated with Tetanus?

A

Early stages: sudden spastic paralysis
Later stages: continuous muscle spasms and rigidity, head and neck lockjaw with 3rd eyelid prolapse, Sawhorse stance, tail elevation

38
Q

How is tetanus diagnosed?

A

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

39
Q

What treatment methods are associated with tetanus?

A

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)

40
Q

How do you prevent tetanus?

A

it is considered a core vaccine!

Booster following injury

41
Q

What is the causative agent of botulism

A

Clostridium botulinum

42
Q

What is the MOA of Clostridium botulinum?

A

Prevents Ach release at the neuromuscular junction and leads to flaccid paralysis

43
Q

Clinical signs associated with Botulism

A

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.

44
Q

how is botulism diagnosed/

A

PCR and elisa of serum or feed is common

45
Q

Treatment methods for Botulism

A

Early administration of antitoxin (prior to recumbency)
supportive care
Recovery of dysphagia 1-2 weeks, 4 weeks for limb strength

46
Q

Prevention and control for Botulism

A

Vaccination: commercial toxins for “at risk barns:”

3 dose initial series, with annual revaccination

Infectious Disease (12 decks)

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