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LA Infectious Disease > Unit 4 - Equine CNS > Flashcards

Unit 4 - Equine CNS Flashcards

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
Q

How is WNV diagnosed?

A 
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
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26
Q

What will the CSF tap show in patients with WNV?

A

Non-specific lymphocytic pleocytosis and elevated TP, possibly mononuclear pleocytosis

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27
Q

How is WNV treated?

A

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

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28
Q

How is WNV prevented and controlled?

A

Mosquito control

Vaccination

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29
Q

What is the etiologic agent of rabies?

A

Rabies virus - neurotropic rhabdovirus

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30
Q

What species is rabies most commonly associated with in the midwest?

A

skunks and raccoons

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31
Q

What is the most common form of transmission of rabies in the US?

A

Bite of the infected animal

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32
Q

What is the range for the incubation period for rabies?

A

It ranges from 2-9 weeks depending on the location of bite

33
Q

Rabies is considered the great imitator. Why?

A

It can initially present as a lameness, colic fever of unknown origin, pharyngeal paralysis, hyperesthesia, ataxia, recumbency, any neurologic sign, abnormal vocalization

34
Q

What are the three main forms of rabies?

A

Furious - infects brain
Dumb - infects brain stem
Paralytic - infects spine

35
Q

T/F: Rabies is always fatal

A

True

36
Q

How is rabies diagnosed?

A

Clinical signs
Direct or indirect FA test at necropsy
Negri bodies

37
Q

How is rabies treated?

A

It isnt

38
Q

How is rabies prevented?

A

Vaccination
Re-vaccinate post-exposure and quarantine for 45 days
Contact public health officials if not vaccinate and exposed

39
Q

What are the infectious causes of brainstem/CN neurologic disease?

A

Guttural pouch mycosis

Otitis media

40
Q

T/F: There are no infectious causes of cerebellar neurologic disease.

A

True

41
Q

What are the infectious causes of spinal and peripheral nerve neurologic disease?

A 
EHM
EPM
Tetanus
Spinal abscesses
Verminous meningoencephalomyelitis
42
Q

How is EHV-1 myeloencephalopathy transmitted?

A

Respiratory, direct contact, or fomites

43
Q

EHV-1 myeloencephalopathy is a ______ associated viremia. ______ cell damage causes an inflammatory cascade and _____ causing ______ injury.

A

Leukocyte
Endothelial
Thrombosis
Ischemic

44
Q

What age group of horses are more commonly affected by EHM?

A

Older horses

45
Q

What clinical signs are associated with EHM?

A

Transient fever
Acute onset of ataxia and tetraparesis that may progress to recumbency
Urinary incontinence, bladder distension, weak tail/anal tone

46
Q

When does the onset of EHM clinical signs occur?

A

6-10 days after infection

47
Q

What is the average mortality rate of EHM?

A

50%

48
Q

How is EHM diagnosed?

A 
Tentative based on CS and history
CSF
PCR
4 fold increase in titers
Necropsy
49
Q

What will a CSF tap show in a patient with EHM?

A

Xanthochromia with increased protein and normal cell count

50
Q

How is EHM treated?

A 
Immediate isolation
Supportive care - fluids and nutritional support
Anti-inflammatories
Antivirals
\+/- Heparin
51
Q

How is EHM prevented and controled?

A

Prevent introduction of new virus strains

52
Q

What is the protocol for EHM prevention/control in case of outbreaks?

A

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
Q

What is the etiologic agent of equine protozoal myeloencephalitis (EPM)?

A

Sarcocystis neurona

54
Q

What is the definitive host of Sarcocystis neurona?

A

Opossum

55
Q

How is Sarcocystis neurona transmitted?

A

Ingestion of feed or water contaminated with opossum feces

56
Q

What clinical signs are associated with EPM?

A

They vary greatly - can infect any part of the CNS so almost any neurologic sign is possible (spinal cord&raquo_space; brain, asymmetric > symmetric)
Limb weakness and ataxia

57
Q

How is EPM diagnosed?

A

Serology
CSF antibody titers
PCR on CSG
Necropsy - may find protozoa but absence doesn’t rule it out

58
Q

How is EPM treated?

A

Anti-protozoal medications (28 days)

Supportive care - NSAIDs, Vitamin E, corn oil

59
Q

How is EPM prevented and controlled?

A

Protect feed and water sources from opossum feces
Avoid stress and steroid use
+/- preventative utilization of ponazuril or diclazuril

60
Q

What is the etiologic agent of tetanus?

A

Clostridium tetani

61
Q

How can horses become infected with tetanus?

A

Via spore formation in the environment or contamination of wounds with spores from environment

62
Q

What is the pathogenesis of tetanus infection?

A

Tetanospasmin binds irreversibly to presynaptic inhibitory neurons resulting in muscle rigidity and spasms

63
Q

Tetanus clinical signs can develop up to ___ months after wound inoculation.

A

2

64
Q

What clinical signs are associated with the early stages of tetanus?

A

Startling by loud noises leads to sudden spastic paralysis

65
Q

What clinical signs are associated with later stages of tetanus?

A

Continuous muscle spasms and rigidity
Head and neck - lockjaw, 3rd eyelid prolapse
Sawhorse stance
Tail elevation

66
Q

How is tetanus diagnosed?

A

Lack of ID of wounds in many cases

Clinical signs in the absence of recent vaccination

67
Q

How is tetanus treated?

A

Administration of antitoxin if unvaccinated or status unknown
Debride wounds
Penicillin
Supportive care

68
Q

T/F: There is a low mortality rate associated with tetanus, but a prolonged recovery time.

A

False - high mortality rate

69
Q

How is tetanus prevented and controlled?

A

Vaccination, booster vax following injury

70
Q

What are the infectious causes of motor unit/peripheral nerve neurologic disease?

A

Botulism

71
Q

What is the etiologic agent of Botulism?

A

Clostridium botulinum

72
Q

T/F: Botulism is contagious.

A

False - tis not

73
Q

What are the 3 routes of infection of botulism?

A

Ingestion, wounds, ingestion of performed toxin

74
Q

What clinical signs (general) are associated with botulism?

A

Flaccid paralysis and death from paralysis of respiratory muscles within 48-72 hours

75
Q

What clinical signs are associated with foals that have botulism?

A

Initially less active, rest with head on the ground
Drag hooves when walking
Progress to down and unable to rise

76
Q

What clinical signs are associated with Botulism in adults?

A

Dysphagia, tongue weakness, muscle tremors, abnormal great, progress to ataxia and recumbency

77
Q

How is botulism diagnosed?

A

Detection of toxin in serum or feed - PCR or ELISA

78
Q

How is botulism treated?

A

Early administration of antitoxin

Supportive care

79
Q

How is botulism prevented and controlled?

A

Vaccination in endemic areas

LA Infectious Disease (33 decks)

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