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Equine Medicine > Infectious Diseases of the Nervous System, Pt. 2 > Flashcards

Infectious Diseases of the Nervous System, Pt. 2 Flashcards

1
Q

What are the main 2 groups of mosquito-borne viral infections that affect the equine nervous system?

A
  1. ALPHAVIRUSES - Eastern Equine Encephalomyelitis (EEE), Western Equine Encephalomyelitis (WEE), Venezuelan Equine Encephalomyelitis (VEE)
  2. FLAVIVIRUS - West Nile Virus
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2
Q

What geographical area is most affected by Eastern Equine Encephalomyelitis? What animals act as reservoirs? Vectors?

A
  • North, South, Central America
  • Caribbean
  • “East of the Mississippi River”

birds, rodents, snakes

Aedes spp

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3
Q

What geographical area is most affected by Western Equine Encephalomyelitis? What animals act as reservoirs? Vectors?

A
  • North, South America
  • “West of the Mississippi River”

birds, rodents, snakes

Culex tarsalis

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4
Q

What geographical area is most affected by Venezuelan Equine Encephalomyelitis? What animals act as reservoirs? Vectors?

A
  • Central, South America
  • Caribbean

cotton rat

  • Culex melaconium
  • Aedes spp.
  • Phosphora spp.
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5
Q

What geographical area is most affected by West Nile Virus? What animals act as reservoirs? Vectors?

A
  • Africa, Middle East, Europe
  • North, Central, South America
  • Australia

Passerine birds

biting insects

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6
Q

Which of the 4 mosquito-borne neurologic viruses have a unique method of spreading/transmission?

A

VEE- high viremia allows for spread by mosquitoes from horse to horse after feeding on a positive horse

(all 4 are reportable, part of the core AAEP vaccines, and cause similar signs)

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7
Q

What horse and environmental risk factors are associated by mosquito-borne neurologic infections?

A

HORSE: any breed/sex, not common in foals (protected by maternal Ab), vaccination history

ENVIRONMENT: region, season, weather, landscape

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8
Q

How does region affect vaccination regimen for mosquito-borne neurologic infections?

A

northeast = vaccinate for vector season (safe during winter when mosquitoes are dead)

southeast = year-round vaccinations (2x year)

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9
Q

What horses are most vulnerable to developing mosquito-borne neurologic infections?

A

young horses recently moved to an endemic area with incomplete vaccination

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10
Q

What are the amplifying and dead-end hosts of mosquito-borne neurologic viruses?

A

AMPLIFYING = birds

DEAD-END = horses and humans, usually cannot transmit to others due to low-level of viremia (not VEE!)

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11
Q

What are the 5 most common clinical signs associated with mosquito-borne neurologic infections?

A
  1. fever
  2. change in mentation (sleeping sickness) - depression, somnolence, head pressing, circling, leaning, convulsion, hyperexcitability, apprehension, drowsiness
  3. gait - weakness, ataxia, incoordination, paralysis, recumbency
  4. colic
  5. death
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12
Q

What 3 clinical signs are especially associated with WNV?

A
  1. cranial nerve deficits - pharyngeal, laryngeal, tongue, and facial nerve paralysis
  2. facial and neck tremors
  3. head tilt
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13
Q

What 4 diseases must be ruled out before diagnosing mosquito-borne nerologic disease?

A
  1. liver/kidney disease - CBC, serum biochem, blood ammonia
  2. cervical vertebral malformation - radiographs
  3. EPM - CSF tap
  4. EHM - nasal swab, EDTA blood
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14
Q

What serological tests are used to diagnose mosquito-borne neurologic viral disease?

A
  • titers = 4x increase of 2-3 wks
  • IgM capture ELISA = can differentiate between vaccinated, IgM will not be high in these horses (IgG!)
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15
Q

What diagnostics are used postmortem to diagnose mosquito-borne neurologic viral disease?

A
  • find virus on PCR or IHC on brain tissue
  • viral isolation from brain tissue
  • gross and microscopic lesions
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16
Q

How can mosquito-borne neurologic viral disease be prevented?

A
  • vaccination
  • eliminate standing water where mosquitoes breed
  • clean watering troughs monthly
  • larvicides, mosquito-eating fish, eliminate brush and litter
  • keep horses indoors at dusk and dawn
  • screen stalls and install fans, avoid turning on lights in stables
  • insect repellants
  • keep birds away
  • protect yourself
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17
Q

What is important to note when planning mosquito-borne neurologic viral disease vaccination?

A

typically annual before the seasion, but adapt schedule to region

  • NORTH = once a year before season
  • SOUTH = endemic, 2x a year
  • increased vaccinations per year for immunocompromised and older horses
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18
Q

Core vaccination schedule:

A
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19
Q

What causes rabies? What animals act as reservoirs?

A

ssRNA Lyssa virus

  • raccoons
  • skunks
  • foxes
  • coyotes
  • bats
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20
Q

What are some risk factors that contribute to developing rabies?

A
  • younger horses tend to be more curious and would find themselves in contact with reservoirs
  • vaccination history
  • pasture access
  • endemic areas

(ZOONOTIC, 100% fatality, reportable)

21
Q

What is the pathogenesis of rabies infection?

A
  • bite infliction introduces virus within MM and skin lesions, allowing for replication
  • retrograde axonal transport along axons takes the virus to the spinal cord where it replicates more
  • continual movement up the spinal cord allows the virus to reach the brain
  • retrograde axonal transport sends virus to the salivary glands (salivation, spread through bite!)

long incubation time = bite wound not often seen

22
Q

What are the 3 forms of rabies? What portion of the CNS is affected by each?

A
  1. furious - cerebrum
  2. dumb - brainstem
  3. paralytic - spine
23
Q

What are common clinical signs seen with furious rabies?

A
  • aggression
  • photo/hydrophobia
  • hyperesthesia
  • self-mutilation
  • straining, tremors, convulsions
  • blindness
24
Q

What are common clinical signs seen with dumb rabies?

A
  • obtundation
  • anorexia
  • head tilt, circling
  • excessive salivation
  • facial or pharyngeal paralysis
25
What are common clinical signs seen with paralytic rabies?
- ascending paralysis - ataxia - shifting lameness - hyperesthesia - cauda equina
26
How is rabies diagnosed antemortem?
NO CONFIRMATION AVAILABLE ANTEMORTEM - history, clinical signs - CBC, biochem are usually normal - CSF
27
How is rabies diagnosed postmortem?
- half of the brain preserved in 10% formaldehyde for histology and the other half frozen for direct IFAT - mild non-suppurative encephalomyelitis - Negri bodies
28
How can rabies be prevented? How are exposed horses treated depending on vaccination status?
- vaccinate ---> yearly core vaccine - contact tracing for zoonosis VACCINATED = immediate revaccination with observation as directed by state public health official UNVACCINATED = contact public health state official
29
What causes botulism?
neurotoxins (A, B, Ca, Cb, D) from G+, anaerobic, spore-forming Clostridium botulinum
30
What are the 3 forms of botulism?
1. forage poisoning 2. wound contamination 3. toxiinfectious (Shaker foal)
31
What causes forage poisoning botulism?
toxin preformed in food or water with decaying vegetable matter or carcass (most common!)
32
What causes wound contamination botulism?
contamination of a wound with Clostridium botulinum where the anaerobic environment allows it to germinate and produce toxins
33
What causes toxiinfectious botulism?
food with spores or bacteria allows for germination in necrotic, hypoxic conditions (ulcers) and production of toxins
34
What is the mechanism of botulism?
- binding and internalization of bacteria - translocation - inhibition of presynaptic action at peripheral cholinergic neuromuscular junction blocking of Ach = flaccid neuroparalysis
35
What clinical signs are associated with botulism?
- generalized symmetric weakness with normal mentation - decreased tail, anal, eyelid, and tongue tone - trembling worsened with exertion - recumbency - dysphagia = eating slow, unable to swallow, drooling - mydriasis, sluggish pupillary light reflec - hypoventilation, respiratory arrest (intercostal muscle paralysis) - colic, decreased GI motility - sudden death
36
What 2 tests are commonly used to diagnose botulism?
1. tongue stress test = increased time to correct tongue position after it was pulled out of the mouth 2. grain test = takes longer to eat, sluggish
37
How is botulism definitively diagnosed?
identification of toxins - feces - stomach or intestinal content - dead animals, feed, water, soil - mouse toxin assay**
38
How is botulism medically treated? What are some cons?
neutralizing circulating toxin with antitoxin - trivalent (A, B, C) - Ag Select, BOTABC - monovalent (B) - Equiplas B may initially worsen signs, $$$ and not readily available
39
What supportive care is recommended for botulism?
- decrease stress with stall confinement - remove food to avoid aspiration and use tube feeding and fluids - position in a sling for respiratory support - pain medications, sedation - antimicrobials for secondary infection
40
What antibiotics are avoided when treating secondary infections caused by botulism? What is used?
- Aminoglycosides - PPG - Tetracyclines Ceftiofur, TMS
41
What affects the prognosis of botulism?
FOALS - antitoxins + standing = good; respiratory distress = poor ADULTS = mild weakness + standing = fair-good; recumbent or peracute signs = poor
42
How is botulism prevented?
- feed and water management - vaccination in endemic areas with type B strain
43
What causes tetanus? What toxins are responsible?
Clostridium tetani - G+, anaerobic, spore-forming, ubiquitous (horses > ruminants) - tetanospasmin - tetanolysin - non-spasmogenic toxin
44
What risk factors are associated with tetanus?
- unvaccinated horses - WOUNDS: deep contaminated puncture on lower legs + burns - SOFT TISSUE: surgical, post-partum, injection site
45
What is the pathogenesis of tetanus?
- germination of spores - exotoxin formation and spread - retrograde transport by alpha motoneuron - toxins bind irreversibly to presynaptic inhibitory interneurons, resulting in spastic paralysis (stiff)
46
What clinical signs are associated with tetanus?
- colic, stiffness - trembling, spasm, paralysis - protruding 3rd eyelid upon stimulation, eyelid retraction - grimace - flared nostril - locked jaw - sawhorse stance, stiff/spastic gait - erect tail - rigid recumbency, panic
47
How is tetanus diagnosed? What are some differential diagnoses?
no diagnostic tests available - history, clinical signs, anaerobic culture can be attempted - severe neck pain - hypocalcemia - myopathy - EMND - stiff horse syndrome - shiver - encephalitis
48
What are the 6 treatments used for tetanus?
1. environmental - quiet, good footing, deep bedding, dark stall, cotton in ears 2. muscle relaxation/tranquilization - Acepromazine, Phenobarbital, Diazepam, Methocarbamol 3. remove source of infection - debride, local PPG, systemic K-Pen 4. neutralized unbound toxin - IV, IM, intrathecal antitoxin 5. maintain hydration and nutrition 6. vaccinate
49
What affected prognosis with tetanus?
fair to poor overall ---> depends on severity of clinical signs and affected horse - recumbent = grave

Equine Medicine (33 decks)

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