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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
Q

What are common clinical signs seen with paralytic rabies?

A
  • ascending paralysis
  • ataxia
  • shifting lameness
  • hyperesthesia
  • cauda equina
26
Q

How is rabies diagnosed antemortem?

A

NO CONFIRMATION AVAILABLE ANTEMORTEM

  • history, clinical signs
  • CBC, biochem are usually normal
  • CSF
27
Q

How is rabies diagnosed postmortem?

A
  • 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
Q

How can rabies be prevented? How are exposed horses treated depending on vaccination status?

A
  • 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
Q

What causes botulism?

A

neurotoxins (A, B, Ca, Cb, D) from G+, anaerobic, spore-forming Clostridium botulinum

30
Q

What are the 3 forms of botulism?

A
  1. forage poisoning
  2. wound contamination
  3. toxiinfectious (Shaker foal)
31
Q

What causes forage poisoning botulism?

A

toxin preformed in food or water with decaying vegetable matter or carcass

(most common!)

32
Q

What causes wound contamination botulism?

A

contamination of a wound with Clostridium botulinum where the anaerobic environment allows it to germinate and produce toxins

33
Q

What causes toxiinfectious botulism?

A

food with spores or bacteria allows for germination in necrotic, hypoxic conditions (ulcers) and production of toxins

34
Q

What is the mechanism of botulism?

A
  • binding and internalization of bacteria
  • translocation
  • inhibition of presynaptic action at peripheral cholinergic neuromuscular junction

blocking of Ach = flaccid neuroparalysis

35
Q

What clinical signs are associated with botulism?

A
  • 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
Q

What 2 tests are commonly used to diagnose botulism?

A
  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
Q

How is botulism definitively diagnosed?

A

identification of toxins

  • feces
  • stomach or intestinal content
  • dead animals, feed, water, soil
  • mouse toxin assay**
38
Q

How is botulism medically treated? What are some cons?

A

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
Q

What supportive care is recommended for botulism?

A
  • 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
Q

What antibiotics are avoided when treating secondary infections caused by botulism? What is used?

A
  • Aminoglycosides
  • PPG
  • Tetracyclines

Ceftiofur, TMS

41
Q

What affects the prognosis of botulism?

A

FOALS - antitoxins + standing = good; respiratory distress = poor

ADULTS = mild weakness + standing = fair-good; recumbent or peracute signs = poor

42
Q

How is botulism prevented?

A
  • feed and water management
  • vaccination in endemic areas with type B strain
43
Q

What causes tetanus? What toxins are responsible?

A

Clostridium tetani - G+, anaerobic, spore-forming, ubiquitous (horses > ruminants)

  • tetanospasmin
  • tetanolysin
  • non-spasmogenic toxin
44
Q

What risk factors are associated with tetanus?

A
  • unvaccinated horses
  • WOUNDS: deep contaminated puncture on lower legs + burns
  • SOFT TISSUE: surgical, post-partum, injection site
45
Q

What is the pathogenesis of tetanus?

A
  • 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
Q

What clinical signs are associated with tetanus?

A
  • 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
Q

How is tetanus diagnosed? What are some differential diagnoses?

A

no diagnostic tests available - history, clinical signs, anaerobic culture can be attempted

  • severe neck pain
  • hypocalcemia
  • myopathy
  • EMND
  • stiff horse syndrome
  • shiver
  • encephalitis
48
Q

What are the 6 treatments used for tetanus?

A
  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
Q

What affected prognosis with tetanus?

A

fair to poor overall —> depends on severity of clinical signs and affected horse

  • recumbent = grave

Equine Medicine (33 decks)

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