Toxin induced neuro disease Flashcards

1
Q

What is the cause of tetnus in horses?

A
  • Disease caused by Clostridium tetani exotoxin (tetanospasmin)
  • C. tetani is ubiquitous in soil, ruminants faeces (GI): toxin only produced in specific circumstances and anaerobic environment
  • Spores are long-lived and resistant to most disinfectants
  • Associated with dirty wounds
  • Incubation: 7-21 days
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2
Q

What is the mechanism of action of tetanospasmin within the body?

A

tetanospasmin diffuses in the blood from site of production within the body to the presynaptic membrane of inhibitory neurons (Renshaw cells), these cells fine tune movement by fine tuning movements (by balancing extension and flexion)
These cells are activated GABA and glycine neurotransmitter and tenanus blocks the release of both of these . Hyperactivity of the alpha motor neurone and spams and rigidity is the result.
Also affects autonomic nerves
The binding of the neurotoxin is irriversible to new nerves have to grow - recovery is several weeks

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3
Q

What are the clinicla signs of tenenus in horses?

A
  • Prolapse Nictitating membrane
  • Tight facial expression (risus sardonicus)
  • Limb Spasticity (“Sawhorse”)
  • Fixed extended neck
  • Tight jaw (trismus)
  • Laryngeal spasm (stridor), drooling
  • Dysphagia
  • Elevated tail head
  • Recumbency, dyspnoea, hyperthermia
  • Profuse sweating and tachy/bradycardia (autonomic storms)
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4
Q

What is the treatment and management of a horse with tetenus?

A
  • Tetanus antitoxin >10 000IU IV slow
    • Intrathecal LS: 400-1000IU/Kg
  • Muscle relaxants: Dantrolene, methocarbamol,
  • acepromazine
  • Magnesium sulphate:
    • Blocks neuromuscular transmission
    • Decrease catecholamine release
    • Antagonises Ca
  • Supportive
    • IV fluids and dextrose
    • Quiet environment
    • Thick bedding
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5
Q

If you find a horse with mild signs of tetenus with a wound what should you do?

A

If you detect a suspicious wound:
Open, clean and debridement (to stop the production of futher toxins
Systemic Antibiotics: Metronidazol (Better than Penicillin in human clinical trials)

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6
Q

What is the prevention for tetenus?

A
  • Pregnant mares: 4 weeks before delivery
  • Foals: @ 4-6 months: first dose, followed by 2nd 4 weeks apart, then 3rd @12 months then biannual

Non-vaccinated mares:
* Tetanus anti-toxin at birth
* Foals: @ 1-3 months : 3 doses 4 weeks apart, then 12 months after, then biannual

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7
Q

What is the cause of botulism?
what are the causes of the differnt types?
How does botulism cause its effects?

A

Disease caused by Clostridium botulinum exotoxin (Botulinum neurotoxin)
Type A & B: forage contamination, soil, wounds, injections
Type C: rodent or birds carcases on forage/feed

  • Ingestion of preformed toxins in spoiled feedstuffs,
  • Spores with contaminated wounds (umbilicus)
  • B type most common in horses “Foal shaker syndrome”
  • Toxin (BoNT) Inhibits Acetylcholine release (therfore no contraction in smooth or skeletal muscle, parasympathetic nerves also use ACh as neurotransmiter)
  • Toxin crosses GI but no BBB
  • Incubation 3-7 days and half-life 12 days
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8
Q

What are the clinical signs of botulism in horses?
How can you test a horse with minimal clinical signs?

A

Clinical signs:
* Mydriasis
* Slow pupillary light reflexes
* Tongue hypotonia
* Dysphagia
* Weakness
* Muscle tremors
* Recumbency

Feed challenge test
Give 8 oz of grain in a shallow pan. A normal horse should be able to eat it in less than 2 minutes

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9
Q

how is botulism diagnosed?
What is the treatment?

A

DIAGNOSIS
Only in 30-40% cases toxin is found
* Faecal samples
* GI fluid samples
* Liver samples
PCR +/- bioassays

TREATMENT
* Time is of essence: 70% survival if early treatment
* Serum anti-toxin 500ml-1L > only for unbound toxin (in the USA)
* Nutritional support: NGT (be careful>decrease motility) or parenteral nutrition
* Support recumbency: bedding, head elevation, slings, padded helmet

Vaccines can be given in endemic areas

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10
Q

What is stringhalt? What are two types?

A

Disorders characterised by a sudden and exaggerated flexion of the pelvic limbs during swing phase of locomotion

Classical stringhalt: unilateral: toxic or trauma?: blunt trauma or fibrosis/adhesions on extensor muscles, OA hock?
Pasture-associated: bilateral, outbreaks in horses at pasture, some might have obtundation, stridor> long nerves axonopathy. Muscle atrophy within 2 weeks:
* Ingestion of plant neurotoxin: demyelination of long nerves (Hypochaeris radicata, also known as catsear or false dandelion)
* Peroneal/Tibial
* Recurrent laryngeal nerve
* Muscle atrophy within 2 weeks: gaskin, thigh

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11
Q

What are the clinicla signs of stringhalt
what is the prognosis?
What is the treatment?

A

Clinicla signs:
* Forward walking: Flexing limbs snaps forward and upward in an adducted and sagittal plane
* Determine whether toxic or mechanic: nerve block, IA block, several horses, bilateral vs unilateral….

Prognosis
* Toxic: 50 % fully recovered within 12 months
* Mechanical: 50% recovered with lateral extensor

TREATMENT
* Mechanical: OA treatment, splitting of lateral digital extensor
* Toxic: Phenytoin (10-15mg/kg BID PO)

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12
Q

What is Rye-grass staggers?
When and where does this occur?
What are the clinical signs?

A

Tremorgenic mycotoxins: secondary diterpenoid metabolites produced by endophyte fungi affecting Perennial rye-grass, Paspalum, Bermuda grass..

Commonly in australia and new zeland, can occur in europe when feild is reseeded
Dry summer/autumn after very wet spring
Initial signs: 5-10 days after consumption

Clinical signs:
Coarse muscle tremors, thoracic limbs, muzzle> cerebellar damage
Jerky hindlimb movement, base wide stance, exaggerated truncal sway
Abortion in pregnant mares

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13
Q
A
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