Toxin induced neurological disease Flashcards
(22 cards)
Toxin induced nerve dz examples
- tetanus
- botulism
- string halt
- rye-grass staggers
Tetanus - cause
Clostridium tetani endotoxin (tetanospasmin)
- horses are particularly sensitive
- tetanospasmin blocks Renshaw neurons -> irreversible
- associated with dirty wounds
- necrotic tissue and pus favour the sporulation of clostridium, and the release of toxin
- it diffuses from the site of production into the vascular system to reach the presynaptic membrane of inhibitory cells or inhibitory neurones called Renshaw cells in the spinal cord
Tetanus - where is the cause found?
- ubiquitous in soil, ruminant faeces: toxin only produced in specific circumstances and anaerobic environment
- spores are long lived and resistant to most disinfectants
Tetanus - incubation
- 7-21d
Tetanus - mortality
-~70%
– the neuronal binding of the toxin is irreversible, and therefore requires a complete sprouting and regrowth of the nerve terminal
– this process is complicated and can take weeks-months
– this definitely accounts for the high mortality rate
Tetanus - CS
- prolapsed nictitans membrane
- tight facial expression
- 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)
Tetanus - tx
Tetanus antitoxin >10,000IU IV slow
- intrathecal LS: 400-1000IU/kg
Muscle relaxants
- dantrolene
- methocarbamol
- ace-romaine
Magnesium sulphate
- blocks neuromuscular transmission
- decreases catecholamine release
- antagonises Ca
- i.e. eases muscle spasm
Supportive
- IVFT & dextrose
- quiet environment
- thick bedding
If detect a suspicious wound
- open, clean, debridement
- antibiotic: metronidazole (better than penicillin in human clinical trials)
Tx often unsuccessful but early recognition and aggressive tx in initial stages might determine a better outcome
Tetanus - prevention
Pregnant mares: 4w before delivery
- foals: @4-6mo 1st dose, followed by 2nd 4w apart, then 3rd 12mo, then biannual
Non-vaccinated mares
- tetanus anti-toxin at birth
- foals: @1-3mo, 3 doses 4w apart, then 12mo after, then biannual
Biannual vaccination for adult horses
Botulism - cause
Clostridium botulinum exotoxin (Botulinum neurotoxin)
- A & B: forage contamination, soil, wounds, injections
- C: carcases on forage
- ingestion of preformed toxins in spoiled feedstuffs
- spores with contaminated wounds (e.g. umbilicus)
- horses are very sensitive, B type most common in horses
- ‘foal shaker syndrome’
- toxin inhibits acetylcholine release at the NMJ
- toxin cross GI but not BBB (i.e. signs exclusively peripheral)
Botulism - incubation
- 3-7d
- half-life 12d
Botulism - CS
- mydriasis
- slow PLR
- tongue hypotonia
- dysphagia
- weakness
- muscle tremors
- recumbency
- hypometric gait (short and slow stride)
- low head carriage
- resp distress can be seen within 48h
Botulism - diagnosis
Feed challenge test
- give 8oz of grain in shallow pan
- a normal horse should be able to eat it in less than 2 mins
- horses with botulism will take significantly longer to finish a small amount of food
- used for those with minimal or initial CS
– used to determine if the horse has a normal eating capacity
Only in 30-40% cases toxin is found
- faecal samples (AM diagnosis)
- GI fluid samples (PM diagnosis)
- liver samples (PM diagnosis)
- PCR ± bioassays
- currently no labs in the uk that perform this test
Botulism - tx
70% survival if early tx
Serum anti-toxin 500ml-1L
- only for unbound toxin
- not available in the UK atm
Nutritional support
- NGT (be careful with decreased motility)
- or parenteral nutrition
Support recumbency
- bedding
- head elevation
- slings
- padded helmets
If wound
- open
- clean
- debride
Antibiotics
- metronidazole or penicillin often not indicated as although clostridium sensitive, in botulism they might magnify toxin release and worsening of CS, esp if pts haven’t received antitoxin
- tetracyclines and ahminoglycosides should be used with care or avoided as they seem to potentiate neuromuscular blockade
Stringhalt - what is it?
- disorders characterised by a sudden and exaggerated flexion of the pelvic limbs during swing phase of locomotion
Stringhalt - types
Classical stringhalt
- unilateral
- toxic or trauma?
- blunt trauma or fibrosis/adhesions on extensor muscles
- hock OA?
Pasture-associated
- bilateral
- outbreaks in horses at pasture
- some might have obtundation
- stridor > long nerves axonopathy
- muscle atrophy 2w
Stringhalt - pasture associated cause
Ingestion of plant neurotoxin (dandelion): demyelination of long nerves
- peroneal/tibial
- recurrent laryngeal nerve
- muscle atrophy within 2w: gaskin, thigh
Stringhalt - prognosis
Toxic
- 50% fully recovered within 12 after removal from offending pasture
Mechanical
- 50% recovered with lateral extensor
Stringhalt - CS & diagnosis
Forward walking:
- flexing limbs snap forward and upward in an adducted and sagittal plane
Determine whether toxic or mechanic
- nerve block
- IA block
- several horses
- uni vs bilateral
For cases of unilateral stringhalt
- a thorough MSK workup is needed including nerve blocks and radiographs
Stringhalt - tx
Mechanical
- OA tx
- splitting of lateral digital flexor
Toxic
- phenytoin 10-15mg/kg BID PO
Rye-grass staggers - what is it / cause?
Tremorgenic mycotoxins
- secondary diterpenoid metabolites produced by endophyte fungi affecting Perennial rye-grass, Parpalum, Bermuda grass
- dry summer/autumn after very wet spring
- these types of grass are common in areas of Australia and NZ
Rye-grass staggers - CS
- initial signs: 5-10d after consumption
- coarse muscle tremors, thoracic limbs, muzzle > cerebellar damage
- jerky hindlimb movement, base wide stance, exaggerated truncal sway
- abortion in pregnant mares
Rye-grass staggers - tx
- remove from pasture: resolution within 2w
- reduce handling: quiet environment
- provide water & feed: IV if necessary over 1st 48h
- remove infested pasture: mowing and burning
