OOD 27.6.4: Toxin-induced neurological disease Flashcards
Cause and pathogenesis of tetanus
Cause:Clostridium tetani exotoxin (tetanospasmin)
* This bacterium is ubiquitous in soil and ruminant faeces but toxin only produced in specific circumstances and anaerobic environment
* Spores are long-lived and resistant to most disinfection
* Tetanospasmin inhibits Renshaw neurones and this is irreversible
* Horses are particularly sensitive
* Infection generally associated with dirty wounds
Incubation and mortality of tetanus
- Incubation: 7-21 days
- Mortality: 70%
Clinical signs of tetanus
- Prolapsed nictitating membrane
- Tight facial expression (Risus sardonicus)
- Limp spasticity (“sawhorse” stance)
- Fixed extended neck
- Tight jaw (trismus)
- Laryngeal spasm (stridor), drooling
- Dysphagia
- Elevated tail head
- Recumbency
- Dyspnoea
- Hyperthermia
- Profuse sweating and tachy/bradycardia (autonomic storms)
Treatment of tetanus
- Tetanus antitoxin slow IV >10,000 IU needed
- Muscle relaxants e.g. Dantrolene, methocarbamol, acepromazine
- Magnesium sulphate: blocks neuromuscular transmission, catecholamine release, antagonises Ca
- Supportive care: IV fluids and dextrose, quiet environment, thick bedding
What to do if you find a suspicious wound and are worried about tetanus?
- Open, clean, debride
- Provide antibiotics: in humans trials, metronidazole performed better compared to penicillin
- (Penicillin = drug of choice in ruminants / anything that may enter the food chain)
Prevention of tetanus
- Vaccination of pregnant mares 4 weeks before delivery
- Vaccinate foals at 4-6 months, then 4 weeks later, then at 12 months. Then give biannually.
- If mare not vaccinated, provide TAT at birth and vaccinate foals at 1-3 months with 3 doses 4 weeks apart, then at 12 months, then biannually.
Causative agent of Botulism
- Causative agent: Clostridium botulinum exotoxin (Botulism neurotoxin)
- Toxins A&B are found in contaminated forage, soil, wounds, injections etc.
- Toxin C is found in carcasses on forage
Pathogenesis of botulism
- Ingestion of preformed toxins in spoiled feedstuffs, or entry of spores to body via contaminated wounds, or umbilicus
- Horses are very sensitive; most common form is Type B (“foal shaker syndrome”)
- Toxin (BoNT) inhibits acetylcholine release
- The toxin crosses the GIT but not the BBB
Incubation and half life of botulism
- Incubation: 3-7 days
- Half-life: 12 days
Clinical signs of botulism
- Mydriasis
- Slow PLR
- Tongue hypotonia
- Dysphagia
- Weakness
- Muscle tremors
- Recumbency
What is the feed challenge test, when would you use it and what is a normal result?
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 mins.
Could use if suspicious of tongue hypotonia / dysphagia e.g. in botulism
Diagnosis of botulism
- Toxin is only found in 30-40% cases
- Can check faecal / GI fluid / liver samples and send for PCR ± bioassays
Treatment of botulism
- Time-critical: 70% survival if early treatment
- Serum antitoxin: 500ml-1L - only works on unbound toxin
- Nutritional support: e.g. NGT but care due to decreased motility, or parenteral nutrition
- Support recumbency: with deep bedding, head elevation, slings, padded helmets
Prevention of botulism
Vaccination in endemic areas
What is stringhalt and what are the possible causes?
Stringhalt: disorders characterised by sudden and exaggerated flexion of the pelvic limbs during the swing phase of locomotion.
* Classical stringhalt: unilateral and possibly due to trauma of extensor muscles, OA of hock
* Pasture-associated stringhalt: bilateral and associated with ingestion of plant neurotoxin at pasture
Epidemiology and pathogenesis of pasture-associated stringhalt
- Outbreaks seen in horses at pasture
- Occurs due to ingestion of plant neurotoxin (Hypochoeris radicata, false daffofil) which leads to demyelination of long nerves
- There is long nerve axonopathy and muscle atrophy within 2 weeks
- Particularly seen in peroneal, tibial nerves, recurrent laryngeal nerve, and atrophy in the gaskin and thigh
Clinical signs of stringhalt
- During forward walking: flexing limb snaps forwards and upwards in an adducted and sagittal plane
- Muscle atrophy within 2 weeks
Diagnosis of stringhalt
- Determine whether toxic or mechanical: use nerve blocks, intra-articular blocks; see if unilateral or bilateral; see if multiple horses affected
Treatment of stringhalt
- Mechanical: OA treatment, splinting of the lateral digital flexor
- Toxic: phenytoin PO BID
Prognosis for stringhalt
- Mechanical: 50% recovered
- Toxic: 50% fully recovered within 12 months
Epidemiology and pathogenesis of rye-grass staggers
- Initial signs occur 5-10 days after consumption
- Ingestion of tremorgenic mycotoxins (secondary diterpenoid metabolites produced by endophyte fungi affecting perennial rye-grass, paspalum, bermude grass)
- Initial signs are seen 5-10 days after consumption
Clinical signs of rye-grass staggers
- Coarse muscle tremors esp in thoracic limbs and muzzle (cerebellar damage)
- Jerky hindlimb movement
- Wide-based stance
- Exaggerated truncal sway
- Abortion in pregnant mares
Treatment of rye-grass staggers
- Remove from pasture - should see resolution within 2 weeks
- Reduce handling and keep in quiet environment
- Provide water and feed: IV if necessary over first 48hrs
- Remove infested pasture via mowing and burning
