Equine Neuropathies Flashcards
Why do we need to know about tetanus?
Compromises welfare.
Compromises ability to eat or move.
Pain.
Tetanus aetiopathogenesis.
Clostridium tetani is a common soil inhabitant.
- It is a strict anaerobe.
- It can sporulate and survive for years in adverse conditions.
- Usually enters via a deep wound.
- necrosis and pus makes an anaerobic environment and leads to spore germination.
– produce exotoxin.
– exotoxin into bloodstream and nerve axons.
– CNS presynaptic inhibitory interneurones.
–> inhibits NT release here.
—> this inhibits inhibition.
—-> leads to spastic paralysis (7-10d later so may not have a wound anymore).
Tetanus clinical signs.
Hypertonia of muscles w/ spasms.
- worse w/ stimulation.
‘Sawhorse’ stance
Extended, rigid tail.
Stiff gait, can progress to recumbent, which can progress to respiratory paralysis.
Trismus (lockjaw).
Prolapse nictitating membrane.
Pyrexia.
Complications of tetanus.
Complications:
- decubital ulcers.
- dysphagia.
- dysuria.
- impaction and gaseous distension.
- What is the cause of morbidity in tetanus?
- Prognostic indicators in tetanus.
- Respiratory failure.
Aspiration pneumonia (dysphagia). - Age {young - poor as vac less likely).
Dyspnoea.
Dysphagia.
Recumbency.
Time and money - may not be insured.
Tetanus Dx.
By exclusion.
Hx and clinical signs.
- ?presence of a wound (may have healed or be very small)
Response to tx.
? gram stain exudate at wound (could just be contaminant).
May be able to gauge if becoming stiffer as they walk.
Tx of tetanus.
Toxin remains bound so have to manage them until get new receptors.
- slow recovery (~1month).
5 goals of tx:
- Interrupt toxin production.
– Local and parenteral abx therapy w/ penicillin.
- Neutralise unbound toxin.
– Tetanus antitoxin produces from sera of hyperimmunised horses.
– Ab’s neutralise unbound toxin.
– Systemic and local to wound.
– High dose, expensive.
- Control muscular spasms.
– Phenothiazines (at brainstem, depress descending excitatory input).
– Benzodiazepines.
– Keep them calm and quiet.
- Supportive care.
– vital.
– minimal stimulation!
– manage recumbency, dysuria, dysphagia, hyperthermia.
- Generation of active immunity to tetanus toxins.
– Start vac protocol.
Tetanus prevention.
Vaccine.
- rare dz even though horses v susceptible.
All horses:
- primary vac at 4-6m old.
- booster 4-6w later.
- 1yr later.
- then bi or tri annual.
Pregnant mares:
- booster 4-6w before foaling.
– for passive transfer to foal via colostrum.
Foals:
- if unvaccinated mare, but good colostral uptake, vaccinate foal and may give TAT dependent on management.
– can mount a good immune response as good passive transfer.
- if unvaccinated mare, and FPT, give hyperimmune plasma.
Horse w/ wound/surgery.
- check vac status.
- vac at risk again if more than 6m ago.
- ?TAT.
– 3w protection.
– give away from vac site.
– unlikely to do harm but small risk of Theiler’s dz.
Botulism aetiopathogenesis.
Clostridium botulinum.
- gram+ spore forming obligate anaerobe.
- soil, agricultural products.
- produce exotoxins A, B, C1, C2, D, E, F, G.
- most horse dz is type B.
Clostridia bacteria release toxin which acts pre-synaptically at the peripheral cholinergic neuromuscular junction.
- prevents synaptic vesicle from releasing acetylcholine.
- get flaccid paralysis.
- once toxin bound, recovery only by regeneration of new motor end plates (4-10days).
What are the 3 mechanisms of clinical botulism aetiopathogenesis?
Forage poisoning.
- ingestion of pre-formed toxin in feed that has been contaminated by bacteria.
- feed often decaying / carcasses.
- haylage (plastic bags).
- horses more susceptible than cattle.
Wound botulism:
- almost unique to horses.
- wounds become contaminated w/ C. botulinum, producing toxin in vivo.
Toxicoinfectious botulism (shaker foal syndrome):
- rare (US only?)
- Foals days to months old.
- Ingest contaminated soils.
- toxin production w/in intestinal tract.
Botulism clinical signs.
Similar, regardless of source of contamination or type of toxin.
Onset usually w/in 24hrs of exposure.
Weakness - but not ataxic.
Dysphagia.
Poor muscle tone.
Recumbency.
Death from resp. failure.
Dx of botulism.
Difficult.
Clinical signs.
Detect toxin in feed, serum, GI content, faeces, debris from wound.
Tx for botulism.
Antitoxin (US).
Nursing.
Tube feeding.
Laxatives.
?mechanical ventilation.
Time and money.
Px poor.
Prevention of botulism.
Type B vac (US).
Cattle vac (C and D).
Most important:
- good husbandry.
- proper processing and storage of feed material.
Equine Grass Sickness.
Equine Dysautonomia.
Acquired degenerative polyneuropathy.
Neurons of autonomic and enteric nervous system.
Ileum.
EGS pathogenesis.
(Causative agents have not been identified yet).
Neurotoxin causes altered autonomic activity.
Leads to decrease intestinal peristalsis.
Leads to ileus and colonic impaction.
EGS risk factors.
3-5yrs old.
In contacts:
- outbreaks.
- but if in contact and no dz, 10x less likely to develop dz.
Recently moved premises.
Live out.
Soil disturbance.
Spring and autumn.
Acute EGS clinical signs.
Acute onset GI ileus leads to gastric and SI distension leads to colic and hypovolaemia.
Tachycardia.
Sweating.
Muscle fasciculations.
Pyrexia.
Dysphagia.
Ptosis.
Secondary impaction.
Subacute EGS clinical signs.
3-7d.
Similar signs, less severe, often no reflux.
Large colon impactions.
Rhinitis sicca.
Chronic EGS clinical signs.
Weeks to months.
Cachexia.
Empty GIT.
Rhinitis sicca.
Muscle tremors.
Base narrow stance.
Dx of EGS.
Can be difficult unless invasive.
Clinical signs, hx.
?Phenylephrine eye drops.
Ileal biopsy (laparotomy / assisted laparoscopy).
PM.
EGS Px.
Usually fatal.
- acute, 100% – euthanised, gastric rupture, circulatory failure, in ~48hrs.
- subacute, 100%, 5-7d.
- chronic, 50% may survive but not always fully recover.
EGS tx and prevention.
No effective cure.
- acute cases respond initially to gastric decompression and fluid therapy.
- nursing.
Promising work on vac.
Trigeminal-mediated headshaking.
Neuropathic facial pain condition (varying intensities of pins and needles, burning, electric shock pain).
- this pain is occurring due to the threshold potential for firing of the infra-orbital nerve being about 10x lower than normal.
Reason and mechanism for nerve sensitisation is unknown.
Structurally normal and functionally abnormal.
Complex interaction w/ environment but not allergy.
Some seasonally affected (usually spring-summer) only.
Acquired in young adulthood.
