Neuromuscular and Peripheral Neuropathies Flashcards
Fill in the following for Botulism:
1. Gram (+/-)
2. spore-forming or non-sporeforming
3. aerobic or anaerobic
4. cocci, rod, bacillus, spirochete
Clostridium botulinum is a gram positive, spore-forming, anareobic bacillus bacteria
C. botulinum has 8 toxin types (A-G). Which (of those 8) is the MOST common cause of botulism in horses?
B
Why/How does C. botulinum cause flaccid paralysis?
Toxin created by the bacteria prevents the release of acetylcholine at the neuromuscular junction which prevents skeletal and smooth muscle contraction and leads to progressive flaccid paralysis
how do horses obtain botulism?
- ingest the pre-formed toxin in poorly-made silage, feed contaminated with carcasses, rotting hay/grain, spoiled round bales*
(anaerobic conditions) - growth of the organism in a wound
- ingest bacteria but produce toxin in the GI tract (toxicoinfectious – foals)
You are presented with a 1 month old foal that had an acute onset of weakness and dragging his toes late last night. This morning, the foal is recumbent. You presumptively diagnose this foal with botulism. What is the prognosis that you convey to the owners?
Most of them need supplemenetal oxygen (50%), but with intensive care, most survive (96%) so the prognosis can be good.
what is the progression of clinical signs associated with botulism in ADULT horses?
First sign = dysphagia
Then, lowered head, dull appearance
becoming weak, shuffling their gait/dragging their toes.
Their PLR will be decreased, weak tail and anal tone, ileus
Lastly, recumbency (which carries a much worse prognosis)
T/F: botulism may be hard to diagnose in adult horses because it is difficult to distinguish from other diseases (choke, neuro diseases, colic, etc.)
true
how can you diagnose botulism in adult horses?
- grain test (normal horses eat 250 mL sweet feed < 2 min)
- toxin detection in GI contents, feces, or wounds (PCR)
why might a PCR test be more likely to be falsely negative for botulism in an adult horse as opposed to a foal?
Foals ingest the bacteria and produce the toxins in their GI tract, so a positive is more likely in foals. Adults ingest the preformed toxin, not the bacteria itself.
what is the treatment for botulism?
- botulism antitoxin (plasma from hyperimmunized horses with antiboies against the botulism toxin)
ONLY binds circulating toxin, not the toxin that has already bound to the NMJ, so not really helpful for resolving clinical signs, just prevents horse from getting worse.
- supportive care – nutritional/fluid support, oxygen, urinary catheter, ocular care, wound management (cant eat/drink, breathe, urinate, blink, or stand)
why are antibiotics NOT indicated in botulism cases?
the TOXIN is what is causing the disease, not the bacteria
T/F: there is a botulism vaccine
true.
It is only against type B (the most common).
Requires an initial 3 boosters, then boostered annually.
In addition to vaccination, what are other ways you can reduce the risk of botulism in your horse herd?
properly store feed
caution with round bales.
____________ is progressive granulomatous polyradiculoneuritis of the cauda equina and less commonly the cranial nerves.
polyneuritis equi
what is the etiology/cause of polyneuritis equi?
unknown really.
may have something to do with cytotoxic T cells and macrophage infiltrates, autoimmune, or hypersensitivity reactions.
A horse presents to you with hyperesthesia of the skin and muscles around the hindquarters, progressive densensitization, and progressive paresis. This horse has asymmetric muscle atrophy around the body, fecal retention, and urinary incontinence. What is your presumptive diagnosis?
polyneuritis equi
how can you diagnose polyneuritis equi?
- clinical signs
- CSF: mononuclear pleo, high TP
- necropsy: thickened, discolored, edematous cauda equina; granulomatous inflammation; axonal degeneration and demyelination of nerve roots
what is the treatment for polyneuritis equi?
- corticosteroids
- immunosuppressants (gold salts, azathioprine)
- supportive care – ucath, manual removal of feces
what is the prognosis for polyneuritis equi and why?
grave
the treatments are palliative, not curative.
what are the most common peripheral nerves to be injured in horses?
- facial nerve
- suprascapular nerve
- radial nerve
- femoral nerve
- sciatic nerve
- obturator nerve
__________ is the bruising and inflammation of the nerves
neuropraxia
_________ is the crushing of the nerve, but the epineurium and perineurium remain intact
axonotmesis
________ is severing of the whole nerve fiber and wallerian degeneration occuring in the distal segment.
neurotmesis
how quickly do nerves regenerate?
axons grow 1 mm/day (super slowly), so it can take ~6 months for horse nerve to regenerate completely.
What is the significance of nerve injuries?
- Loss of proprioceptive function (placement deficits and ataxia)
- paresis or paralysis of voluntary or reflex movements
- desensitization (deep pain lost)
- muscle mass loss (50% by two weeks) and muscle fibrosis can prevent healing
T/F: failure of nerves to heal beyond 12 months has a poor prognosis
true
what is the treatment for nerve injury in horses?
During the acute phase:
1. NSAIDs and cold therapy
2. physical therapy (passive ROM, exercise to help develop compensatory mechanisms and strength)
During the chronic phase:
1. TIME
2. adjunctive treatments: laser, etc. may help
T/F: corticosteroids are significantly beneficial in nerve regeneration
false – they do not help with regeneration
what are potential etiologies of facial nerve paralysis in horses?
- traumatic compression over facial crest (lat recumbency, halter)
- inflammation of middle ear or guttural pouch
- brainstem disease
T/F: with facial paralysis, the muzzle will deviate towards the side of the lesion
false – away from the lesion
ex. Right facial nerve paralysis will cause muzzle deviation to the Left
Why does it matter to localize the lesions associated with facial nerve paralysis?
You can tell more about the inciting cause
For example, if a horse has No ear deficits and no ptosis, but has muzzle deviation towards the right; this would indicate a right sided facial nerve lesion that is distal to the brainstem/inner ear/guttural pouch since you dont see signs assoc with those systems.
What nerve is injured in a case of sweeny?
trauma to the suprascpular nerve (innervates the supra- and infraspinatus muscles)
What are the clinical signs assoc with suprascapular nerve damage?
- atrophy of supra and infraspinatus muscles
- ABduction of shoulder while weight bearing
- Subluxation of shoulder
- difficulty advancing the limb
how do you treat shoulder sweeny?
scapular notch surgery.
releases a sheath of fascia to decrease compression of the nerve.
What clinical sign would indicate radial nerve paralysis?
Elbow, knee and fetlock FLEXION
Elbow Dropped
dorsum of foot rested on ground
bearing weight poorly or not at all.
