Neuromuscular and Peripheral Neuropathies

Question 1

Fill in the following for Botulism:
1. Gram (+/-)
2. spore-forming or non-sporeforming
3. aerobic or anaerobic
4. cocci, rod, bacillus, spirochete

Answer 1

Clostridium botulinum is a gram positive, spore-forming, anareobic bacillus bacteria

Question 2

C. botulinum has 8 toxin types (A-G). Which (of those 8) is the MOST common cause of botulism in horses?

Answer 2

B

Question 3

Why/How does C. botulinum cause flaccid paralysis?

Answer 3

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

Question 4

how do horses obtain botulism?

Answer 4

1. ingest the pre-formed toxin in poorly-made silage, feed contaminated with carcasses, rotting hay/grain, spoiled round bales*
   (anaerobic conditions)
2. growth of the organism in a wound
3. ingest bacteria but produce toxin in the GI tract (toxicoinfectious – foals)

Question 5

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?

Answer 5

Most of them need supplemenetal oxygen (50%), but with intensive care, most survive (96%) so the prognosis can be good.

Question 6

what is the progression of clinical signs associated with botulism in ADULT horses?

Answer 6

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)

Question 7

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.)

Answer 7

true

Question 8

how can you diagnose botulism in adult horses?

Answer 8

1. grain test (normal horses eat 250 mL sweet feed < 2 min)
2. toxin detection in GI contents, feces, or wounds (PCR)

Question 9

why might a PCR test be more likely to be falsely negative for botulism in an adult horse as opposed to a foal?

Answer 9

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.

Question 10

what is the treatment for botulism?

Answer 10

1. 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.

2. supportive care – nutritional/fluid support, oxygen, urinary catheter, ocular care, wound management (cant eat/drink, breathe, urinate, blink, or stand)

Question 11

why are antibiotics NOT indicated in botulism cases?

Answer 11

the TOXIN is what is causing the disease, not the bacteria

Question 12

T/F: there is a botulism vaccine

Answer 12

true.
It is only against type B (the most common).
Requires an initial 3 boosters, then boostered annually.

Question 13

In addition to vaccination, what are other ways you can reduce the risk of botulism in your horse herd?

Answer 13

properly store feed
caution with round bales.

Question 14

____________ is progressive granulomatous polyradiculoneuritis of the cauda equina and less commonly the cranial nerves.

Answer 14

polyneuritis equi

Question 15

what is the etiology/cause of polyneuritis equi?

Answer 15

unknown really.

may have something to do with cytotoxic T cells and macrophage infiltrates, autoimmune, or hypersensitivity reactions.

Question 16

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?

Answer 16

polyneuritis equi

Question 17

how can you diagnose polyneuritis equi?

Answer 17

• clinical signs
• CSF: mononuclear pleo, high TP
• necropsy: thickened, discolored, edematous cauda equina; granulomatous inflammation; axonal degeneration and demyelination of nerve roots

Question 18

what is the treatment for polyneuritis equi?

Answer 18

1. corticosteroids
2. immunosuppressants (gold salts, azathioprine)
3. supportive care – ucath, manual removal of feces

Question 19

what is the prognosis for polyneuritis equi and why?

Answer 19

grave

the treatments are palliative, not curative.

Question 20

what are the most common peripheral nerves to be injured in horses?

Answer 20

1. facial nerve
2. suprascapular nerve
3. radial nerve
4. femoral nerve
5. sciatic nerve
6. obturator nerve

Question 21

__________ is the bruising and inflammation of the nerves

Answer 21

neuropraxia

Question 22

_________ is the crushing of the nerve, but the epineurium and perineurium remain intact

Answer 22

axonotmesis

Question 23

________ is severing of the whole nerve fiber and wallerian degeneration occuring in the distal segment.

Answer 23

neurotmesis

Question 24

how quickly do nerves regenerate?

Answer 24

axons grow 1 mm/day (super slowly), so it can take ~6 months for horse nerve to regenerate completely.

Question 25

What is the significance of nerve injuries?

Answer 25

1. Loss of proprioceptive function (placement deficits and ataxia)
2. paresis or paralysis of voluntary or reflex movements
3. desensitization (deep pain lost)
4. muscle mass loss (50% by two weeks) and muscle fibrosis can prevent healing

Question 26

T/F: failure of nerves to heal beyond 12 months has a poor prognosis

Answer 26

true

Question 27

what is the treatment for nerve injury in horses?

Answer 27

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

Question 28

T/F: corticosteroids are significantly beneficial in nerve regeneration

Answer 28

false – they do not help with regeneration

Question 29

what are potential etiologies of facial nerve paralysis in horses?

Answer 29

• traumatic compression over facial crest (lat recumbency, halter)
• inflammation of middle ear or guttural pouch
• brainstem disease

Question 30

T/F: with facial paralysis, the muzzle will deviate towards the side of the lesion

Answer 30

false – away from the lesion
ex. Right facial nerve paralysis will cause muzzle deviation to the Left

Question 31

Why does it matter to localize the lesions associated with facial nerve paralysis?

Answer 31

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.

Question 32

What nerve is injured in a case of sweeny?

Answer 32

trauma to the suprascpular nerve (innervates the supra- and infraspinatus muscles)

Question 33

What are the clinical signs assoc with suprascapular nerve damage?

Answer 33

• atrophy of supra and infraspinatus muscles
• ABduction of shoulder while weight bearing
• Subluxation of shoulder
• difficulty advancing the limb

Question 34

how do you treat shoulder sweeny?

Answer 34

scapular notch surgery.
releases a sheath of fascia to decrease compression of the nerve.

Question 35

What clinical sign would indicate radial nerve paralysis?

Answer 35

Elbow, knee and fetlock FLEXION
Elbow Dropped
dorsum of foot rested on ground

bearing weight poorly or not at all.