13. Neuromuscular Disorders and Peripheral Myelopathies Flashcards

1
Q

What is the etiology of Botulism? What kind of bacteria is it? Where is it normally found?

A

Gram positive, spore forming, anaerobic bacillus
-Normal in soil
-Eight toxins (A-G)
-B most common

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2
Q

What is the pathophysiology of Botulism? What is affected and what signs does that cause?

A

-Toxin prevent release of ACH at neuromuscular junction (no smooth muscle contraction)
-Flaccid Paralysis

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3
Q

How do horses get botulism?

A

Ingestion of pre-formed toxin
-Silage, feed with carcass, rotten or spoiled feed, spoiled round bale, poultry litter
-Growth of organism in a wound
-Organism in GIT (foal)
(think anaerobic conditions)

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4
Q

What is the most common presentation of botulism in foals?

A

Toxicoinfectious
-1-2 months
-rapid onset
-stumble, weak, dragging toes
-Recumbency
-dehydrated and hypoglycemic
-prognosis good intensive care

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5
Q

What type of intensive care do foals need if they have Botulism?

A

Oxygen and ventilator

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6
Q

What are some clinical signs of botulism in horses?

A

Dysphagia - decreased tongue tone
Lowered head, dul
Weak, shuffling gate, dragging toes
Decerased PLR
Weak tail and anal tone
Ileus - present for colic
Recumbency (60-90% mortality)

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7
Q

Is Botulism a straightforward diagnosis?

A

No, may not be thinking it until multiple horses have it and you ask the right history questions

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8
Q

How do you diagnose Botulism?

A

Clinical signs - tongue, weakness, gait
Grain test - normal horse eat 250ml sweet feed in <2 min (Infected = hard to swallow/drop grain)
Toxin detection in GI content, feces, wound (mouse, PCR)
Post-mortem exam

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9
Q

How do you treat Botulism?

A

Botulism antitoxin - plasma from hyperimmunixed horse, antibodies, only bind circulating
Supportive care

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10
Q

What kind of supportive care can you provide for botulism?

A

Nutritional and Fluid - cant eat or drink
Oxygen - cant breath
Urinary Catheter - cant urinate
Ocular care - cant blink
Wound Management - cant stand
Antibiotics?

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11
Q

How long may you need to provide this supportive care?

A

Can be greater than 2 weeks for the end plate to regenerate ACH receptors

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12
Q

Do Botulism horses recover?

A

Yes, quite well if you take the time and support

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13
Q

Can you prevent Botulism?

A

Vaccination - Type B
-No cross protection
-3 boosters, then annually prior to round bale season
-Proper storage of feed
-Care when using round bales

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14
Q

What is polyneuritis equi?
Who does it affect?

A

Progressive granulomatous polyradiculoneuritis of the cauda equina and cranial nerves

Adult horses of any breed

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15
Q

What causes Polyneuritis Equi?

A

-Unknown
-Cytotoxic T cell and macrophage infiltrates
-Autoimmune - allergic, gullian barre
-Hypersensitivity - systemic inflammation, parasite migration, EHV

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16
Q

What are the clinical signs of polyneuritis equi?

A

-Cutaneous and muscular hyperesthesia around the hindquarters
-Progressive desensitization
-Progressive Paresis
-Progressive neurogenic atrophy
-Fecal retention with urinary incontinent
-Weakness and Ataxia
-Asymmetric muscle atrophy (Temporal or gluteal)
-Perfuse sweating

17
Q

What are some differentials for polyneuritis equi?

A

EPM, EHV, Encephalitis, trauma, Botulism

18
Q

How do you diagnose Polyneuritis Equi?

A

Clinical signs
CSF - mononuclear pleocytosis with high TP
Necropsy - thickened, discolored, edematous cauda equina, granulomatous inflammation, axonal degeneration and demyelination

19
Q

How do you treat polyneuritis equi?

A

Anti-inflammatories - steroids
Immunosuppressive Drugs
Palliative but not curative
Supportive Care - bladder cath, manual feces removal
Prognosis - hopeless

20
Q

What are some nerves that are affected by a peripheral neuropathy?

A

Facial, suprascapular (sweeney), Radial, Femoral, Sciatic (peroneal and tibial), obturator (foaling)

21
Q

What causes nerve injury?

A

Trauma, stretching, compression or severance

22
Q

Define the following:
Neuropraxia:
Axonotmesis:
Neurotmesis:

A

Neuropraxia: Brusing and inflammation of nerves (transient 3-6wk)
Axonotmesis: Crushing of nerve, epineurium and perineurium intact
Neurotmesis: Whole fiber severed, Wallerian degeneration expected

23
Q

How fast do regenerating axons grow?

24
Q

What is the progression of nerve dysfunction and damage?

A

-Loss of proprioceptive function (placement and mild ataxia)
-Paresis or paralysis of voluntary and reflex movements
-Desensitization

25
Q

What percent of muscle mass is lost by 2 weeks after denervation?

A

50%
-Fibrosis will prevent healing and failure to heal beyond 12 months is a poor prognosis

26
Q

What causes facial nerve paralysis and what are the clinical signs?

A

Traumatic compression of facial crest, inflammation middle ear or guttural pouch, brainstem disease

Signs: Ear droop, ptosis, muzzle deviation away from lesion, quidding

27
Q

What is the term for paralysis of the suprascapular nerve?

A

Sweeney - trauma to suprascapular nerve (trauma or chronic concussion)
-Look like leg is asleep

28
Q

What are some clinical signs of Sweeny or suprascapular Nerve Paralysis?

A

-Walk like leg is asleep
-Atrophy nerve
-Abduction shoulder while weight bearing
-Subluxation shoulder
-Difficulty advancing limb

29
Q

What is the treatment for sweeny?

A

Acute
Chronic (oa)

Time and antinflammatories

30
Q

When does radial nerve paralysis occur?

A

Shoulder trauma/post anesthesia

31
Q

What are clinical signs of nerve paralysis?

A

Brachial plexus injury, elbow, knee or fetlock flexed, dorsum food on ground, elbow dropped
bear weight poorly and not on all limbs

32
Q

What are some differentials for radial nerve paralysis?

A

Olecranon fracture
Lameness (abscess)

33
Q

What is treatment for radial nerve paralysis?

A

Time and NSAID
Support other limb to prevent laminitis