13. Neuromuscular Disorders and Peripheral Myelopathies Flashcards

(33 cards)

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
What percent of muscle mass is lost by 2 weeks after denervation?
50% -Fibrosis will prevent healing and failure to heal beyond 12 months is a poor prognosis
26
What causes facial nerve paralysis and what are the clinical signs?
Traumatic compression of facial crest, inflammation middle ear or guttural pouch, brainstem disease Signs: Ear droop, ptosis, muzzle deviation away from lesion, quidding
27
What is the term for paralysis of the suprascapular nerve?
Sweeney - trauma to suprascapular nerve (trauma or chronic concussion) -Look like leg is asleep
28
What are some clinical signs of Sweeny or suprascapular Nerve Paralysis?
-Walk like leg is asleep -Atrophy nerve -Abduction shoulder while weight bearing -Subluxation shoulder -Difficulty advancing limb
29
What is the treatment for sweeny?
Acute Chronic (oa) Time and antinflammatories
30
When does radial nerve paralysis occur?
Shoulder trauma/post anesthesia
31
What are clinical signs of nerve paralysis?
Brachial plexus injury, elbow, knee or fetlock flexed, dorsum food on ground, elbow dropped bear weight poorly and not on all limbs
32
What are some differentials for radial nerve paralysis?
Olecranon fracture Lameness (abscess)
33
What is treatment for radial nerve paralysis?
Time and NSAID Support other limb to prevent laminitis