13. Neuromuscular Disorders and Peripheral Myelopathies Flashcards
(33 cards)
What is the etiology of Botulism? What kind of bacteria is it? Where is it normally found?
Gram positive, spore forming, anaerobic bacillus
-Normal in soil
-Eight toxins (A-G)
-B most common
What is the pathophysiology of Botulism? What is affected and what signs does that cause?
-Toxin prevent release of ACH at neuromuscular junction (no smooth muscle contraction)
-Flaccid Paralysis
How do horses get botulism?
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)
What is the most common presentation of botulism in foals?
Toxicoinfectious
-1-2 months
-rapid onset
-stumble, weak, dragging toes
-Recumbency
-dehydrated and hypoglycemic
-prognosis good intensive care
What type of intensive care do foals need if they have Botulism?
Oxygen and ventilator
What are some clinical signs of botulism in horses?
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)
Is Botulism a straightforward diagnosis?
No, may not be thinking it until multiple horses have it and you ask the right history questions
How do you diagnose Botulism?
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
How do you treat Botulism?
Botulism antitoxin - plasma from hyperimmunixed horse, antibodies, only bind circulating
Supportive care
What kind of supportive care can you provide for botulism?
Nutritional and Fluid - cant eat or drink
Oxygen - cant breath
Urinary Catheter - cant urinate
Ocular care - cant blink
Wound Management - cant stand
Antibiotics?
How long may you need to provide this supportive care?
Can be greater than 2 weeks for the end plate to regenerate ACH receptors
Do Botulism horses recover?
Yes, quite well if you take the time and support
Can you prevent Botulism?
Vaccination - Type B
-No cross protection
-3 boosters, then annually prior to round bale season
-Proper storage of feed
-Care when using round bales
What is polyneuritis equi?
Who does it affect?
Progressive granulomatous polyradiculoneuritis of the cauda equina and cranial nerves
Adult horses of any breed
What causes Polyneuritis Equi?
-Unknown
-Cytotoxic T cell and macrophage infiltrates
-Autoimmune - allergic, gullian barre
-Hypersensitivity - systemic inflammation, parasite migration, EHV
What are the clinical signs of polyneuritis equi?
-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
What are some differentials for polyneuritis equi?
EPM, EHV, Encephalitis, trauma, Botulism
How do you diagnose Polyneuritis Equi?
Clinical signs
CSF - mononuclear pleocytosis with high TP
Necropsy - thickened, discolored, edematous cauda equina, granulomatous inflammation, axonal degeneration and demyelination
How do you treat polyneuritis equi?
Anti-inflammatories - steroids
Immunosuppressive Drugs
Palliative but not curative
Supportive Care - bladder cath, manual feces removal
Prognosis - hopeless
What are some nerves that are affected by a peripheral neuropathy?
Facial, suprascapular (sweeney), Radial, Femoral, Sciatic (peroneal and tibial), obturator (foaling)
What causes nerve injury?
Trauma, stretching, compression or severance
Define the following:
Neuropraxia:
Axonotmesis:
Neurotmesis:
Neuropraxia: Brusing and inflammation of nerves (transient 3-6wk)
Axonotmesis: Crushing of nerve, epineurium and perineurium intact
Neurotmesis: Whole fiber severed, Wallerian degeneration expected
How fast do regenerating axons grow?
1mm/day
What is the progression of nerve dysfunction and damage?
-Loss of proprioceptive function (placement and mild ataxia)
-Paresis or paralysis of voluntary and reflex movements
-Desensitization