AVS 271 Anatomy and Physiology

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AVS 271 Anatomy and Physiology

• October 6, 2008
• Pathophysiology of the Nervous System

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Tetanus (lock jaw)

• Caused by the gram positive anaerobic
  bacterium Clostridium tetani
• Produces a potent exotoxin
• Present in soil
• Organism grows in dirty / necrotic anaerobic
  wounds
• Especially puncture wounds
• Tail docking / castration wounds
• All species of domestic animals are
  susceptible
• Horses are exquisitely sensitive

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Pathogenesis

• The exotoxin is a neuro toxin that blocks
  neurotransmitter release of pre synaptic
  inhibitory interneurons that influence
  efferent somatic (motor) neurons

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Clinical Signs

• Evident two weeks to one month from
  bacterial inoculation
• Loss of inhibition of somatic (motor)
  neurons leads to muscle spasms and hyper
  tonia
• Masseter muscle most commonly affected,
  along with other facial muscles
• Lock jaw
• Prolapse of the third eyelid, flared
  nostrils
• Progresses to the muscles of the neck,
  trunk and limbs
• Sawhorse stance, difficulty walking
• Death due to respiratory failure

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Clinical Signs
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Treatment

• Provide muscle relaxation
• Sedation and muscle relaxants
• Provide good footing / bedding
• Eliminate the inciting infection
• Neutralize unbound toxin
• Anti toxin (anti serum)
• Supportive care
• Maintain hydration and nutrition

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Prognosis

• 50 to 80 mortality

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Prevention

• Vaccination with tetanus toxoid (inactivated
  toxin)

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Botulism

• Caused by the gram positive anaerobic
  bacterium Clostridium botulinum
• Produces several potent exotoxins
• Present in soil, decaying vegetable matter
  (bad silage) or animal carcasses
  (geographic distribution)
• All species of domestic animals are
  susceptible
• Horses more susceptible than ruminants
• Three forms of the disease
• Forage poisoning (ingestion of pre formed
  toxin)
• Toxico infectious botulism
• Wound botulism

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Pathogenesis

• Toxins block acetylcholine release at
  peripheral synapses (esp. somatic motor
  neurons)
• Interferes with exocytosis of acetylcholine
  vesicles, preventing release of the
  neurotransmitter

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Clinical Signs

• Evident within 1 to 7 days from ingestion
  / formation of the toxin
• Hypotonia of all skeletal muscles
• Progressive generalized weakness and ataxia
  (loss of muscle coordination)
• Inability to eat, protrusion of the tongue,
  drooling
• Horses show weakness and trembling, which
  subside after a period of recumbency
  (laying down) and then reappear
• Shaker foal syndrome

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Treatment

• Supportive care
• Maintain hydration and nutrition
• Antibiotic therapy
• For toxico infectious or wound form of
  the disease
• Anti toxin (anti serum)

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Prognosis

• Slow onset of clinical signs is associated
  with a better prognosis than with rapid
  onset of clinical signs

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Prevention

• Vaccination with botulism toxoid (inactivated
  toxin)
• Generally only used in areas where the
  disease has been a problem
• E.g., Kentucky and other areas of the
  Eastern United States

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Intervertebral Disk Disease(herniated disk)
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Pathogenesis

• Physical bulging and / or extrusion
  (herniation) of interveterbral disk material
  into the spinal canal that compresses and /
  or damages the spinal cord

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Clinical Signs

• Pain
• Crying, loss of appetite, reluctance to
  move
• Ataxia
• Incoordination of muscle movement / control
• Paresis
• Muscle weakness
• Paralysis
• Urinary and / or fecal incontinence

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Clinical Signs
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Diagnosis

• Signalment and history
• Breed e.g., Dachshund
• Physical examination
• Neural function testing
• Radiography

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Treatment

• Cage rest
• Anti inflammatory and / or analgesic
  medication
• NSAIDs, cortisone, muscle relaxants
• Surgery
• Relieve pressure on spinal cord

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