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Saturday, September 14, 2013

BOTULISM

Botulism is an acute neurologic disorder that causes potentially life-threatening neuroparalysis due to a neurotoxin produced by Clostridium botulinum. The 3 main clinical presentations of botulism are as follows:
  • Infant botulism
  • Foodborne botulism
  • Wound botulism

Essential update: FDA approves first heptavalent botulism antitoxin

On March 22, 2013, the FDA approved the first botulism antitoxin that can neutralize all 7 known botulinum nerve toxin serotypes. The heptavalent antitoxin is derived from horse plasma and is the only drug available for treating botulism patients over 1 year of age, including adults. It is also the only available drug for treating infant botulism that is not caused by nerve toxin type A or B.[1, 2, 3, 4]

Signs and symptoms

More than 90% of patients with botulism have 3-5 of the following signs or symptoms:
  • Nausea
  • Vomiting
  • Dysphagia
  • Diplopia
  • Dilated/fixed pupils
  • Extremely dry mouth unrelieved by drinking fluids
Generally, botulism progresses as follows:
  • Preceding or following the onset of paralysis are nonspecific findings such as nausea, vomiting, abdominal pain, malaise, dizziness, dry mouth, dry throat, and, occasionally, sore throat
  • Cranial nerve paralysis manifests as blurred vision, diplopia, ptosis, extraocular muscle weakness or paresis, fixed/dilated pupils, dysarthria, dysphagia, and/or suppressed gag reflex
  • Additional neurologic manifestations include symmetrical descending paralysis or weakness of motor and autonomic nerves
  • Respiratory muscle weakness may be subtle or progressive, advancing rapidly to respiratory failure
The autonomic nervous system is also involved in botulism, with manifestations that include the following:
  • Paralytic ileus advancing to severe constipation
  • Gastric dilatation
  • Bladder distention advancing to urinary retention
  • Orthostatic hypotension
  • Reduced salivation
  • Reduced lacrimation
Other neurologic findings include the following:

  • Changes in deep tendon reflexes, which may be either intact or diminished
  • Incoordination due to muscle weakness
  • Absence of pathologic reflexes and normal findings on sensory and gait examinations
  • Normal results on mental status examination

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