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Botulism

Botulism. Botulinim toxin. History. Neurologic disease from botulinum toxin Most lethal substance known. History. Neurologic disease from botulinum toxin Most lethal substance known History as bioweapon. History. Neurologic disease from botulinum toxin Most lethal substance known

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Botulism

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  1. Botulism Botulinim toxin

  2. History • Neurologic disease from botulinum toxin • Most lethal substance known

  3. History • Neurologic disease from botulinum toxin • Most lethal substance known • History as bioweapon

  4. History • Neurologic disease from botulinum toxin • Most lethal substance known • History as bioweapon • Japanese in WWII (Unit 731)

  5. History • Neurologic disease from botulinum toxin • Most lethal substance known • History as bioweapon • Japanese in WWII (Unit 731) • Former US and USSR programs

  6. History • Neurologic disease from botulinum toxin • Most lethal substance known • History as bioweapon • Japanese in WWII (Unit 731) • Former US and USSR programs • Iraqi deployed weapons

  7. History • Neurologic disease from botulinum toxin • Most lethal substance known • History as bioweapon • Japanese in WWII (Unit 731) • Former US and USSR programs • Iraqi deployed weapons • Japanese cult in early 1990’s

  8. Epidemiology • Found worldwide • U.S. incidence • ~100 cases annually (1/4 foodborne)

  9. Epidemiology • Mechanisms of intoxication • No person-to-person transmission

  10. Epidemiology • Mechanisms of intoxication • No person-to-person transmission • Toxin ingestion (foodborne)

  11. Epidemiology • Mechanisms of intoxication • No person-to-person transmission • Toxin ingestion (foodborne) • Toxin generated from wound infection (wound)

  12. Epidemiology • Mechanisms of intoxication • No person-to-person transmission • Toxin ingestion (foodborne) • Toxin generated from wound infection (wound) • Toxin from intestinal colonization (infant, intestinal)

  13. Epidemiology • Mechanisms of intoxication • No person-to-person transmission • Toxin ingestion (foodborne) • Toxin generated from wound infection (wound) • Toxin from intestinal colonization (infant, intestinal) • Toxin inhalation (aerosol release)

  14. Epidemiology • Mechanisms of intoxication • No person-to-person transmission • Toxin ingestion (foodborne) • Toxin generated from wound infection (wound) • Toxin from intestinal colonization (infant, intestinal) • Toxin inhalation (aerosol release) • Mortality <10%

  15. Microbiology • Clostridium botulinum

  16. Microbiology • Clostridium botulinum • Large, anaerobic Gram positive bacillus • Spore-forming

  17. Microbiology • Clostridium botulinum • Large, anaerobic Gram positive bacillus • Spore-forming • Rarely infects humans

  18. Microbiology • Clostridium botulinum • Large, anaerobic Gram positive bacillus • Spore-forming • Rarely infects humans • Produces potent neurotoxin • 7 types (A-G)

  19. Microbiology • Clostridium botulinum • Large, anaerobic Gram positive bacillus • Spore-forming • Rarely infects humans • Produces potent neurotoxin • 7 types (A-G) • Types A, E, B most common in U.S.

  20. Microbiology • Clostridium botulinum • Large, anaerobic Gram positive bacillus • Spore-forming • Rarely infects humans • Produces potent neurotoxin • 7 types (A-G) • Types A, E, B most common in U.S. • Same general mechanism

  21. Arnon S, et al. JAMA. 2001;285:1059-70.

  22. Clinical Features • Incubation 12-72 hours • Probably faster if inhalational exposure

  23. Clinical Features • Classic syndrome

  24. Clinical Features • Classic syndrome • Acute symmetric cranial nerve palsies

  25. Clinical Features • Classic syndrome • Acute symmetric cranial nerve palsies • Blurry vision, ptosis, dysphasia

  26. Clinical Features • Classic syndrome • Acute symmetric cranial nerve palsies • Blurry vision, ptosis, dysphasia • Descending flaccid paralysis

  27. Clinical Features • Classic syndrome • Acute symmetric cranial nerve palsies • Blurry vision, ptosis, dysphasia • Descending flaccid paralysis • Complete skeletal muscle paralysis

  28. Clinical Features • Classic syndrome • Acute symmetric cranial nerve palsies • Blurry vision, ptosis, dysphasia • Descending flaccid paralysis • Complete skeletal muscle paralysis • Respiratory (ventilatory) failure

  29. Clinical Features • Classic syndrome • Acute symmetric cranial nerve palsies • Blurry vision, ptosis, dysphasia • Descending flaccid paralysis • Complete skeletal muscle paralysis • Respiratory (ventilatory) failure • Autonomic – urinary retention, orthostasis

  30. Clinical Features • Classic syndrome • Acute symmetric cranial nerve palsies • Blurry vision, ptosis, dysphasia • Descending flaccid paralysis • Complete skeletal muscle paralysis • Respiratory (ventilatory) failure • Autonomic – urinary retention, orthostasis • Afebrile, normal mentation

  31. Clinical Features • Differential Diagnosis

  32. Clinical Features • Differential Diagnosis • Myasthenia Gravis – anticholinesterase response

  33. Clinical Features • Differential Diagnosis • Myasthenia Gravis – anticholinesterase response • Guillaine-Barre Syndrome - ascending

  34. Clinical Features • Differential Diagnosis • Myasthenia Gravis – anticholinesterase response • Guillaine-Barre Syndrome - ascending • Stroke – asymmetric, abnormal brain imaging

  35. Clinical Features • Differential Diagnosis • Myasthenia Gravis – anticholinesterase response • Guillaine-Barre Syndrome - ascending • Stroke – asymmetric, abnormal brain imaging • Tick paralysis – ascending, presence of tick

  36. Clinical Features • Differential Diagnosis • Myasthenia Gravis – anticholinesterase response • Guillaine-Barre Syndrome - ascending • Stroke – asymmetric, abnormal brain imaging • Tick paralysis – ascending, presence of tick • Poliomyelitis – asymmetric, preceding viral illness

  37. Clinical Features • Other features • Foodborne – nausea, diarrhea, dry mouth

  38. Clinical Features • Other features • Foodborne – nausea, diarrhea, dry mouth • Infant - constipation

  39. Diagnosis • High index of suspicion necessary • No readily available rapid confirmatory tests

  40. Diagnosis • High index of suspicion necessary • No readily available rapid confirmatory tests • Clinical diagnosis

  41. Diagnosis • Laboratory confirmation • Specimens – blood, stool • At reference labs • Mouse bioassay • ELISA

  42. Treatment • Supportive care

  43. Treatment • Supportive care • Mechanical ventilation, nutritional support • Prevention of secondary infections

  44. Treatment • Supportive care • Mechanical ventilation, nutritional support • Prevention of secondary infections • Avoid aminoglycosides, clindamycin

  45. Treatment • Passive immunization (antitoxin)

  46. Treatment • Passive immunization (antitoxin) • Halts paralysis, doesn’t reverse

  47. Treatment • Passive immunization (antitoxin) • Halts paralysis, doesn’t reverse • Must be given ASAP

  48. Treatment • Passive immunization (antitoxin) • Halts paralysis, doesn’t reverse • Must be given ASAP • Equine antitoxin (Types A, B and E toxins) • Serum sickness (9%), anaphylaxis (2%)

  49. Treatment • Passive immunization (antitoxin) • Halts paralysis, doesn’t reverse • Must be given ASAP • Equine antitoxin (Types A, B and E toxins) • Serum sickness (9%), anaphylaxis (2%) • Heptavalent antitoxin (Types A-G) • Investigational, less hypersensitivity

  50. Post-Exposure Prophylaxis • Antitoxin not recommended • High incidence hypersensitivity • Limited supplies

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