Canis ISSN: 2398-2942

Botulism

Contributor(s): Bryn Tennant

Introduction

  • Flaccid neuromuscular paralysis caused by a clostridial neurotoxin.
  • Rare in carnivores.
  • Cause: all reported natural cases in dogs due to ingestion of preformed toxin produced byClostridium botulinum Clostridium botulinum.
  • Signs: symmetrical ascending weakness; death may result from respiratory paralysis.
  • Diagnosis: clinical signs, history, presence of toxin in body fluids or ingested food.
  • Treatment: supportive therapy; antitoxin not always available.
  • Prognosis: fair to guarded, depending on ingested dose and rapidity of treatment.

Pathogenesis

Etiology

  • Neurotoxin produced byClostridium botulinum Clostridium botulinum.
  • Bacterium survives in neutral or alkaline soil and aquatic sediments.
  • Produces toxin in anaerobic environments, eg animal carcasses, rotting vegetation.
  • Predominant toxin type varies by geographic region.
  • Most canine cases due to types C or D toxin.

Predisposing factors

General
  • Ingestion of carrion or raw meat.
  • Geographical region.

Specific

  • Foxhounds, often fed raw meat.
  • Contaminated wound → anaerobic conditions.

Pathophysiology

  • Toxin → interference with acetylcholine release → neuromuscular paralysis → generalized lower motor neurone disease and parasympathetic dysfunction.
  • Natural cases in dogs usually due to ingestion of preformed toxin, eg in carrion.
  • Contamination of wounds byClostridium botulinumalso possible → toxin productionin situ.
  • Ingested toxin absorbed from stomach and upper small intestine → lymphatics.
  • Toxin binds to receptors, possibly gangliosides, and blocks acetylcholine release at:
    • Neuromuscular junctions.
    • Peripheral cholinergic nerve terminals in preganglionic nerve endings.
    • Postganglionic parasympathetic nerve endings.
  • Proposed mechanisms of toxin action:
    • Presynaptic inhibition of acetylcholine release.
    • Interference with function of calcium ions at nerve terminal.
    • Blocks exocytosis of synaptic vesicles.
  • Sensory nerves are not affected.

Timecourse

  • Timecourse is related to dose of toxin.
  • In dogs that recover, illness usually lasts 1-3 weeks.

Epidemiology

  • Reservoirs ofC. botulinumare soil and aquatic sediments.
  • Spores present in gut and tissues of mammals and birds.
  • Following death of animal spores germinate and generate toxin → carrion ingested by carnivores.
  • Spores also germinate in rotting vegetation.
  • Spore ingestion and wound contamination may lead to botulism.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • VanNes J J (1986) Electrophysiological evidence of peripheral nerve dysfunction in 6 dogs with botulism type C. Res Vet Sci 40 (3), 372-6 PubMed.
  • Farrow B R, Murrell W G, Revington M L et al (1983) Type C botulism in young dogs. Aust Vet J 60 (12), 374-7 PubMed.
  • Barsanti J A, Walser M, Hatheway C L et al (1978) Type C botulism in American Foxhounds. JAVMA 172 (7), 809-13 PubMed.
  • Darke P G, Roberts T A, Smart J L & Bradshaw P R (1976) Suspected botulism in foxhounds. Vet Rec 99 (6), 98-9 PubMed.


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