ISSN 2398-2985      

Botulism

4ferrets

Introduction

  • Cause: ingestion of preformed toxin produced by Clostridium botulinum. Rarely seen and this topic is scarce in the literature for botulism in exotics species.
  • Signs: symmetrical ascending weakness/paralysis. Death due to respiratory paralysis.
  • Diagnosis: clinical signs, history, presence of toxin in ingested food or body fluids.
  • Treatment: supportive therapy. Antitoxin not always available and off license for exotics species.
  • Prognosis: depends on the amount of toxin ingested and the speed of treatment. Prognosis is fair to poor.

Pathogenesis

Etiology

  • Ingestion of carrion or spoiled food containing the preformed Clostridium botulinum neurotoxin.
  • Bacteria survive in aquatic environments and neutral or alkaline soil.
  • Botulism cases due to preformed Clostridium botulinum types A, B and C neurotoxin were reported. Ferrets are moderately susceptible to types A and B, and they are highly susceptible to botulism type C. It has been reported that they are refractory to type E neurotoxin.
  • Botulism in mink usually is caused by type C strains that have produced toxin in chopped raw meat or fish.

Predisposing factors

General

  • Exposure of carcasses.
  • Working ferrets more susceptible.
  • Deaths in ferrets due to botulism were reportedly associated with ingestion of wild bird carcasses in England.

Specific

  • Ingestion of spoiled foodstuff, eg raw meat, or carrion.

Pathophysiology

  • Ingestion of carrion or spoiled food containing the neurotoxin.
  • Toxin is absorbed from the stomach and upper small intestine into the lymphatic system.
  • Acetylcholine release at neuromuscular junctions and autonomic cholinergic synapses is inhibited by the botulinal neurotoxin.
  • Diffuse neuromuscular blockade and dysfunction of the autonomic nervous system, resulting in neuromuscular paralysis, generalized motor neuron disease and parasympathetic dysfunction.
  • Sensory nerves are not affected.
  • Contamination by Clostridium botulinum in wounds is possible.

Timecourse

  • Onset of clinical signs is related to the dose of the toxin ingested.
  • Clinical signs (ascending LMN paralysis) were seen within 12-96 h after ingestion of contaminated feed.
  • Muscle atrophy will occur from disuse within 5-7 days.

Epidemiology

  • Clostridium botulinum are present in aquatic environments and the soil.
  • Spores may be present in the gastrointestinal tract and tissues of mammals and birds.
  • Spores can germinate upon the death of the animal and generate a toxin. The carcass is then potentially ingested by another animal or fed raw meat (especially working ferrets).
  • Botulism can result from both spore ingestion and wound contamination of Clostridium botulinum.

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.
  • Papageorgiou S, Quinton J-F & Gnirs K (2018) Motor and sensory nerve conduction study in the ferret. J Exotic Pet Med 27 (4), 38-47 VetMedResource.
  • Powers L (2009) Bacterial and parasitic diseases of ferrets. Vet Clin Exot Anim 12 (3), 531-561 PubMed.
  • Diaz-Figueroa O & Smith M O (2007) Clinical neurology of ferrets. Vet Clin North Am Exotic Anim Pract 10 (3), 759-773 PubMed.
  • Harrison S G & Borland E D (1973) Deaths in ferrets (Mustela putorius) due to Clostridium botulinum type C. Vet Rec 93 (22), 576-577 PubMed.

Other sources of information

  • Quesnel A D (2004) Botulism. In: The 5-Minute Veterinary Consult. Canine and Feline. 3rd edn. Eds: Tilley L P & Smith F W K Jr. Lippincott, Williams & Wilkins, USA. pp 164.

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