Equis ISSN 2398-2977

Botulism

Contributor(s): Rachael Conwell, Caroline Hahn, Robert J MacKay, Graham Munroe, Wilson Rumbeiha

Introduction

  • Flaccid neuromuscular paralysis caused by a clostridial neurotoxin.
  • Incidence: uncommon; sporadic.
  • Cause: Clostridium botulinum Clostridium botulinum - 3 routes of infection:
    • Ingestion of pre-formed toxin in contaminated feed (classic botulism most common - especially in big bale silage).
    • Ingestion of spores with local toxin production and absorption in the gastrointestinal tract (toxicoinfectious botulism - foals).
    • Wound contamination by spores.
  • Signs: foals - paralysis and inability to stand, severe muscle tremors ('Shaker foal'), sudden death; adults - acute onset flaccid quadriplegia, pharyngeal paralysis, sudden death, tongue paresis. More gradual progression possible with generalized, symmetric weakness and dysphagia.
  • Diagnosis: clinical signs and history.
  • Treatment: specific botulism antitoxin.
  • Prognosis: guarded - dependent upon 'dose' of toxin, rapidity of onset of symptoms, speed of treatment. Fair/good with small toxin 'dose' and rapid administration of antitoxin.
Print off the Owner factsheet on Botulism to give to your clients.

Pathogenesis

Etiology

  • Toxin produced by Clostridium botulinum Clostridium botulinum.
  • Toxin type varies in different areas/countries:
    • Type B - Kentucky, mid-Atlantic seaboard.
    • Type C - Europe, Florida.
    • Type D.
  • Grows in preferably neutral or alkaline soils.
  • Rapidly forms spores.
  • Will produce toxin in anerobic environments, eg decaying vegetable matter, animal carcasses, damaged tissues.

Predisposing factors

General

  • Geographical environment especially neutral to alkaline soil type.
  • Moist or spoiled feeds.
  • Feed source contaminated by anaerobic decaying vegetable or animal matter.
  • Stagnant water sources contaminated by carcasses.

Specific

  • Feeding spoiled or contaminated forage especially round bale hay or silage - toxin Types A and B (if organism present before fermentation reduces pH to 4.5 or less).
  • Decomposing carcasses - Type C toxin.
  • Presence of gastric ulcers especially in foals Stomach: gastric ulceration.
  • Wounds especially abscesses; damaged tissue →  anaerobic conditions, eg infected umbilical remnants (foals), castration wounds (adults).
  • Stress - onset of clinical signs has been associated with stress, eg racing, foaling, weaning.

Pathophysiology

  • Toxin → interference with acetylcholine release at a variety of nerve endings/junctions → neuromuscular paralysis.
  • CNS and sensory nerves are not affected.
  • There are three recognized routes of botulism exposure.

Ingestion of pre-formed toxin

  • Most common in adults (forage poisoning).
  • In US, involves either processed feed contaminated by animal carcass or big bales.
  • In UK usually involves big bale silage or similar products.
  • Cases occur sporadically or as outbreaks.

Toxicoinfectious botulism

  • Ingestion of spores that germinate → toxin within digestive tract.
  • Especially seen when local GI environment is favorable for overgrowth, eg gastric ulceration Stomach: gastric ulceration, especially in foals (normal intestinal flora of adults inhibits spore growth).

Wound infection

  • Contamination of wound → toxin production (rare).
  • Neurotoxin spreads throughout body → blocks acetylcholine release at:
    • Neuromuscular junctions.
    • Peripheral cholinergic nerve terminals in preganglionic nerve endings.
    • Postganglionic parasympathetic nerve endings.
  • CNS and sensory nerves are not affected.
  • Proposed mechanisms of toxin action include:
    • Interference with calcium function at nerve terminal.
    • Inhibition of acetylcholine release.
    • Blockage of exocytosis of synaptic vesicles.

Timecourse

  • Incubation periods from 2 h to 2 weeks; symptoms usually develop within 12-24 h of exposure.
  • Related to toxin dose, ie patients with gradual presentation and slow progression of signs have probably been exposed to small doses of toxin; rapid onset and severe signs are more common with large toxin doses.

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.
  • Stratford C H, Mayhew I G & Hudson N P H (2014) Equine botulism: A clinical approach to diagnosis and management. Equine Vet Educ 26 (8), 441-448 WileyBlackwell.
  • Johnson A L et al (2012) Quantitive real-time PCR for detection of the neurotoxin gene ofClostridium botulinumtype B in equine and bovine samples. The Vet J 194 (1), 118-120 PubMed.
  • Aleman M et al (2011) Repetitive stimulation of the common peroneal nerve as a diagnostic aid for botulism in foals. J Vet Intern Med 25 (2), 365-372 PubMed.
  • Frey J et al (2007) Alternative vaccination against equine botulism (BoNT/C). Equine Vet J 39 (6), 516-520 PubMed.
  • Wilkins P A & Palmer J E (2003) Mechanised ventilation in foals with botulism: 9 cases (1989-2002). J Vet Intern Med 17 (5), 708-712 PubMed.
  • Wilkins P A & Palmer J E (2003) Botulism in foals less than 6 months of age: 30 cases (1989-2002). J Vet Intern Med 17 (5), 702-707 PubMed.
  • McCann J L (2000) A suspected case of botulism in a horse. Equine Vet Educ 12 (3), 114-119 VetMedResource.
  • Dyson S, Marr C M & Barr T J (1997) Equine botulism. Vet Rec 141 (2), 56 PubMed.
  • Whitlock R H & Buckley C (1997) Botulism. Vet Clin North Am Equine Pract 13 (1), 107-128 PubMed.
  • Szabo E A, Pemberton J M, Gibson A M, Thomas R J, Pascoe R R & Desmarchelier P M (1994) Application of PCR to a clinical and environmental investigation of a case of equine botulism. J Clin Microbiol 32 (8), 1086-1991 PubMed.
  • Roblot P, Roblot F, Fauchere J L, Devilleger A, Marechaud R, Breux J P, Grollier G & Becq-Giraudon B (1994) Retrospective study of 108 cases of botulism in Poitiers, France. J Med Microbiol 40 (6), 379-384 PubMed.
  • Wichtel J J & Whitlock R H (1991) Botulism associated with feeding alfalfa hay to horses. JAVMA 199 (4), 471-472 PubMed.

Other sources of information

  • Hurcombe S (2010) Botulism in foals and adult horses. In: Proc NAVC. pp150-152.
  • Bernard W V (2003) Botulism in the foal. In: Proc NAVC. pp 128.

Organisation(s)

  • British Equine Veterinary Association, UK - Polyvalent equine-origin botulism antitoxin Botulinus antiserum available here.
  • University of Pennsylvannia, School of Veterinary Medicine, New Bolton Center, Kennet Square, PA, USA. Polyvalent equine-origin botulism antitoxin Botulinus antiserum available here.


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