equis - Articles
Botulism
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.
Presenting signs
Shaker foal- Flaccid neuromuscular paralysis.
- Foal at least 1-2 weeks old.
- Bright and alert.
- Dysphagia.
- Muscular weakness: initial muscle tremors progressing to recumbency.
- Endemic area.
- Variable clinical signs dependent upon toxin 'dose'.
- Stress.
- Gastric ulcers.
- Unvaccinated dam.
Adult
- Endemic area.
- Acute onset flaccid quadriparesis.
- Pharyngeal paralysis and dysphagia.
- Muscle tremors.
- Unvaccinated.
- Ingestion of contaminated feed.
- Sudden death.
- Contaminated wound(s).
Acute presentation
- Recumbency.
- Sudden death.
Geographic incidence
- USA - found in 18.5% of soil samples: central Kentucky, mid-Atlantic seaboard (mainly type B toxin).
- Florida/California (type C toxin).
- Europe (mainly type C toxin).
- Toxicoinfectious botulism in foals has not been reported in the UK.
Age predisposition
- Foals: >1-2 weeks old (70% cases between 2-5 weeks old).
- Adults: any age.
Public health considerations
- Botulism in humans due to Types A, B, E and F and result from contaminated food, wounds and ingestions of spores in infants (honey commonly implicated) - not contagious.
Cost considerations
- Loss of animal(s) - outbreaks financially devastating on studs.
- Treatment, especially antitoxin.
Special risks
- Progressive paralysis of respiratory muscles, therefore not suitable for anesthesia.
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 et al (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 et al (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. pp 150-152.
- 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.