Clostridium botulinum

Introduction

Botulism is caused by the ingestion of the neurotoxin of the pathogen Clostridium botulinum, which is a spore-forming, gram positive bacteria. Clostridium botulinum is found ubiquitously in the soil worldwide. It is one of the most lethal substances known on earth as only 1.0 micrograms is the lethal dose for humans. Therefore the disease is zoonotic and a public health issue.
The toxin works by binding to gangliosides at the neuromuscular junction and irreversibly inhibiting acetyl choline release, following absorption into the bloodstream. This inhibition of Ach, causes flaccid paralysis and death.
There are three ways that botulism can arise, firstly and most commonly (only one of the three that does occur in the UK) is ingested of the preformed toxin. Secondly, the spores can be ingested and the toxin can proliferation in the intestine, but this tends only to occur in neonates or young stock. Thirdly, the bacteria can enter the body through a wound and then prilferate again, once inside the body. The previous two types of infection are rare and neither occur in the UK. In the UK, infection usually arises when animals e.g. cattle or horses have ingested contamination big bale silage, that has been contaminated with soil or carcasses.

Signalment

Any animal of any age, sex or breed can contract this disease. In the UK access to big bale silage is the main cause of the disease, so therefore cattle and horses are most likely to develop the disease in this country.

Clinical Signs

The characteristic clinical sign is generalised flaccid paralysis. Most clinicians consider the reduction in tongue tone to be the most characteristic sign (pull tongue out of side of mouth and let go; the animal will not pull it back in cases of botulism. Sudden death may be the only clinical sign in some cases, especially farm animals.

Diagnosis

History of big bale silage or knowledge of previous clostridium botulinum on farm, plus characteristic clinical signs are indicative of the disease.
Any differentials should be ruled out. Faecal samples can be taken for detection of the toxin.

Treatment and Control

Antiserum to Clostridium botulinum can be given, but this will only work very early on, when the toxin is free. When the toxin has fixed to the gangliosides, antiserum is not effective.
In countries where botulism is endemic, a toxoid vaccine is avaliable for livestock. This is not the cases in the UK.
Management of the recumbent animal, plus fluid therapy and nutrition can be undertaken if considered economically viable. Most livestock and horses that contract the disease are destroyed on humane grounds.

References

Blood, D.C. and Studdert, V. P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition), Elsevier Science.
Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students, University of Liverpool.
Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
Piercy, R (2008) The Nervous System and Special Senses Study Guide, Royal Veterinary College.
Quinn, P.J., Markey, B.K., Carter, M.E., Donnelly, W.J., Leonard, F.C. (2007) Veterinary Microbiology and Microbial Disease, Blackwell Publishing.
Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses, Elsevier Health Sciences.
Rycroft, A (2007) Principles of Microbiology Part I; Fundamentals of Veterinary Microbiology, Royal Veterainry College.

• Ubiquitous organism
• Oval, subterminal endospores; spores survive boiling for hours
• Causes botulism, a potentially fatal intoxication
• Germination of endospores, growth of bacterial cells and toxin production in anaerobic conditions e.g. decaying carcasses and vegetation
• Disease in animals consuming rotting carcasses and in herbivores through contamination of feed
• Pathogenesis:
  • Intoxication on ingestion and absorbtion of toxin from GIT into the blood
  • Occasionally germination of spores in wounds or GIT
  • Neurotoxin carried to peripheral nervous system
  • Toxin binds gangliosides irreversibly at the neuromuscular junction
  • Blocks release of acetylcholine
• Clinical signs:
  • Dilated pupils, dry mucus membranes, decreased salivation, tongue flacidity, dysphagia in farm animals
  • Incoordination and knuckling followed by flacid paralysis and recumbency
  • Paralysis of respiratory muscles leads to death
  • Flacid paralysis of legs and wings in birds
• Diagnosis:
  • Mouse inoculation with infected serum
  • Toxin detection by PCR, ELISA
  • Toxin neutralisation tests in mice
• Treatment: polyvalent antiserum neutralises unbound toxin
• Toxoid vaccine used in endemic regions
• Implicated in equine grass sickness