Botulism (Proceedings)


Botulism (Proceedings)

Apr 01, 2010


Botulism is a neuromuscular disease characterized by flaccid paralysis that is caused by neurotoxins produced by strains of Clostridium botulinum. Horses are one of the most susceptible species, with both individual and group outbreaks reported.


Clostridium botulinum is a Gram positive, sporeforming anaerobic bacterium. Spores are found in the soil throughout most of the world with the distribution of strains dependent on temperature and soil pH. Eight serotypes of botulinum neurotoxin exist and are labeled A, B, C1, C 2 , D, E, F and G, all of which have similar toxicity. There is geographic variation in the predominant serotypes. In North America, botulism in horses is most often caused by type B toxin and less often by toxin types A and C1.


There are two main forms of botulism. Toxicoinfectious botulism, also known as 'shaker-foal syndrome' occurs almost exclusively foals as a result of overgrowth of C. botulinum in the intestinal tract, followed by production of neurotoxins. The disease most often affects fast growing foals from 1-2 months of age, although cases outside this age range have been seen. The mature, protective gastrointestinal microflora of adult horses typically prevents overgrowth of C. botulinum following ingestion. In adult horses, botulism occurs following ingestion of pre-formed toxins in feed. Spoiled hay or silage are most commonly implicated in botulism caused by types A and B. Silage with a pH greater than 4.5 is favorable for sporulation and toxin production. This is known as "forage poisoning". It has also been suggested that birds may be able to carry preformed toxin from carrion to the feed of horses. Type C botulism is associated with ingestion of feed or water contaminated by the carcass of a rodent or other small animal. Less commonly, botulism can occur when neurotoxins are produced in wounds infected with C. botulinum. Proliferation of C. botulinum type B organisms in gastric ulcers, foci of hepatic necrosis, abscesses in the navel or lungs and wounds in skin and muscle have been associated with toxicoinfectious botulism.

Botulinum neurotoxins bind to presynaptic membranes at neuromuscular junctions, irreversibly blocking the release of the neurotransmitter acetylcholine resulting in flaccid paralysis. Botulinum neurotoxin has also been linked to equine grass sickness.

Clinical presentation

The clinical picture of symmetrical flaccid paralysis is consistent, with the onset and rate of progression dependent on the amount of toxin that is absorbed. The initial clinical signs include dysphagia with apparent excess salivation, weak eyelid tone, weak tail tone and exercise intolerance. Affected animals also spend increased amounts of time resting due to generalized muscle weakness, which is also associated with tremors, carpal buckling and ataxia. Pharyngeal and lingual paralysis causes marked dysphagia and predisposes to aspiration pneumonia. The affected animals tend to quid their food. Paralysis of the diaphragm and intercostal muscles results in an increased respiratory rate and decreased chest wall expansion. Severely affected animals die from respiratory paralysis and cardiac failure.

Differential diagnosis

Differential diagnoses for botulism include viral causes of encephalitis, protozoal causes of encephalomyelitis, and toxic causes of sudden death or neurologic dysfunction.


Botulism should be suspected in animals with flaccid paralysis displaying the above clinical signs. Botulinum toxin does not affect the central nervous system but does affect the cranial nerves; thus symmetrical cranial nerve deficits in an animal with normal mentation can help differentiate botulism from other disorders. Botulism is often a clinical diagnosis. Definitive diagnosis can be achieved by the mouse inoculation test using serum or gastrointestinal contents. However, horses are extremely sensitive to the toxin and this test is often negative. The traditional mouse bioassay identifies Clostridium botulinum in only about 30% of feces collected from adult horses with clinical disease. If the toxin is demonstrated with mouse inoculation, the serotype can be determined through inoculation of mice passively protected with different serotypes of antitoxin. Detection of antibody titers in a recovering unvaccinated horse is also evidence for the diagnosis of botulism. Demonstration of spores in the intestine is not diagnostic, as they can be ingested and observed as contaminants.

Dr. Whitlock at the University of Pennsylvania is currently developing a quantitative real-time PCR (qPCR) test for the detection of Clostridium botulinum neurotoxin type B in equine diagnostic samples. This assay should be more economical, time efficient and sensitive than the traditional mouse bioassay