During my final year of university studying Bachelor of Systems Agriculture majoring in Equine Studies I undertook a project which identified problems within the horse industry. Botulism in horses is an issue that rears its head every few years resulting in major mortality. Having an equine establisment in the Hawkesbury district were outbreaks have occured many times I felt it was necessary for me to learn more about the disease and how it affects horses. If the article creates any concern or would like to know more please don't hesitate in contacting me (by email) through my web site at www.homebushpark.cjb.net .

Only when outbreaks of endemic disease receive publicity do we become aware of the problem.Horses have not been considered as livestock by the NSW Agriculture thus resulting in little information on the occurrences of diseases in horses.

Botulism has been a silent and deadly disease that has been around for many years, not only in horses but in humans and cattle as well. Botulism is not only an Australian disease, but also affects horses from all over the world. The clinical signs of the disease give horse's pain and depressions.

What is Botulism?

Botulism is a disease that affects not only horses but also a wide variety of animals. It is a tiny microorganism that has been a silent, but deadly killer, the casual agent identified as Clostridium botulinum. It is closely related to the bacterium that causes tetanus only it is more deadly. As with the tetanus bacteria, which are always present in the environment, so it is with Clostridium botulinum. Once the horses have the toxins in the system the incubation period for the organism is from 24 hours to several days. When it is within the horses system, the toxins reproduce repeatedly and rapidly in the horse's gut.

Eight distinct toxins of botulism have been identified, they are A, B, Ca, Cb, D, E, F and G. Some bacterial subtypes can produce more than one type of toxin. Types C and D are most common in Australia. The organism seems to grow best in neutral or alkaline conditions. It grows and produces toxins in anaerobic (minus oxygen) environments, such as both decaying vegetable matter and animal carcasses.

History of Botulism

In April 1994 Australia's thoroughbred industry was rocked by an outbreak of botulism at the Easter Yearling Sales. Four hundred and sixty yearlings were presented at the 1994 Australian Easter Yearling sales of William Inglis and Son Ltd, which took place at Newmarket on the 5th, 6th and 7th of April. Forty-one yearlings exhibited signs of the disease and 33 of those horses died or were humanly destroyed. The vendors and auctioneers had to not only deal with the loss of the yearlings but also a monetary loss of over $2.46 million.

In 1999, another cluster of Botulism poisoning in the Hawkesbury and Bowral area were documented. Fourteen Standardbred horses were diagnosed with the disease in the Hawkesbury district and two of those horses were destroyed due to the symptoms of the disease (Hoare, 1995).

Botulism is not just a recent event, but reports date back to as far as and earlier than 1983, 11 years prior to the yearling sale disaster and most reported occurrences are overseas. In the South east of England between December 1983 and January 1984 thirteen cases of suspected Botulism poisoning occurred. Nine of the horses died and a mouse inoculation test confirmed the presence of type B toxins in the serum of one horse. The horses had been fed big bale silage, wrapped in plastic, which was inadequate to prevent the fermentation and growth of Clostridium Botulinum (Ricketts et al, 1984). In California eight horses died with signs of botulism over six days after eating contaminated grass clippings(Ricketts et al, 1984).

In Australia in 1984, over a two-week period 11 horses in four training stables were affected with the clinical sign of botulism. Eight of the 11 died. In the investigation following the deaths, the Clostridium botulinum toxins were food-borne as a result of contaminated oaten chaff (Kelly et al, 1984).

An episode of nervous system dysfunction was observed in horses on 17 premises in 4 countries of southern California. 38 horses were affected and 31 of those died. Later investigations revealed the exposure to a common batch of Lucerne hay cubes on the 17 premises was the cause for manifestation of botulism. Strains of C.Botulinum type-C were isolated from intestinal contents of 5 affected horses, one of which also contain type-Ca and type-Cb toxins (Kinde, et al, 1991).

Germany in the years between 1995 and 1998 had 122 cases of botulism reported. Of that 66 were positive. Type C and D toxins were identified in 57 of the horses. The results of an enquiry of the animal owners showed that modern agricultural technology had an important impact on the toxinogenesis in feed (Source of Information: CAB Abstracts).

How do horses get Botulism?

There are three basic modes of intoxication.

1. Ingestion of a pre-formed toxin, also know as forage poisoning.

2. Growth of the agent in the gastrointestinal system, also known as toxicoinfectious botulism.

3. Contamination of wounds, also known as wound botulism

The ingestion of pre-formed toxins is the usual route of infection in adult horses. This would normally occur when the animal actually consumes bits of decayed or decaying material that harbored the bacteria. This explains why one horse will die from the disease, but another in the same paddock wont. The toxins have to be eaten to have any effect.

In cases where toxicoinfection is the route of attack, the horse ingests the spores that then germinate and produce toxins within the gastrointestinal tract. This route is most often the implication of the Shaker Foal Syndrome. Occurring at three to eight weeks of age, causing muscle tremors thus resulting in the name.

Wound infection is less common; toxins are produced at the site and absorbed into the horses system.

Clinical Signs

Dr Hutchins (1994) prepared a report on the clinical signs the yearlings presented at Newmarket. He reported the following; the indication of Botulism is that the horse shows mild depression; muscle fasciculations of varying severity seen most commonly affecting the tricep muscles, muscles of the forearm, muscles of the flank and hindquarters. There were signs of a mild wobbly gait, prolonged periods of sternal and lateral recumbency with difficulty in rising and the tongue hanging out. Eventually the horse cant get up and may die of breathing failure

The toxins affect the nerve endings where it joins onto the muscle of the horse and blocks transmission from the nerves to the muscle similar to symptoms of "tying up". The yearlings at the sales exhibited signs of dilation of the pupils and difficulty with the prehension of food in the later stages. Self-inflicted head trauma was common due to repeated and futile efforts to raise the head or neck.


The treatment used at the 1994 Yearling sales was unsuccessful in most of the cases. But that was due to not knowing what type of botulism was evident until after the incident. There are two sorts of treatment, first being supportive care which is given to the horse that have gone too far, making them as comfortable as possible and the second treatment is a more specific treatment with antiserum. But the problem being that there eight distinct toxins and a particular antiserum will only match the distinct toxin (Hutchins, 1994).

Why is the problem getting more frequent?

An article written by Dr Hoare proposed and explanation as to why botulism is getting more frequent.

  • Rabbits get killed during the mowing process and incorporated in the hay:

  • When farmers made small bales of hay the carcasses were easily detected as the bales were hand fed into the chaffer and the bales were rejected.

  • Increasing technology allows farmers to make larger square bales.

  • Increasing size of bales provides anaerobic conditions necessary for the botulism organism to grow

  • Chaffing manufacturers are saving labor by using automation and the hay is fed into the chaffer by hydraulic rams

  • The contaminated chaff is put into large bins and could be distributed into many 40kg bags of chaff.

The smallest amount of decaying or decayed carcass could be distributed into many bags of chaff and will go undetected but will contain sufficient toxins to kill many horses. No matter how careful you and the feed supplier may be, the toxins could still be distributed (Hoare, 1999).

As detection of the organism is impossible, the ideal solution would be a botulism vaccine for horses.

For a company to produce a vaccine, there needs to be a market.


Buchta, R; Weibye, R; Coleman, G. "A novel vaccine for the control of botulism in cattle" Cyanamid Websters Pty Ltd.
Hoare. R, 1995. Botulism in Horses NSW Agriculture Elizabeth Macurther Agricultural Institute.
Kelly. AP, Jones. RT, Gillick. JC & Sims. LD. Outbreak of Botulism in horses Equine Veterinary Journal. 1984, 16:6, 519-521.
NRA. "Registering Agricultural and Veterinary Chemical Products" 2000.
Ricketts. SW, Greet. TRC, Ginnett. CDR, McAllister. EP, McCraig. J, Skinner.Ph, Webbon. PM, Frape. DL, Smith. GR & Murry. LG. Thirteen Cases of botulism in horses fed big bale silage Equine Veterinary Journal. 1984, 16: 6, 515518.
RIRDC, "R&D plan for the equine Industry Program 1996-2000 RIRDC, Barton ACT, 1996.
RIRDC, "Annual Report 1998 - Shaping the Future" RIRDC, Barton Act, 1998.
Vets Corner "Botulism Poisoning from Lucerne Chaff" Rod Hoare.EFA Newsletter, 1999.

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Updated: October 2005.