Botulism in Horses

Filed Under: Horses, Diseases

Is your horse showing clinical signs of weakness?  Does your horse appear to have difficulty controlling movements of its tongue or show any other signs of dysphagia (difficulty eating)?  These may be the early warning signs that you horse is suffering from a toxin produced by a type of bacteria known as Clostridium botulinum
Known as the cause of “Shaker Foals” when seen in fast-growing young foals being fed grain, or “Forage Poisoning” in adult horses, botulism is a disease syndrome produced by cub-shaped, anaerobic, spore-forming bacteria.  The bacteria live only in the absence of oxygen and are therefore termed “anaerobic”.  In the presence of oxygen, this bacteria enters a dormant state as a spore which is resistant to environmental conditions adverse to its survival.  When living conditions become suitable, this bacterium emerges from the spore to actively metabolize and reproduce.  A side effect of its metabolism is the production of a potent neurotoxin, of which there are up to eight antigenically distinct toxins.
Clostridium botulinum is a normal inhabitant of the soil.  There are three types of Clostridium botulinum (Types A, B, and C) that affect horses.  In the United States, types A and C are the most common found bacteria in the soil west of the Mississippi River.  Clostridium botulinum type B is found on the Eastern Seaboard, in Mid-Atlantic areas, and in the Ohio Valley.  Outbreaks may occur in non-native areas due to the sale of hay cubes, round hay bales, and haylage to other parts of the country.  The forage is believed to become contaminated by the inclusion of soil or through contamination with rodent carcasses and/or subsequent moisture and spoilage.  Hay cut from areas fertilized with chicken manure is also more commonly affected.
Horses are the most sensitive domestic animals affected by the botulism toxin.  Horses become affected by C. botulinum by one of three distinct routes:  ingestion of the bacteria which grows in the intestines and is typically seen in Shaker foals,  puncture wounds contaminated with the bacteria, which is rare, or ingestion of the toxin in food, primarily haylage.   
The neurotoxin causes weakness and dysphagia.  The tongue may become paralyzed and hang from the mouth, causing an inability to swallow and subsequent drooling of saliva. Facial nerve paralysis may occur, leading to droopy eyelids and muscles of the face.  The pupils are often dilated.  Colic may occur.   Muscle tremors and a flaccid paralysis soon follow, leading to recumbency (the horse will be unable to get up).  The paralysis begins in the hindquarters and progresses to the front legs.   Finally there is paralysis of the chest muscles which leads to respiratory paralysis.  Death ensues 1 to 4 days following the onset of clinical signs due to the respiratory paralysis or complicating aspiration pneumonia.
The toxin interferes with the transmission of impulses from nerves to muscles of the body and is believed to be mediated by the toxin’s ability to cause interference with acetylcholine’s activity at the neuromuscular junction.  The toxin does not interfere with sensory function, leaving the patient aware of all that is occurring.
A diagnosis may be confirmed by detecting the toxin in serum, the gastric contents, or in feedstuff.  Unfortunately, disease confirmation takes time, typically days to weeks, and the animal should be treated immediately in suspected cases for optimal survival.  Antitoxin can bind to toxin molecules in the blood circulation and thereby neutralize them.  Once the toxin molecule has bound to a nerve cell, the damage to the motor end plate is irreversible and not even an antitoxin may reverse the effects.   New neuromuscular junctions can be formed in 7 to 10 days if a horse is able to survive with dedicated nursing care.
Treatment consists of the early administration of antitoxin before complete recumbency occurs.  The availability of antitoxin varies, for it is not universally available and is expensive.  Hospitals often stock the antitoxin for human patients.  Affected animals should be treated with intensive supportive care including fluid therapy and parenteral feeding.  Oxygen and mechanical ventilation may be required in advanced or refractory cases.    
The prognosis for horses with mild to moderate cases of intoxication is usually good for recovery.
There is a toxoid available for Clostridium botulinum type B manufactured by Neogen Corp™ under the name BotVax B®.  This vaccine is currently the only USDA-approved vaccine for the prevention of equine botulism.  The vaccine is currently unavailable in the United Kingdom.  Bot Vax B should not be used in pregnant mares during the first two trimesters of pregnancy.  Vaccinating is much less expensive than having to treat a horse once it has become intoxicated.  In endemic areas, horses should definitely be vaccinated. 

Catcott, E.J. and J.F. Smithcors, Eds.  Equine Medicine and Surgery.  American Veterinary Publications, Inc.  1972. P. 99.
Sprayberry, Kim.  “The Perfect Killer.”  The Horse.  December 2007. Pp. 39-42.
Radostits, Otto, and Clive Gay, et al.  “Veterinary Medicine.”  Saunders/Elsevier.  2007. Pp. 824-827.
Smith, Bradford.  Large Animal Internal Medicine.  2nd Edition.  Mosby.  1996. Pp. 1159-1162.
Tiffany, Lynn.  “More Clients Vaccinating Own Horses.”  Veterinary Practice News.  August 2009.  Pp. 39-40.

Topics: botulism

Symptoms: difficulty controlling tongue, difficulty eating

Similar entries

  • Tetanus is caused by a neurotoxin produced by club-shaped bacteria, known as Clostridium tetani. In the presence of oxygen or other adverse environmental conditions such as cold or a lack of humidity, this bacterium will produce a single inactive spore. The spore is a defense mechanism by which the bacteria are able to survive conditions that would result in their death.

  • Ticks in North America may cause an acute flaccid paralysis. Engorged female ticks are believed to secrete a neurotoxin that prevents the release of acetylcholine and thereby causes a paralysis of skeletal muscles. Acetylcholine is a necessary neurotransmitter for skeletal muscle contraction. When acetylchole is absent, the result is loss of motor control. This paralysis begins in the hind legs and will progress to the front end of the patient within 24 - 48 hours and is therefore termed an ascending paralysis.

  • Raising avocados may be detrimental to the health of your horse. Avocado leaves, fruit, bark, and seeds all contain persin and an unidentified cardiac toxin. In lactating mares, persin produces a non-infectious mastitis (inflammation of the mammary glands), epithelial necrosis (skin cell death over the mammary glands) and agalactia (decrease in milk production). Occasionally gastritis and colic may occur.

  • Are your horses on a poor pasture this fall?  Is there a beautiful red maple tree in the field?  You might want to think twice about this tree being a pasture-mate to your horses.  Green or wilted leaves of the red maple tree can be hazardous to your horse’s health.  

    Consumption of the wilted leaves of the red maple will cause an acute and profound Heinz body anemia (destruction of red blood cells) and methemoglobin production.

    The toxin involved in the poisoning has, to-date, not been identified.

  • Gastric ulcers may be an important source of gastrointestional problems in foals and adult horses under stress. The prevalence and severity of ulcers in an adult horse will increase as stress increases. A horses with a nervous disposition is more likely to have ulcers than a quiet or easygoing animal. Horses under intense training, such as race horses, tend to have moderate to severe gastric changes and up to 90% of racing horses may be affected.