- Jan 1, 1999
It was a grim sight. My wife's handsome young National Show Horse gelding lay writhing on the ground, unable to rise. He appeared to be in the grip of partial paralysis that allowed movement of the front legs, but not the rear. We immediately called for a veterinarian, then attempted to assist the gelding in rising. We couldn't do it. He had no control over his rear end.
First one veterinarian, then another, from our local equine clinic were soon on the scene. Fluids were administered to battle signs of dehydration. And, if memory serves correctly, some antibiotics also might have been given. It was raining at the time, so we erected a makeshift tent with plastic tarps to keep the young gelding dry during the night. The dawn of another day brought no improvement in the horse's condition. Instead, it appeared that the paralysis was spreading.
It was time to admit that we were fighting a losing battle and the gelding was humanely put down.
We were living in Kentucky at this time, so we had the horse's body shipped to the diagnostic laboratory at the University of Kentucky in Lexington. The results of the necropsy were not long in coming.
The gelding had been infected by one of the most toxic bacteria known to the human and animal world. Once ingested, the bacteria had basically handed down a death sentence.
"How does a horse get botulism?" we asked. Spores of the deadly bacteria, we were told, can live in the soil for years and can be ingested through grazing in a spot where a dead animal might have decomposed. He could have ingested the spores or he could have ingested decayed or decaying material that contained the bacteria itself. Ingestion of only small amounts of infected decayed material can bring about deadly results.
"But," we argued, "our horses had been grazing in this particular pasture for a couple of years and there had never been a problem before." But, wait. Early that particular summer, the property adjoining ours had been sold. The newcomers, a friendly young couple, generously offered to open the fence between our pasture and their newly purchased 10-acre field that had lain idle for several years. There was lush grass in the field and they suggested that our horses might as well be grazing on it. They intended to plant trees in the future, but for now we were welcome to make use of it.
We had jumped at the opportunity and our horses were allowed into the field. It was a month or two after that the gelding was fatally afflicted.
The prevailing theory was that an animal could have died in the field and decomposed, with the botulism-causing organisms taking up residence in the warm, moist soil as spores. Along came our gelding, who might have ingested them while grazing, or, as mentioned earlier, had ingested some of the decayed material itself, and a fatal affliction was the result.
Or, perhaps he had picked up the organism in a remote part of our own small pasture that had not been grazed before.
Whatever the source, he was gone, and we had learned about a deadly organism that is insidious and can kill quickly.
Botulism does not strike adult horses only. It also can be a fatal disease for foals. For many years, practitioners referred to a particular malady of foals as the "Shaker Foal Syndrome."
When it strikes, it is often when the foal is three to eight weeks of age. Typical symptoms include inability to rise, weakness, and profound muscle tremors with flaccidity. In the early stages, the foal often can be assisted to its feet, but it normally can only nurse feebly. The uncontrollable shaking often causes the foal to tumble back to the ground. In fatal cases, death usually comes as the result of respiratory paralysis and occurs about three days after the foal is stricken.
There generally are at least five basic clinical signs that occur when an adult horse or foal is afflicted with botulism:
- Muscular tremors and stilted gait.
- Difficulty eating or swallowing.
- Progressive muscular weakness, then recumbency.
- Decreased tail and tongue tone.
- Respiratory paralysis generally followed by death within 48 to 72 hours.
Botulism appears to be on the rise in the equine world. The organism seems to thrive in moist soil and high humidity. Two states that have reported an increase in equine botulism are Georgia and Alabama, both of which have a lot of rain and humidity. Kentucky also has its fair share of cases.
There have been numerous cases in other parts of this country, as well. In February of 1997, for example, the United States Department of Agriculture's Animal and Plant Health Inspection Service (APHIS) reported that the apparent cause of death of 12 horses in New Mexico was botulism (see The Horse of March 1997).
All the horses which died were stabled at the Crownpoint Community Stables in Crownpoint, N.M., on the Navajo Nation. According to the USDA, the first death occurred on Jan. 10, 1997, and six horses were reported dead to the Veterinary Services office in Albuquerque on Jan. 15. Horses showing signs of illness usually died within a 24- to 72-hour period.
All horses showed similar signs in the early stages of the disease, including normal temperature, pulse, and respiration, and vague symptoms similar to a mild colic, such as restlessness and mild lethargy. In the later stages, the familiar clinical signs of staggering gait, trembling, poor or weak tail and tongue tone, excessive lying down, and finally, paralysis, were observed. Death followed.
Two of the horses were treated with a botulism anti-toxin that is now available. Both responded immediately to treatment, but one of the horses subsequently collapsed and died. The other horse recovered. The remaining horses at the stable also were treated with the anti-toxin even though they showed no clinical signs of botulism. No further cases were reported at the stable in the wake of the anti-toxin treatment.
An Early Response Team from the USDA went to the scene in an effort to determine the cause of the outbreak. Hundreds of samples were collected, including tissues, grain, hay, water, soil, and blood from the horses stabled there. Laboratory results were negative for heavy metals, pesticides, and organophosphates.
The team reported that a large number of crows, predators of mice, had been reported in the area. This resulted in the killing of 15 crows by tribal veterinarians who were still trying to pinpoint the origin of the outbreak. The result was more religiously significant than scientific. The Navajo hold the crow in high regard as crows play a significant role in two traditional Navajo healing ceremonies. The Navajo Veterinary Services announced that it had no plans to kill more crows. Ernest Sandigo, a veterinarian who was working with the veterinary services program, issued this statement:
"What we have been able to determine so far is that the crows are eating dead animals' carcasses and carcasses are known to harbor botulism. In that area, there seems to be a high number of dead animal carcasses. We are in no means suggesting that crows are spreading the illness. We are testing to determine how the horses were exposed, if, indeed, the cause of death is botulism."
Botulism that attacks horses is not restricted to the United States. It was reported from Australia in 1994 that 30 yearlings died of botulism at the Australian Easter Sale.
Botulism is caused by toxins produced by the bacterium Clostridium botulinum. It is closely related to the bacteria that cause tetanus, only it is even more deadly. It is one of the most potent toxins known. As with the tetanus bacteria, which are always present in the environment, so it is with Clostridium botulinum. Horses are particularly susceptible to its attacks.
As mentioned, there are several ways for a horse to become infected. More about that in a moment.
Once ingested, the incubation period for the organism is from 24 hours to seven days. Once it is within the horse's system, the toxin reproduces repeatedly and rapidly in the horse's gut.
Eight distinct toxins produced by the various subtypes of C. botulinum 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. Each of the toxins seems to have its own agenda for harm. Types B, C, and D have been shown to cause disease in cattle. Type C also is potent in sheep.
Horses are most susceptible to Types B and C. Horses, incidentally, seem to be much more susceptible to botulism than are cattle.
Geography also seems to determine which strains are found. In North America, Type A is most commonly found west of the Rocky Mountains. Type B is found in Kentucky and the mid-Atlantic seaboard, and Type C is found in Florida. 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.
In cattle and adult horses, the disease sometimes occurs as a herd outbreak, such as was the case on the Navajo Nation. Sometimes the cause of such a herd outbreak is an infected pasture or a particular food source. It has been found, for example, that silage can provide a suitable medium for growth and toxin production before it reaches a particular stage of fermentation. In one outbreak in cattle, it was found that botulism was related to ingestion of silage that was in contact with contaminated water. The worst confirmed botulism outbreak in North America occurred in 1996 in Canada, when 11 broodmares died after consuming contaminated haylage (The Horse of March 1997).
There have been botulism outbreaks in dairy herds where up to 65% of the animals involved died six to 72 hours after recumbency. In those incidents, forage poisoning was implicated.
Researchers also have found that animals with phosphorus deficiencies might be more apt to ingest decaying flesh or even bones. A case in point involves cattle ranges in South Africa, where a combination of extensive agriculture and phosphorus deficiency in the soil provides ideal conditions for the proliferation of Type D toxins. The phosphorus-deficient cattle chew bones with their accompanying tags of flesh that they find on the grasslands. If the bones and flesh came from animals carrying the Type D strain, botulism intoxication is the result. A gram or so of dried flesh from such a carcass can harbor enough toxin to kill a cow.
That isn't the end of the story. Animals eating such material also ingest spores that germinate in the intestine. After death of the host, the organisms invade the muscle structure, which, in turn, becomes toxic for other animals consuming it. Fortunately, this type of botulism is rare in the United States, with only a few cases occurring in Texas and Montana.
In Australia, botulism has occurred as a result of protein and carbohydrate deficiency rather than phosphorus deficiency. It was found that sheep with these deficiencies were eating the carcasses of rabbits and other small animals found on the range.
Climate also can be a factor in the proliferation of spores in the soil. A cold, wet winter, for example, is thought to produce conditions favorable to the growth of botulism organisms.
In horses, there are three basic modes of intoxication.
1. Ingestion of pre-formed toxin, also known 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 toxin is the usual route of infection in adult animals and is probably the only form that occurs in adult cattle. This would normally occur when the animal actually consumed bits of decayed or decaying material that harbored the bacteria.
In cases where toxicoinfection is the route of attack, the horse ingests spores that then germinate and produce toxin within the gastrointestinal tract. When lesions, such as gastric ulcers, liver disease, abscesses in the navel or lungs, and wounds of the skin and muscle are present, the organisms have additional opportunity for proliferation.
It is this route of infection--toxicoinfection--that is most often implicated in the "Shaker Foal Syndrome."
Wound infection by C. botulinum, with toxins being produced at the site and absorbed by the horse's system, is a less common route of infection.
While no one is totally certain just how the toxin does its dirty work, it is believed that it might block the release of acetylcholine at certain nerve junctions, terminals, and nerve ends. Acetylcholine serves as a neurotransmitter.
The toxin also could act by interfering with the function of calcium at the synaptic nerve terminal, thus inhibiting the release of acetylcholine. (The synapse is the site of transfer between neurons where an impulse is transmitted from one neuron to another by either electrical or chemical means. In the typical synapse, the impulse is transmitted by a neurotransmitter, such as acetylcholine.)
What this all means is that the nerves are unable to stimulate the muscles into action and paralysis is the end result.
In the past, treatment for botulism was rarely successful. It usually involved administration of fluids and nutritional support, something that remains important in treatment today. However, the end result was usually the same--death.
Today, there is an anti-toxin available that can be effective when the disease is correctly diagnosed at an early stage. It was this form of anti-toxin that was administered to some of the horses at the Navajo Nation during the outbreak.
The problem is that the anti-toxin is very expensive. The cost of the anti-toxin to treat a foal has been estimated at $1,000 to $1,500, and the cost to treat an adult horse can run as high as $2,000.
In addition, there would be the cost of additional forms of treatment, such as the administration of fluids and antibiotics and the cost of intensive care. The anti-toxin administration works best when given early in the course of the disease. The problem is that a definitive diagnosis often isn't made until the disease has progressed to an advanced stage.
Large Animal Medicine, edited by Bradford P. Smith, DVM, Diplomate ACVIM, University of California, Davis, includes a section dealing with treatment of botulism cases. The following recommendations were made by contributing editor Lisle W. George, DVM, PhD, Dip. ACVIM:
"Therapy is mainly symptomatic and should include fluid and nutritional support, general nursing care, and ventilatory support if required. In cases of wound contamination or toxicoinfectious botulism, antibiotic therapy is indicated.
"Metronidazole has been suggested as a suitable antibiotic because of its effectiveness against C. botulinum in vitro. In one experimental study, it was shown to have some efficacy if given shortly after wound infection with C. botulinum, but was not useful once clinical signs had developed. Antibiotics that have been associated with neuromuscular weakness should be avoided. These include aminoglycosides, tetracyclines, and procaine penicillin.
"Polyvalent anti-toxin is useful in the early stages of the disease and in animals that are believed to be at risk. Once the toxin has entered the synaptic terminal and clinical signs are present, anti-toxin therapy is ineffective. However, anti-toxin should be administered even to animals showing clinical signs to neutralize any toxin (that has) not yet been taken up at the nerve terminal."
Definitive diagnosis of botulism is confirmed by identification of the toxin in serum, gastrointestinal contents, or food. One of the approaches is to inoculate mice with samples of serum, gut contents, or organs from affected animals or feed extracts. If the toxins are present, the mice develop respiratory distress and die.
Toxin can be demonstrated in serum up to six days after the onset of clinical signs. Levels of toxin in the serum of some horses, however, might be so low that they give negative results on a mouse inoculation. Horses are so sensitive to the toxin that they can suffer ill effects even though the level is so low that it doesn't show up in the mouse.
Culture of the toxin from feeds is difficult.
Other, more sophisticated diagnostic tests also can be conducted, such as electrophysiologic testing, which helps differentiate botulism from other nerve, neuromuscular, and muscular disorders.
Development of the anti-toxin, along with increased knowledge about caring for afflicted horses, has increased the survival rate. In the past, it was estimated that at least 90% of infected horses succumbed to the disease. With good care in assisting nursing, drinking, and eating, the survival rate now is a good deal higher.
The good news is that there is a vaccine for equines for the type of toxin found most frequently in the United States--Type B. As mentioned earlier, Type B is found in Central Kentucky and along the Eastern Seaboard. (Type C is common in Europe and is believed to be the type that killed the yearlings in Australia. It is rare in the United States, other than in Florida.)
The vaccine is marketed as Bot Tox-B. The manufacturer, Neogen Corporation, recommends use of the vaccine on pregnant mares as well as on foals, weanlings, and yearlings.
A vaccination program for mares, officials say, should be a series of three doses given at least one month apart, with the third dose administered 204 days before parturition. They also recommend that owners re-vaccinate annually within two to four weeks of the mare foaling.
Young horses, the company recommends, should be given the three-dose series to establish initial immunity. After that, yearly booster shots will maintain ongoing protection. For a foal from a non-immunized mare, it is recommended that the vaccination program should begin a week to 10 days following birth.
While vaccination for the Type B strain is perhaps the best deterrent for that form of botulism, there also are preventive steps that all farms can put in place.
The American Association of Equine Practitioners recommends, for example, that horses be fed in feed tubs rather than on the ground to minimize the potential for ingesting harmful material.
Then, there is the simple matter of good husbandry. While it is impossible to clear every small rodent carcass from a pasture, one can make certain that all known animal carcasses are removed from the premises and properly destroyed. An ongoing control approach to rodent populations in the barn and paddocks also can be effective.
It should go without saying that one should avoid feeding spoiled feed of any kind. Carefully checking hay bales when feeding can be helpful in locating any rodent carcasses that might be contained therein.
The same can be true of bags of corn and oats. It is rare that one will find a rodent carcass in a bag of processed feed, but it can occur. Special care should be taken in examining bags of non-processed horse feed.
An immunization program, combined with good husbandry around the stable and in pastures, as well as a careful feeding program, can do much to cut down on the incidence of an insidious affliction that often carries a death sentence.
About the Author
Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.
POLL: University Equine Hospitals