Vaccination Essentials: Rabies, Tetanus, and Botulism


Ask veterinarians anywhere in North America and they'll likely agree: If you vaccinate for nothing else, at the very least vaccinate for tetanus and rabies. The two diseases have much in common. They're endemic--meaning your horse could be exposed to the causative organisms at any time, anywhere in his environment. They're exquisitely painful, have no cure, and are almost certainly fatal. And it's completely unnecessary for your horse to suffer from these diseases since the vaccines available to protect against them are inexpensive, extremely effective, and are part of every veterinarian's arsenal.

There's a third disease--botulism--that is caused by an organism closely related to the one that causes tetanus. It shares many of the same characteristics (it's painful, has a high mortality rate, and horses are exposed to the organism daily). But at the moment, it's not routinely vaccinated against except in parts of North America where incidence is high (Kentucky and Ohio, for example). Yet, given some of the risk factors for the disease, vaccinating against botulism ought to be as much a part of our yearly health care routine for our horses as protecting them against tetanus and rabies.

Let's look at each disease in more detail.

Terrible Tetanus

Once upon a time it was called lockjaw, and even 200 years ago horse owners knew it was a terrible way for a horse to die.

Clostridium tetani, the organism that causes tetanus, is an anaerobic bacterium found in soil and fecal material. Ordinarily it's harmless because it dies on exposure to the air--but if it finds a hospitable, moist, airless environment in which to live, it flourishes and gives off one of the most potent natural toxins known to man. Its preference? A puncture wound, sometimes one so small you might not notice it on your horse, as such wounds tend to bleed very little and close over quickly. C. tetani can also infect unvaccinated stallions following castration, and it can infect foals with failure of passive transfer via the umbilical stalk (hence the practice of dipping a newborn's umbilical stalk with antiseptic).

Tetanus can incubate for one to three weeks before signs start appearing. Once the toxin begins to work, it impairs the inhibition of excitatory signals to the nerves--meaning that muscles, once contracted, will tend to stay contracted and not be able to relax. A horse with tetanus will show a classic "startled" expression and a straddled, "sawhorse" stance, might have ears pulled permanently forward or back and down, retracted lips, flared nostrils, and difficulty opening jaws (lockjaw). He might also seem colicky.

Within 24 hours of the appearance of the initial symptoms, he'll experience spasms of his third eyelid, a retraction of the eyeball into the socket (which makes the eyes look sunken), and he'll be over-reactive to any sudden noises, going into spasms or seizures. His temperature might rise to 110ºF, and eventually he'll go down, lying on his side with his legs extended rigidly and his neck stretched awkwardly upward. Death follows soon afterward.

Horses that contract tetanus have an 80% mortality rate, and few treatment options apart from emergency administration of tetanus anti-toxin (more on this in a moment) and supportive therapies. He might need to be fed intravenously because he'll be unable to relax his jaw. Even if your horse does recover, he'll need more than six weeks to get anywhere near back to normal, and his experience will not grant him long-lasting immunity from further tetanus infections.

Equine tetanus anti-toxin is a treatment, not a vaccine; it confers passive immunity to an unvaccinated horse that might have been exposed to C. tetani. Stephanie Thompson, DVM, manager of technical services for Merial pharmaceutical company, describes it like this: "Instead of stimulating an immune response, an anti-toxin provides the animal with the short-term immune response. The antibodies contained in an anti-toxin are meant only as help in a crisis."

Anti-toxins are expensive, not always readily available, and can only do so much. They can bind to circulating toxins in the horse's bloodstream, but once the toxin binds to the nerve cells, anti-toxins have no way to dislodge it. Thus, early administration is crucial if you think you have an unvaccinated horse that is at risk for tetanus. But apart from exceptional circumstances--say, you rescue a neglected horse at auction who has a visible puncture wound and no medical history--you should never find yourself in the position of having to get your veterinarian to administer anti-toxin because your horses should be routinely protected against tetanus through vaccination. It's a no-brainer, says Thompson.

"Because the exposure risk is so high in horses--and all farm animals--there really is no reason not to vaccinate against tetanus," she says. "Tetanus vaccine is readily available (usually along with other vaccines in a combined injection), and it's extremely effective in protecting (horses) from the disease." Furthermore, there's very little danger of reaction, and no risk whatsoever of contracting the disease from receiving the injection because the tetanus vaccine is a toxoid, formulated from proteins in the toxin rather than from the bacteria itself. Since there are no live components in the formulation, and only selected proteins from the toxin (enough to stimulate the immune system to recognize it as "foreign" and attack it, but not enough to cause disease), the vaccine is one of the safest available, with a track record decades long.

Why a toxoid instead of a killed-bacteria vaccine? Thompson explains that with tetanus, the bacteria tend to stay in the wound where they initially take hold; it's the toxin that circulates in the horse's system. Therefore, it's the toxin the immune system needs to recognize and attack, particularly because it can linger in the system even after you kill the organism itself.

Incidentally, although the disease is not transmissible between humans and horses, our two species are considered among the most vulnerable to its effects, so if you work around a barn, you should make sure your own tetanus protection is up-to-date as well as your horse's! Consult your physician for a human-approved vaccine.

Rabies: No Way for a Friend to Die!

If tetanus sounds like a horrific disease, it might just be surpassed by rabies, a true nightmare with no hope of a happy ending.

Historically one of man's most feared diseases, rabies was described by the ancient Greeks as lyssa, meaning "frenzy." The Romans gave us its present name by adapting their Latin word meaning "to rage." It's a form of viral encephalitis that is transmitted by the saliva of infected animals, meaning that in almost all cases you must be bitten to contract it. Rabies exists in populations of all sorts of wildlife with which horses might come into contact--skunks, raccoons, bats, foxes, coyotes, groundhogs, and feral cats and dogs, to name only a few--and the disease is considered endemic in most parts of North America.

The rabies virus, once introduced to the system by the bite of an infected animal, takes aim at the cells of the central nervous system. It enters nerve cells at the wound site and travels to the brain, then follows nerve pathways to the muscles and organs, wreaking havoc in the process.

The virus concentrates in salivary glands, which explains why it is usually spread by bites, but it also invades the muscles used for drinking and swallowing, causing extreme pain when the animal tries to swallow liquids. The result is that although the animal might be desperately thirsty, the pain on trying to drink induces a fear response to the mere sight of water--hence one of the other historical names for rabies: Hydrophobia (fear of water).

The incubation period for rabies is usually two to six weeks (according to an extension publication from the University of Kentucky), depending on the site of the bite from the rabid animal. A bite on the muzzle means the virus hasn't got far to travel to reach the brain, while a chomp on a hind leg presents the virus with a longer journey and a longer incubation time.

Broadly described, there are two ways rabies is expressed: The "furious" form and the "dumb" form. In the furious form, animals become abnormally aggressive, even vicious, as well as super-sensitive to stimuli, especially touch. Horses usually, but not always, exhibit the dumb form, which is less dramatic. The animal becomes lethargic and weak, and he soon is unable to raise his head or vocalize because the throat and neck muscles are paralyzed. He might show photophobia (an aversion to light), develop a high fever, become colicky, or go temporarily or permanently blind. Excessive salivation, heart arrhythmias, even seizures can all be present. It's often said that the only thing typical about rabies is that it's atypical.

As the virus spreads, it destroys the brain matter, with symptoms depending on what parts of the brain are targeted. By the time any symptoms are evident, one thing is for sure: Death is three to five days away, and there is no treatment. Rabies is 100% fatal!

Rabies also has the distinction of being a "zoonose"--a disease transmissible between animals and humans. That makes it extremely dangerous for horse owners, especially since, as Thompson explains, "The dumb form in horses can be mistaken for choking--so owners might stick their hands in these horses' mouths trying to locate a blockage."

There have been rare cases of horses with the furious form as well; in one shocking case in Ontario a few years ago, a rabid Belgian horse savaged and killed his owner.

As with tetanus, Thompson emphasizes the value of vaccination. "Rabies is a horrible, horrible disease, and the vaccine is extremely safe and virtually 100% effective," she says. "It's surprising how many people don't routinely give rabies vaccinations to their horses, saying there isn't much of it in their area. It's the law to vaccinate for rabies in most places for dogs, and even for cats, but there's no such legislation for horses.

"I think part of the reason people don't vaccinate is that they don't truly understand the risk, because they've never seen a case of rabies," continues Thompson.4 "If you see it, you will never, ever forget it. Vaccinating is so inexpensive and has such a low reaction rate...the disease risk far outweighs any risk inherent in vaccination."

The rabies vaccine used for horses in North America is a killed-virus formulation with an adjuvant (a substance added to a vaccine to boost the immune response). This means there is no risk of live organisms in the solution, so it's extremely safe. If your horse does react to the injection, he's probably reacting to the adjuvant. Since each manufacturer has its own proprietary adjuvant formula, choosing a vaccine from another manufacturer next time will generally take care of the problem.

The AAEP Guidelines state: "None of the licensed vaccines are labeled for administration to pregnant mares; therefore, it is recommended that mares be vaccinated before breeding. However, it should be recognized that some veterinarians administer the killed-virus vaccine to pregnant mares without reports of adversity. Modified live rabies vaccines are not licensed for horses and should not be used."

It's reassuring to know that although there are several different strains of rabies (you might have heard of "skunk rabies" or "bat rabies," for example), there are enough common proteins in the various strains that the commercially available rabies vaccines will protect against all of them.

Beware of Botulism

The dark horse in our trio of deadly diseases is botulism, which is still not considered a common disease in horses. That, unfortunately, is changing.

Botulism is caused by a neurotoxin produced by the anaerobic bacterium Clostridium botulinum, first identified in 1897 in Belgium during an outbreak of food poisoning. It's closely related to C. tetani, the bacterium that causes tetanus, and like C. tetani, produces one of the most potent poisons known to man. Horses are particularly sensitive to botulinum toxin; untreated foals can suffer up to 90% mortality. Mortality is also high in untreated adults.

Eight toxin types, each produced by a different bacterial strain, have been identified: Types A, B, C1, C2, D, E, F, and G. Each type is unique in its geographic distribution and species susceptibility. Type B accounts for more than 80% of equine cases, with Types A and C making up the rest.

The clinical signs of botulism can easily be confused with other conditions such as rabies, equine protozoal myelitis (EPM), tetanus, and azoturia (tying-up). Unlike most of these, however, botulism can strike very swiftly. The toxin works by inhibiting the release of acetylcholine (a neurotransmitter) at the neuromuscular junction, the point at which nerve endings meet muscle fibers. Without acetylcholine, muscles are not stimulated to contract, and become progressively weaker and finally paralyzed. Affected horses lose the ability to swallow food or water, dribbling grain and saliva from their lips; move in a shuffling fashion or drag their toes; and can suffer other signs such as depression, muscle tremors, a protruding tongue, dilated pupils, constipation, colic, shortness of breath, and violent spasms or seizures. Physical activity may worsen clinical signs.

In as little as 48 hours, horses affected with botulism are recumbent and unable to rise, typically with their chins resting on the ground. Respiratory paralysis usually forces euthanasia. The severity of symptoms, however, is largely dependent on the amount of toxin, and less severely affected horses might decline slowly--a characteristic that can confuse diagnosis.

Horses can get botulism in three ways. The most common is ingestion of the toxin (not the bacterial spores themselves) in contaminated feed or water. Decomposing carcasses of rodents or birds in baled hay are often blamed, but it is far more common for hay or silage to be contaminated through improper storage or poor fermentation. The risk increases markedly when horses are fed large round bales, especially the wrapped silage type, which can become infected with C. botulinum when their plastic wrapping is compromised. Outbreaks of botulism in several horses on a farm are almost always due to this type of feed.

More rarely, horses can contract botulism through the entrance of C. botulinum from the soil into a puncture wound. In young foals, botulism can be contracted by the entrance of the organism through the tissue of the umbilical stump. The result is called "shaker foal syndrome" because the foal develops violent muscle tremors, a stilted walk, and an inability to swallow (milk dribbling from a foal's mouth and nose is a classic sign of botulism). Death usually occurs within 72 hours.

As with tetanus, the vaccine is an inactivated toxoid, which is extremely effective. There is also a botulism anti-toxin for treating horses and foals with suspected botulism, but it's prohibitively expensive for most, difficult to get, and must be specific to the type of toxin causing the disease (which is a challenge with lab results often taking several days to determine this).

Currently, the only botulism toxoid readily available in North America protects only against the B strain, which luckily is the serotype most commonly associated with forage contamination. Although vaccinating for botulism might not be as widely recommended as for tetanus and rabies, any farm considering feeding cost-effective haylage or silage products, or round hay bales, should consider protecting their animals from this disease, especially broodmares, who can pass their antibodies on to their nursing foals and thus protect them from shaker foal syndrome.

It can also be useful to test your forage for pH (acidity) before you feed. C. botulinum is very pH-sensitive and thrives at levels over 4.5. Feedstuffs that test at a pH level below 4.5 are probably acidic enough not to be contaminated with the toxin.

In sum, there's virtually nothing to lose and everything to gain by vaccinating all horses against tetanus and rabies. Botulism guidelines are fuzzier, but your veterinarian can help you decide whether you should vaccinate against this often fatal disease.

Vaccination Schedules for Tetanus, Rabies, and Botulism

TETANUS TOXOID Foals from nonvaccinated mares: First dose given at 3-4 months, second dose given at 4-5 months Annual Annual Annual Annual, 4-6 weeks before foaling Booster at time of penetrating injury or surgery if the last dose was not administered within six months

Foals from vaccinated mares: First dose given at 6 months, second dose given at 7 months, third dose given at 8-9 months Annual Annual Annual
 RABIES Foals born to nonvaccinated mares: First dose given at 3-4 months, second dose given at 12 months Annual Annual Annual Annual, before breeding

Vaccination recommended in endemic areas. Do not use modified-live virus vaccines in horses.

Foals born to vaccinated mares: First dose given at 6 months, second dose given at 7 months, third dose given at 12 months Annual Annual Annual
BOTULISM Foals from non-vaccinated mares: See comments Consult your veterinarian Consult your veterinarian Consult your veterinarian Initial 3-dose series at 30-day intervals with last dose 4 to 6 weeks before foaling; annually thereafter, 4-6 weeks before foaling

Only in endemic areas. A third dose administered 4-6 weeks after the second dose may improve the response of foals to primary immunization.

Foals from non-vaccinated mares may benefit from toxoid at 2, 4, and 8 weeks of age; transfusion of plasma from vaccinated horse; or antitoxin. Efficacy needs further study.

Foals from vaccinated mares: Three-dose series of toxoid at 30-day intervals starting at 2-3 months of age Consult your veterinarian Consult your veterinarian Consult your veterinarian


About the Author

Karen Briggs



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