Tetanus is a disease that is easily prevented, but can also be extremely lethal to horsesA lot of what veterinarians domost of what we dois routine and repetitious, so much so, in fact, that we (I, anyhow) forget that these things are not necessarily routine or repetitious to others. Clients, for example.
A short time ago, a new client asked me, Why do I need to vaccinate for tetanus? What is tetanus?
Wow, I thought, where has this guy been? Everyone knows about tetanus.
Within a week, another client, this being one of several years standing, asked, What if a horse gets tetanus? What is it?
Well, I knew where this guy had been, so maybe, I thought, there is a communication problem of some sort. I had assumed that everyone knew what tetanus was and why we vaccinate, but obviously that is not the case.
So, on the odd chance that there are others out there not familiar with tetanus and the reason to vaccinate against it, here is the story.

Cause
Tetanus is caused by the bacterium Clostridium tetani. (Clostridium is a fun genus; diseases caused by other clostridial species include botulism, anthrax, and gas gangrene.) The disease can occur in all animals, but the horse is the most susceptible, which is too bad because Cl. tetani is a normal inhabitant of the equine intestinal tract. Every time a horse defecates, he introduces the organism into his environment.
Tetanus is classified as an infectious disease, but it cannot be spread from animal to animal. Cl. tetani is an anaerobe; i.e., it grows in the absence of oxygen, so in the normal course of things it is not a problem. Puncture wounds are the major cause of the disease, especially punctures of the sole of the foot, but any integumentary alteration is a potential access route. The organism, everywhere in the horses environment, enters the wound where it finds all of its requirements for reproduction and proliferation: no air and devitalized tissue.
The organism itself does not actually cause the disease; as it grows, a toxin (tetanospasmin) is produced and released into the tissue, where it is spread by both the blood and retrograde axonal migration to the central nervous system (CNS), where it eventually takes up residence in the gray matter itself, from whence signs of the disease are produced.
Incubation ranges from a few days to several months. As with rabies, the incubation period of tetanus depends on point of entry of the organism; the closer to the CNS, the sooner clinical signs will be seen. Also important in the incubation period are the initial amount of bacteria introduced and the condition of the wound itself; a clean, open wound is much less apt to be the source of a case of tetanus.

Diagnosis
Diagnosis is made by the clinical signs and history. Culturing the organism from a lesion is difficult and often not rewarding, and the inability to grow Cl. tetani in the laboratory in no way eliminates the disease from a differential diagnosis. History is important in the diagnosis of any disease, but it is especially helpful in tetanus. A nonexistent or incorrect immunization program, coupled with a puncture wound or other laceration in the horses past, lead to a fairly conclusive diagnosis of tetanus when accompanied by the physical findings.
These findings are several and include rigid, erect ears, flared nostrils, retracted eyelids, prolapse of the third eyelid, difficulty in swallowing (or inability to, hence lockjaw), and rigid extension of the legs (sawhorse stance), making walking difficult. Also, there may be cessation of urination and defecation. The animal has an anxious look and even minimal external stimuli (sudden sights or sounds) may cause lengthy muscle spasms. If startled suddenly, the horse may fall onto its side and be unable to rise.
Tetanus itself will not kill the horse, but death will occur as the result
of several possibilities: respiratory paralysis, starvation or dehydration (swallowing is not possible), or pneumonia resulting from the aspiration of feed or water as swallowing is attempted.

Treatment
Treatment is prolonged, can be difficult and expensive, and fails as much as 80% of the time, but must be attempted. Tetanus antitoxin (TAT) is routinely administered, but it will not affect toxin that has already reached nerves or the CNS. It only functions to neutralize toxin in the circulatory system which has not yet reached the nervous system, making it most effective when given to a non-vaccinated horse at the time a laceration or puncture occurs.
There is a potential risk in the use of TAT, however. In certain instances, serum hepatitis will develop in horses who have received it. This may even be a better reason than the threat of tetanus for the use of a proper vaccination program.
Also, a tetanus toxoid injection should be given as part of the treatment. I do not know why; my teachers in school said to do it, the books say to do it, journal articles say to do it, so I guess you do it.
The horse should be placed in a dark, quiet, isolated (if possible) stall to lessen or eliminate external stimuli and any people who must work with or around the animal should do so slowly and silently. Plugging the horses ears with cotton is helpful in reducing the impact of auditory stimuli.
Penicillin will do nothing to combat the toxin already produced but it will kill any vegetative Cl. tetani organisms which may still be present, so high levels of the antibiotic should be given.
Tranquilizers, sedatives, and/or muscle relaxants should be used to control muscle spasms and convulsions. Your veterinarian will instruct as to what, when, and how much. Bute can be used to control fever and pain.
Nutrition and hydration must be maintained. If the horse cannot swallow, it must be fed and watered via a stomach tube. Also, the end products of metabolism need to be addressed; if the horse cannot urinate and defecate, these functions must be done for it. Manual emptying of the rectum two or three times daily is necessary, and catheterization of the bladder is needed.
Prognosis varies. An animal that can eat, drink, and eliminate will usually come along well; one that cannot, and especially one that goes down, is not a promising patient.
We are dealing with a disease which has a mortality rate of 30%-to-80%, depending on whose study you read, but recent work with a 16th-century Chinese herbal remedy has shown promise in reducing the mortality rate to be-
low 20%. The local veterinary sup-
ply house is fresh out of Chinese herbs, however; I will check again next week.
Recovery is slow. Full return to normalcy may take months, but once a horse is recovered, there are usually no residual effects. Likewise, there is no immunity acquired from having the disease; the next rusty nail can start it all over again.

Prevention
Prevention is easy: properly vaccinate. Vaccinate mares 1-to--2 months before foaling and, should they not conceive, give an annual booster anyway. The foal receives passive protection via its dams late-gestation booster, but should be given additional boosters at three and six months and then annually.
If a horse receives a tetanus-susceptible injury (i.e., almost any break in the skin) more than four months after its most recent booster, a booster should be given at that time. If a horse suffers a puncture or laceration and it is known that the animal has not been vaccinated, or the vaccination history is unknown, TAT, unfortunately, must be given. Also, if the tetanus toxoid vaccination program has not been completed, administer TAT. It is also of extreme importance to thoroughly cleanse the wound; a peroxide flush in the case of a puncture is a good idea.
Some people balk at the nominal cost of the vaccination program and others do not keep proper records so they do not know when boosters are needed. The cost, length, and inconvenience of treating a horse with tetanus, not to mention the real possibility of the animal dying, should make these considerations inconsequential.