Tetanus is caused by the tetanus neurotoxin (TeNT, or tetanospasmin) produced by the sporulating anaerobic bacterium Clostridium tetani, which is found in soil and intestinal tracts and usually introduced into tissues through deep puncture wounds. The toxin causes a generalized muscular spastic paralysis. Clinical signs and history are usually sufficient for diagnosis. Treatment is supportive, including thorough flushing of the wound, along with injection of tetanus antitoxin. Tetanus toxoid is administered for active vaccination.
Tetanus toxemia is caused by the tetanus neurotoxin (TeNT, or tetanospasmin) produced by Clostridium tetani in necrotic tissue.
Almost all mammals are susceptible to tetanus; however, dogs and cats are relatively more resistant than any other domestic or laboratory mammal. Birds are quite resistant; the lethal dose for pigeons and chickens is 10,000–300,000 times greater (on a body weight basis) than that for horses (1). Horses, guinea pigs, pigs, monkeys, and sheep seem to be the most susceptible of all species, with the possible exception of humans.
Although tetanus is worldwide in distribution, in some areas, such as the northern Rocky Mountains of the US, the organism is rarely found in the soil and tetanus is almost unknown. In general, the occurrence of C tetani in the soil, especially in cultivated soil, and the incidence of tetanus in humans, horses, and lambs is higher in the warmer parts of the various continents.
Etiology and Pathogenesis of Tetanus
Clostridium tetani, an anaerobe with terminal, spherical spores, is found in soil (especially cultivated soil) and intestinal tracts. In most cases, C tetanispores are introduced into tissues through wounds, particularly deep puncture wounds, that provide a suitable anaerobic environment.
In lambs and sometimes in other species, tetanus often follows tail docking or castration (see ). The umbilicus is a common site of tetanus spore entry in neonates. Sometimes, the point of entry cannot be found because the wound is minor or healed.
A. The site of banding castration, performed on a bull, that resulted in tetanus. Note the wound created by the band that enabled the introduction of Clostridium tetani spores from the environment. B. Full body image of the same bull. Note the generalized stiffness of the limbs, as well as of the back and neck muscles, resulting in extension of the head and neck.
Courtesy of Dr. Mary Smith.
The spores of C tetani are unable to grow in healthy tissue or even in wounds if the tissue remains at the normal oxidation-reduction potential of the circulating blood. Suitable conditions for multiplication occur when a small amount of soil or a foreign object causes tissue necrosis. The bacteria remain localized in the necrotic tissue at the original site of infection and multiply. As bacterial cells undergo autolysis, the potent TeNT is released.
TeNT is a zinc-binding protease that cleaves synaptobrevin, a vesicle-associated membrane protein. Usually, the toxin is absorbed by the motor nerves in the area and travels retrograde up the nerve tract to the spinal cord, where it causes ascending tetanus. C tetani also produces tetanolysin, a hemolysin that induces membrane damage in macrophages, assisting with local colonization of tissue.
TeNT causes spasmodic, tonic contractions of the voluntary muscles by interfering with the release of inhibitory neurotransmitters from presynaptic nerve endings. If more toxin is released at the site of the infection than the surrounding nerves can take up, the excess is carried off by the lymph to the bloodstream and thus to the CNS, where it causes descending tetanus.
Even minor stimulation, such as touch, light, or noise, can trigger the characteristic tetanic muscular spasms, which are shorter-lasting muscle contractions. The spasms can be severe enough to cause bone fractures. Spasms affecting the larynx, diaphragm, and intercostal muscles lead to respiratory failure. Involvement of the autonomic nervous system results in cardiac arrhythmias, tachycardia, and hypertension.
Clinical Findings of Tetanus
The incubation period of tetanus varies from one to several weeks, usually averaging 10–14 days.
Localized stiffness, often involving the masseter muscles and muscles of the neck, the hindlimbs, and the region of the infected wound, is the first clinical sign; general stiffness becomes pronounced approximately 1 day later, and tonic spasms and hyperesthesia develop.
Because of their high resistance to tetanus toxin, dogs and cats often have a long incubation period and develop localized tetanus; however, generalized tetanus can develop in these species.
In tetanus cases, reflexes increase in intensity, and the animal is easily excited into more violent, general spasms by sudden movement or noise. Spasms of head muscles cause difficulty in prehension and mastication of food—hence the common name lockjaw.
In horses and ruminants with tetanus, the ears are erect, the tail stiff and extended, the external nares dilated, and the third eyelid prolapsed (see ). An anxious expression due to the ears being held back and eyelids being held open widely might be evident (see ).
Close-up of the head of a calf, showing the anxious expression characteristic of tetanus. The ears are held back, and the eyes are held open widely.
Courtesy of Dr. Mary Smith.
Walking, turning, and backing up are difficult for animals with tetanus. Spasms of the neck and back muscles cause extension of the head and neck, and stiffness of the leg muscles causes the animal to assume a “sawhorse” stance (see ). Sweating is common.
Calf showing the stiffness of leg muscles resulting in the "sawhorse" stance that is characteristic of tetanus.
Courtesy of Dr. Mary Smith.
Limb stiffness and rigid gait are the most common clinical signs of tetanus in sheep. These signs can progress to lateral recumbency and death from respiratory failure. Outbreaks can be caused by iatrogenic interventions such as ear tagging.
In ruminants with tetanus, bloat is common, and trismus (painful spasms in jaw muscles that make opening the mouth difficult) is often very evident. Outbreaks associated with herdwide interventions such as vaccinations, dehorning, or castration events are also possible.
In pigs, tetanus usually progresses very rapidly.
General spasms due to tetanus disturb circulation and respiration, resulting in increased heart rate, rapid breathing, and congestion of mucous membranes. Sheep, goats, and pigs often fall to the ground and exhibit opisthotonos when startled.
Consciousness is not affected by tetanus.
Pearls & Pitfalls
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In dogs and cats, localized tetanus often presents as stiffness and rigidity in a limb with a wound. The stiffness can progress from localized to generalized. The animal's appearance in generalized tetanus is similar to that described for horses, except that the partially open mouth with lips drawn back (as in humans) is usually evident. Young, large-breed dogs seem to be the most commonly affected.
Usually, body temperature remains slightly above normal in tetanus cases; toward the end of a fatal attack, however, it can rise up to 43°C (110°F). In mild attacks of tetanus, the pulse and body temperature remain nearly normal.
The mortality rate in tetanus cases averages approximately 80% (approximately 50% in dogs in one study) (2). In animals that recover, there is a convalescent period of 2–6 weeks; protective immunity usually does not develop after recovery.
Diagnosis of Tetanus
Clinical evaluation
Gram stain
Anaerobic culture
PCR assay
Clinical signs and a history of recent trauma, in combination with negative vaccination status, are usually adequate for a clinical diagnosis of tetanus. TeNT is typically not detected in the blood of affected animals.
When a wound is apparent, verification of the bacterium in Gram-stained smears and by anaerobic culture may be attempted. PCR assay for the Clostridium tetani organism or to target the organism's gene that codes for TeNT can be performed on wound material.
Detection of the organism alone does not confirm a tetanus diagnosis; with compatible history and clinical signs, however, it is strongly supportive.
Treatment and Control of Tetanus
Wound cleaning
Antimicrobial therapy
Parenteral antitoxin administration
Muscle relaxants
Vaccination
Treatment of tetanus should target elimination of Clostridium tetani, neutralization of any remaining unbound TeNT in circulation, and supportive care aimed at muscle relaxation and analgesia. If a wound or site of infection is evident, it should be properly debrided and cleaned.
Procaine penicillin G (PPG) and metronidazole are the antimicrobials of choice to target any remaining C tetani:
For horses, the most common dosing regimen for PPG is 22,000 U/kg, IM, every 12 hours (3). In tetanus cases, however, dosages up to 50,000 U/kg during the first 2 days of treatment have been recommended (4).
The dose of metronidazole for horses ranges from 15–20 mg/kg, IV or PO, every 8–12 hours up to 20 mg/kg, PO, every 6 hours (5).
Antimicrobial treatment of tetanus is typically continued for at least 10 days.
Tetanus antitoxin may be administered to provide passive immunity to horses or other affected animals. It works to prevent free TeNT in circulation from entering neurons; however, it has no effect on toxin that has already been taken up into neurons, so it is most useful when administered to unvaccinated animals that need immediate, short-term protection.
Tetanus antitoxin can also be administered very early in the course of disease in conjunction with other treatments.
Tetanus antitoxin is derived from horse blood, so there is a risk of allergic reaction. Donor horses should also be tested annually for equine hepacivirus and equine parvovirus to avoid the production of contaminated antitoxin, which can result in Theiler disease (viral hepatitis) in recipient foals and horses.
In addition, animals with tetanus should be kept in an environment with limited auditory, tactile, and visual stimulation, to minimize muscle spasms. Muscle relaxants, sedatives, and analgesics might also be indicated, along with additional supportive care to address effects on other body systems.
For horses, vaccinations against tetanus should be administered according to current recommendations from the American Association of Equine Practitioners. Mares should be vaccinated during the last 4–6 weeks of pregnancy. Foals should be vaccinated at the age of 4–6 months, followed by a booster 4–6 weeks later and a third booster at the age of 10–12 months, then annually. Adult horses otherwise should receive an initial two-dose series 4–6 weeks apart, followed by annual boosters.
Small ruminants typically receive tetanus toxoid as part of a multivalent clostridial vaccine. The vaccination strategy is outlined above under control strategies for Clostridium perfringens type C and type D.
Although veterinarians might want to be familiar with human tetanus prophylaxis because of their occupational risk of exposure and the need to advise clients after animal-related injuries, recommendations for tetanus toxoid booster vaccination in humans are beyond the scope of this chapter; for more information, see the current human medical guidelines.
Tetanus toxoid boosters should also be administered to highly susceptible species anytime there is a penetrating injury or before surgery, if the previous dose of vaccine was given > 6 months previously. In high-risk areas, foals may be administered tetanus antitoxin immediately after birth and every 2–3 weeks until they are 3 months old, at which time they can be administered toxoid.
Pearls & Pitfalls
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The decision to vaccinate calves against tetanus depends on the prevalence of the disease in the area. All animals that have recovered from tetanus should be regularly vaccinated. Animals that survive tetanus do not develop natural immunity and should be vaccinated with tetanus toxoid.
To prevent tetanus, all surgical procedures should be conducted with the best possible aseptic techniques. After surgery, patients should be turned out on clean ground, preferably grass pastures. Only oxidizing disinfectants such as iodine or chlorine dependably kill C tetani spores.
Key Points
Horses are highly susceptible to tetanus; dogs and cats are relatively resistant.
Treatment includes wound cleaning, antimicrobials, tetanus antitoxin, muscle relaxants, and intensive supportive care.
Early recognition and treatment improve the chances of recovery; however, severe cases can be life-threatening.
For More Information
Tetanus. Centers for Disease Control and Prevention.
Tetanus Vaccination Guidelines. American Association of Equine Practitioners.
Furr M. Clostridial neurotoxins: botulism and tetanus. In: Furr M, Reed S, eds. Equine Neurology. Blackwell Publishing; 2007:221-229.
Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.
Also see pet owner content regarding tetanus in dogs, cats, horses, and potbellied pigs.
References
Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.
Bandt C, Rozanski EA, Steinberg T, Shaw SP. Retrospective study of tetanus in 20 dogs: 1988–2004. J Am Anim Hosp Assoc. 2007;43(3):143-148. https://doi.org/10.5326/0430143
Uboh CE, Soma LR, Luo Y, et al. Pharmacokinetics of penicillin G procaine versus penicillin G potassium and procaine hydrochloride in horses. Am J Vet Res. 2000;61(7):811-815. doi:10.2460/ajvr.2000.61.811
de Melo UP, Ferreira C. Clinical findings and response to treatment of 17 cases of tetanus in horses (2012–2021). Braz J Vet Med. 2022;44:e005321. doi:10.29374/2527-2179.bjvm005321
Sweeney RW, Sweeney CR, Weiher J. Clinical use of metronidazole in horses: 200 cases (1984–1989). J Am Vet Med Assoc. 1991;198(6):1045-1048. doi:10.2460/javma.1991.198.06.1045
Stein F, Gilliam L, Davis J, Taylor J. Rectal administration of metronidazole with and without rectal evacuation prior to use in horses. J Vet Pharmacol Ther. 2018;41(6):838-842. doi:10.1111/jvp.12697
Auvinen JRE, Kritchevsky JE, Reinhart JM, Gochenauer AE, Jannasch AS, Han-Hallett Y. Pharmacokinetic analysis and steady-state predictions of different preparations of metronidazole administered per rectum in adult horses. J Vet Intern Med. 2026;40(1):aalaf032. doi:10.1093/jvimsj/aalaf032
Swain EA, Magdesian KG, Kass PH, Edman JE, Knych HK. Pharmacokinetics of metronidazole in foals: influence of age within the neonatal period. J Vet Pharmacol Ther. 2015;38(3):227-234. doi:10.1111/jvp.12164
Magdesian KG. Antimicrobial pharmacology for the neonatal foal. Vet Clin North Am Equine Pract. 2017;33(1):47-65. doi:10.1016/j.cveq.2016.12.004
