Tetanus toxemia is caused by a specific poison, or toxin, that blocks transmission of inhibitory nerve signals. This leads to severe muscle contraction and an exaggerated response to stimuli. The toxin is produced by the bacterium Clostridium tetani in dead tissue. Most mammals are susceptible, but horses and humans appear to be the most sensitive of all species. Although tetanus occurs worldwide, there are some areas, such as the northern Rocky Mountain section of the United States, where the organism is rarely found in the soil and where tetanus is almost unknown. In general, the occurrence of the bacteria in the soil and the frequency of tetanus in humans and horses are higher in the warmer parts of the various continents.
Clostridium tetani is found in soil and intestinal tracts. In most cases, it is introduced into the body through wounds, particularly deep puncture wounds. Sometimes, the point of entry cannot be found because the wound itself may be minor or healed. The bacteria remain in the dead tissue at the original site of infection and multiply. As bacterial cells die and disintegrate, the potent nerve toxin is released. The toxin spreads and causes spasms of the voluntary muscles.
The incubation period varies from 1 to several weeks but usually averages 10 to 14 days. Localized stiffness, often involving the jaw muscles and muscles of the neck, the hind limbs, and the region of the infected wound, is seen first. General stiffness becomes pronounced about 1 day later, and then spasms and painful sensitivity to touch become evident.
As the disease progresses, the reflexes increase in intensity and the animal is easily excited into more violent, general spasms by sudden movement or noise. The spasms may be so severe that they cause bone fractures. Spasms of head muscles cause difficulty in grasping and chewing of food, hence the common name, lockjaw.
In horses, the ears are erect, the tail stiff and extended, the nostrils dilated, and the third eyelid sunken. Walking, turning, and backing are difficult. Spasms of the neck and back muscles cause extension of the head and neck, while stiffness of the leg muscles causes the animal to assume a “sawhorse” stance. Sweating is common. General spasms disturb blood circulation and breathing, which results in increased heart rate, rapid breathing, congestion of mucous membranes, and possible respiratory failure. About 80% of affected animals die. In horses that recover, there is a recovery period of 2 to 6 weeks.
The diagnosis of tetanus is usually based on the distinctive signs and history of recent trauma. Your veterinarian may be able to confirm the diagnosis by finding the tetanus toxin in a blood sample taken from the affected animal. Treatment involves thorough cleaning and disinfection of the wound, the use of antibiotics, and tetanus antitoxin (which helps protect against the effects of additional toxin being released). Whether or not the horse has been immunized, another injection of toxoid is usually given to increase the production of antibodies to the toxin. In the early stages of the disease, your veterinarian may recommend muscle relaxants, tranquilizers, or sedatives, in conjunction with tetanus antitoxin. Good results with tetanus antitoxin injections have been obtained in horses.
Recovering horses require supportive nursing care and should be kept in a dark, quiet stall. Feeding and watering devices should be high enough to allow the horse to use them without lowering the head. Slings may be useful for horses having difficulty standing or rising. Ask for and follow your veterinarian's advice regarding any other steps you should take.
Immunization can be accomplished with tetanus toxoid and is usually recommended for all horses. Yearly booster injections of toxoid are advisable. Mares should be vaccinated during the last 6 weeks of pregnancy and the foals vaccinated at 5 to 8 weeks of age. In high-risk areas, foals may be given tetanus antitoxin immediately after birth and every 2 to 3 weeks until they are 3 months old, at which time they can be given toxoid.
Last full review/revision July 2011 by Otto M. Radostits, CM, DVM, MSc, DACVIM (Deceased); Delores E. Hill, PhD; Barton W. Rohrbach, VMD, MPH, DACVPM; Charles J. Issel, DVM, PhD; Max J. Appel, DMV, PhD; David A. Ashford, DVM, MPH, DS; Daniela Bedenice, DVM, DACVIM, DACVECC; Farouk M. Hamdy, DVM, MSc, PhD, MPA (Deceased); Kenneth R. Harkin, DVM, DACVIM; Johnny D. Hoskins, DVM, PhD; Eugene D. Janzen, DVM, MVS; Jodie Low Choy, BVMS; John E. Madigan, DVM, MS; Dale A. Moore, MS, DVM, MPVM, PhD; J. Glenn Songer, PhD; Joseph Taboada, DVM, DACVIM; Charles O. Thoen, DVM, PhD; John F. Timoney, MVB, PhD, Dsc, MRCVS; Ian Tizard, BVMS, PhD, DACVM; Brian J. McCluskey, DVM, MS, PhD, DACVPM; Bert E. Stromberg, PhD; Peter J. Timoney, MVB (Hons), MS, PhD, FRCVS