Tetanus

C. D. STEIN.

TETANUS, commonly called lockjaw, is a wound infection disease that is usually accompanied by a fatal toxemia. The toxemia causes contractions of the voluntary muscles, mainly those of the face, neck, body, legs, and tail. Spasms are the result of steady and prolonged contractions of the affected muscles.

Tetanus is caused by a rod-shaped germ, Clostridium tetani, which produces an extremely potent toxin. The germs form highly resistant, large terminal spores, which give the organism a peculiar drumstick appearance. The tetanus germs and spores remain localized at the place of the wound where they enter the body. They multiply and produce the powerful toxin. The poison is absorbed and carried by the blood to all parts of the body. It acts directly on the nervous system. It is so potent that a mere prick with a hypodermic needle contaminated with it may be enough to cause symptoms of tetanus in people.

C. tetani, like the germs that cause blackleg and malignant edema, thrive in the absence of air. They become especially active and dangerous when they are implanted in injured tissue from which the air is excluded. Deep punctured or lacerated wounds contaminated with foreign material or soil such as may result from nail or splinter punctures, fractured bones, gunshot wounds, castration, and harness and saddle galls therefore are more apt to produce tetanus than superficial open wounds.

The disease occurs all over the world. It is most common in old farming areas, especially in sections where truck gardens, heavily manured land, and swamps are contaminated with tetanus germs. The organisms or their spores are scattered in the top layers of soil and in street dust and hay. They often are in manure.

The disease is common in people and horses. It may attack other warm-blooded animals.

Horses, mules, and asses, which are highly susceptible, may contract the disease from any type of wound but most frequently from wounds of the feet.

In sheep, which are rather susceptible, the infection sometimes occurs after castration, docking, and shearing; in the umbilical (navel) cord of lambs during birth; or in ewes during parturition. Cows may get infection following parturition and calves after castration.

Cases are observed occasionally in swine, dogs, and cats.

Poultry is highly resistant.

SYMPTOMS appear in most cases in 1 to 2 weeks after the germs enter the body. Sometimes depending on the type of primary injury, the character of the healing process, and the degree of infection the symptoms may not appear for several weeks. Very young animals may develop symptoms in less than a week.

The first signs of the disease usually are manifested about the head. Chewing is difficult at first, and swallowing is slow and awkward. Spasms spread rapidly from one group of muscles to another and make them rigid. Eating may become impossible when the muscles used in chewing are affected and the jaws are "locked."

The nictitating membrane (the inner, or third, eyelid between the lower eyelid and the eyeball proper) protrudes up on the surface of the eyeball. This is noticeable especially in the horse.

The legs are spread and stiffened, giving a straddling gait and the appearance of a sawhorse. The tail is elevated and stiff. The ears are held rigidly erect. Constipation commonly occurs. The breathing is rapid and forced. The heart action may or may not be quickened. Usually there is little or no fever except in the severe cases and then just before death.

The muscles may tend to relax at intervals, but they contract instantly, like a spring, at the slightest noise, a ray of light, or a touch. Death is usually due to exhaustion or nonfunction of the vital organs. Pneumonia, which results from the inhalation of water, saliva, feed, or improperly administered medicines, is a frequent complication.

Death usually comes 7 or 10 days after the first symptoms appear. Mortality is 55 to 90 percent, depending on the individuals, the species of animal, and severity of the infection. Animals that recover often are sick a month.

Tetanus is not hard to diagnose because its symptoms are unusual. Rigidity of the muscles is one of the most constant and typical symptoms. No typical lesions are found on postmortem examination, but microscopic examination of stained smears made from deep portions of wounds may reveal the typical drumstick-shaped organisms of tetanus.

PREVENTION of tetanus depends first on cleanliness. Cleanliness in all operations includes strict aseptic surgical procedures and the use of sterile surgical instruments.

Animals should be housed during parturition and following surgery in clean, dust-free quarters.

Prompt and proper attention should be given to deep wounds the removal of dirt and other foreign material, proper drainage with surgery, and irrigation of the wound with suitable medicaments, such as hydrogen peroxide.

Stables, corrals, paddocks, or pastures used by horses and other livestock should be kept free of sharp objects which are apt to cause injuries.

In known tetanus districts, routine preventive immunization of animals against tetanus and immediate treatment of injured animals with tetanus antitoxin following wounds will materially reduce the chances of infection.

THE PREVENTIVE immunizing agents against tetanus are of two types, tetanus antitoxin and tetanus toxoid.

Tetanus antitoxin is produced from the blood serum of horses. It is standardized as to potency, so that a given amount neutralizes a specific amount of toxin. Injected into susceptible animals, it confers a passive or temporary immunity against the disease. As a preventive, it should be injected immediately following an injury and not after symptoms occur.

The tetanus toxoid is prepared by treating the toxin with formalin to inactivate its toxicity. The refined formalized toxoid, which has largely replaced antitoxin for immunization, especially in man, confers an active immunity against the toxin in about 2 weeks after its injection. The immunity lasts about a year and can be increased by booster injections. The use of tetanus toxoid in animals and man has become a routine practice in some areas where tetanus is prevalent.

The prevalence of tetanus in animals and man has decreased because of improved methods of wound treatment, better hygiene, and preventive vaccination with tetanus toxoid. The incidence of tetanus in troops during the First World War was greatly reduced by better treatment of battle wounds and administration of tetanus antitoxin. Its incidence in the Second World War was negligible, because immunization of all the troops with tetanus toxoid was a routine measure.

TREATMENT of an established case of tetanus in an animal that shows well-marked symptoms has little value.

Chances for recovery are improved if treatment is started early. It is first essential to open the wound through which the infection entered, if it can be located, to provide adequate drainage and to keep it open by irrigation with a suitable antiseptic.

Confinement of affected animals in clean, cool, quiet, darkened quarters is advantageous.

If tetanus antitoxin is indicated, it should be given in large, repeated doses. Sedatives of various types are commonly employed to produce relaxation of the muscles. Artificial feeding may be required.

Veterinarians have reported that the administration of penicillin, alone or as an adjunct to antitoxin, has given good results in the treatment of some cases that show early symptoms of tetanus.

When attempts are made to treat a case of tetanus, the procedure should be carried out under the supervision of a veterinarian.

C. D. STEIN, a graduate of the University of Pennsylvania, is a veterinarian in the Animal Disease and Parasite Research Branch of the Agricultural Research Service. He has been with the Department of Agriculture since 1911, during which time his research has contributed fundamental information for a better understanding of anthrax, equine infectious anemia, and other infectious diseases of livestock.