Botulism in Animals

Botulism in most cases is an intoxication, not an infection, and results from ingestion of toxin in food. There are seven types of C botulinum, differentiated by the antigenic specificity of the toxins: A, B, C₁, D, E, F, and G. Types A, B, and E are most important in humans; C₁ in most animal species, notably wild ducks, pheasants, chickens, mink, cattle, and horses; and D in cattle. In horses, the most common type in North America and Europe is type B (>85% of US cases), and in the western US type A has been reported in only two outbreaks, both in humans, known to have been caused by type F. Type G, isolated from soil in Argentina, is not known to have been involved in any outbreak of botulism.

The usual source of the toxin is decaying carcasses or vegetable materials such as decaying grass, hay, grain, or spoiled silage. Toxins of all types have the same pharmacologic action. Like tetanus toxin, botulinum toxin is a zinc-binding metalloprotease that cleaves specific proteins in synaptic vesicles. Motor neuron surface receptors vary for the different botulinum toxins; therefore, some of the species differ in susceptibility to the various toxins.

The exact incidence of botulism in animals is not known, but it is relatively low in cattle and horses, probably more frequent in chickens, and high in wild waterfowl. Probably 10,000–50,000 birds die in most years, with deaths reaching 1 million or more during the great outbreaks in the western US. Most affected birds are ducks, although loons, mergansers, geese, and gulls also are susceptible. (Also see Botulism.) Dogs, cats, and pigs are comparatively resistant to all types of botulinum toxin when challenged orally; however, individual case reports mention botulism in dogs.

Most botulism in cattle occurs in South Africa and South America, where a combination of extensive agriculture, phosphorus deficiency in soil, and C botulinum type D in animals creates conditions ideal for the disease. The phosphorus-deficient cattle chew any bones with accompanying bits of flesh they find on the range; if these came from an animal carrying type D strains of C botulinum, intoxication is likely to result. Any animal eating such material also ingests spores, which germinate in the intestine and, after death of the host, invade the musculature, which in turn becomes toxic for other cattle.

Type C strains also cause botulism in cattle in a similar fashion. This type of botulism in cattle is rare in the US, although a few cases have been reported from Texas under the term loin disease, and a few cases have occurred in Montana. Hay or silage contaminated with toxin-containing carcasses of birds or mammals and poultry litter fed to cattle have also been sources of type C or type D toxin for cattle (“forage botulism”). Big bale silage and haylage seem to be a particular risk and result in botulism problems if fermentation fails to produce a low and stable pH (< 4.5).

Botulism in sheep has occurred in Australia, associated not with phosphorus deficiency as in cattle, but with protein and carbohydrate deficiency, which results in sheep eating carcasses of rabbits and other small animals found on the range. Botulism in horses often results from forage contaminated with type C or D toxin. In six of eight outbreaks of equine botulism associated with type A, the source of infection was confirmed to be hay or silage.

Toxicoinfectious botulism is the term given the disease in which C botulinum grows in tissues of a living animal and produces toxins there. The toxins are liberated from the lesions and cause typical botulism. This has been suggested as a means of producing the shaker foal syndrome. Gastric ulcers, foci of necrosis in the liver, abscesses in the navel and lungs, wounds of the skin and muscle, and necrotic lesions of the GI tract are predisposing sites for development of toxicoinfectious botulism. This disease of foals and adult horses appears to resemble “wound botulism” in humans. Type B toxin is often implicated in botulism in horses and foals in the eastern US. Toxicoinfection is also suggested as a cause of equine grass sickness (equine dysautonomia) and recently in Japan as a cause of botulism in cattle.

Botulism in mink usually is caused by type C strains that have produced toxin in chopped raw meat or fish. Type A and E strains are occasionally involved. Botulism has not been reported in cats but occurs sporadically in dogs. Type C toxin is usually responsible, but there have been reports in which type D was the source.

Clinical signs of botulism are caused by flaccid muscle paralysis and include progressive motor paralysis, disturbed vision, difficulty in chewing and swallowing, and generalized progressive paresis. Death is usually due to respiratory or cardiac paralysis. The toxin prevents release of acetylcholine at motor endplates (neuromuscular junction). Passage of impulses down the motor nerves and contractility of muscles are not hindered. No characteristic gross and histologic lesions develop, and pathologic changes may be ascribed to the general paralytic action of toxin, particularly in the muscles of the respiratory system, rather than to the specific effect of toxin on any particular organ.

Epidemics have occurred in dairy herds in which up to 65% of adult cows developed clinical botulism and died 6–72 hours after the onset of recumbency. Major clinical findings included drooling, decreased tongue tone, dysphagia, inability to urinate, and sternal recumbency that progressed to lateral recumbency just before death. Skin sensation is usually normal, and withdrawal reflexes of the limbs are weak. Initially, clinical signs resemble second-stage parturient paresis, but the cows do not respond to parenteral administration of calcium.

Reported clinical signs in horses are very similar, with progressive muscle paresis, recumbency, dysphagia, and decreased muscle tone (tail, tongue, jaw), respiratory distress, and death.

In shaker foal syndrome, foals are usually < 4 weeks old. Affected foals may be found dead without premonitory clinical signs; most often, they exhibit signs of progressive symmetric motor paralysis. Stilted gait, muscular tremors, and the inability to stand for >4–5 minutes are salient features. Other clinical signs include dysphagia, constipation, mydriasis, and frequent urination. As the disease course progresses, dyspnea with extension of the head and neck, tachycardia, and respiratory arrest occur. Death ensues most often 24–72 hours after the onset of clinical signs due to respiratory failure. The most consistent necropsy findings are pulmonary edema and congestion and excessive pericardial fluid, which contains free-floating strands of fibrin.

• Clinical evaluation with characteristic motor paralysis is suggestive but not confirmatory

• The mouse inoculation test is the traditional diagnostic test

Although sporadic cases of botulism are often suspected because of the characteristic motor paralysis; however, it is difficult to establish the diagnosis via detection of the toxin in animal tissues or serum samples or in the suspect feed. Commonly, diagnosis is made by eliminating other causes of motor (flaccid) paralysis. Filtrates of the stomach and intestinal contents should be tested for signs of toxicosis in mice, but a negative result is unreliable. Primary supportive evidence is provided if feeding suspect material to susceptible animals produces similar clinical signs. In peracute cases, the toxin may be detectable in the blood by use of the mouse inoculation tests but usually is not useful in the typical field case in animals on farms. Use of ELISA testing for detection of the toxin makes it feasible to test large numbers of samples, increasing the chances of diagnostic confirmation. In toxicoinfectious botulism, the organism may be cultured from tissues of affected animals.

• Control and correction of dietary deficiencies

• Immunization with region-specific type toxoid

• Supportive care

• Sometimes, botulinum antitoxin

Any dietary deficiencies in range animals should be corrected and carcasses disposed of, if possible. Decaying grass or spoiled silage should be removed from the diet. Immunization of cattle with types C and D toxoid has proved successful in South Africa and Australia. Toxoid is also effective in immunizing mink and has been used in pheasants.

Botulinum antitoxin has been used for treatment with varying degrees of success, depending on the type of toxin involved and the species of host. Treatment involves hydration, correcting electrolyte disturbances, and general supportive measures. Treatment of ducks and mink with type C antitoxin is often successful; however, such treatment is rarely used in cattle. Early administration of antitoxin (type B) specific or polyvalent to foals before recumbency (30,000 IU, IV) is reported to be successful. Supportive care in valuable animals is essential; prognosis is poor in recumbent animals. In endemic areas (eg, Kentucky), vaccination with type B toxoid appears to be effective.

• Western Australia Department of Industries and Regional Development: Botulism in Cattle

• Ontario Ministry of Agriculture, Food, and Rural Affairs: Animal Health—Botulism

• Anniballi F, Fiore A, Löfström C, et al. Management of Animal Botulism Outbreaks: From Clinical Suspicion to Practical Countermeasures to Prevent or Minimize Outbreaks. Biosecur Bioterror. 2013;11(S1):S191-S199.

• Also see pet health content regarding botulism in dogs and horses.