Botulism is a rapidly fatal motor paralysis caused by ingestion of the toxin produced by Clostridium botulinum types A-G. The spore-forming anaerobic organism proliferates in decomposing animal tissue and sometimes in plant material.
Botulism is in most cases an intoxication, not an infection, and results from ingestion of toxin in food. There are 7 types of C botulinum, differentiated on the antigenic specificity of the toxins: A, B, C1, D, E, F, and G. Types A, B, and E are most important in people; C1 in most animal species, notably wild ducks, pheasants, chickens, mink, cattle, and horses; and D in cattle. Only 2 outbreaks, both in humans, are known to have been caused by type F. Type G, which was isolated from soil in Argentina, is not known to have been involved in any outbreak of botulism either in humans or other animals. 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, explaining some of the species differences in susceptibility to the different 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 are lost in most years, with losses reaching 1 million or more during the great outbreaks in the western USA. Most affected birds are ducks, although loons, mergansers, geese, and gulls also are susceptible. (See also
botulism in poultry, see Botulism.) Dogs, cats, and pigs are comparatively resistant to all types of botulinum toxin when administered orally.
Most botulism in cattle occurs in South Africa, 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 that they find on the range; if these came from an animal that had been 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 USA, although a few cases have been reported from Texas under the name of 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 been encountered 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.
Toxicoinfectious botulism is the name 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 USA. Toxicoinfection is also suggested as a cause of equine grass sickness (equine dysautonomia, see Dysautonomia: Equine Dysautonomia).
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 incriminated.
Clinical Findings and Lesions
The signs of botulism are caused by flaccid muscle paralysis and include progressive motor paralysis, disturbed vision, difficulty in chewing and swallowing, and generalized progressive weakness. Death is usually due to respiratory or cardiac paralysis. The toxin prevents release of acetylcholine at motor endplates (the 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 hr 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 (see Disorders of Calcium Metabolism: Parturient Paresis in Cows), but the cows do not respond to calcium therapy.
In the shaker foal syndrome, foals are usually <4 wk old. They may be found dead without premonitory signs; most often, they exhibit signs of progressive symmetric motor paralysis. Stilted gait, muscular tremors, and the inability to stand for >4–5 min are salient features. Other clinical signs include dysphagia, constipation, mydriasis, and frequent urination. As the disease progresses, dyspnea with extension of the head and neck, tachycardia, and respiratory arrest occur. Death ensues most often 24–72 hr 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.
Although sporadic cases of botulism often are suspected because of the characteristic motor paralysis, it is sometimes difficult to establish the diagnosis by demonstrating the toxin in animal tissues or sera or in the suspect feed. Commonly, the diagnosis is made by eliminating other causes of motor paralysis. Filtrates of the stomach and intestinal contents should be tested for toxicity in mice, but a negative answer is unreliable. Primary supportive evidence is provided by feeding suspect material to susceptible animals. In peracute cases, the toxin may be detectable in the blood by mouse inoculation tests but usually is not detectable in the average field case in farm animals. Use of ELISA methodology for detection of the toxin makes it feasible to test large numbers of samples, increasing the chances of diagnosis confirmation. In toxicoinfectious botulism, the organism may be cultured from tissues of affected animals.
Treatment and Control
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 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 patients. In endemic areas (eg, Kentucky), vaccination with type B toxoid appears to be effective.
Last full review/revision March 2012 by Henry R. Stämpfli, DVM, DrMedVet, DACVIM