Botulism is an intoxication caused by ingesting Clostridium botulinum exotoxin or by absorbing toxin produced in the alimentary tract (toxico-infection). Between 1910 and 1997, 4,881,000 waterfowl, primarily ducks, are known to have drowned due to loss of motor control and ensuing paralysis of the neck caused by botulism. Deaths occurred in Europe, North America, Australia, Sweden, Denmark, Great Britain, New Zealand, the Netherlands, Japan, Russia, Argentina, and Brazil. Avian botulism has been found in 28 countries, and there is concern that endangered species may be lost. (Also see Clostridial Diseases: Botulism.)
C botulinum is a gram-positive, sporeforming, anaerobic bacterium that inhabits soils and marine and freshwater sediments. It is commonly found in the gut of poultry and wild birds and in litter, feed, and water in broiler chicken houses. Intoxications are sporadic in poultry, but massive mortality has occurred in waterfowl in western North America. Outbreaks in poultry and waterfowl are predominately caused by type C toxin, and types A and E are less frequently incriminated.
Type C intoxications are found in chickens, turkeys, ducks, and pheasants. However, the disease has been identified in 117 species of feral birds representing 22 families. Mammalian species affected by type C toxin include mink, ferrets, cattle, pigs, dogs, horses, laboratory rodents, and various zoo animals. Botulism was reported in ruminants fed poultry manure contaminated with C botulinum type C spores.
Transmission, Epidemiology, and Pathogenesis
Ingested preformed toxin, absorbed into the blood, binds to nerve terminals and blocks release of acetylcholine. The result is flaccid muscle paralysis. Death is due to cardiac and respiratory arrest.
Toxin is elaborated in dead carcasses after postmortem release of the organism from the gut. Maggots acquire toxin from carcass tissues and, when eaten by scavenging poultry, serve as a source of neurotoxin. Alternatively, if toxin levels are sufficiently high in carcass tissues, cannibalism can initiate disease. Other feed sources have been implicated in outbreaks in backyard poultry flocks. Botulism in waterfowl may result after ingesting dead invertebrates found in water that contains decaying vegetation.
Toxico-infectious botulism is reported to occur in intensively reared broiler flocks housed on litter. Mortality may range from a few birds to 40% of a flock. The conditions that allow toxin elaboration in the alimentary tract are not clearly understood because C botulinum can be recovered from normal chickens on farms without histories of outbreaks. However, two outbreaks of type C botulism in commercial broiler flocks were associated with elevated iron content from feed and water sources. Iron promotes the proliferation of enteric bacteria, including C botulinum.
Clinical signs in poultry and wild birds are similar. Flaccid paralysis of the legs, wings, neck, and eyelids is seen. Paralytic signs progress cranially from the legs to include the wings, neck, and eyelids. “Limberneck,” the common name of botulism, describes neck paralysis. In affected waterfowl, neck paralysis can lead to drowning. Affected chickens have ruffled feathers. Signs in broiler chickens may also include diarrhea with excess urates in the loose droppings.
No characteristic gross lesions develop.
Definitive diagnosis requires demonstration of the toxin in serum, liver homogenates, or crop or GI washings from sick birds. Mice injected with samples of such material become paralyzed and die unless protected with specific typing serum.
Leg paralysis is the only sign in mild intoxications, which must be differentiated from Marek's disease, drug and chemical toxicities, or appendicular skeletal problems. In waterfowl, botulism must be differentiated from fowl cholera and chemical toxicities, especially lead poisoning.
Treatment and Prevention
Affected birds may recover without treatment. Numerous treatments have been reported, including use of bacitracin (100 g/ton in feed) or streptomycin (1 g/L in water), but none have been uniformly successful.
Collection and disposal of dead birds is important in preventing and limiting outbreaks, especially in pheasant and broiler chicken flocks. Fly control may reduce the risk of toxic maggots in the environment. Some, but not all, recurrent outbreaks in broiler flocks may be prevented by cleaning and disinfecting with products effective against spore-forming bacteria. Disinfection around poultry houses is suggested because spores are found outside the houses and can be reintroduced into housing. Litter treatments, although not always effective, have included sodium bisulfate at 1 lb/1,000 sq ft (1 kg/200 m2). In waterfowl outbreaks, ducks should be dispersed from affected areas and water levels stabilized. Elimination of large shallow areas may prevent conditions favorable for decay of vegetation and die-off of invertebrates.
Active immunization with inactivated type C bacterin-toxoids has been successful in pheasant operations but is not cost effective in commercial chickens and wild ducks. Treatment with type-specific antitoxin is effective but not practical.
The zoonotic potential of type C botulism is minimal. Only 4 poorly documented type C botulism intoxications have been reported in people, but cases have occurred in nonhuman primates.
Last full review/revision March 2012 by John E. Dohms, PhD