Synonyms
Limber neck, bulbar paralysis, western duck sickness, alkali disease.
Aetiology
The toxin of clostridium botulism. This bacterium(Clostridium botulinum) is a spore forming, gram positive bacterium capable of elaborating potent exotoxins under appropriate environmental conditions. The species consist of a diverse groups of bacteria in 8 antigenically different groupings A, B, C alpha, C beta, D, E, F and G. Human disease is caused by types A, B, E, F while A, C, E cause disease in birds. Cases of botulism in poultry have been caused in natural setting by type C. The organism is naturally common and is widely disseminated in the soils. Ingestion of the organism is not harmful. It becomes dangerous only when conditions are supportive for its growth and consequent toxin formation. The organism grows best under relatively high temperature and high humidity and in an environment that contains decaying organic material(plant or animal) for example carcasses and plant waste, and material that contains toxin(such as carcasses maggots, pond-mud) is consumed by the birds. Toxin may be formed by the bacteria in the caecum.
Age/host species affected
All fowls of any age. Botulism is common in wild ducks and is frequent killer of waterfowl, humans and other animals are highly susceptible. The vulture is the only animal host to be resistant to the disease.
Transmission
Eating of spoiled food, decaying bird carcasses on poultry houses, pens, wet litter or other organic substance and fly maggots from decaying substances harbouring a neurotoxin formed by the Clostridium botulinum leads to botulism.
Morbidity and mortality
Morbidity and mortality is usually low when low levels of the toxin are ingested but mortality is high up to 40% in severe cases. Mortality in waterfowl and pheasants and other game birds are very high.
Clinical signs
Incubation periods are dose related. With high levels of the toxin, the disease appears within few hours, with low toxin doses, onset of paralysis occurs within 1-2 days.
Clinical signs include the following;
Nervous signs, weakness
Progressive flaccid paralysis of legs, wings, neck and eyelids are the most common clinical sign; this paralysis progress cranially from legs to include wings, neck and eyelids.
Droopy wings and limber neck
Because of the eyelid paralysis, birds appear comatose, prostration and death follow in 12 to 24 hours. Respiratory muscle paralysis leads to death.
Ruffled feathers which may fall out with handling.
Diarrhea with excess urates in loose droppings.
Post-mortem lesions
Possibly, no significant lesions except maggots or decayed ingesta may be found in the crop.
Diagnosis
Tentative diagnosis is by clinical history, clinical signs and lack of post-mortem lesions.
Mouse toxicology on serum or extract of intestinal contents: groups of mice are inoculated with the suspected serum or extract; a group received samples treated with type specific antiserum while other group was not treated with the antiserum. If toxin is present, the untreated group will show signs of disease within 48 hours while the treated group will be protected.
Isolation of the Clostridium botulinum in an anaerobic culture is confirmatory.
Differential diagnosis
Epidemic tremor
Treatment
Remove the source of toxin such as spoiled food or decaying matter.
Flush the flock with Epsom salts(1 Ib/1000 hens) in water or in wet marsh.
It has been reported that potassium permanganate(1:3000) in the drinking water is helpful.
Prevention
Preventing access to toxin, suspected food and stagnant ponds especially in hot weather.
The most significant measure is careful pick-up and removal of all dead birds on a daily basis. Incinerate or bury dead birds promptly. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread.
Control flies.
Vaccination with inactivated bacterin-toxoids has been successfully used in pheasants, chickens and ducks.