Identifying & Treating Avian Botulism
Avian botulism is a paralytic disease caused by ingestion of a toxin produced by the bacterium Clostridium botulinum - an anaerobic, Gram positive, spore-forming rod. It acts by blocking nerve function and leads to respiratory and musculoskeletal paralysis.
In all cases, illness is caused by the toxin made by C. botulinum, not by the bacterium itself. There are several types of toxin produced by strains of this bacteria with birds being most commonly affected by type C and to a lesser extent type E.
This bacteria is widespread in soil and requires warm temperatures, a protein source and an anaerobic (no oxygen) environment in order to become active and produce toxin.
Decomposing vegetation and invertebrates (i.e., insects) combined with warm temperatures can provide ideal conditions for the botulism bacteria to activate and produce toxin.
Birds either ingest the toxin directly or may eat invertebrates (e.g. chironomids, fly larvae) containing the toxin. Invertebrates are not affected by the toxin and store it in their body. A cycle develops in a botulism outbreak when fly larvae (maggots), feed on animal carcasses and ingest toxin. Ducks that consume toxin-laden maggots can develop botulism after eating as few as 3 or 4 maggots.
- Foodborne botulism results from contaminated foodstuffs in which C. botulinum spores have been allowed to germinate.
- Wound botulism results from the contamination of a wound with the bacteria, which then secrete the toxin into the bloodstream.
- Inhalation: Isolated cases of botulism have been described after inhalation.
Fowls, turkeys, water fowl, pheasants and also most wild birds are susceptible. Death from botulism is common in waterfowl; an estimated 10 to 100 thousand birds die of botulism annually. In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. Botulism also affects commercially raised poultry. Carrion-eating birds, such as vultures, can withstand large doses of the toxin without showing any symptoms.
Botulism occurs sporadically in domestic poultry / fowl, particularly commercially raised poultry raised under conditions where hygiene is poor and where birds have access to rotting carcasses or other contaminated or decaying material. It also occurs occasionally in wild birds particularly if they are feeding in stagnant water holes. Botulism is usually more common in the warmer months. In chickens, the mortality rate varies from a few birds to 40% of the flock. Some affected birds may recover without treatment.
Clinical Signs/Field Signs
The pattern of damage occurs because the toxin affects nerves that are firing more often. For example, the inhibition of the release of Acetylcholine from motor neurons results in a loss of muscle function and paralysis. In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck (twisting) and eyelids. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess urates and respiratory problems.
Healthy birds, affected birds, and dead birds in various stages of decay are commonly found in the same area.
Consequently, birds are unable to use their wings and legs normally or control the third eyelid, neck muscles, and other muscles. Birds with paralyzed neck muscles cannot hold their heads up and often drown. Death can also result from water deprivation, electrolyte imbalance, respiratory failure, or predation.
Diagnosis of botulism is based on demonstration of the toxin in serum from sick birds, or tissue samples from dead birds such as clotted heart blood, stomach contents or liver.
Treatment / Recovery:
Birds which live through 48 hours of illness usually recover.
At this time, there are two primary Botulinum Antitoxins available for treatment of wound and food borne botulism:
Trivalent (A,B,E) Botulinum Antitoxin - derived from equine sources utilizing whole antibodies (Fab & Fc portions). This antitoxin is available from the local health department via the CDC.
Heptavalent (A,B,C,D,E,F,G) Botulinum Antitoxin - derived from "depreciated" equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This is a less immunogenic* antitoxin that is effective against all known strains of botulism where not contraindicated. (*Immunogenicity is the ability of a particular substance to provoke an immune response.)
Under favourable environmental conditions - access to clean water, fair weather conditions and no predation - birds can recover from low doses of the toxin without treatment. Birds that do recover from avian botulism do not show any increased tolerance for the poison and are not resistant to subsequent exposures. There is some evidence that birds may be protected for short periods of time with a vaccine.
The following cause of action is recommended:
- Sick birds should be isolated and provided with food and water.
- Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria.
- Good supportive care with antibiotics and vitamins has been helpful in some cases.
- Remove the source of the toxin. Keep birds away from suspect sources that cannot be removed.
- Remove dead birds, supply clean feed and water, clean up around stagnant pools and ensure that all feed is fed in containers and not on the ground.
- The toxin is also found in maggots and litter beetles so these must also be controlled