Botulism is a disease caused by the ingestion of a toxin produced by the Clostridium botulinum bacterium. All domestic fowl and most wild birds are susceptible to the toxin’s effects. Many human deaths have also been attributed to the consumption of food or water containing the toxin.

Botulism is not a bacterial infection, but a condition produced by a byproduct of the bacteria’s growth. The organism is common in nature and is widely dispersed in soils. Ingestion of the organism is not harmful. It becomes dangerous only when conditions are favorable for its growth and subsequent toxin formation. The organism grows best under high humidity and relatively high temperature and in an environment containing decaying organic material (plant or animal). The organism requires an environment in which all atmospheric oxygen is eliminated. The organism cannot multiply in the presence of air. Stagnant pools or damp areas with buried decaying matter are danger areas for toxin development. Botulism results after the decaying animal or plant material containing the toxin is consumed. Decaying carcasses are a frequent source of the toxin, as are many insects feeding in the same tissue. The insects may contain enough toxin to cause the disease in any bird that ingests it. Since the toxin is water soluble, water sources may become contaminated and provide a reservoir for the disease.

The toxin is one of the most potent discovered by scientists. The toxin is relatively heat stable but may be destroyed by boiling. There are different types of the toxin; types A and C cause the disease in birds while type B frequently produces the disease in man.

Weakness is generally the first sign of the illness and is followed by progressive flaccid paralysis of the legs, wings and neck. When neck muscles are affected the head hangs limp, thus causing a condition referred to as “limberneck”. Affected birds may have a peculiar trembling, loose feathers that are pulled out easily and dull partly closed eyes. Some birds (turkey) do not develop loose feathers or limberneck symptoms. Because of the paralysis, birds are unable to swallow and mucous accumulates in the mouth. Fatally affected birds may lie in a profound coma appearing lifeless for several hours before death. Significant lesions are not usually observed in affected birds. Examining digestive contents may reveal insects, decomposed animal or vegetable material or other matter suggesting that the birds have consumed the toxin.

A tentative diagnosis can be made from the history, symptoms and post-mortem findings. As an aid to diagnosis, sick birds may be given water into the crop, kept in a cool environment and treated intravenously with antitoxin. Recovery of a large percentage of the affected birds would substantiate diagnosis.

Prevention should be aimed at eliminating sources of toxin production and preventing access of birds to such materials. These practices include prompt removal of all dead animals from houses and pens, debeaking the birds, controlling fly and insect populations and avoiding access to decaying organic material. Contaminated water supplies are particularly dangerous.

If the disease strikes, locate and remove the source of the toxin and separate all visibly affected birds from the flock for treatment. Place sick birds in a cool shaded area and give fresh water into the crop, twice daily. Mild laxatives may be used for birds that have been exposed but do not show disease symptoms. Epsom salts (one pound per 100 birds) may be mixed into feed. Adding a level teaspoonful of Epsom salts in one ounce of water and placing in the crops of sick birds has been beneficial in many instances. Antitoxin therapy is indicated only in birds that have high individual value since the antitoxin is difficult to obtain and is expensive.

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