Botulism is a food poisoning caused by the ingestion of the toxin produced by the bacterium Clostridium botulinum of any of six strains, designated A through F. The disease, as it occurs in epidemic proportion in wild birds, is most commonly of the C type, although outbreaks caused by type E botulism have been observed on the Great Lakes.

C. botulinum is a widely distributed anaerobic bacterium which is capable of existence for many years in spore form. Its vegetative cells grow and synthesize toxin, whenever and wherever the proper conditions exist in their environment. Outbreaks of botulism occur when aquatic birds consume this toxin which has been preformed in their food. Botulism is, therefore, an intoxication rather than an infection and is not a contagious disease. Botulism can be diagnosed conclusively only by demonstration of the toxin in the blood or serum of live affected birds, and a diagnostic laboratory should be contacted to confirm field diagnoses. A conclusive diagnosis cannot be reached by demonstrating the toxin or the organism in dead animals.

The 'microenvironment concept' assumes that C. botulinum produces toxin in small, discrete, particulate food items which provide the requirements for growth of the bacteria independent of the surrounding wetland environment and which protect the toxin from dilution or inactivation. Optimum conditions for C. botulinum growth and toxin production include the absence of oxygen, a temperature of 76 deg. to 98 deg. F and suitable organic media, especially those composed of animal protein. Such conditions may be met in decaying invertebrate carcasses even though external conditions are unfavorable for toxin production. Vertebrate carcasses also may provide suitable conditions for the production of toxin, and maggots collected from duck carcasses during botulism outbreaks frequently contain extremely high levels of toxin. In determining the specific source of toxin and recommending control measures in the dynamic, complex, and diverse conditions of specific wetland ecosystem where botulism occurs, one's conclusions must necessarily become more speculative. Possibilities for reducing waterfowl losses due to botulism--Complete elimination of the causative organism, C. botulinum, from the wetland ecosystem is neither practical nor possible. Control methods may sometimes be profitably directed at prevention of toxin production, and the quantity of suitable media can be influenced. Rising water levels may drown terrestrial invertebrates, or flood vegetation thereby releasing nutrients which stimulate the increase in aquatic invertebrate populations to unstable levels which collapse. In other situations decreasing water levels may increase the numbers of invertebrate carcasses by increasing water temperatures or salinity which had been marginal for survival of previously thriving invertebrate populations or by stranding invertebrates on mud flats subject to periodic wind flooding. Therefore, a basic and important step in controlling botulism is stabilization of the wetland ecosystem in order to avoid the accumulation of decaying animal protein, especially during periods when temperatures are favorable for toxin production in these media. This can sometimes be accomplished by water level manipulation.

If toxin production cannot be controlled by reducing the quantity of suitable media, another step is to prevent the ingestion of the toxic food items. Birds may be chased or lured from areas of toxin source or areas can be made less attractive by rapid and complete drainage, or draw down to a stable shoreline, where wind flooding does not occur. Removal of vertebrate carcasses, especially those of birds dying during the outbreak, reduces the availability of toxic maggots but carcass removal must be carried out frequently and diligently.Prevention of the effects of the toxin can be accomplished in some instances. Some degree of active immunity can be produced by injections of specific toxoi