Making wetlands safe from avian botulism.

More and more birds are dying of avian botulism, the most serious disease of wetland bird species. Wetland managers have few good strategies for combating the threat, but they may soon have some effective weapons against the toxin that causes the disease, says animal disease specialist Tonie E. Rocke.

Rocke and her colleagues at the National Wildlife Health Research Center in Madison, Wis., have developed new genetic techniques for studying the botulism toxin, and they report new findings on the importance of salinity and pH in the life of the poison.

A problem worldwide, avian botulism kills hundreds of thousands of birds, including zoo animals, every year in the United States alone. A single outbreak in Russia in 1981 killed more than 1 million birds. The botulism toxin acts by disrupting the nervous system and causing paralysis.

During the last 5 years, Rocke and her colleagues have compared 31 wetlands in the United States where botulism outbreaks have occurred and similar locations where they haven't. She reported the results at the American Society of Zoologists meeting last week in Washington, D. C.

The scientists found that the risk of a botulism outbreak peaks when wetlands have a relatively neutral pH-between 7 and 8 for soil and between 7.5 and 8.5 for water. Also, the risk of botulism decreases when wetlands are salty.

A virus carries the gene that codes for the botulism toxin, but the virus must enter an anaerobic bacterium, Clostridium botulinum, in order to produce the toxin. Most soil and many wetland inhabitants carry the bacterium, but it often remains dormant until, for example, an animal dies and its tissue becomes anaerobic. Birds may get sick after ingesting insects that obtained the toxin by eating carrion.

Laboratory studies suggest that C. botulinum grows best in neutral pH conditions and that the gene-carrying virus is sensitive to salt, Rocke says. But the researchers have yet to determine whether pH and salinity alter toxin production. Salinity and pH may, for example, change the behavior of insects carrying the toxin or influence the populations of bacteria that compete with C. botulinum.

The team has recently developed genetic tools to help untangle the relationship between soil and water conditions and toxin production. Using a technique for amplifying DNA segments, Rocke and her colleagues can now detect the gene responsible for the toxin. They are also developing methods for determining whether the gene is producing the poison.

To help prevent outbreaks, the group is planning to explore how managers might change the pH and salinity of wetlands. Rocke wouldn't recommend adding chemicals to a wetland but might suggest instead encouraging different vegetation to grow or managing existing vegetation differently.

"We don't understand what factors are conducive to outbreaks . . . so the kind of work [Rocke] is doing is really important," says Mary Ann Ottinger of the University of Maryland in College Park.