Avian Botulism Epizootiology on Sewage Oxidation Ponds in Utah1

In the microenvironment concept of avian botulism epizootiology, it is hypothesized that invertebrate carcasses may serve both as a substrate for toxin production by Clostridium botulinum type C and as a vehicle for toxin transmission to water birds. We field-tested that hypothesis by attempting to induce botulism in wing-clipped mallard ducks (Anas platyrhynchos) on sewage oxidation ponds in Utah. The experimental ponds were inoculated with C. botulinum spores in June 1974. Aquatic insect populations were monitored throughout the summer. Rotenone was used in August to kill insects in two ponds (one served as control), thereby providing potential substrate for clostridial growth and toxin production. Botulism was not detected among the birds even though they routinely ingested invertebrate carcasses. Samples of dead invertebrates contained no botulinum toxin. We concluded that the microenvironment concept, as it now stands, cannot always be a sufficient explanation of how type C botulism epizootics are initiated in nature. Other microbes may inhibit the growth of clostridial cells or destroy botulinum toxin. J. WILDL. MANAGE. 40(4):735-742 Avian botulism has been recognized as a significant cause of waterfowl mortality in North America for at least 60 years (Wetmore 1915). The etiology of the disease was defined nearly 50 years ago (Giltner and Couch 1930, Kalmbach 1930). The ecology of the disease, including the natural substrates used by C. botulinum type C for growth and toxin production and the natural modes of toxin transmission to birds, has yet to be defined clearly. Research on avian botulism has been reviewed extensively by several authors (Sciple 1953, Kalmbach 1968, Rosen 1971, Enright 1971). Studies designed to delineate the epizootiology of type C botulism have been few. Kalmbach and Gunderson (1934) originally suggested that aquatic invertebrate carcasses might serve both as a substrate for toxin produc1 A contribution of the Utah Cooperative Wildlife Research Unit: Utah State University, U.S. Fish and Wildlife Service, Utah Division of Wildlife Resources, and the Wildlife Management Institute, cooperating. 2 Present address: Department of Entomology, Fisheries, and Wildlife, University of Minnesota, St. Paul 55108. tion and as a vehicle for toxin transmission to birds. This hypothesis was supported and elaborated by the microenvironment concept of Bell et al. (1955:353), which stated: "(1) that C. botulinum type C germinates, reproduces, and synthesizes its toxin in small discrete particulate substances, possibly invertebrate carcasses; (2) that the particulate substances are in no wise dependent upon the ambient medium for nurture of the bacteria, but contain all of the requisites within them; and (3) that the toxin is probably in the bacteria which reside in the particulate materials, rather than in the form of soluble, freely diffused toxin." The microenvironment concept has become the generally accepted, but inadequately tested, working hypothesis of type C botulism epizootiology (Enright 1971). The objective of this study was to fieldtest the microenvironment hypothesis of type C botulism epizootiology. We attempted to induce botulism in wing-clipped flocks of mallard ducks on sewage oxidation ponds in Utah. The ponds represented newly created aquatic habitats supporting abundant aquatic insect populations, a poJ. Wildl. Manage. 40(4): 1976 735 736 AVIAN BOTULISM EPIZOOTIOLOGY * Moulton et al.