Experimental Avian Botulism Studies on Sewage Oxidation Ponds in Utah

The objective of this study was to field-test the microenvironment concept of avian botulism epizootiology. The microenvironment concept hypothesizes that aquatic invertebrate carcasses may serve both as a substrate for toxin production by Clostridium botulinum type C in nature and as a vehicle for toxin transmission to waterbirds. This concept has become the generally accepted, but inadequately tested, working hypothesis of type C botulism epizootiology. This study attempted to experimentally induce type C botulism in sentinel flocks of mallard ducks (Anas platyrhynchos) and American coots (Fulica americana) on sewage oxidation ponds in northern Utah. The three experimental oxidation ponds were inoculated with Cl. botulinum type C (strain X220B2) endospores in June, 1974. Aquatic invertebrate populations were monitored throughout the summer. Rotenone was used in August in two of the experimental ponds (one pond served as a control) to kill aquatic invertebrates and thereby provide a large amount of substrate for clostridial growth and toxin production. No botulism was detected among the sentinel birds even though they routinely ingested invertebrate carcasses. None of the samples of dead invertebrates collected from the experimental ponds contained detectable (in white mice) botulinum toxin. It was 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. Microbiological experiments designed to determine why the invertebrate carcasses collected from the study ponds contained no botulinum toxin were started and are now ongoing. Early results indicate that Cl. botulinum (X220B2) cells may not normally be able to effectively compete (at least in terms of toxin production) with other microorganisms present in the sewage ponds. It is suggested that the initiation of a type C botulism epizootic in nature may require the alleviation of the inhibitory effects of other putrefactive microorganisms upon clostridial metabolism and/ or toxin. This hypothesis is highly speculative and requires much further experimentation