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Environmental Characteristics Associated with the Occurrence of Avian Botulism in Wetlands of a Northern California Refuge


Since the early 1900s, Type C avian botulism has caused the largest disease losses known to occur in North American waterfowl, killing tens of thousands to millions of birds in a single outbreak (Locke and Friend 1987). During the last 5 years, losses from botulism outbreaks in several U.S. and Canadian wetlands have been estimated in the millions (National Wildlife Health Center [NWHC], unpublished data). Avian botulism is a paralytic disease of birds resulting from ingestion of neurotoxin produced by the bacterium, Clostridium botulinum, Type C. This bacterium is a strict anaerobe that forms dormant spores in aerobic or other adverse environmental conditions. Dormant spores are resistant to heating and drying, can remain viable for years, and are widely distributed in wetland sediments (Mitchell and Rosendal 1987). C. botulinum spores can also be found in the tissues of many wetland inhabitants (Jensen and Allen 1960), such as aquatic insects, mollusks and crustacea, birds, and other vertebrates (Reed and Rocke 1992). Botulinum toxin is produced only when environmental conditions are suitable for spore germination and cell growth.

Despite the widespread distribution of spores of C. botulinum Type C, outbreaks of avian botulism in waterbirds are sporadic and unpredictable, occurring annually in some wetlands, but not in adjacent wetlands. Several ecological factors are thought to play a critical role in the timing and location of outbreaks by favoring spore germination and bacterial replication, providing a suitable energy source or substrate for bacterial growth and toxin production, and a means to transfer the toxin from the substrate to birds. Toxin is presumably transferred to waterfowl via invertebrates consumed as food or incidentally while feeding on other food items. The most suitable conditions for bacterial growth and toxin production in wetlands and the ecological features that precipitate outbreaks are unclear. For many years, avian botulism was thought to occur in shallow, stagnant waters with low dissolved oxygen, alkaline wetlands, and when mud flats were flooded or drained during warm summer months (Kalmbach and Gunderson 1934, Quortrup and Holt 1941, Bell et al. 1955, Rosen 1971). However, these conditions do not adequately characterize the timing and location of many botulism outbreaks in wetlands with deep, well-oxygenated water and stable water levels, or outbreaks that occur in late winter or spring.

From 1987–89, we conducted studies on the occurrence of avian botulism in several wetlands at SNWR. Our objectives were: (1) monitor the occurrence and severity of botulism mortality in captive-reared mallards placed as sentinels in wetland enclosures; (2) compare specific environmental characteristics, including invertebrate populations and sediment and water conditions, between wetland enclosures in outbreak wetlands and in nonoutbreak wetlands; (3) determine if botulism outbreaks in sentinel birds were associated with temporal changes in environmental characteristics in wetland enclosures; and (4) correlate environmental characteristics with botulism mortality rates in sentinel mallards.

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