Ecology and Management of Avian Botulism on the Canadian Prairies

102seasonal wetl<strong>and</strong>s. Williamson et al. (1999) found the toxin gene in 16 <strong>of</strong> 18 wetl<strong>and</strong> sediments<strong>and</strong> confirmed its presence in both outbreak <strong>and</strong> non-outbreak wetl<strong>and</strong>s. However, the botulismhistory for non-outbreak marshes was not given, <strong>and</strong> too few samples were analyzed fromindividual wetl<strong>and</strong>s to make comparisons among them.Wobeser (1997) proposed a simple model to account for transfer <strong>of</strong> toxin to susceptible hosts.Making an analogy to infectious diseases, he suggested that the basic reproductive rate (R; theaverage number <strong>of</strong> secondary infections arising from a single infection in a naïve population)could be used to describe the number <strong>of</strong> secondary intoxications attributed to a single carcass as:R = M 2 /M 1 ,where M 2 is the number <strong>of</strong> individuals dying <strong>of</strong> secondary intoxications arising from M 1, <strong>and</strong> M 1is the number <strong>of</strong> carcasses on a wetl<strong>and</strong>. Disease incidence increases if R > 1, whereas itdeclines if R < 1. Furthermore, M 2 was defined as:M 2 = M 1 (P s )(P m )(β),where P s is the proportion <strong>of</strong> carcasses that contain spores <strong>of</strong> toxigenic C. botulinum, <strong>and</strong> P m isthe proportion <strong>of</strong> carcasses that become infested with maggots <strong>and</strong> persist until toxin-ladenmaggots emerge. The β term is an intoxication coefficient that consists <strong>of</strong> two components: 1)the frequency <strong>of</strong> contacts between live birds <strong>and</strong> toxic material (C) <strong>and</strong> 2) the proportion <strong>of</strong> suchcontacts that result in intoxication (P i ). In this model, the proportion <strong>of</strong> carcasses that containspores is a key determinant <strong>of</strong> botulism outbreaks.Our objectives were to determine: 1) whether the prevalence <strong>of</strong> toxin-laden carcasses <strong>and</strong> levels<strong>of</strong> toxin varied among wetl<strong>and</strong>s, during botulism outbreaks <strong>and</strong> between years, <strong>and</strong> 2) if, duringan outbreak, birds that died <strong>of</strong> botulism had a higher probability <strong>of</strong> producing type C than birdsthat died for other reasons (e.g., gunshot). This would suggest that the bacterium is“transmitted” along with the toxin, leading to further objectives to determine: 3) whether ducksfrom wetl<strong>and</strong>s with a previous history <strong>of</strong> botulism were more likely to produce type C toxin th<strong>and</strong>ucks from wetl<strong>and</strong>s with no previous history <strong>of</strong> botulism (i.e., whether the bacterium isacquired locally) <strong>and</strong> 4) the role that factors such as P S <strong>and</strong> P M play in determining theoccurrence <strong>of</strong> botulism outbreaks <strong>and</strong> survival <strong>of</strong> waterfowl.METHODSWork was conducted from 1999 to 2003 at wetl<strong>and</strong>s or lakes on the Canadian Prairies. Allwetl<strong>and</strong>s provided habitat for dabbling ducks during the summer months <strong>and</strong> were used tovarying degrees for brood rearing, moulting <strong>and</strong> migration. They were chosen because they hadsufficient numbers <strong>of</strong> ducks for our sampling efforts <strong>and</strong> because they were subjected to ongoingmonitoring, which enabled us to determine if they had previously experienced botulismoutbreaks. From 1999 to 2001 inclusive, this research was part <strong>of</strong> a larger study evaluatingaspects <strong>of</strong> botulism management <strong>and</strong> impacts, including clean-up efficiency, estimating