Ecology and Management of Avian Botulism on the Canadian Prairies

88birds <strong>and</strong> toxic material, C, <strong>and</strong> proportion <strong>of</strong> contacts resulting in intoxication <strong>and</strong> death, P i(Wobeser 1997a). If R o >1, then a botulism outbreak may occur (Wobeser 1997a). For example,during the week prior to the first detected cases <strong>of</strong> botulism in 2001, HY FG carcasses had a0.9 (9/10) probability (P m ) <strong>of</strong> developing maggots, which had a 0.67 (6/9) probability (P tox ) <strong>of</strong>containing toxin (see Table 5, trial initiated 30 June 2001). R o for HY FG carcasses wastherefore (0.9)(0.67)(β) or 0.6β, hence for R o to be >1, β was >1.7. If each contact resulted indeath, >1.7 contacts per HY FG carcass (on average) would have been required to initiate abotulism outbreak in 2001. Contact rate was likely high during the week prior to botulism in2001 because there was approximately 93 kg <strong>of</strong> toxic maggot-laden carcass material from HYFGs within the colony (estimated using the product <strong>of</strong> adjusted carcass density[4.6 carcasses/ha], mean carcass mass [214 g/carcass], P m [0.9], P tox [0.67], <strong>and</strong> colony area[156 ha]), concurrent with a high density <strong>of</strong> susceptible birds.For a given lake <strong>and</strong> population density <strong>of</strong> susceptible birds, there may be a ‘threshold’ carcassdensity, below which botulism outbreaks are unlikely to occur. We could not assess this becausea botulism outbreak (preceded by high FG carcass density) occurred every year <strong>of</strong> this study. Ifcarcass density is a key factor initiating botulism outbreaks, attempts should be made toinvestigate the relationship between population density <strong>and</strong> the density <strong>of</strong> toxic material (hencetaking into account P m , P tox , <strong>and</strong> carcass mass). Other factors such as aquatic invertebrateabundance, temperature, redox potential, pH, <strong>and</strong> salinity should be considered; however, furtherresearch is required to evaluate their relationship with density <strong>of</strong> toxic material, or the effects <strong>of</strong>abiotic factors on P m <strong>and</strong> P tox .Temperature is important in the ecology <strong>of</strong> botulism outbreaks because it influences C.botulinum type C proliferation <strong>and</strong> toxigenesis, as well as blowfly (Calliphora spp.) activity.Optimal temperatures for proliferation <strong>and</strong> toxigenesis are >30 C (Cato et al. 1986; Smith <strong>and</strong>Turner 1987); however, low levels <strong>of</strong> toxin production may occur at 12.5 C (Haagsma 1973). Inthe current study, gull carcasses were 22.2 times more likely to develop maggots when averagewater temperature was ≥20 C than when it was