Ecology and Management of Avian Botulism on the Canadian Prairies

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4(Coburn <strong>and</strong> Quortrup 1938; Bell et al. 1955). In the absence <strong>of</strong> these conditions, a reversion tothe spore form occurs. Vegetative growth can also be inhibited by other factors that are not wellunderstood. How these limiting factors might apply to type C C. botulinum growth in differentsubstrates, such as within carcasses, is also largely unknown.<strong>Botulism</strong> in wetl<strong>and</strong>s <strong>and</strong> waterfowlType C C. botulinum spores are readily available in wetl<strong>and</strong>s, <strong>and</strong> a wide range <strong>of</strong> wildlifespecies ingest them continuously. Spores have been detected in the liver <strong>of</strong> birds not affectedwith botulism (Gunderson 1933), as well as in the intestines <strong>of</strong> fish (Itoh et al. 1978) <strong>and</strong> withinthe liver <strong>and</strong> intestines <strong>of</strong> healthy mallards (Anas platyrhynchos) (Reed <strong>and</strong> Rocke 1992). Thefrequency <strong>of</strong> occurrence, as well as the density <strong>and</strong> residency time <strong>of</strong> spores in different animals,have not been established; nor has the relationship between the prevalence <strong>of</strong> spores in theenvironment <strong>and</strong> the prevalence <strong>of</strong> spores in animals.When an animal with spores in its gut or tissue dies, its carcass becomes anaerobic <strong>and</strong> its tissuesare invaded by C. botulinum spores, which then begin vegetative growth <strong>and</strong> toxin production ifconditions are favourable (Smith <strong>and</strong> Turner 1987). This process <strong>of</strong> toxin development has beenreproduced in various insects, birds, <strong>and</strong> mammals (Hunter 1970; Notermans et al. 1980; Reed<strong>and</strong> Rocke 1992). Vertebrate carcasses tend to support particularly high levels <strong>of</strong> C. botulinumtoxin production; mostly likely because they provide a large amount <strong>of</strong> suitable substrate, a selfcontainedmicroenvironment, <strong>and</strong> high temperatures that are optimal for growth <strong>and</strong> toxinproduction (Duncan <strong>and</strong> Jensen 1976; Wobeser <strong>and</strong> Galmut 1984). The amount <strong>of</strong> toxinproduced in different types <strong>of</strong> animal carcasses may vary (Smith <strong>and</strong> Turner 1989), but this hasnot been examined carefully.When the type Cneurotoxin is ingested by abird, it is absorbed intotheir blood <strong>and</strong> binds tospecific receptors on theirmotor neurons. The toxinsthen block the transmission<strong>of</strong> nerve impulses involvedin muscle activation, whichresults in the flaccidparalysis seen in birdsaffected by botulism(Schiavo et al. 1995) (seeleft). Ingestion <strong>of</strong> preformedtoxin is the majorroute <strong>of</strong> botulismintoxication in all wildlifespecies, including wild
5birds. There is no evidence that birds become intoxicated through drinking water, possiblybecause toxins do not reach high enough concentrations in water to cause poisoning. The mostlikely source <strong>of</strong> toxin is toxin-bearing invertebrates, <strong>and</strong> bird species differ markedly in theprobability <strong>of</strong> ingesting these due to differences in feeding behaviour. All birds, with thepossible exception <strong>of</strong> vultures (Kalmbach 1939; Cohen et al. 1969), are susceptible toingested type C neurotoxin, but there is very little information on interspecific differencesin susceptibility.In California, Rocke et al. (1999) determined that certain wetl<strong>and</strong> environmental conditions wereassociated with botulism outbreaks. They found an association, in time, between the occurrence<strong>of</strong> outbreaks <strong>and</strong>: increasing sediment <strong>and</strong> water temperature; increasing abundance or biomass<strong>of</strong> invertebrates; <strong>and</strong> decreasing turbidity. Wetl<strong>and</strong>s with botulism outbreaks also had lowerredox potential than non-outbreak wetl<strong>and</strong>s. In later studies, which were conducted on a largergeographic scale, outbreaks were more likely when water pH was in the 7.5-8.5 range, redoxpotential was negative, <strong>and</strong> temperature exceeded 20 C, although the relationship among thesevariables was complex (Rocke <strong>and</strong> Samuel 1999). How these physiochemical factors mightrelate to bacterial abundance, growth <strong>and</strong> toxin production, as well as the availability <strong>of</strong> toxin tobirds, is unknown.Models <strong>of</strong> botulism ecologyThe most basic conceptual model <strong>of</strong> avian botulism has three components: i) the bacterium,ii) the substrate within which the bacterium grows <strong>and</strong> produces toxin, <strong>and</strong> iii) a population <strong>of</strong>susceptible birds. Each <strong>of</strong> these three components is influenced by many other environmentalfactors, <strong>and</strong> botulism only occurs when all three components are present <strong>and</strong> environmentalconditions are favourable.For example, toxin may beproduced if toxin-producingbacteria <strong>and</strong> substrate arepresent, but the disease won’toccur if birds are absent.Similarly, if the bacterium<strong>and</strong> birds are present butsubstrate is not available forbacterial growth, no toxin willbe formed. In a simpleschematic model, the risk <strong>of</strong>botulism is dependent uponthe overlap among all threecomponents (see right).SubstrateBacteriaBirds<strong>Botulism</strong> occurs inthe area <strong>of</strong> overlapThere are two distinct phases in the ecology <strong>of</strong> botulism: an initiation phase <strong>and</strong> a propagationphase. The basic bacteria-substrate-birds model (see above) applies to both phases, but theydiffer in the type <strong>of</strong> substrate involved. In the initiation phase, any protein-rich organic matter
Page 1: Ecology an
Page 4 and 5: iiThe model of bot
Page 6 and 7: ivTABLE OF CONTENTSEXECUTIVE SUMMAR
Page 8 and 9: 2Research from the 1970s supported
Page 12 and 13: 6could potentially serve as substra
Page 14 and 15: 8additional lakes and</stro
Page 16 and 17: 10challenge because management assu
Page 18 and 19: 12Rocke TE, Bollinger TK. 2007. <st
Page 20 and 21: 14Table 1. Names and</stron
Page 22 and 23: 16PART IEFFICACY OF CARCASS CLEAN-U
Page 24 and 25: 18Our objectives were to determine:
Page 26 and 27: 20marked carcasses potentially avai
Page 28 and 29: 22Intensive search studyOn 18 Augus
Page 30 and 31: 24if extrapolated to Whitewater Lak
Page 32 and 33: 26Table 1. Characteristics
Page 34 and 35: 28Table 3. Number of</stron
Page 36 and 37: 30Table 5. Estimates of</st
Page 38 and 39: Figure 2. Map of W
Page 40 and 41: Figure 4. Variation of</str
Page 42 and 43: 36PART IISURVIVAL OF RADIO-MARKED M
Page 44 and 45: 38two lakes were subjected to carca
Page 46 and 47: 40NecropsiesDead birds were include
Page 48 and 49: 42were right censored. One hundred
Page 50 and 51: 44design, possibly with a treatment
Page 52 and 53: 46Rocke TE, Bollinger TK. 2007. <st
Page 54 and 55: 48Table 2. Models used to assess ef
Page 56 and 57: 50Table 4. Models used to evaluate
Page 58 and 59: 52INTRODUCTIONMaggot-laden carcasse
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54among categories after creating a
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56LITERATURE CITEDBurnham KP, Ander
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58Table 2. Candida
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60PART IVLATE-SUMMER SURVIVAL OF MA
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62In each year of
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64Recovery rate comparisons - 1999D
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66between the present study <strong
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68Table 1. Number of</stron
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70Table 3. Logistic analyses evalua
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72Table 5. Direct recovery rates <s
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741210ControlBotulism</stro
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761614ControlBotulism</stro
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78INTRODUCTIONAvian</strong
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80(GPS) receivers (eTrex Venture, e
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82mortality rate was calculated by
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84samples from FG carcasses collect
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86outbreaks in waterfowl (Table 4;
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88birds and toxic
Page 96 and 97:
90LITERATURE CITEDBall G, Bollinger
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92Williamson JL, Rocke TE, Aiken JM
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94Table 2. Species composition <str
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96Table 4. Estimates of</st
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98iiviiiii1 0 1 2 km1 0 1 21 0 1 21
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100PART VIVARIABILITY OF TYPE C CLO
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102seasonal wetland</strong
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104clinical signs of</stron
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106RESULTSThe proportion of
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108sediments in basins of</
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110Williamson JL, Rocke TE, Aiken J
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112Chaplin, SK botulism 3/5 (60) 1/
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114Table 3. Annual and</str
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116MAIN CONCLUSIONS AND RECOMMENDAT
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Recommendation 8:The model
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120APPENDIX 1AVIAN BOTULISM IN ALBE
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122July 15, 2002ISBN: 0-7785-0962-1
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1242BackgroundMunro (1927) provides
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1264SUMMARY OF ALBERTA BOTULISM OUT
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128Moyles, D. 1989. Avian</
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13081) 1980 (Calverley 1980)Appendi
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1321010) 1990 (F&W files)LakeDetect
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134123 probable blue-green algal po
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136APPENDIX 2EXPOSURE OF MALLARD DU
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138Toxin was administered orally us
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140LITERATURE CITEDCarmichael WW, B
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