Ecology and Management of Avian Botulism on the Canadian Prairies

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iEXECUTIVE SUMMARY<strong>Avian</strong> botulism (Clostridium botulinum, Type C; hereafter ‘botulism’) has occurred on thePrairies <strong>and</strong> elsewhere for centuries. <strong>Botulism</strong> affects varying numbers <strong>of</strong> birds, <strong>of</strong>ten inmultiple locations, at some time virtually every year. After the formation <strong>of</strong> the Prairie HabitatJoint Venture (PHJV) in 1988, <strong>and</strong> as early as 1994, it was becoming increasingly apparentthat very large numbers <strong>of</strong> ducks <strong>and</strong> shorebirds were dying annually during botulismoutbreaks at several large wetl<strong>and</strong>s on the Canadian Prairies. The magnitude <strong>of</strong> these lossescreated considerable consternation in the North American waterfowl <strong>and</strong> wildlifemanagement community.At the time, wetl<strong>and</strong> surveillance <strong>and</strong> carcass removal (or ‘clean-up’) were used to try to limitthe severity <strong>of</strong> these outbreaks, but the efficacy <strong>of</strong> this approach was unknown. In 1997, thePHJV Advisory Board responded by creating an <strong>Avian</strong> <strong>Botulism</strong> Working Group to identifycritical research needs <strong>and</strong> management objectives. From 1998 to 2001, this group coordinated aPrairie-wide investigation to determine whether carcass removal could reduce waterfowl losses<strong>and</strong> whether late-summer survival <strong>of</strong> mallards (Anas platyrhynchos) was reduced duringbotulism outbreaks. The group also sought to learn more about the basic ecology <strong>of</strong> avianbotulism, with the goal <strong>of</strong> providing clues about other management options.<strong>Botulism</strong> <strong>Ecology</strong>Initial investigations <strong>of</strong> botulism ecology focused on whether <strong>and</strong> why abiotic <strong>and</strong> biotic factorscould trigger <strong>and</strong> perpetuate botulism outbreaks. The source <strong>of</strong> substrate for initial proliferation<strong>and</strong> toxigenesis <strong>of</strong> botulism prior to outbreaks was unknown.One study investigated the factors involved in the initiation <strong>of</strong> avian botulism outbreaks, byfocussing on the role <strong>of</strong> Franklin’s gull (Larus pipixcan) mortality as a source <strong>of</strong> initial substratefor C. botulinum. Hatch-year Franklin's gull carcasses were the predominant source <strong>of</strong> toxinladenmaggots found prior to outbreaks <strong>of</strong> avian botulism in waterfowl. Peak carcass density <strong>of</strong>gulls occurred one to two weeks prior to the onset <strong>of</strong> botulism outbreaks in waterfowl.Gull carcasses were 22.7 times more likely to become maggot-laden at ambient temperatures≥20 C than were carcasses exposed to lower temperatures. High C. botulinum toxicity <strong>of</strong>maggots produced in gull (or eared grebes [Podiceps nigricollis]) chick carcasses coincided withhigh densities <strong>of</strong> susceptible birds. Hence, mortality <strong>of</strong> gulls or other birds may be a majorinitiating factor to trigger some botulism outbreaks.In controlled studies <strong>of</strong> mallards collected from a range <strong>of</strong> wetl<strong>and</strong>s, abundance <strong>of</strong> botulismspores <strong>and</strong> the potency <strong>of</strong> toxins produced from spores in birds varied considerably among studywetl<strong>and</strong>s. The proportion <strong>of</strong> carcasses producing type C C. botulinum toxin under controlledconditions in mallard carcasses varied from 0 to 100% across lakes. The prevalence <strong>of</strong> toxinproduction on non-botulism lakes ranged from 0 to 38% (median = 17%), whereas lakeswith a history <strong>of</strong> botulism had prevalences ranging from 15 to 100% (median = 71%).
Page 1: Ecology an
Page 5 and 6: iii[Anas acuta]). Impacts o
Page 7 and 8: 1GENERAL INTRODUCTIONType C Clostri
Page 9 and 10: 3Initially, the working group revie
Page 11 and 12: 5birds. There is no evidence that b
Page 13 and 14: 7carcasses are removed by larger sc
Page 15 and 16: 9Priority areasIn order to move for
Page 17 and 18: 11LITERATURE CITEDBell GF, Sciple G
Page 19 and 20: Figure 1. Map indicating lakes wher
Page 21 and 22: 15Lake # Location Province* Latitud
Page 23 and 24: 17INTRODUCTIONIn Type C Clostridium
Page 25 and 26: 19visited the site daily. This stra
Page 27 and 28: 21searched the area thoroughly, col
Page 29 and 30: 23time. Our experiment differed in
Page 31 and 32: 25LITERATURE CITEDCliplef DJ, Wobes
Page 33 and 34: 27Table 2. Total and</stron
Page 35 and 36: 29Table 4. Number of</stron
Page 37 and 38: 31NFigure 1. Maps of</stron
Page 39 and 40: 33ANWEWater TransectsShoreline Tran
Page 41 and 42: Figure 5. Variation in carcass dens
Page 43 and 44: 37INTRODUCTIONWhere logistically fe
Page 45 and 46: 39mallards occurred on all study la
Page 47 and 48: 41Weighted carcass density for each
Page 49 and 50: 43longer than did light-weight mall
Page 51 and 52: 45LITERATURE CITEDBurnham KP, Ander
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47Table 1. Body mass (g) an
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49Table 3. Estimated survival proba
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51PART IIIRELATIONSHIPS BETWEEN LOC
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53and the carcass
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55not well supported (∆AIC c = 4.
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57Table 1. Estimates of</st
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595040Control (65 plots)Clean-up (9
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61INTRODUCTIONAvian</strong
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63We used the rate of</stro
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65Results from the 2000 field seaso
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67LITERATURE CITEDAnderson DR. 1975
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69Table 2. Logistic analyses evalua
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71Table 4. Logistic analyses evalua
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73Table 6. Results of</stro
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751210ControlBotulism</stro
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77PART VIDENTIFICATION OF PRIMARY S
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79During the mid-1990s, extensive m
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81each dead or sick animal found, s
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83Sudheimer (1943). The control mou
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85Carcass densityModelling
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87laden maggots when mean daily wat
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89While we did not assess all possi
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91Rasbah J, Browne W, Goldstein H,
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93Table 1. Adjusted estimates <stro
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95Table 3. Unadjusted estimates <st
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97Table 5. Fate of
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Figure 2. Weekly pattern of
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101INTRODUCTIONAvian</stron
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103mortality, effects on population
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105series or simple polynomial seri
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1072.73), indicating that the addit
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109LITERATURE CITEDCox JRR, Afton A
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111Table 1. Prevalence and<
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113Table 2. Numbers of</str
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115Table 4. Lake-adjusted associati
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117Recommendation 4:Population mode
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119ACKNOWLEDGEMENTSLeadership <stro
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121Avian botulism
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1231AVIAN BOTULISM IN ALBERTA: A HI
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125Alberta Records of</stro
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1275Literature reporting waterfowl
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129-----. 1998b. Waterfowl disease
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13194) 1984 (Calverley 1985)LakeDet
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1331114) 1994 to 1997 Pakowki Lake
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1351318) 2001Lake Location Detectio
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137INTRODUCTIONAlthough blue-green
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139used, as would be more appropria
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Ecology and Management of Avian Botulism on the Canadian Prairies

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