Abstract
Objective: Wildlife death from organophosphate and carbamate pesticide exposure has been documented previously in Canada. Wildlife exposure to these agents can occur through primary toxicity (i.e., inhalation), ingestion of contaminated water or food, or secondary toxicity through scavenging on toxic carrion. This paper describes epidemiologic information pertaining to confirmed acetyl cholinesterase inhibitor pesticide lethality in the coyote and bald eagle over a 16-year period in the Canadian Prairies. Methods: Epidemiologic case information from the diagnostic records of Prairie Diagnostic Services confirmed lethal acetyl cholinesterase inhibitor poisoning in 58 coyotes (Canis latrans) and 60 bald eagles (Haliaeetus leucocephalus) from 1998 to 2013. Brain acetyl cholinesterase enzyme activity suppressed to 50% or greater was indicative of toxicity and death. Results: Coyote case submissions varied both annually (p<0.0001) and temporally (p<0.0001). Submissions were highest in the years of 2000, 200, and 2002 (collectively 46.6%). The months of most frequent submission were May and April (36.2%). Bald eagle cases were also influenced annually (p<0.0001) and temporally (p<0.0001). Confirmed poisoning in bald eagle carcasses was most frequent during two seasonal periods: May through April and December through January. Years 2000, 200, and 2004 comprised 43.3% of the bald eagle poisonings during the investigational period. Annual and temporal distribution of coyote and bald eagle cases were comparable but were not significantly correlated. Brain acetyl cholinesterase activities within 20% of the mean in unaffected cases were considered background. These activities were 3.44 ± 1.52 μmol/min/g in the coyote and 15.18 ± 3.37 μmol/g/min in the bald eagle. Conclusion: Poisoning in wildlife with acetyl cholinesterase inhibitor pesticides continues to be a regular occurrence in the Canadian prairies. Increased surveillance and monitoring of pesticide use should be considered to mitigate future poisonings.
Highlights
Acetyl cholinesterase inhibitor insecticides have a longstanding history of use in Canadian agriculture
The primary objective of this paper is to describe epidemiological information on the occurrence of poisoning cases with anticholinesterase pesticides in coyotes and bald eagles in Western Canada
Epidemiologic case information from confirmed lethal anticholinesterase poisoning in coyotes and bald eagles across the Canadian prairies was obtained from the records of Prairie Diagnostic Services (PDS) located in the Western College of Veterinary Medicine (WCVM) in Saskatoon, Saskatchewan
Summary
Acetyl cholinesterase inhibitor insecticides have a longstanding history of use in Canadian agriculture. Following the nation-wide ban of the organochlorine class of insecticides in the early 1970s, organophosphate and carbamate insecticides were introduced as alternatives for pest management [1,2]. The major advantage associated with the introduction of these insecticides was low environmental persistence coupled with efficacious insect control. The major disadvantage associated with use of acetyl cholinesterase inhibitor pesticides is the non-target poisoning in domestic and wildlife animal species. The nervous system of vertebrates is highly conserved throughout evolution and renders any animal species vulnerable to poisoning. Phosphorylation (by organophosphate agents) or carbamylation (by carbamate agents) of acetyl cholinesterase prevents the enzyme’s ability to hydrolyse acetylcholine [3,4]. Uncontrolled binding of acetylcholine to post-synaptic neurons will occur. Stimulation of nicotinic acetylcholine receptors and muscarinic acetylcholine receptors at the postsynaptic neurons results in the rapid onset of classical symptomatology [3]
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