Secondary Poisoning of Eagles Following Intentional Poisoning of Coyotes With Anticholinesterase Pesticides in Western Canada

Abstract

ABSTRACT:Records of eagles, coyotes (Canis latrans), and red foxes (Vulpes vulpes) necropsied at the Western College of Veterinary Medicine, Saskatoon, Saskatchewan, Canada, between 1967 and2002 were reviewed for cases suggestive of anticholinesterase poisoning. From 1993 to 2002, 54 putative poisoning incidents involving 70 bald eagles (Haliaeetus leucocephalus) and 10 golden eagles (Aquila chrysaetus) were identified. Of these, 50 incidents occurred in Saskatchewan, two were in Manitoba, and one occurred in each of Alberta and the Northwest Territories. The diagnosis was confirmed in eight instances by demonstration of pesticide in ingesta from eagles or known use of pesticide at the site together with brain cholinesterase (AChE) reduction of Ͼ50% in at least one animal. A presumptive diagnosis of poisoning was made in 33 incidents based on brain AChE reduction of Ͼ50% in at least one animal; 13 incidents were considered suspicious because of circumstantial evidence of the death of eagles in association with other species and limited AChE reduction. Other wild species were found dead in 85% of the incidents involving eagles. Coyotes, foxes, black-billed magpies (Pica pica), and striped skunks (Mephitis mephitis) were associated with 34, six, six, and three incidents, respectively. There were eight additional incidents that did not involve eagles in which poisoning was diagnosed in coyotes. Carbofuran was identified in nine incidents. Carbamate poisoning was indicated on the basis of reactivation of brain AChE activity in two additional incidents. Brain AChE activity was not reduced from normal in eagles in four of seven incidents in which carbofuran was identified. The organophosphorous insecticide terbufos was found together with carbofuran in one incident. Brain AChE activity was measured in wild canids and in eagles in 15 incidents; in all of these incidents, brain AChE was reduced by Ͼ50% in at least one mammal, whereas this level of reduction occurred in eagles in only four incidents. Use of anticholinesterase pesticides to poison coyotes is illegal, but the practice continues and secondary poisoning of eagles is a problem of unknown proportions in western North America.

A Retrospective Study of Cases of Acetyl Cholinesterase Inhibitor Poisoning in the Coyote (Canis latrans) and the Bald Eagle (Haliaeetus leucocephalus) in the Canadian Prairies

“…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.…”

“…A consequence of off-label pesticide use may be the secondary poisoning of scavenger species [2]. Scavengers, including eagles, magpies, ravens, foxes, and skunks, may opportunistically feed on animal carcasses.…”

“…Targeted poisoning of coyotes (Canis latrans) with organophosphate and carbamate pesticides has been identified in Canada and the United States [1][2][3][4][5][6][7][8]. The continued economic losses from coyote-related livestock kills have deemed the animal a nuisance for livestock producers.…”

“…Registered lethal poisons for coyote control include sodium cyanide gas injection cartridges (Alberta only), sodium fluoroacetate tablets (Alberta and Saskatchewan only), and toxic neck collars [9,10]. Despite the availability and potency of approved pesticides for coyote control, occurrence of illegal coyote poisoning with acetyl cholinesterase inhibitor pesticides remains a regular occurrence [2].…”

“…rat oral LD50 of carbofuran=6.0-7.8 mg/kg body weight) and extensive availability of acetyl cholinesterase inhibitor insecticides enables the accidental and intentional animal poisoning with these agents [5]. Exposure to animals can occur through multiple routes: inhalation of sprayed agricultural pesticides (i.e., primary toxicity), consumption of contaminated water or food, dermal contact for insect control in fur (depending on the agent or formulation used), and secondary toxicity from the ingestion of animals previously poisoned with acetyl cholinesterase inhibitor pesticides [1][2][3][4][5][6].…”