No abstract

Seabird tissues, collected during the 1988 breeding season from colonies on the Atlantic coast of Canada, were analyzed for toxic metals--Cd, Hg and Pb--and 18 other trace elements. Metallothionein (MT) was measured in kidney, and kidneys and livers underwent histopathological examination. Levels of most essential trace elements appear to be closely regulated in seabird tissues; values were in good agreement with those previously reported in the published literature. Liver-Se concentrations in Leach's storm-petrels (Oceanodroma leukorrhea) (77.6 + 7.49 micrograms/g dry weight) were much higher than values normally reported for free-living birds and mammals. Cd levels varied greatly among individuals, but were always higher in kidney than in liver. Highest mean Cd concentrations (183 + 65 micrograms/g dry weight) were in kidneys of the planktivorous Leach's storm-petrels from the Gulf of St. Lawrence. A few individuals of this species had values greater than 300 micrograms/g dry weight. Cd and metallothionein (MT) concentrations were positively correlated in kidneys of Leach's storm-petrels (r = 0.692), Atlantic puffin (Fratercula arctica) (r = 0.845) and herring gull (Larus argentatus) (r = 0.866). Concentrations of total Hg varied greatly among species and individuals, but were consistently higher in liver than in kidney. Highest mean levels (21 + 28 micrograms/g) were in livers of the piscivorous double-crested cormorant (Phalacrocorax auritus) from Saint John Harbour in the Bay of Fundy. Concentrations of Hg and Se were positively correlated (r = 0.736) in livers of Leach's storm-petrel, but not in other species. Pb concentrations were consistently greatest in bone, with mean levels being highest in herring gulls from a colony in the Bay of Fundy (63 + 36 micrograms/g). Histological examination of liver and kidney failed to reveal indications of tissue damage associated with elevated levels of heavy metals.

Oral doses of 0, 1, 4, 5, 10, or 20 ml of Prudhoe Bay crude oil/kg body weight/day were given to herring gull and Atlantic puffin nestlings for 5 to 7 consecutive days. Gulls defecated substantial amounts of oil within 10 to 15 minutes after receiving a dose. Clinical signs and lesions occurred only in birds given greater than or equal to 10 ml oil/kg body weight/day. Gulls consumed less food and lost weight. Two categories of lesions were observed: those considered secondary to a primary toxic hemolytic disease, and those considered nonspecific reactions to stress. The former included phagocytosis of degenerate erythrocytes in the liver and spleen, hemoglobin resorption droplets in renal proximal tubule cells, and erythroid hyperplasia in the bone marrow; the latter included lymphocyte depletion in primary lymphoid tissues, an increase in heterophil: lymphocyte ratio in peripheral blood, lipid depletion and necrosis in adrenal steroidogenic cells, and an increased prevalence and severity of lesions in the bursa of Fabricius. These findings indicated that the primary target of oil toxicity was the peripheral red blood cell, but that significant stress-related lesions were also associated with ingestion of oil.

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.