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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.

From 2000 to 2004, over 10,000 seabirds, primarily Herring Gulls (Larus argentatus), died from an undetermined cause in the Blekinge archipelago in southeastern Sweden. In June 2004, 24 affected Herring Gulls were examined clinically, killed humanely, and 23 were examined by necropsy. Seven and 10 unaffected Herring Gulls collected from a local landfill site and from Iceland, respectively, served as controls. All affected birds showed similar neurologic signs, ranging from mild incoordination and weakness to severe flaccid paralysis of legs and wings, but generally were alert and responsive. All affected gulls were in normal nutritional condition, but were dehydrated and had empty stomachs. No gross or microscopic lesions, and no bacterial or viral pathogens were identified. Type C botulinum toxin was detected in the sera of 11 of 16 (69%) affected gulls by mouse inoculation. Type C botulism was the proximate cause of disease in 2004. Sera from 31% of birds tested from outbreaks in 2000 to 2003 also had detectable type C botulinum toxin by mouse inoculation. No large-scale botulism outbreak has been documented previously in this area. The source of toxin, initiating conditions, and thus, the ultimate cause of this outbreak are not known. This epidemic might signal environmental change in the Baltic Sea.

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Norway (Rattus norvegicus) and black rats (Rattus rattus) are common peridomestic species, yet little is known about wild rat ecology, including their natural diseases. We describe gross and histological lesions in the respiratory tract of a sample of 711 wild urban rats. A subset was examined for 19 distinct categories of histological lesions in the respiratory tract. Testing for known respiratory pathogens included serology and polymerase chain reaction (PCR) of lung samples. Grossly evident lesions were rare (8/711; 1%). Upper respiratory tract inflammation was present in 93 of 107 (87%) rats and included rhinitis, submucosal and periglandular lymphoplasmacytic tracheitis, and/or tracheal intraluminal necrotic debris and was significantly associated (P < .05) with the presence of cilia-associated respiratory bacillus (CARB), Mycoplasma pulmonis, and increased body mass (odds ratio [OR] ¼ 1.09; 95% confidence interval [CI] ¼ 1.05-1.14 per 10 g). Within the lungs, peribronchiolar and/or perivascular lymphoplasmacytic cuffs were present in 152 of 199 rats (76%) and were also significantly associated (P .02) with CARB, M. pulmonis, and increased body mass (OR ¼ 1.20; 95% CI ¼ 1.14-1.27 per 10 g). Rats were frequently coinfected with M. pulmonis and CARB, and lesions associated with these pathogens were histologically indistinguishable. Pneumocystis sp was detected in 48 of 102 (47%) rats using PCR but was not significantly associated with lesions. This description of pathology in the respiratory system of wild rats demonstrates that respiratory disease is common. Although the impact of these lesions on individual and population health remains to be investigated, respiratory disease may be an important contributor to wild rat morbidity and mortality.Keywords cilia-associated respiratory bacillus; lung; Mycoplasma pulmonis, pathology; Pneumocystis; rats; Rattus norvegicus; Rattus rattus; respiratory diseases; wild Norway and black rats (Rattus norvegicus and Rattus rattus) are cosmopolitan peridomestic species that are well adapted to living in urban habitats.12 Negative impacts of rats on human society range from economic losses through agricultural crop destruction to zoonotic diseases. 12,13,22 Even though rats have lived in cities with people for centuries, many details of urban rat ecology remain unexplored. Specifically, little is known about the causes of natural morbidity and mortality in rats.The life span of wild urban rats is considerably shorter than that of laboratory rats, with few individuals living beyond 1 year of age.12 Conversely, laboratory rats live up to 3 years. 43Factors contributing to the rapid population turnover among wild rats are unclear. Due to the high fecundity of rats, predation and human rat control activities, including trapping and poisoning, have limited effects on population size. 12 Mortality associated with resource competition does not explain why mature rats die, since they would be expected to outcompete juvenile rats.12 Natural disease may be a key component to

This report describes West Nile virus (WNV)-associated mortality in captive lesser scaup (Aythya affinis) ducklings that occurred in Saskatchewan, Canada, in July and August 2007. There were no clinical signs or gross necropsy findings suggestive of the cause of death; however, microscopic lesions were consistent with WNV infection, including nonsuppurative encephalitis and myocardial, pancreatic, and splenic necrosis. Necrosis of the thymus and thyroid was also observed in some birds, which has not previously been reported in association with WNV infection. Immunohistochemistry revealed WNV antigen in multiple tissues, including thymus and thyroid, and reverse transcription polymerase chain reaction resulted in the identification of WNV gene sequence in all of the ducklings that were tested. This outbreak is of interest because waterfowl (Anseriformes) are not thought to be particularly susceptible to WNV, and there is little information about WNV infection in prefledging birds. The apparent susceptibility of lesser scaup to WNV demonstrated in this study may have implications for declining lesser scaup populations in the wild.