Experimentally induced selenosis of adult mallard ducks: clinical signs, lesions, and toxicology.
Selenosis is thought to be a significant problem among waterfowl populations in selenium-contaminated wetlands in the western United States. Chemical analysis of avian tissues is currently the principal basis for diagnosis. The purpose of these two 150-day studies was to establish whether morphological criteria for selenosis could be developed to supplement chemical analysis. Forty-eight flightling male mallard ducks were fed either a proprietary waterfowl ration (< 1 ppm selenium) or the same ration amended to contain 10, 25, and 60 ppm selenium supplied as seleno-L-methionine (n = 12/group). In a separate study, 12 birds fed twice daily were offered either a proprietary ration or a selenium-supplemented ration (120 microg/g) for one of two daily feedings. Selenium in whole blood increased from baseline concentrations (< 0.4 microg/ml) to means of 4.5, 8.9, and 16.0 microg/ml in the 10-, 25-, and 60-ppm groups, respectively. All birds in the 60-ppm-dose group rapidly lost weight and were killed (11/12) or died (1/12) between 22 and 50 days of dietary exposure. In addition to emaciation, six of 12 birds (50%) fed the 60-microg/g diet developed mild to moderate generalized hepatopathy with single-cell necrosis, karyomegaly of hepatocytes, hyperplastic bile duct epithelium, and/or iron accumulation in Kupffer cells. The principal lesions in birds exposed to other dietary concentrations of selenium involved integumentary structures containing hard keratin. Gross lesions developed after 76 days of dietary exposure and consisted of bilaterally symmetrical alopecia of the scalp and dorsal cervical midline, broken or lost digital nails, and necrosis of the tip of the beak (maxillary nail). One or more of these three lesions were present in 0/12 birds (0%) fed 10 ppm selenium, 5/12 birds (42%) fed 25 ppm selenium, and 4/9 (44%) birds fed a split-feed diet containing 120 ppm selenium. Controls were unaffected. Histologic lesions in digital and maxillary nails consisted of single-cell to full-thickness necrosis of keratinocytes and multifocal parakeratosis in stratum corneum. Histologic lesions in alopecic skin (necrosis of the epidermal collar, inflammation of the feather pulp, and follicular keratosis) were mild. Some birds with alopecia had no detectable lesions in feather follicles from affected areas of skin. The highest tissue concentrations of selenium were in liver, kidney, and feathers, respectively. Mean hepatic tissue concentrations were 14.5 microg/g (10 ppm group), 29.6 microg/g (25 ppm group), 60.6 microg/g (60 ppm group), 13.0 microg/g (120 ppm split-feed group), and 2.0 microg/g (controls). Integumentary and hepatic lesions may be of value in corroborating a diagnosis of selenosis based on chemical analysis of tissues from naturally intoxicated waterfowl. Some birds with fatal selenosis may have no morphologic lesions other than emaciation.
O'Toole
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The Wyoming State Veterinary Laboratory, Laramie 82070, USA. dot@uwyo.edu
Raisbeck
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MF
D000505:Alopecia / Q000139:chemically induced; D000821:Animal Feed; D000818:Animals; D001715:Bird Diseases / Q000139:chemically induced*; D001835:Body Weight / Q000187:drug effects; D004372:Ducks; D004435:Eating / Q000187:drug effects; D004781:Environmental Exposure; D005241:Feathers / Q000187:drug effects; D005528:Foot; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008297:Male; D011041:Poisoning / Q000662:veterinary*; D012643:Selenium / Q000097:blood / Q000506:poisoning*; D018036:Selenium Compounds / Q000506:poisoning*; D012645:Selenomethionine / Q000506:poisoning*; D014018:Tissue Distribution
D018036:Selenium Compounds; D012645:Selenomethionine; D012643:Selenium