EXPERIMENTALLY-INDUCED SELENOSIS OF ADULT MALLARD DUCKS - CLINICAL SIGNS, LESIONS, AND TOXICOLOGY

Selenosis is thought to be a significant problem among waterfowl popul ations in selenium-contaminated wetlands in the western United States. Chemical analysis of avian tissues is currently the principal basis f or diagnosis. The purpose of these two 150-day studies was to establis h whether morphological criteria for selenosis could be developed to s upplement 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 supplie d as seleno-L-methionine (n = 12/group). In a separate study, 12 birds fed twice daily were offered either a proprietary ration or a seleniu m-supplemented ration (120 mu g/g) for one of two daily feedings. Sele nium in whole blood increased from baseline concentrations (< 0.4 mu g /ml) to means of 4.5, 8.9, and 16.0 mu g/ml in the 10-, 25-, and 60-pp m groups, respectively. All birds in the 60-ppm-dose group rapidly los t 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-mu g/g diet developed mild to moderate generalized hepatop athy with single-cell necrosis, karyomegaly of hepatocytes, hyperplast ic bile duct epithelium, and/or iron accumulation in Kupffer cells. Th e principal lesions in birds exposed to other dietary concentrations o f selenium involved integumentary structures containing hard keratin. Gross lesions developed after 76 days of dietary exposure and consiste d 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 presen t 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 o f keratinocytes and multifocal parakeratosis in stratum corneum. Histo logic lesions in alopecic skin (necrosis of the epidermal collar, infl ammation of the feather pulp, and follicular keratosis) were mild. Som e birds with alopecia had no detectable lesions in feather follicles f rom affected areas of skin. The highest tissue concentrations of selen ium were in liver, kidney, and feathers, respectively. Mean hepatic ti ssue concentrations were 14.5 mu g/g (10 ppm group), 29.6 mu g/g (25 p pm group), 60.6 mu g/g (60 ppm group), 13.0 mu g/g (120 ppm split-feed group), and 2.0 mu g/g (controls). Integumentary and hepatic lesions may be of value in corroborating a diagnosis of selenosis based on che mical analysis of tissues from naturally intoxicated waterfowl. Some b irds with fatal selenosis may have no morphologic lesions other than e maciation.