D. Otoole et Mf. Raisbeck, EXPERIMENTALLY-INDUCED SELENOSIS OF ADULT MALLARD DUCKS - CLINICAL SIGNS, LESIONS, AND TOXICOLOGY, Veterinary pathology, 34(4), 1997, pp. 330-340
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.