Sm. Honour et al., EXPERIMENTAL VITAMIN-A-DEFICIENCY IN MALLARDS (ANAS-PLATYRHYNCHOS) - LESIONS AND TISSUE VITAMIN-A LEVELS, Journal of wildlife diseases, 31(3), 1995, pp. 277-288
Captive mallards (Anas platyrhynchos), fed an all-grain diet for up to
5 months during the winters of 1991 to 1992 and 1992 to 1993, develop
ed lesions of squamous metaplasia; some had no detectable hepatic vita
min A. Vitamin A deficiency in mallards was defined as hepatic levels
of retinyl palmitate <2 mu g/g liver. Lesions were found only in ducks
with low levels of hepatic vitamin A, but not all ducks with these lo
w levels of hepatic vitamin A had histological lesions. The prevalence
of lesions in the esophagus was greatest cranially and caudally and l
ess common in the central region. Palatine salivary glands rarely were
affected. Mallards with liver stores >600 mu g of hepatic retinyl pal
mitate per g liver, fed a diet deficient in vitamin A were unlikely to
become deficient over a 5 month period. Birds fed an all-grain diet h
ad significantly lower vitamin A concentrations in their liver compare
d to those fed an all-grain diet with vitamin A added. Liver weight, w
hen corrected for body size, did not affect vitamin A concentration. S
erum retinol levels were conserved over a large range of hepatic vitam
in A levels but levels below 300 mu g retinol/l were useful in detecti
ng vitamin A deficiency in captive mallards. Based on the findings, th
e presence of lesions provides a conservative measure of vitamin A sta
tus in ducks and tissue levels should be measured in instances when ma
llards have questionable vitamin A status.