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Vitamin E-Selenium Deficiency and Its Influence on Avian Malarial Infection in the Duck^1,2,

Departments of Pathology and Microbiology and Public Health, Michigan State University, East Lansing, Michigan 48823

The effect of feeding to ducklings a Torula yeast, cod-liver oil basal diet, deficient or supplemented with vitamin E and selenium, and its influence during acute avian malarial infection were determined in three experiments. Ducklings fed the basal, deficient diet developed clinical signs of deficiency in 9 days. Prominent clinical signs included poor growth and skeletal muscular weakness in ducklings fed the deficient diet and an anemia in malarious ducks, irrespective of their diet. The main lesions associated with the vitamin E-selenium-deficient diet were skeletal and smooth (gizzard and duodenum) muscle necrosis and myocarditis. Severe muscle lesions undergoing mineralization and extensive reparative processes were more apparent in muscles of malarious, deficient ducklings than of noninfected, deficient ones. A prominent lesion associated with malarial infection was necrotizing pancreatitis. No nutritionally-related lesions of exudative diathesis, hepatic necrosis or encephalomalacia occurred during this study. Ducklings fed the vitamin E-selenium-deficient diet had decreased plasma tocopherol, muscle creatine and muscle glutamic-oxalacetic transaminase. Plasma glutamic-oxalacetic transaminase was markedly increased for ducklings fed the basal, deficient diet and significantly (P < 0.05) elevated during the entire study for malarious ducks fed the same diet. After 3 days of malarial infection, plasma tocopherol for vitamin E-selenium-supplemented ducklings tended to increase. For the duration of each experiment despite marked influences on other parameters, dietary vitamin E-selenium did not affect the death rate of acutely infected ducks.

KEY WORDS: • vitamin E-selenium deficiency • duck • avian malaria

¹ Michigan Agricultural Experiment Station Journal Article no. 5925. Supported in part by a Postdoctoral Fellowship, U. S. Public Health Service General Research Support Grant no. 5-501-RR-05623-09.

² From a thesis submitted by the senior author in partial fulfillment of the requirements for the M.S. degree in Pathology, Michigan State University, 1971. Present address: Department of Veterinary Pathology, The Ohio State University, Columbus, Ohio 43210.

Manuscript received 16 May 1972.