The physiological and production effects of increased dietary intake of vitamins E and C in feedlot cattle challenged with bovine herpesvirus 1.

ABSTRACT

The physiological and production effects of feeding additional vitamin E and ruminally protected vitamin C were examined in cattle challenged with bovine herpesvirus 1 (BHV 1). Forty-eight individually penned 6-mo-old Angus and Angus crossbred heifer calves with a mean BW of 151 kg were allocated randomly to four diets in a 2 x 2 factorial arrangement of treatments. Pelleted diets provided either 15 or 185 IU/kg of DM of vitamin E, with or without 3.7 g of ruminally protected vitamin C/kg of DM. Blood samples were taken at start of the experiment and at wk 4, 5, and 6. At the start of wk 5, half of each of the dietary groups was challenged with BHV 1. Feeding additional vitamin E was associated with greater (P < 0.001) mean plasma alpha-tocopherol. In contrast, feeding ruminally protected vitamin C was not associated with greater (P = 0.59) mean plasma ascorbate concentration; however, feeding ruminally protected vitamin C was associated with lower (P = 0.03) mean blood total superoxide dismutase (Cu/Zn SOD and Mn SOD) concentration. Calves fed additional vitamin E had greater (P = 0.05) mean plasma beta-carotene concentrations. There were interactions between dietary intake of vitamins E and C with respect to serum ceruloplasmin concentration (P = 0.01) and GF (P = 0.05). Bovine herpesvirus 1 challenge was associated with lower white cell count (P = 0.007), lymphocyte count (P < 0.001), and DMI (P = 0.03). Feeding additional vitamin E to calves challenged with BHV 1 was associated with a lower (P = 0.03) serum ceruloplasmin concentration. There was a non-significant trend towards an interaction (P = 0.06) between the feeding of vitamins E and C, with virus-challenged calves fed additional vitamin E alone having greater plasma retinol concentrations. The feeding of vitamins E and/or C in calves challenged with BHV 1 was associated with alterations in the concentrations of other antioxidants. More severe disease may have translated these cellular effects to changes in health and performance.