Abstract
The rise in morbidity and mortality rates in pre-weaned calves related to poor colostrum management and subsequent transportation may be attenuated by the pre-transport administration of meloxicam (MEL). Our objective was to determine the effects and potential interaction of colostrum management (CM) and NSAID administration (NA; Meloxicam) on indicators of stress, inflammation, health measures, and fatty acid profile in transported pre-weaned calves. Male dairy calves (n = 48) were collected at birth and used in a randomized block design with a 2 2 factorial arrangement of treatments; colostrum (COL) feeding according to recommendations or milk replacer (MR) in place of colostrum, and administration of MEL or a placebo prior to transportation at each level of CM. Blood samples were collected (<2 d old) prior to transportation (300 km), on arrival, 12 h, and 36 h post arrival and were analyzed for glucose, betahyroxybutyrate (BHBA), cortisol, total antioxidant capacity (TAC), thiobarbituric acid reactive substances (TBARS), hematological parameters, and fatty acid profile. After harvest (36 h post-arrival), liver and gut tissue were used to quantify transcript abundance of markers of inflammation including tumor necrosis factor alpha (TNFα), interleukin (IL) 6, IL-8, IL-1β, intercellular adhesion molecule-1(ICAM-1), and nuclear factor kappa B (NFkB). Data was analyzed using PROC MIXED of SAS. There were no CM NA interactions (P ≥ 0.34) for plasma cortisol, BHBA, glucose, TAC, TBARS, white blood cells (WBC), and transcript abundance of markers of inflammation. However, there was a tendency for a CM NA (P = 0.07) interaction for mean corpuscular volume (MCV); MCV was lowest for calves fed COL and administered MEL compared to calves fed COL and administered a placebo, and also MR fed calves with or without MEL. Further investigation beyond CM NA interactions, we observed a CM time (P 0.04) interaction for glucose, BHBA, WBC count, basophil (BAS) count, red blood cell (RBC) count, hemoglobin (HGB), and C16:0 fatty acid, and a tendency for a CM time (P = 0.09) interaction for monocyte (MON) count. Although glucose concentration was lower in COL than MR calves prior to transport, COL fed calves had a greater glucose concentration at arrival and harvest than MR fed calves. Colostrum fed calves had a greater BHBA concentration prior to transport and at arrival; however, no differences were observed among treatments at harvest. No differences in WBC and MON count were observed prior to transportation or at arrival, however, COL fed calves had a greater WBC and MON count at harvest than MR fed calves. Basophil count was lower prior to transportation in COL than MR calves, but did not differ at arrival; however, basophil count was greater at harvest in COL than MR fed calves. Colostrum fed calves had a lower RBC count prior to transportation, at arrival, and at harvest than MR fed calves; however, RBC count in colostrum calves decreased during transportation whereas it increased in MR calves during transportation. Plasma HGB content, which did not differ in COL compared to MR fed calves prior to transport, was lower at arrival and harvest in COL compared to MR fed calves. Lastly, C16:0 fatty acid concentration was greater in COL than MR calves prior to transport and at arrival, but no differences were observed between treatments at harvest. There was a CM (P < 0.01) effect for TAC and a tendency for a CM (P = 0.06) effect for TBARS; total antioxidant capacity was greater in COL than MR fed calves and TBARS concentration tended to be lower in COL than MR calves. Feeding colostrum also downregulated (P ≤ 0.02) the expression of markers of inflammation in the liver (TNFα, IL-6, IL-8, IL-1β, ICAM-1), rumen (IL-6, ICAM-1), and jejunum (IL-6). In addition, there was a CM (P < 0.01) effect and tendency for a NA (P = 0.08) effect for cortisol concentration. Cortisol concentration was lower in COL compared to MR fed calves and tended to be lower in MEL compared to placebo calves. Overall, feeding colostrum reduced blood cortisol and TBARS concentration, RBC count, HGB content, and gene expression of pro-inflammatory markers in liver and gut tissue, and increased TAC, glucose, BHBA, WBC, MON, and BAS counts. Pre-transport administration of MEL also reduced blood cortisol and MCV. This suggests that proper colostrum management is key to limiting the negative health impact of transportation stress. When COL is not provided, MEL administration may not reduce the negative impact of transport related stress.