Physiological effects of starter-induced ruminal acidosis in calves before, during, and after weaning.
2019
ABSTRACT The objectives were to nutritionally induce or blunt ruminal acidosis in young calves and to compare indicators of rumen and systemic health. Ten bull calves (n = 5/diet) were ruminally cannulated at 3 wk of age and received milk replacer and 1 of 2 calf starter diets that were designed to cause (AC; pelleted, 42.7% starch, 15.1% neutral detergent fiber, 57.8% nonfiber carbohydrates) or blunt (BL; texturized, 35.3% starch, 25.3% neutral detergent fiber, 48.1% nonfiber carbohydrates) ruminal acidosis. Mean birth weight was 38.7 ± 1.3 kg. Body weight and calf starter intake were measured weekly. Rumen contents were sampled at −8, −4, 0, 2, 4, 8, 12, and 24 h relative to starter feeding during wk 6, 8, 10, 12, 14, and 16 of age. Blood was collected from the jugular vein during the same weeks for complete blood cell count, blood pH, and partial pressures of oxygen and carbon dioxide. Rate of starter consumption was assessed during wk 16. Marker systems were used to estimate liquid passage and volatile fatty acid absorption rates. Calves were slaughtered at 17 wk, and rumen tissue was collected and assessed for papillae length, width, and degree of tissue degradation. Mean ruminal pH ± standard error was 5.37 ± 0.24 and 5.63 ± 0.24 for AC and BL calves, respectively. Lowest pH values were observed the week after weaning. Total ruminal volatile fatty acid concentrations were 131.5 and 124.8 ± 2.4 mM in AC and BL calves, respectively, and increased with age and time after feeding. Dry matter intake was lower in AC calves at wk 4 and remained lower through wk 16. Rate of starter consumption was also lower in AC calves at wk 16. Body weight also was also lower for AC calves from wk 5 through 16. Blood hemoglobin and hematocrit were lower in AC calves, but other blood characteristics were not different. Rumen volume increased with age and tended to be greater in BL calves. Passage rate and papillae length and width were not different between diets, but AC calves experienced a greater degree of tissue degradation. Ruminal acidosis symptoms in calves appear similar to those in adult cattle, and the etiology of the disease seems to follow similar mechanisms. It is clear from this study that symptoms can be moderated by diet, but further research is needed to determine whether symptoms can be nutritionally prevented or whether calves that experience ruminal acidosis are more susceptible to the disease as adults.
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