Abstract

The main objective of this study was to determine the association of dry matter intake as percentage of body weight (DMI%BW) and energy balance (EB) prepartum (-21 d relative to parturition) and postpartum (28 d) with ketosis (n = 189) and clinical mastitis (n = 79). For this, DMI%BW and EB were the independent variables and ketosis and clinical mastitis were the dependent variables. A secondary objective was to evaluate prepartum DMI%BW and EB as predictors of ketosis and clinical mastitis. For this, ketosis and clinical mastitis were the independent variables and DMI%BW and EB were the dependent variables. Data from 476 cows from 9 experiments were compiled. Clinical mastitis was diagnosed if milk from 1 or more quarters was abnormal in color, viscosity, or consistency, with or without accompanying heat, pain, redness, or swelling of the quarter or generalized illness, during the first 28 d postpartum. Ketosis was defined as the presence of acetoacetate in urine that resulted in any color change [5 mg/dL (trace) or higher] in the urine test strip (Ketostix, Bayer, Leverkusen, Germany). Cows that developed ketosis had lesser DMI%BW and lesser EB on d -5, -3, -2, and -1 than cows without ketosis. Each 0.1-percentage point decrease in the average DMI%BW and each 1-Mcal decrease in the average of EB in the last 3 d prepartum increased the odds of having ketosis by 8 and 5%, respectively. Cut-offs for DMI%BW and EB during the last 3 d prepartum to predict ketosis were established and were ≤1.5%/d and ≤1.1 Mcal/d, respectively. Cows that developed ketosis had lesser postpartum DMI%BW and EB and greater energy-corrected milk (ECM) than cows without ketosis. Cows that developed clinical mastitis had lesser DMI%BW but similar prepartum EB compared with cows without clinical mastitis. Each 0.1-percentage point decrease in the average DMI%BW and each 1-Mcal decrease in the average EB in the last 3 d prepartum increased the odds of having clinical mastitis by 10 and 8%, respectively. The average DMI%BW and EB during the last 3 d prepartum produced significant cut-offs to predict clinical mastitis postpartum, which were ≤1.2%/d and ≤1.0 Mcal/d, respectively. Cows that developed clinical mastitis had lesser postpartum DMI%BW from d 3 to 15 and on d 17; greater EB on d 18, from d 21 to 23, and on d 26; and lesser ECM. The main limitation in this study is that the time-order of disease relative to DMI%BW and ECM is inconsistent such that postpartum outcomes were measured before and after disease, which was diagnosed at variable intervals after calving. In summary, measures of prepartum DMI were associated with and were predictors of ketosis and clinical mastitis postpartum, although the effect sizes were small.

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