A total of 1010 dry cows and pregnant heifers was randomly selected from 25 dairy farms near Guelph, Ontario, Canada to receive either a controlled-release capsule of monensin or a placebo at 3 wk prior to expected calving. Serum samples were obtained at the time of treatment administration, and both serum and milk samples were collected at wk 1, 2, 3, 6, and 9 postcalving. The threshold used to define subclinical ketosis was selected a priori at a concentration of > or = 1200 mumol/L of beta-hydroxybutyrate. Using this threshold, the prevalence and incidence of subclinical ketosis were significantly reduced (50%) by monensin treatment. The duration of subclinical ketosis for cows that had been treated with monensin was also shorter than that for cows treated with the placebo. Monensin treatment significantly reduced the incidence of subclinical ketosis when the threshold was defined using higher concentrations of serum beta-hydroxybutyrate (1400 and 2000 mumol/L). In addition, monensin significantly reduced the prevalence of positive milk ketone tests.

An experiment was designed to examine subclinical ketosis in periparturient dairy cows and the antiketogenic effects of monensin. Subclinical ketosis was induced through a 10% feed restriction and was quantitatively determined using a blood beta-hydroxybutyrate (BHBA) threshold of 1200 mumol/L. Monensin decreased the BHBA concentration by 35% and increased the glucose concentration by 15%. No effect of monensin on milk production was detected, but rumen fermentation was altered. Monensin decreased the acetate to propionate ratio, decreased the butyrate concentration, and increased pH. The lower concentration of BHBA in blood and higher concentration of blood glucose in cows treated with a monensin controlled-release capsule decreased subclinical ketosis in early lactation cows.

The effects of monensin on the energy metabolism of dairy cows in early lactation were investigated in a large clinical trial that was randomized and double-blinded. A total of 1010 Holstein cows and first lactation heifers were allocated to receive a controlled-release capsule of monensin or a placebo at 3 wk prior to expected calving date. Treatments were randomized across 25 dairy farms located near Guelph, Ontario, Canada. Serum samples obtained at the time of treatment administration and at wk 1, 2, 3, 6, and 9 postcalving were analyzed for beta-hydroxybutyrate, glucose, aspartate aminotransferase, urea, total protein, calcium, and phosphorus. Cows were also assigned a body condition score at the time each sample was obtained. Monensin treatment significantly reduced serum beta-hydroxy-butyrate concentrations at wk 1, 2, and 3 postpartum and significantly raised serum glucose concentrations during wk 1 and 2 of lactation. In addition, monensin treatment significantly reduced the loss of body condition score and decreased serum activity of aspartate aminotransferase during the postpartum period. Concentrations of serum urea were significantly higher during wk 2 and 3 postpartum for the cows that were treated with monensin. Monensin treatment had no effect on the concentrations of calcium, phosphorus, or total protein.

Dry cows and pregnant heifers from 25 farms near Guelph, Ontario, Canada were enrolled in a large double-blind, randomized clinical trial that was designed to evaluate the impact of monensin on energy metabolism, health, and production. A total of 503 cows was given monensin in controlled-release capsules, and 507 were administered placebo capsules 3 wk prior to the expected calving date. The effects of treatment on milk production and milk components at the first three Dairy Herd Improvement (DHI) tests were evaluated using repeated measures analysis of variance. Treatment with monensin increased milk production, but this effect was dependent on body condition score prior to calving. Cows that were classified as thin (score of < or = 3.0) did not have increased production in response to monensin treatment. Cows with fair body condition (score of 3.25 to 3.75) produced significantly more milk at the second DHI test (+0.85 kg), but cows that were fat (score of > or = 4.0) produced significantly more milk than did controls for all three DHI tests (+1.25 kg) in early lactation. Monensin significantly increased projected 305-d milk production in cows from herds at increased risk of ketosis. Treatment with monensin had no significant effect on either milk fat percentage or milk protein percentage.

Dry cows and pregnant heifers from 25 farms near Guelph, Ontario, Canada were enrolled in a large, double-blind, randomized clinical trial designed to evaluate the impact of monensin on energy metabolism, health, and production. A total of 503 cows was given monensin in controlled-release capsules, and 507 cows were administered placebo capsules 3 wk before expected calving date. The effects of treatment on health were evaluated using a logistic regression model. Treatment with monensin significantly reduced the incidence of abomasal displacement (OR = 0.41-0.84) and multiple illnesses (OR = 0.38-0.89). Monensin treatment tended to reduce the incidence of clinical ketosis (P = 0.11) and the risk of being culled (P = 0.09) in the first 94 d of lactation. Reproductive performance was analyzed with both a logistic regression model for conception rate and a survival analysis for days to first breeding and days from calving to conception. Treatment with monensin had no significant effect on any measure of reproductive performance.