Abstract

The effect of Monensin on clinical mastitis in dairy cattle was evaluated from data collected at nine geographical clinical field trials using 966 Holstein cows and heifers in the United States and Canada. At each site, a randomized complete block design was conducted. Monensin (Rumensin®) was fed at concentrations of 0, 8, 16, or 24 ppm in a total mixed ration beginning 21 days before first calving for all nine sites, up to 7 days after second calving for six sites, and 203 days after second calving for three sites. Quarter milk samples were taken and cultured to determine the causative pathogen for each mastitis case and if clinical signs were observed the disease data were grouped according to etiology and analyses conducted. Analyses were conducted for all clinical mastitis cases as well as for a breakdown of the clinical mastitis cases into microorganism group levels. A generalized linear mixed model and a linear mixed model were used to determine if there were significant differences in clinical mastitis between the non-zero concentrations of Monensin and controls. Response variables for the clinical mastitis cases that were analyzed using a generalized linear mixed model were Animal rate, Quarter rate, Observation rate, and Incident rate. An additional response variable, Average case duration, was analyzed using a linear mixed model. Inferences from the analyses indicate that Monensin does not influence the susceptibility of dairy cattle to clinical mastitis.

Keywords

Monensin, Rumensin, Clinical Mastitis, Generalized Linear Mixed Model, Linear Mixed Model, Dairy Cattle

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Apr 24th, 11:00 AM

EVALUATING CLINICAL MASTITIS IN DAIRY CATTLE FED MONENSIN

The effect of Monensin on clinical mastitis in dairy cattle was evaluated from data collected at nine geographical clinical field trials using 966 Holstein cows and heifers in the United States and Canada. At each site, a randomized complete block design was conducted. Monensin (Rumensin®) was fed at concentrations of 0, 8, 16, or 24 ppm in a total mixed ration beginning 21 days before first calving for all nine sites, up to 7 days after second calving for six sites, and 203 days after second calving for three sites. Quarter milk samples were taken and cultured to determine the causative pathogen for each mastitis case and if clinical signs were observed the disease data were grouped according to etiology and analyses conducted. Analyses were conducted for all clinical mastitis cases as well as for a breakdown of the clinical mastitis cases into microorganism group levels. A generalized linear mixed model and a linear mixed model were used to determine if there were significant differences in clinical mastitis between the non-zero concentrations of Monensin and controls. Response variables for the clinical mastitis cases that were analyzed using a generalized linear mixed model were Animal rate, Quarter rate, Observation rate, and Incident rate. An additional response variable, Average case duration, was analyzed using a linear mixed model. Inferences from the analyses indicate that Monensin does not influence the susceptibility of dairy cattle to clinical mastitis.