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Canadian Bovine Mastitis Research Network
 

All about Mastitis I Others

Can we Identify Sire Families With Increased Resistance to Mastitis?

Many nongenetic factors influence mastitis. However, recent studies have shown that significant genetic variation exists among sire families.

At present, only the Nordic countries practice selection based on the actual incidence of mastitis, using information from their national veterinary databases. All other leading dairy countries use somatic cell count as an indicator of mastitis.
 
In a recent study by Zwald et al. (Journal of Dairy Science, 2006), scientists at the University of Wisconsin investigated the possibility of genetic selection for mastitis resistance using producer-reported incidence data from herd management software programs. Data from 77,791 Holstein cows in 418 herds that were either progeny test cooperators of Alta Genetics (Watertown, WI) or customers of Dairy Records Management Systems (Raleigh, NC) were used in the study. The incidence rate of mastitis, which was computed as the percentage of cows with at least one reported clinical case during the lactation, averaged 16% in the first lactation, 20% in second lactation, and 24% in third lactation in these herds. As one would expect, incidence rates were highest in the first 50 days postpartum.

Estimated heritability of clinical mastitis was 12% in first lactation, 10% in second lactation, and 9% in third lactation. These heritability estimates from producer-reported mastitis events match, and even exceed published estimates from the Nordic countries. Those countries have national veterinary recording systems, but average herd size is much smaller. Predicted transmitting abilities of individual Holstein sires, expressed as the percentage of daughters that will make it through their first lactation without a case of mastitis, ranged from 77% to 88%. When expressed as the percentage of daughters that will make it through first, second and third lactation without a case of mastitis, the range among sire families was 36% to 55%. That is, the best and worst sire families differ by 10% in mastitis rate per lactation, genetically, and this is similar to what we would expect based on differences among sires in genetic evaluations for somatic cell score.

It is important to note that differences exist among farms in the diagnosis, treatment and reporting of disease events, and this can lead to real challenges in interpreting across-farm comparisons of incidence rates, as well as within-farm trends. Fortunately, a key aspect of our genetic improvement programs is that each young bull has approximately 100 progeny test daughters distributed randomly over 75 or more cooperator herds. More importantly, genetic comparisons are based on the “herdmate deviation” method, which means that daughters of a given bull are compared with other cows that are housed in the same herd at the same time. As such, the impact of differences in diagnosis, treatment and reporting of disease among farms on genetic evaluations of dairy sires is quite small, and based on this study it appears that genetic selection for improved mastitis resistance using producer-recorded health events on commercial U.S. dairy farms is possible.
 
Source: Udder Topics, The NMC Newsletter, August 2007, Volume 30, No. 4. Article written by Dr. Kent A. Weigel, University of Wisconsin, Dairy Science Department, Madison, Wisconsin.

 





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