Epsilon Open Archive

Abstract

This thesis aims to advance our understanding of the genetic background of mastitis resistance in dairy cattle. More particularly, it seeks to improve the potential of genetic evaluation of clinical mastitis (CM) both by utilizing more of the available information and by applying appropriate methodology. A linear cross-sectional model was used to estimate genetic parameters for binary CM, somatic cell count (SCC) and milk production in the first three lactations of Swedish Holstein cows. The unfavorable genetic correlations found between udder health and production traits emphasize the need to include mastitis resistance in the breeding goal. The higher heritability of SCC (0.10-0.14) than CM (0.01-0.03) and the high genetic correlation between these two traits (average 0.70) imply that SCC is a useful indicator trait in breeding for improved mastitis resistance. The method of survival analysis was used to analyze time to first CM and was compared with a linear cross-sectional model on field data and with linear and threshold cross-sectional models in a simulation study. Despite the theoretical advantages of survival analysis, there was no difference in the accuracy of genetic evaluation when methods were compared within the same length of opportunity period. The correlation between true and predicted sire breeding values in the simulation study was, however, 8% greater when data from the full lactation rather than the first 150 days were used. Longitudinal binary CM data in 12 intervals of first lactation were analyzed as repeated observations in a linear random regression model. This method has some appealing features so far as genetic evaluation of CM is concerned, but it was found rather sensitive for parameter estimation in the current setting. Genetic parameters from the chosen random regression model agreed rather well, however, with the corresponding estimates from a linear longitudinal multivariate model in which records of CM in the different intervals were considered as different traits. Both longitudinal models indicated clearly that CM is not the same trait genetically throughout lactation, something that is ignored in a cross-sectional model.