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Published 2008

Read in Norwegian

Publication details

Journal : Journal of Dairy Science (JDS) , vol. 91 , p. 4355–4364–10 , 2008

Publisher : Elsevier

International Standard Numbers :
Printed : 0022-0302
Electronic : 1525-3198

Publication type : Academic article

Contributors : Madsen, Per; Shariati, M.M.; Ødegård, Jørgen

Issue : 11

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Kjetil Aune
Chief Librarian


Mixture models are appealing for identifying hidden structures affecting somatic cell score (SCS) data, such as unrecorded cases of subclinical mastitis. Thus, liability-normal mixture (LNM) models were used for genetic analysis of SCS data, with the aim of predicting breeding values for such cases of mastitis. Here, putative mastitis statuses and breeding values for liability to putative mastitis were inferred solely from SCS observations. In total, there were 395,906 test-day records for SCS from 50,607 Danish Holstein cows. Four different statistical models were fitted: A) a classical (nonmixture) random regression model for test-day SCS; B1) an LNM test-day model assuming homogeneous (co) variance components for SCS from healthy (IMI-) and infected (IMI+) udders; B2) an LNM model identical to B1, but assuming heterogeneous residual variances for SCS from IMI- and IMI+ udders; and C) an LNM model assuming fully heterogeneous (co) variance components of SCS from IMI- and IMI+ udders. For the LNM models, parameters were estimated with Gibbs sampling. For model C, variance components for SCS were lower, and the corresponding heritabilities and repeatabilities were substantially greater for SCS from IMI- udders relative to SCS from IMI+ udders. Further, the genetic correlation between SCS of IMI-and SCS of IMI+ was 0.61, and heritability for liability to putative mastitis was 0.07. Models B2 and C allocated approximately 30% of SCS records to IMI+, but for model B1 this fraction was only 10%. The correlation between estimated breeding values for liability to putative mastitis based on the model (SCS for model A) and estimated breeding values for liability to clinical mastitis from the national evaluation was greatest for model B1, followed by models A, C, and B2. This may be explained by model B1 categorizing only the most extreme SCS observations as mastitic, and such cases of subclinical infections may be the most closely related to clinical (treated) mastitis.