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Effects of trait definition on genetic parameter estimates and sire evaluation for clinical mastitis with threshold models

Published online by Cambridge University Press:  18 August 2016

Y. M. Chang*
Affiliation:
Department of Dairy Science, University of Wisconsin, 1675 Observatory Drive Madison, WI53706, USA
D. Gianola
Affiliation:
Department of Dairy Science, University of Wisconsin, 1675 Observatory Drive Madison, WI53706, USA department of Animal and Aquacultural Sciences, Agricultural University of Norway, PO Box 5025, N-1432, As, Norway
B. Heringstad
Affiliation:
department of Animal and Aquacultural Sciences, Agricultural University of Norway, PO Box 5025, N-1432, As, Norway
G. Klemetsdal
Affiliation:
department of Animal and Aquacultural Sciences, Agricultural University of Norway, PO Box 5025, N-1432, As, Norway
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Abstract

Clinical mastitis records on 36 178 first-lactation Norwegian dairy cattle (NRF) cows, daughters of 245 sires from 5286 herds, were analysed to study the impact of trait definition on estimates of genetic parameters and sire evaluations for clinical mastitis. The opportunity interval for infection, going from 30 days pre-calving to 300 days post partum, was divided into either 11 periods (each 30 days long); four periods ((-30, 0), (1, 30), (31, 120), (121, 300)); a single period (-30, 300) or defined as the interval currently used for sire evaluation in Norway (-15,120). Within each period, clinical mastitis was scored as 1 if it occurred at least once and 0 otherwise. Analysis was with Bayesian threshold models, assuming that mastitis (presence v. absence) was a different trait in each period. By use of multivariate or univariate normal link functions, unobserved liabilities to disease were modelled as a linear function of year of calving, age-season of calving, herd, sire of cow and residual effects. Estimates of heritability of liability to clinical mastitis ranged from 0-06 to 0-14, depending on the model and stage of lactation. In multi-period models, estimates of genetic correlations between periods were positive and ranged from 0-13 to 0-55. This suggests that clinical mastitis resistance is not the same trait in different periods of the first lactation, which is not captured by the single-interval models. The single-interval (-30, 300) model gave slightly smaller sire-specific posterior probabilities of clinical mastitis during the first lactation than the multi-period models. Furthermore, the interval used in current Norwegian sire evaluation understated the posterior probabilities of clinical mastitis, relative to the multi-period specifications. This led to some differences in sire rankings between the four models, although there was agreement between the four- and 11-period models. In conclusion, the multi-period models captured more genetic variation than the single-interval models, but the four-period model gave sire rankings that differed little from those obtained with an 11-period definition of clinical mastitis.

Type
Research Article
Copyright
Copyright © British Society of Animal Science 2004

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