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Phenotypic and genetic relationships of common health disorders with milk and fat yield persistencies from producer-recorded health data and test-day yields

J. A. D. R. N. Appuhamy^*,1, B. G. Cassell^* and J. B. Cole

^* Department of Dairy Science, Virginia Polytechnic Institute and State University, Blacksburg 24061
Animal Improvement Programs Laboratory, Agricultural Research Service, USDA, Beltsville, MD 20705-2350

¹ Corresponding author: appuhamy{at}vt.edu

The objective of this study was to investigate phenotypic and genetic relationships of common health disorders in dairy cows with milk (PMY) and fat (PFY) yield persistencies. Health and production data from 398 commercial dairy herds were used. Disease traits were defined in binary form for individual lactations considering mastitis only during the first 100 d in milk (MAST1), only after 100 d in milk (MAST2), and at any stage of lactation (MAST), and reproductive disorders (REPRO), metabolic disorders (METAB), and lameness (LAME). The persistencies were defined to be uncorrelated with 305-d yields. Impact of the diseases on PMY and PFY were investigated separately in first (FL) and later (LL) lactations. Phenotypic associations of PMY and PFY with likelihood of diseases in current and subsequent lactations were examined using odds ratios from a logistic regression model. Linear-threshold sire-maternal grandsire models were used to estimate genetic correlations of displaced abomasums (DA), ketosis (KET), metritis (MET), MAST, MAST1, and MAST2 with PMY and PFY across parities. Metabolic diseases and REPRO had significantly positive relationships with PMY and PFY in both FL and LL. Significantly greater PMY and PFY were associated with MAST1 in LL. Significantly lower PMY and PFY were related to MAST2 in both FL and LL, whereas cows affected by MAST had significantly less persistent lactations. Incidence of MAST and MAST2 decreased with increasing PMY and PFY in the present and previous lactation. Heritability of disease incidences were 0.03 (DA), 0.01 (KET), 0.10 (MAST), 0.02 to 0.05 (MAST1), 0.02 (MAST2), and 0.04 to 0.10 (MET). Displaced abomasum, KET, MAST, MAST1, and MET had unfavorable genetic correlations of 0.35, 0.46, 0.17, 0.02, and 0.27 with PMY, and 0.16, 0.21, 0.07, 0.06, and 0.12 with PFY, respectively. Favorable genetic correlations were found for MAST2 with PMY (–0.24) and PFY (–0.04). Results suggest that diseases in early lactation increase persistency of milk and fat yield. Selection for greater lactation persistency must consider these antagonistic relationships.

Key Words: persistency • disease • genetic correlation • phenotypic correlation