Abstract #27

# 27
Genetic analysis of subclinical mastitis resistance in early lactation in first-parity cows.
Saranya G. Narayana*1,2, Filippo Miglior2,3, Syed A. Naqvi1, Francesca Malchiodi2, Pauline Martin2, Herman W. Barkema1, 1Department of Production Animal Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada, 2CGIL, Department of Animal Biosciences, University of Guelph, Guelph, ON, Canada, 3Canadian Dairy Network, Guelph, ON, Canada.

Subclinical mastitis (SCM) causes economic losses for producers by affecting milk production and leading to higher incidence of clinical mastitis and premature culling. The incidence of SCM in first-lactating cows is usually higher during early lactation. The SCC can be used for the diagnosis of subclinical mastitis. The objective of this study was to estimate genetic parameters for SCM in early lactation in first parity Holsteins. Test-day records for SCC were collected monthly between 2005 and 2009 in 90 Canadian herds participating in the national cohort of dairy farms of the Canadian Bovine Mastitis Research Network. Only the first test-day record available between 5 to 30 DIM was considered for the analysis. The final data set contained 8,518 records from first lactating Holstein heifers. Six alternative traits were defined as indicators of subclinical mastitis using different cut-off values of SCC (between 150,000 to 400,000 cells/mL). Linear and threshold animal models were used for the analysis. The prevalence of subclinical mastitis ranged from 15 to 24%. Estimated heritabilities from linear and threshold model ranged from 0.037 to 0.057 and 0.040 to 0.050, respectively. Strong genetic correlations were found among alternative SCC traits (from 0.90 to 0.99), indicating that these 6 traits were genetically similar. Despite a low heritability, estimated breeding values (EBV) predicted from both models showed a large genetic variation among sires. Higher EBV of SCM resistance corresponded to sires with higher percentage of healthy daughters. The percentage of diseased daughters varied between 5 to 13% and 19 to 33% among sires with best and worst EBV. The Spearman’s rank correlations between EBVs of sires predicted from linear (0.76 to 0.95) and threshold (0.74 to 0.95) models were moderate to high. These results indicates that although the heritabilities were low, an exploitable genetic variation for SCM in early lactation exists.

Key Words: mastitis, heritability, somatic cell count