Genetic analysis of pathogen-specific intramammary infections in dairy cows.

Mastitis is one of the most common diseases in dairy cattle, causing severe economic losses to dairy farmers. Mastitis usually occurs due to intramammary infection (IMI) caused by a variety of pathogenic bacteria. Although good progress has been made in understanding genetics of pathogen-specific clinical mastitis, studies involving genetic analysis of pathogen-specific IMI are scarce. The overall objective of this study was, therefore, to assess genetic variation of overall and pathogen-specific IMI in nonclinical primiparous and multiparous cows using bacterial culture. Data and milk samples were collected over a 2-yr interval as part of the Canadian Bovine Mastitis Research Network. The final data set contained records of 46,900 quarter milk samples from 3,382 clinically healthy primiparous and multiparous Holstein cows from 84 dairy herds. For the genetic analysis, we considered the following 7 traits: overall IMI, non-aureus staphylococci (NAS) IMI, contagious pathogen IMI, environmental pathogen IMI, major pathogen IMI, minor pathogen IMI and somatic cell score (SCS). Data were analyzed at the quarter level using a threshold-probit model via Gibbs sampling in BLUPF90. Prevalence of IMI traits at the quarter level in multiparous cow from 0 to 400 DIM ranged from 6.8 to 45.5%. Posterior mean of quarter heritability estimates (on the underlying scale, posterior SD in brackets) of overall IMI and pathogen-specific IMI traits ranged from 0.017 to 0.073 (±0.009 to 0.030). Weak to strong genetic correlations [ranging from 0.18 to 0.97 (±0.01 to 0.29)] among pathogen-specific IMI traits and with overall IMI indicated that not all of these traits were genetically similar. Weak to moderate Spearman rank correlations between estimated breeding values for overall IMI and pathogen-specific IMI traits (from 0.31 to 0.87) indicated possible substantial reranking of sires. The percentage of daughters with IMI caused by various pathogen groups ranged from 13 to 80% and from 38 to 94% for the best (10% decile) and worst sires (90% decile) according to their IMI trait-specific estimated breeding values, respectively. Pathogen-specific IMI traits and overall IMI had weak to moderate positive genetic correlations [ranging from 0.11 to 0.81 (±0.11 to 0.22)] with SCS. Therefore, selection for lower SCS will improve resistance to IMI. However, based on the observed weak to moderate rank correlations (0.04 to 0.47) between pathogen-specific IMI traits and SCS, selection for lower SCC will not improve resistance to IMI from every pathogen-specific IMI group in the same manner. Therefore, despite low heritability estimates, there was sizeable genetic variation for pathogen-specific IMI traits, indicating that long-term direct genetic selection for pathogen-specific IMI can improve pathogen-specific IMI resistance.