Genetic analysis of longitudinal trajectory of clinical mastitis in first-lactation Norwegian cattle

Clinical mastitis records for 36,178 first-lactation daughters of 245 Norwegian Cattle (NRF) sires were analyzed with a Bayesian longitudinal threshold model. For each cow, the period going from 30 d before calving to 300 d after calving was divided into 11 intervals of 30 d length each. Absence or presence of clinical mastitis within each interval was scored as "0" or "1", respectively. A Bayesian threshold model consisting of a set of explanatory variables plus Legendre polynomials on time of order four was used to describe the trajectory of liability to clinical mastitis. Heritability ranged between 0.07 and 0.13 before calving, from 0.04 to 0.15 during the first 270 d after calving, and increased sharply thereafter, as a consequence of the form of the polynomial. Genetic correlations between adjacent days were close to 1, and decreased when days were further apart. Most genetic correlations were moderate to high. A measure of probability of future daughters contracting clinical mastitis during lactation was computed for each sire. A typical curve had a peak near calving followed by a decrease thereafter. The best sires had a low peak around calving and a low expected probability of mastitis among daughters throughout lactation. Expected fraction of days without mastitis was derived from the probability curves and used for ranking of sires. Rank correlations with genetic evaluations of sires obtained from cross-sectional models were high. However, sire selection was affected markedly, especially at high selection intensity. An advantage of the longitudinal model for clinical mastitis is its ability to take multiple treatments and time aspects into account.     

Genetic associations between clinical mastitis and somatic cell score in early first-lactation cows

The objectives of this study were to examine genetic associations between clinical mastitis and somatic cell score (SCS) in early first-lactation cows, to estimate genetic correlations between SCS of cows with and without clinical mastitis, and to compare genetic evaluations of sires based on SCS or clinical mastitis. Clinical mastitis records from 15 d before to 30 d after calving and first test-day SCS records (from 6 to 30 d after calving) from 499,878 first-lactation daughters of 2,043 sires were analyzed. Results from a bivariate linear sire model analysis of SCS in cows with and without clinical mastitis suggest that SCS is a heterogeneous trait. Heritability of SCS was 0.03 for mastitic cows and 0.08 for healthy cows, and the genetic correlation between the 2 traits was 0.78. The difference in rank between sire evaluations based on SCS of cows with and without clinical mastitis varied from −994 to 1,125, with mean 0. A bivariate analysis with a threshold-liability model for clinical mastitis and a linear Gaussian model for SCS indicated that heritability of liability to clinical mastitis is at least as large as that of SCS in early lactation. The mean (standard deviation) of the posterior distribution of heritability was 0.085 (0.006) for liability to clinical mastitis and 0.070 (0.003) for SCS. The posterior mean (standard deviation) of the genetic correlation between liability to clinical mastitis and SCS was 0.62 (0.03). A comparison of sire evaluations showed that genetic evaluation based on SCS was not able to identify the best sires for liability to clinical mastitis. The association between sire posterior means for liability to clinical mastitis and sire predicted transmitting ability for SCS was far from perfect.     

Genetic analysis of fertility-related diseases and disorders in Norwegian Red cows

Heritability of and genetic correlations among silent heat (SH), cystic ovaries (CO), metritis (MET), and retained placenta (RP) were inferred. These traits were chosen because they are the 4 most frequent fertility-related diseases and disorders among first-lactation cows in Norway. Records of 503,683 first-lactation daughters of 1,058 Norwegian Red sires with first calving from 2000 through 2006 were analyzed with a 4-variate threshold sire model. Presence or absence of each of the 4 diseases was scored as 1 or 0 based on whether or not the cow had at least 1 veterinary treatment for the disease. The mean frequency was 3.1% for SH, 0.9% for MET, 0.5% for CO, and 1.5% for RP. The model for liability had effects of age at calving and of month-year of calving, herd, sire of the cow, and a residual. Posterior mean (SD) of heritability of liability was 0.06 (0.01) for SH, 0.03 (0.01) for MET, 0.07 (0.01) for CO, and 0.06 (0.01) for RP. The genetic correlation between MET and RP was strong, with posterior mean (SD) 0.64 (0.10). A negative genetic correlation (−0.26) was found between RP and CO. The posterior distributions of the other genetic correlations included zero with high density, and could not be considered different from zero. The frequency of fertility-related diseases and disorders is very low in the Norwegian Red population at present, so there is limited scope for genetic improvement. However, this study indicates that reasonably precise genetic evaluation of sires is feasible for these traits given information from large daughter groups.     

Short communication: bivariate genetic analysis of clinical mastitis and somatic cell count in Norwegian dairy cattle

Clinical mastitis (CM) and lactation mean somatic cell score (LSCS) were analyzed with a bivariate linear sire model. Nearly 1.4 million primiparous cows of Norwegian Dairy Cattle from 2043 sires were used. The heritability estimates were 0.03 for CM and 0.11 for LSCS. The estimates of genetic and residual correlations between the 2 traits were 0.53 and 0.10, respectively. It is postulated that the genetic correlation probably is highly population-specific.     

Short communication: use of culling information in genetic evaluation of fertility and mastitis in Norwegian red cows

Breeding values for clinical mastitis, interval from calving to first insemination, and 56-d nonreturn rate for heifers and primiparous cows, were predicted using multivariate linear-threshold sire models, with or without including information on culling during the first lactation. Breeding values for 3,064 sires were predicted using 3 data sets with an average of 273, 135, and 68 first-crop daughters per sire, respectively. For each data set, accuracies of selection for health and fertility traits were evaluated through the predictive ability of predicted sire breeding values with respect to phenotypic performance of second-crop daughters. The predictive ability of estimated breeding values for clinical mastitis and interval from calving to first insemination did not improve when including information on early culling, irrespective of the size of first-crop daughter groups. For 56-d nonreturn rates (heifer and primiparous cow), sire evaluations based on reduced size of daughter groups tended to predict performance of the future daughters slightly better when including data on early culling. Hence, for breeding programs with direct selection for health and fertility traits there is little to gain by including early culling as additional information.     

Short communication: Genetic analysis of respiratory disease in Norwegian Red calves

A genetic analysis of respiratory disease (RD) in Norwegian Red calves was conducted. This is the first genetic study of calf diseases based on data from the Norwegian health recording system, and RD was chosen because it is the most frequent disease in calves. Records on absence or presence of RD before 180 d of age for 250,212 calves (progeny of 728 Norwegian Red artifical insemination sires) were analyzed with a threshold model. A total of 0.7% of the calves had veterinary treatment of RD before 180 d of age. Heritability of RD in the underlying scale was 0.05, with a 95% credibility interval from 0.02 to 0.09. The “worst” sire had a predicted probability of RD that was more than twice as high as that of the “best” one (1.15 vs. 0.44%). Their 95% credibility intervals for predicted probability of RD, however, overlapped. With improved and more extensive recording of calf diseases, the precision in genetic evaluation of sires could increase considerably. The frequency of RD is very low in the Norwegian Red population at present, so there is not much scope for genetic improvement. However, this study indicates that reasonably precise genetic evaluation of sires for resistance to RD could be feasible.     

Genetic analysis of calving difficulty and stillbirth in Norwegian Red cows

The objectives of this study were to infer genetic parameters for stillbirth (SB) and calving difficulty (CD) and to evaluate phenotypic and genetic change for these traits in the Norwegian Red breed. Stillbirth is recorded as a binary trait and calving difficulty has 3 categories: 1) easy calving, 2) slight problems, and 3) difficult calving. The overall mean frequency of SB in Norwegian Red was 3% at first calving and 1.5% for second and later calvings; mean frequency of the category “difficult calving” was 2 to 3% for heifers and 1% for cows at second and later calvings. Mean stillbirth rate has remained unchanged from 1978 to 2004. The proportion of the category “difficult calving” has not changed over the years, but the “slight problems” category increased from 4 to 7% for heifers and from 2 to 3% for cows. A total of 528,475 first-calving records were analyzed with a Bayesian bivariate sire-maternal grandsire threshold liability model. Posterior means of direct and maternal heritabilities were 0.13 and 0.09 for CD, and 0.07 and 0.08 for SB, respectively. Strong genetic correlations were found between direct SB and direct CD (0.79), and between maternal SB and maternal CD (0.62), whereas all genetic correlations between direct and maternal effects within or between traits were close to zero. These positive correlations are favorable in the sense that selection for one of the traits would result in a favorable selection response for the second trait. No genetic correlations between direct and maternal effects imply that bulls should be evaluated both as sire of the calf (direct) and sire of the cow (maternal). No genetic change for SB was found, and a slight genetic improvement for CD was detected.     

Genetic change for clinical mastitis in Norwegian cattle: a threshold model analysis

Records of clinical mastitis on 1.6 million first-lactation daughters of 2,411 Norwegian Cattle sires that were progeny tested from 1978 through 1998 were analyzed with a threshold model. The main objective was to infer genetic change for the disease in the population. A Bayesian approach via Gibbs sampling was used. The model for the underlying liability had age at first calving, month x year of calving, herd x 3-year-period, and sire of the cow as explanatory variables. Posterior mean (SD) of heritability of liability to clinical mastitis was 0.066 (0.003). Genetic evaluations (posterior means) of sires both in the liability and observable scales were computed. Annual genetic change of liability to clinical mastitis for progeny tested bulls born from 1973 to 1993 was assessed. The linear regression of mean sire effect on year of birth had a posterior mean (SD) of -0.00018 (0.0004), suggesting a nearly constant genetic level for clinical mastitis. However, an analysis of sire posterior means by birth-year of daughters indicated an approximately constant genetic level in the cow population from 1976 to 1990 (-0.02%/yr), and a genetic improvement thereafter (-0.27%/yr). This reflects more emphasis on mastitis in selection of bulls in recent years. Corresponding results obtained with a standard linear model analysis were -0.01% and -0.23% per year, respectively (regression of sire predicted transmitting ability on birth-year of daughters). Genetic change seems to be slightly understated with the linear model, assuming the threshold model holds true.     

Genetic analysis of number of mastitis cases and number of services to conception using a censored threshold model

The objective of this study was to infer genetic parameters and genetic change for number of clinical mastitis cases (NCM) and number of services to conception (STC) in first-lactation Norwegian Red (NRF) cows. Records on 620,492 daughters of 3,064 NRF sires, with first calving from 1980 through 2004, were analyzed with a bivariate threshold liability model that takes censoring into account. Posterior mean (SD) of heritability of liability was 0.08 (0.004) for NCM and 0.03 (0.002) for STC. The mean (SD) of the posterior distribution of the genetic correlation between the 2 traits was 0.21 (0.04). Posterior means of the correlation between herd-5-yr effects, and between residuals for NCM and STC were 0.17 and 0.05, respectively. To evaluate effects of taking censoring into account, the data were also analyzed with a bivariate ordered threshold model ignoring censoring. The genetic correlation between NCM and STC was lower than in the censored threshold model (0.09 vs. 0.21). Heritability of liability to NCM and STC from this model was also slightly lower, whereas the point estimates of herd-5-yr and residual correlations were 0.15, and −0.01, respectively. These results suggest that genetic (co)variance may be understated in models ignoring censoring. For comparison purposes, the data were analyzed with a bivariate linear sire model and standard REML-BLUP procedures. The correlation (rank correlation) between sire evaluations from the censored threshold model and sire predicted transmitting abilities from the linear model was 0.90 (0.90) for NCM and 0.87 (0.86) for STC. The evolution of average sire posterior means by birth year of daughters was used to assess genetic change, and results indicated genetic reduction (i.e., genetic improvement) of NCM and little or no genetic change for STC in the NRF population.     

Bivariate analysis of liability to clinical mastitis and to culling in first-lactation cows

Records taken on 13,070 first-lactation daughters of 250 Norwegian Cattle sires were used to examine associations between susceptibility to clinical mastitis and to culling. Clinical mastitis was defined as a binary trait, whereas culling was treated as either binary (culled or not culled) or continuous (length of opportunity period) for two sampling periods (120 or 300 d of lactation). Two Bayesian models were employed; 1) a bivariate threshold model with both mastitis and culling as binary traits, and 2) a bivariate model with mastitis as a threshold binary variable and time to culling as Gaussian. The heritability of liability to clinical mastitis was not affected by either the length of sampling period (120 vs. 300 d) or by whether culling (binary) or length of opportunity period was the second trait in the bivariate analysis. The posterior mean (standard deviation) of heritability of liability to clinical mastitis was 0.06 to 0.07 (0.02) in all analyses. The heritability estimate of length of opportunity period was less than 0.001. Culling (threshold trait) in first lactation had a low heritability, but a high genetic correlation with clinical mastitis. The posterior means (standard deviation) for heritability of liability to culling were 0.01 (0.006) for 120 d and 0.02 (0.009) for 300 d, and the posterior means (standard deviation) of the genetic correlation between liability to clinical mastitis and to culling were 0.48 (0.24) and 0.53 (0.21) for 120 and 300 d, respectively.     

Comparison between bivariate models for 56-day nonreturn and interval from calving to first insemination in Norwegian red

A bivariate threshold-linear (TL) and a bivariate linear-linear (LL) model were assessed for the genetic analysis of 56-d nonreturn (NR56) and interval from calving to first insemination (CFI) in first-lactation Norwegian Red (former Norwegian Dairy Cattle) (NRF). Three different datasets were used to infer genetic parameters and to predict transmitting abilities for NRF sires. Mean progeny group sizes were 147.8, 102.7, and 56.5 daughters, and the corresponding number of sires were 746, 743, and 742 in the 3 datasets. Otherwise, the structures of the 3 datasets were similar. When the TL model was used, heritability of liability to NR56 was 2.8% in the 2 larger datasets and 3.8% in the smallest dataset. In the LL model, the heritability of NR56 in the largest dataset and in the 2 smaller datasets was 1.2 and 0.9%, respectively. For CFI, the heritability was similar in TL and LL models, ranging from 2.4 to 2.7%. The small heritability of the 2 reproductive traits implies that most of the variation is environmental and that large progeny groups are required to get accurate sire PTA. The point estimates of the genetic correlation between NR56 and CFI were near zero in both models. The 2 bivariate models were compared in terms of predictive ability using logistic regression and a χ² statistic based on differences between observed and predicted outcomes for NR56 in a separate dataset. Comparison was also with respect to ranking of sires and correlations between sire posterior means (TL model) and PTA (LL model). We found very small differences in ability to predict NR56 between the 2 bivariate models, regardless of the dataset used. Correlations between sire posterior means (TL) and sire PTA (LL) and rank correlations between sire evaluations were all >0.98 in the 3 datasets. At present, the LL model is preferred for sire evaluations of NR56 and CFI in NRF. This is because the LL model is less computationally demanding and more robust with respect to the structure of the data than TL.     

Genetic analysis of clinical mastitis, milk fever, ketosis, and retained placenta in three lactations of Norwegian red cows

The objectives were to infer heritability and genetic correlations between clinical mastitis (CM), milk fever (MF), ketosis (KET), and retained placenta (RP) within and between the first 3 lactations and to estimate genetic change over time for these traits. Records of 372,227 daughters of 2411 Norwegian Red (NRF) sires were analyzed with a 12-variate (4 diseases × 3 lactations) threshold model. Within each lactation, absence or presence of each of the 4 diseases was scored based on the cow's health recordings. Each disease was assumed to be a different trait in each of the 3 lactations. The model for liability had trait-specific effects of year-season of calving and age of calving (first lactation) or month-year of calving and calving interval (second and third lactations), herd-5-yr, sire of the cow, and a residual. Posterior means of heritability of liability in first, second, and third lactations were 0.08, 0.07, and 0.07, respectively, for CM; 0.09, 0.11, and 0.13 for MF; 0.14, 0.16, and 0.15 for KET, and 0.08 in all 3 lactations for RP. Posterior means of genetic correlations between liability to CM, MF, KET, and RP, within disease between lactations, ranged from 0.19 to 0.86, and were highest between KET in different lactations. Correlations involving first lactation MF were low and had higher standard deviations. Genetic correlations between diseases were low or moderate (from −0.10 to 0.40), within as well as between lactations; the largest estimates were for MF and KET, and the lowest involved MF or KET and RP. Positive genetic correlations between diseases suggest that some general disease resistance factor with a genetic component exists. Trends of average sire posterior means by birth-year of daughters were used to assess genetic change, and the results indicated genetic improvement of resistance to CM and KET and no genetic change for MF and RP in the NRF population.     

Correlated selection responses for female fertility after selection for high protein yield or low mastitis frequency in Norwegian Red cows

Correlated selection responses in female fertility were estimated from a selection experiment with 2 groups of Norwegian Red cows selected for high protein yield (HPY) and low mastitis frequency (LCM), respectively. Genetic trends were calculated for nonreturn rate within 56 d after first insemination (NR56) for heifers, first-lactation cows, and second- and third-lactation cows, calving interval between first and second calving (CIN), and interval from calving to first insemination (CFI) for first-lactation cows and for second- and third-lactation cows. A total of 5,001 cows from the selection experiment had estimated breeding values for fertility, of which 2,806 were HPY and 2,195 were LCM cows. Permutation tests showed significant genetic differences between LCM and HPY for all fertility traits except CFI for second- and third-lactation cows. Observed differences between mean EBV in HPY and in LCM were, with few exceptions, far outside the range of the permutation test (i.e., significantly different from zero). LCM cows were, in general, genetically more fertile than HPY cows, with higher NR56 in heifers and cows, shorter CIN, and shorter CFI in first lactation. Genetic differences between HPY and LCM after 6 cow-generations were 2.5 percentage units NR56 in heifers, 2 percentage units NR56 in cows, and 4 d for CIN. No difference was found for CFI in second and third lactation. This is the first report of genetic change in female fertility as a correlated response after selection against mastitis.     

Genetic analyses of claw health in Norwegian Red cows

The aim of this study was genetic analyses of claw health in Norwegian Red. Claw health status at claw trimming has, since 2004, been recorded in the Norwegian Dairy Herd Recording System. The claw trimmer records whether the cow has normal (healthy) claws or if one or more claw disorders are present. Nine defined claw disorders were recorded: corkscrew claw (CSC), heel horn erosion (HH), dermatitis (DE), sole ulcer (SU), white line disorder (WLD), hemorrhage of sole and white line (HSW), interdigital phlegmon (IDP), lameness (LAME), and acute trauma (AT). Data from 2004 to 2011, with a total of 204,892 claw health records, were analyzed. The disorders were defined as binary traits with 1 record per cow per lactation. Further, 3 groups of claw disorders were analyzed: infectious claw disorders (INFEC, containing HH, DE, and IDP); laminitis-related claw disorders (LAMIN, containing SU, WLD, and HSW); and overall claw disorder. The 9 single traits and the 3 groups were analyzed using univariate threshold sire models. Multivariate threshold models were performed for the 5 most frequent single traits (CSC, HH, DE, SU, and WLD) and for CSC together with the grouped traits INFEC and LAMIN. Posterior mean of heritability of liability ranged from 0.04 to 0.23, where CSC had the highest heritability. The posterior standard deviations of heritability were low, between 0.01 and 0.03, except for IDP (0.06). Heritability of liability to INFEC and LAMIN were both 0.11 and for overall claw disorders, the heritability was 0.13. Posterior means of the genetic correlation among the 5 claw disorders varied between 0.02 and 0.79, and the genetic correlations between DE and HH (0.65) and between WLD and SU (0.79) were highest. Genetic correlation between INFEC and CSC was close to zero (0.06), between LAMIN and CSC it was 0.31, and between LAMIN and INFEC it was 0.24. The results show that claw disorders are sufficiently heritable for genetic evaluation and inclusion in the breeding scheme. At present, data are scarce with few recorded daughters per sire. Claw trimming records from more herds would therefore be beneficial for routine genetic evaluation of claw health.     

Short communication: Genetic aspects of milk differential somatic cell count in Holstein cows: A preliminary analysis

The aim of the present study was to assess genetic variation and heritability of a novel indicator of udder health, milk differential somatic cell count (DSCC), which represents the percentage of neutrophils plus lymphocytes in the total somatic cell count (SCC). Furthermore, we estimated genetic and phenotypic correlations of DSCC with other milk traits routinely measured in Italian Holstein cows. Besides DSCC, test-day data included milk yield, composition traits (i.e., fat, protein, casein, and lactose percentages), pH, milk urea nitrogen, and SCC. After editing, the final data set included 10,709 test-day records of 5,142 cows in 299 herds. Mean of DSCC was 62.07%, which means that macrophages were approximately 38% of total SCC. Comparing our results with the literature offered compelling evidence of the importance of acquiring information about the proportion of the different cell types in milk to better define the udder health status. In addition, our analysis revealed, for the first time, that DSCC is a heritable trait, and heritability (0.08 ± 0.02) was higher than that of traditional somatic cell score (0.04 ± 0.02). Nevertheless, heritability of DSCC is still low compared with milk yield and quality traits. Single-trait analysis within parity showed that DSCC was less heritable in primiparous than in multiparous cows, whereas bivariate analysis confirmed that DSCC and somatic cell score were 2 different traits, as their genetic and phenotypic correlations differed from unity. From a genetic point of view, the DSCC was positively weakly associated with milk yield, lactose percentage, and milk urea nitrogen, and negatively associated with pH. Our findings contributed to the understanding of the genetic background of DSCC and are a precursor to the potential use of DSCC in breeding programs to enhance cow resistance to mastitis. However, further research is needed to determine the weight this novel trait should receive in a selection program aimed to reduce udder health problems.     

Short communication: Validation of two animal models for estimation of genetic trends for female fertility in Norwegian dairy cattle

Two animal models were compared with respect to potential bias in genetic trend estimates for female fertility and for their predictive ability. In addition to either a fixed effect for month of first insemination or for month-year of first insemination, the models had fixed effects of age and double insemination and random effects of herd-year and animal. The model with a fixed effect of month of first insemination had a larger positive genetic trend for 56-d nonreturn rate in virgin heifers (0.16% yr), smaller downward bias, and somewhat higher predictive ability. These results demonstrate the importance of verifying models to be used in the calculation of breeding values.     

Short communication: Genetic parameters for mastitis and its predictors in Canadian Holsteins

The objective of this study was to estimate genetic parameters for mastitis and its predictors [mean somatic cell score (SCS) in early lactation, standard deviation of SCS, excessive test-day somatic cell count (SCC), udder depth (UD), fore udder attachment (FUA), and body condition score (BCS)]. Mastitis data recorded by producers were available from the national dairy cattle health system in Canada. Mastitis was defined as a binary variable based on whether or not the cow had at least 1 mastitis case in the period from calving to 305 d after calving. A Bayesian analysis using Gibbs sampling was applied. Threshold liability models were applied for binary traits (mastitis and excessive test-day SCC), and linear models were used for other normally distributed traits. For mastitis, a heritability of 0.07 was obtained. Heritability estimates for mean SCS in early lactation, standard deviation of SCS, excessive test-day SCC, UD, FUA, and BCS were 0.10, 0.04, 0.06, 0.41, 0.21, and 0.18, respectively. Mastitis was highly correlated with mean SCS in early lactation (0.63), standard deviation of SCS (0.74), and excessive test-day SCC (0.76). Moderate genetic correlations of −0.36, −0.24, and −0.28 were found between mastitis and UD, FUA, and BCS, respectively. As much as 72% of the genetic variation in mastitis resistance was explained by all the indirect predictor traits, whereas the most commonly used indirect measures of mastitis resistance (SCS in early lactation, UD, and FUA) explained together only 46% of the genetic variation in mastitis resistance. A combination of mean and standard deviation of SCS seem to be more successful in improving udder health than the traditional indirect measures. The results of the present study highlight that although routine cow SCC is the best measurement to monitor udder health, it cannot explain all the genetic variation in mastitis resistance and, therefore, direct information on mastitis resistance can be expected to yield to a more accurate genetic evaluation for this trait.     

Short communication: genetic correlation between test-day electrical conductivity of milk and mastitis

Electrical conductivity (EC) of milk is an indicator of mastitis. If EC shows genetic variation and is genetically correlated to mastitis, it could be used in a breeding program that includes selection for improved mastitis resistance. In this study, daily records of EC and mastitis from about 1,500 Holstein cows were analyzed. A bivariate animal model was used for estimation of (co)variance components, including fixed effects of age of calving, herd-test-day, and days in milk, in addition to random additive genetic effects and permanent environmental effects. For EC, the estimated heritability was moderate (0.22 to 0.39), whereas for mastitis, the heritability was low (0.013). The genetic correlation between EC and mastitis was estimated to be 0.75, and genetic improvement of mastitis resistance should be feasible through selection for reduced EC.     

Multivariate threshold model analysis of clinical mastitis in multiparous norwegian dairy cattle

A Bayesian multivariate threshold model was fitted to clinical mastitis (CM) records from 372,227 daughters of 2411 Norwegian Dairy Cattle (NRF) sires. All cases of veterinary-treated CM occurring from 30 d before first calving to culling or 300 d after third calving were included. Lactations were divided into 4 intervals: -30 to 0 d, 1 to 30 d, 31 to 120 d, and 121 to 300 d after calving. Within each interval, absence or presence of CM was scored as "0" or "1" based on the CM episodes. A 12-variate (3 lactations x 4 intervals) threshold model was used, assuming that CM was a different trait in each interval. Residuals were assumed correlated within lactation but independent between lactations. The model for liability to CM had interval-specific effects of month-year of calving, age at calving (first lactation), or calving interval (second and third lactations), herd-5-yr-period, sire of the cow, plus a residual. Posterior mean of heritability of liability to CM was 0.09 and 0.05 in the first and last intervals, respectively, and between 0.06 and 0.07 for other intervals. Posterior means of genetic correlations of liability to CM between intervals ranged from 0.24 (between intervals 1 and 12) to 0.73 (between intervals 1 and 2), suggesting interval-specific genetic control of resistance to mastitis. Residual correlations ranged from 0.08 to 0.17 for adjacent intervals, and between -0.01 and 0.03 for nonadjacent intervals. Trends of mean sire posterior means by birth year of daughters were used to assess genetic change. The 12 traits showed similar trends, with little or no genetic change from 1976 to 1986, and genetic improvement in resistance to mastitis thereafter. Annual genetic change was larger for intervals in first lactation when compared with second or third lactation. Within lactation, genetic change was larger for intervals early in lactation, and more so in the first lactation. This reflects that selection against mastitis in NRF has emphasized mainly CM in early first lactation, with favorable correlated selection responses in second and third lactations suggested.     

Genetic analysis of pathogen-specific clinical mastitis in Norwegian Red cows

The objective of this study was to estimate heritabilities and genetic correlations for pathogen-specific clinical mastitis (CM) in Norwegian Red cows. In Norway, breeding values for mastitis are predicted based on records of veterinary treatments of clinical mastitis. Bacteriological milk sample results from the mastitis laboratories have been recorded routinely into the Norwegian Dairy Herd Recording System since 2000, but have so far not been used in genetic analyses. This additional source of data may provide valuable information on pathogen-specific CM. Records from 234,088 first-lactation Norwegian Red cows, daughters of 1,656 sires, were used for genetic analyses of unspecific, Staphylococcus aureus, Streptococcus dysgalactiae, and Escherichia coli CM. The 4 CM traits were defined as binary and scored as 1 if the cow had at least 1 case of the CM in question and 0 otherwise. A Bayesian approach using Gibbs sampling was applied, and a multivariate threshold liability model was used for the analyses. The posterior mean (SD ≤ 0.01) of the heritabilities were 0.06 for liability of unspecific CM, 0.04 for Staph. aureus CM, 0.02 for Strep. dysgalactiae CM, and 0.03 for E. coli CM. The posterior mean (SD) of the genetic correlations were all high, ranging from 0.75 (0.14) to 0.87 (0.07). The highest genetic correlation was found between unspecific CM and Strep. dysgalactiae CM, whereas the lowest was found for E. coli CM and Staph. aureus CM. Genetic correlations lower than 1 indicate that mastitis caused by different pathogens can be considered as partly different traits. In spite of high rank correlations (0.95-0.98), some re-ranking of sires was observed.