Genetic analyses of mastitis data using animal threshold models and genetic correlation with production traits

In the present study, 6 different mastitis data sets of 3 dairy herds with an overall herd size of 3200 German Holstein cows were analyzed. Data collection periods included the first 50, 100, or 300 d of lactation. The 3 data collection periods were analyzed with a lactation model and a test-day model. All models were animal threshold models. Mastitis frequencies in the lactation model data sets varied between 29 and 45%, and varied between 3 and 6% in the test-day model data sets. Depending on the period of data collection, heritabilities of liability to mastitis in the lactation models were 0.05 (50 d), 0.06 (100 d), and 0.07 (300 d). In the test-day models, heritabilities were slightly higher with values of 0.09 (50 and 100 d), and 0.06 (300 d). Between lactation models, the rank correlations between the relative breeding values were high and varied between 0.86 and 0.94. Rank correlations between the relative breeding values of the test-day models ranged from 0.68 to 0.87. The rank correlations between the relative breeding values of lactation models and test-day models varied from 0.51 and 0.80. Genetic correlations between mastitis and milk production traits were estimated with a linear animal test-day model. The correlations with mastitis were 0.29 (milk yield), 0.30 (fat yield), 0.20 (fat content), 0.34 (protein yield), and 0.20 (protein content). The estimated genetic correlation between mastitis and somatic cell score was 0.84.     

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.     

Bayesian analysis of liability of clinical mastitis in Norwegian cattle with a threshold model: effects of data sampling method and model specification.

First-lactation records of Norwegian Cattle were used to infer heritability of liability to clinical mastitis with a threshold sire model. Mastitis was defined as a binary response (presence or absence) in a defined period of first lactation (opportunity period). Length of opportunity period (from 30 d before calving up to 120 or 300 d of lactation) had less effect on heritability estimates than data sampling methods (include or exclude records of cows culled before the end of the opportunity period) whereas sire ranking was more affected by the former. Including all cows, whether culled before the end of the opportunity period or not, gave a sharper and more symmetric posterior distribution of heritability of liability to clinical mastitis. When we analyzed data for all cows, model specification had a small effect on heritability estimates, while sire ranking was affected markedly. Posterior means of heritability range from 0.058 to 0.074. A model regressing on the length of the opportunity period for culled cows without mastitis, was shown favorable for the two opportunity periods using Bayes factors and the deviance information criterion for model comparison. This model, in which liability of mastitis depends on time to culling, may allow utilizing information from all first lactations in genetic evaluation, irrespectively of duration and culling outcome.     

Genetic analysis of clinical mastitis data from on-farm management software using threshold models

Producer-recorded clinical mastitis data from 77,791 cows in 418 herds were used to determine the potential for genetic improvement of mastitis resistance using data from on-farm management software programs. The following threshold sire models were applied: 1) a single-trait lactation model, where mastitis was recorded as 0 or 1 in first lactation only; 2) a 3-trait lactation model, where mastitis was recorded as 0 or 1 in each of the first 3 lactations, and 3) a 12-trait, lactation-segment model, where mastitis was recorded as 0 or 1 in each of 4 segments (0 to 50, 51 to 155, 156 to 260, and 261 to 365 d postpartum) in each of the first 3 lactations. Lactation incidence rates were 0.16, 0.20, and 0.24 in first, second, and third lactation, respectively, and incidence rates within various segments of these lactations ranged from 0.036 in late first lactation to 0.093 in early third lactation. Estimated heritability of liability to clinical mastitis ranged from 0.07 to 0.15, depending on the model and stage of lactation. Heritability estimates were higher in first lactation than in subsequent lactations, but estimates were generally similar for different segments of the same lactation. Genetic correlations between lactations from the 3-trait model ranged from 0.42 to 0.49, while correlations between segments within lactation from the 12-trait model ranged from 0.26 to 0.64. Based on the results presented herein, it appears that at least 2 segments are needed per lactation, because mastitis in early lactation is lowly correlated with mastitis in mid or late lactation. Predicted transmitting abilities of sires ranged from 0.77 to 0.89 for probability of no mastitis during the first lactation and from 0.36 to 0.59 for probability of no mastitis during the first 3 lactations. Overall, this study shows that farmer-recorded clinical mastitis data can make a valuable contribution to genetic selection programs, but additional systems for gathering and storing this information must be developed, and more extensive data recording in progeny test herds should be encouraged.     

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.     

Heritability estimates associated with alternative definitions of mastitis and correlations with somatic cell score and yield

The objectives of this study were to compare alternative mastitis definitions and to estimate genetic correlations of producer-recorded mastitis with somatic cell score (SCS) and yield. Cow health events and lactation records from June 2002 through October 2007 were provided by Dairy Records Management Systems (Raleigh, NC). First- through fifth-lactation records from cows calving between 20 and 120 mo of age and that calved in a herd-year with at least 1% of cows with a clinical mastitis event were retained. The edited data contained 118,516 lactation records and 1,072,741 test-day records of 64,893 cows. Mastitis occurrence (1 = at least one mastitis event during lactation or test-day interval, 0 = no mastitis events), number of mastitis events during lactation, SCS, and yield were analyzed with animal models (single trait) or sire-maternal grandsire models (multiple trait) in ASREML. Comparisons were made among models assuming a normal distribution, a binary distribution, or Poisson distribution (for total episodes). The overall incidence of clinical mastitis was 15.4%; and heritability estimates ranged from 0.73% (test-day interval mastitis with a linear model) to 11.07% (number of mastitis episodes with a Poisson model). Increased mastitis incidence was genetically correlated with higher SCS (range 0.66 to 0.88) and was generally correlated with higher yield (range −0.03 to 0.40), particularly during first lactation (0.04 to 0.40). Significant genetic variation exists for clinical mastitis; and health events recorded by producers could be used to generate genetic evaluations for cow health. Sires ranked similarly for daughter mastitis susceptibility regardless of how mastitis was defined; however, test-day interval mastitis and a total count of mastitis episodes per lactation allow a higher proportion of mastitis treatments to be included in the genetic analysis.     

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.     

Poisson versus threshold models for genetic analysis of clinical mastitis in US Holsteins

Typically, clinical mastitis is coded as the presence or absence of disease in a given lactation, and records are analyzed with either linear models or binary threshold models. Because the presence of mastitis may include cows with multiple episodes, there is a loss of information when counts are treated as binary responses. Poisson models are appropriated for random variables measured as the number of events, and although these models are used extensively in studying the epidemiology of mastitis, they have rarely been used for studying the genetic aspects of mastitis. Ordinal threshold models are pertinent for ordered categorical responses; although one can hypothesize that the number of clinical mastitis episodes per animal reflects a continuous underlying increase in mastitis susceptibility, these models have rarely been used in genetic analysis of mastitis. The objective of this study was to compare probit, Poisson, and ordinal threshold models for the genetic evaluation of US Holstein sires for clinical mastitis. Mastitis was measured as a binary trait or as the number of mastitis cases. Data from 44,908 first-parity cows recorded in on-farm herd management software were gathered, edited, and processed for the present study. The cows were daughters of 1,861 sires, distributed over 94 herds. Predictive ability was assessed via a 5-fold cross-validation using 2 loss functions: mean squared error of prediction (MSEP) as the end point and a cost difference function. The heritability estimates were 0.061 for mastitis measured as a binary trait in the probit model and 0.085 and 0.132 for the number of mastitis cases in the ordinal threshold and Poisson models, respectively; because of scale differences, only the probit and ordinal threshold models are directly comparable. Among healthy animals, MSEP was smallest for the probit model, and the cost function was smallest for the ordinal threshold model. Among diseased animals, MSEP and the cost function were smallest for the Poisson model, followed by the ordinal threshold model. In general, the models for count variables more accurately identified diseased animals and more accurately predicted mastitis costs. Healthy animals were more accurately identified by the probit model.     

Short communication: Genetic analysis of nonreturn rate and mastitis in first-lactation Norwegian Red cows

Associations between clinical mastitis (CM) and nonreturn rate within 56 d after first insemination (NR56) were examined in Norwegian Red (NRF) cows. Records on absence or presence of CM within each of the intervals, −30 to 30, 31 to 150, and 151 to 300 d after first calving, and records on NR56 for 620,492 first-lactation daughters of 3,064 NRF sires were analyzed with a Bayesian multivariate threshold liability model. Point estimates of genetic correlations between NR56 and the 3 CM traits were between −0.05 and −0.02. Residual correlations were close to zero, and correlations between herd-5-yr effects on NR56 and CM in the 3 lactation intervals ranged from −0.15 to −0.17. It appears that CM and NR56 in first lactation are independent traits.     

Genetic analysis of subclinical mastitis in early lactation of heifers using both linear and threshold models

Subclinical mastitis (SCM) causes economic losses for dairy producers by reducing milk production and leading to higher incidence of clinical mastitis and premature culling. The prevalence of SCM in first-lactation heifers is highest during early lactation. The objective of this study was to estimate genetic parameters for SCM in early lactation in first-parity Holsteins. Somatic cell count test-day records were collected monthly in 91 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 and 30 d in milk was considered for analysis. The final data set contained 8,518 records from first lactation Holstein heifers. Six alternative traits were defined as indicators of SCM, using various cutoff values of SCC, ranging from 150,000 to 400,000 cells/mL. Both linear and threshold animal models were used. Overall prevalence of SCM using the 6 traits ranged from 13 to 24%. Heritability estimates (standard error) from linear and threshold models ranged from 0.037 to 0.057 (0.015 to 0.018) and from 0.040 to 0.051 (0.017 to 0.020), respectively. We found strong genetic correlations (standard error) among alternative SCC traits, ranging from 0.90 to 0.99 (0.013 to 0.069), indicating that these 6 traits were genetically similar. Despite low heritability, based on estimated breeding values (EBV) predicted from both models, we noted exploitable genetic variation among sires. Higher EBV of SCM resistance corresponded to sires with a higher percentage of daughters without SCM. Based on a linear model (all 6 traits), percentage of daughters with SCM ranged from 5 to 13% and from 19 to 33% for the top 10% and worst 10% of 69 sires with minimum 20 daughters in at least 5 herds, respectively. Spearman's rank correlations among EBV of sires predicted from linear (from 0.75 to 0.95) and threshold (from 0.74 to 0.95) models were moderate to high, respectively. Very high rank correlations (0.98 to 0.99) between EBV predicted for the same trait from linear and threshold model indicated that reranking of sires based on model used was minimal. In conclusion, despite low heritability, we found utilizable genetic variation in early lactation of heifers. Hence, genetic selection to improve genetic resistance to SCM in early lactation of heifers was deemed possible.     

Effect of increased milking frequency in early lactation with or without recombinant bovine somatotropin

Multiparous Holstein cows (n = 300) were assigned to 1 of 2 milking frequency treatments at parturition. Cows were either milked 6 times (6×) or 3 times (3×) daily to determine effects on early lactation milk yields and subsequent lactation persistency with or without use of recombinant bST (rbST). Treatments included a control group milked 3× and 3 groups milked 6× for either the first 7, 14, or 21 days in milk (DIM). Those 4 groups of cows all received rbST starting at 63 DIM. The fifth treatment group was also milked 6× for the first 21 DIM but those cows received no rbST during the entire lactation. All cows returned to 3× milking after their respective treatment periods ended. Cows milked 3× tended to produce more milk (43.2 vs. 41.5 and 41.0 ± 1.1 kg/d) during the first 9 wk of lactation compared with cows milked 6× for 7 or 21 DIM, respectively. Group milk yields after wk 9 averaged 38.3 ± 0.7 kg/d and did not differ among various groups assigned to an increased milking frequency in early lactation. Percentages of milk fat (3.8 ± 0.12%) and protein (2.9 ± 0.06%) did not differ among treatments during the first 9 wk after calving. Early lactation milk yield (41.9 ± 1.2 kg/d) did not differ between the 2 groups of cows milked 6× for 21 DIM. However, cows subsequently administered rbST (at 63 DIM) produced more milk (38.8 vs. 34.2 ± 0.9 kg/d) from wk 10 to 44. The number of cows sent to the hospital during the 305-d trial for mastitis (97), digestive disorders (14), respiratory issues (9), lameness (22), or retained placenta (16), were not affected by treatments (χ² = 0.49). Under the conditions of this commercial dairy herd in Arizona, increasing milking frequency to 6 times daily for 7 to 21 d at the start of lactation conditions did not increase milk yield nor improve lactation persistency.     

Modeling lactation curves and estimation of genetic parameters for first lactation test-day records of French Holstein cows

Several functions were used to model the fixed part of the lactation curve and genetic parameters of milk test-day records to estimate using French Holstein data. Parametric curves (Legendre polynomials, Ali-Schaeffer curve, Wilmink curve), fixed classes curves (5-d classes), and regression splines were tested. The latter were appealing because they adjusted the data well, were relatively insensitive to outliers, were flexible, and resulted in smooth curves without requiring the estimation of a large number of parameters. Genetic parameters were estimated with an Average Information REML algorithm where the average information matrix and the first derivatives of the likelihood functions were pooled over 10 samples. This approach made it possible to handle larger data sets. The residual variance was modeled as a quadratic function of days in milk. Quartic Legendre polynomials were used to estimate (co)variances of random effects. The estimates were within the range of most other studies. The greatest genetic variance was in the middle of the lactation while residual and permanent environmental variances mostly decreased during the lactation. The resulting heritability ranged from 0.15 to 0.40. The genetic correlation between the extreme parts of the lactation was 0.35 but genetic correlations were higher than 0.90 for a large part of the lactation. The use of the pooling approach resulted in smaller standard errors for the genetic parameters when compared to those obtained with a single sample.     

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 and nongenetic factors associated with lactation length in seasonal-calving,pasture-based dairy cows

Lactation yield estimates standardized to common lactation lengths of 270-d or 305-d equivalents are commonly used in management decision support tools and dairy cow genetic evaluations. The use of such measurements to quantify the (genetic) merit of individual cows fails to penalize cows that do not reach the standardized lactation length, or indeed reward cows that lactate for more than the standardized lactation length. The objective of the present study was to quantify the genetic and nongenetic factors associated with lactation length in seasonal-calving, pasture-based dairy cows. A total of 616,350 lactation length records from 285,598 Irish cows were used. Linear mixed models were used to quantify the associations between lactation length and calving month, parity, age at calving, previous dry period length, calving difficulty score, heterosis, recombination loss, breed, and herd size, as well as to estimate the genetic and residual variance components of lactation length. The median lactation length in the edited data set was 288 d, with 27% of cows achieving lactations of at least 305 d. Relative to cows calving in January, the lactations of cow calving in February, March, or April was, on average, 4.2, 12.7, and 21.9 d shorter, respectively. The lactation length of a first parity cow was, on average, 7.8, 8.6, and 8.4 d shorter than that of second, third, and fourth parity cows, respectively. Norwegian Red and Montbéliarde cows had, on average, a 4.7- and 1.6-d shorter lactation than Holstein-Friesian cows, respectively. The heritability estimate, coefficient of genetic variation, and repeatability estimate of lactation length were 0.02, 1.2%, and 0.04, respectively. Based on the genetic standard deviation for lactation length estimated in the present study (3.3 d), cows ranked in the top 20% for genetic merit for lactation length would be expected to have lactations 9.2 d longer than cows in the bottom 20%, demonstrating exploitable genetic variability. Given the vast array of genetic and nongenetic factors associated with lactation length, an approach which combines improved management practices and selective breeding may be an efficient and effective strategy to lengthen lactations.     

Heritabilities of and genetic correlations among six health problems in Holstein cows

Information from 7712 lactations of Holstein dairy cows was collected from 33 commercial herds around Ithaca, NY in the 3 yr from 1981 to 1983. The data were divided into subsets corresponding to lactation 1, lactation 2, and lactation 3 or greater. To estimate heritabilities of dystocia, retained placenta, metritis, ovarian cysts, milk fever, and mastitis, a mixed linear model (herd-year fixed and sire random effects) with 0 or 1 as the observed response was used. Variance components were estimated using Henderson's Method 3. The results show moderate heritabilities (.15 to .40) for dystocia, metritis, milk fever, and mastitis and low heritability (less than .12) for retained placenta and cystic ovaries. Genetic correlations between dystocia, retained placenta, metritis, and mastitis were moderate in size and positive, whereas cystic ovaries were correlated negatively with dystocia and retained placenta. A general reproductive health trait (dystocia, retained placenta, metritis, cystic ovaries, and milk fever combined in one trait) also was analyzed. The estimated heritability of this trait was .21, .11, and .00 for first calf heifers, second lactation cows, and older cows, respectively.     

Clinical mastitis in Norwegian cattle: frequency, variance components, and genetic correlation with protein yield.

Records of clinical mastitis in first lactation Norwegian Cattle from 1978 onward were analyzed. Variance components for clinical mastitis were estimated with a linear sire model using records of more than 1.2 million cows from 2043 sires, resulting in heritability estimates of 0.035. Different strategies for extracting data gave very similar results, and estimated heritability for mastitis was the same with univariate and bivariate (with protein yield) analyses, which indicates that selection bias caused by correlated responses from other traits in the breeding goal is not a problem with this data set. The estimated genetic correlation between clinical mastitis and protein yield is 0.25.     

Genetic association of clinical mastitis with test-day somatic cell score and milk yield during first lactation of Finnish Ayrshire cows

In this study the genetic association during lactation of 2 clinical mastitis (CM) traits: CM1 (7 d before to 30 d after calving) and CM2 (31 to 300 d after calving) with test-day somatic cell score (SCS) and milk yield (MY) was assessed using multitrait random regression sire models. The data analyzed were from 27,557 first-lactation Finnish Ayrshire cows. Random regressions on second- and third-order Legendre polynomials were used to model the daily genetic and permanent environmental variances of test-day SCS and MY, respectively, while only the intercept term was fitted for CM. Results showed that genetic correlations between CM and the test-day traits varied during lactation. Genetic correlations between CM1 and CM2 and test-day SCS during lactation varied from 0.41 to 0.77 and from 0.34 to 0.71, respectively. Genetic correlations of test-day MY with CM1 and CM2 ranged from 0.13 to 0.51 and from 0.49 to 0.66, respectively. Correlations between CM1 and SCS were strongest during early lactation, whereas correlations between CM2 and SCS were strongest in late lactation. Genetic correlations lower than unity indicate that CM and SCS measure different aspects of the trait mastitis. Milk yield in early lactation was more strongly correlated with both CM1 and CM2 than milk yield in later lactation. This suggests that selection for higher lactation MY through selection on increased milk yield in early lactation will have a more deleterious effect on genetic resistance to mastitis than selection for higher yield in late lactation. The approach used in this study for the estimation of the genetic associations between test-day and CM traits could be used to combine information from traits with different data structures, such as test-day SCS and CM traits in a multitrait random regression model for the genetic evaluation of udder health.     

Genetic parameters for clinical mastitis, somatic cell score, production, udder type traits, and milking ease in first lactation Holsteins.

Genetic parameters were estimated by restricted maximum likelihood with an animal model on first lactation data of 29,284 French Holstein cows for clinical mastitis, lactation somatic cell score, milking ease, production, and nine udder type traits. The heritability was low for clinical mastitis (0.024), moderate for lactation somatic cell score (0.17) and milking ease (0.17), and ranged from 0.17 to 0.30 for type traits. A high (0.72) but lower than unity genetic correlation was found between clinical mastitis and lactation somatic cell score and indicated that both traits were genetically favorably associated. The antagonism with production was stronger for clinical mastitis than for lactation somatic cell score (genetic correlations 0.45 and 0.15, respectively). Udder depth, fore-udder attachment, and udder balance were favorably associated with lactation somatic cell score and clinical mastitis with genetic correlations ranging from -0.29 to -0.46, whereas low correlations were found with teat length. Milking ease was found to be unfavorably correlated with lactation somatic cell score (genetic correlation 0.44) but not with clinical mastitis.     

Recursive relationships between milk yield and somatic cell score of Canadian Holsteins from finite mixture random regression models

Finite mixture, multiple-trait, random regression animal models with recursive links between phenotypes for milk yield and somatic cell score (SCS) on the same test-day were applied to first lactation Canadian Holstein data. All models included fixed herd-test-day effects and fixed regressions within region-age at calving-season of calving classes, and animal additive genetic and permanent environmental regressions with random coefficients. Causal links between phenotypes for milk yield and SCS were fitted separately for records from healthy cows and cows with a putative, subclinical form of mastitis. Bayesian methods via Gibbs sampling were used for the estimation of model parameters. Bayes factors indicated superiority of the model with recursive link from milk to SCS over the reciprocal recursive model and the standard multiple-trait model. Differences between models measured by other, single-trait model comparison criteria (i.e., weighted mean squared error, squared bias, and correlation between observed and expected data) were negligible. Approximately 20% of test-day records were classified as originating from cows with mastitis in recursive mixture models. The proportion of records from cows infected with mastitis was largest at the beginning of lactation. Recursive mixture models exhibited different distributions of data from healthy and infected cows in different parts of lactation. A negative effect of milk to SCS (up to −0.15 score points for every kilogram of milk for healthy cows from 5 to 45 d in milk) was estimated for both mixture components (healthy and infected) in all stages of lactation for the most plausible model. The magnitude of this effect was stronger for healthy cows than for cows infected with mastitis. Different patterns of genetic and environmental correlations between milk and SCS for healthy and infected records were revealed, due to heterogeneity of structural coefficients between mixture components. Estimated breeding values for SCS from the best fitting model for sires of infected daughters were more related to estimated breeding values for the same trait from the regular multiple-trait model than evaluations for sires of mastitis-free cows.     

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.