Genetic analysis of mastitis data with different models

The aim of this study was to analyze different mastitis data sets with different statistical models and compare results. Data recording took place on 3 commercial milk farms with an average herd size of 3,200 German Holstein cows. Recording started in February 1998 and was completed in December 2005. During this period, 63,540 treatments for clinical mastitis were recorded. Five different data sets were analyzed and the number of cows varied between 12,972 and 13,618, depending on the data set. Data collection periods contained either the first 50 or the first 300 d of lactation. When the data-recording period ended after 50 d of lactation, data sets were analyzed with a lactation threshold model (LTM), a multiple threshold lactation model (MTLM), and a test-day threshold model (TDTM). In the LTM analysis, mastitis was treated as a binary trait coded as 0 (no mastitis) or 1 (mastitis), whereas in MTLM mastitis, codes were between 0 and 4, depending on the number of estimated days with mastitis. The TDTM treated each day as a single observation coded similarly to that of the LTM. When the data collection period included the first 300 d of lactation, data sets were analyzed with the LTM or MTLM only, because the TDTM was computationally infeasible. Mastitis frequencies in LTM data sets were 25.8 and 39.2%, and 26.9 and 39.2% in MTLM data sets, when data recording ended after 50 and 300 d of lactation, respectively. The mastitis frequency in the TDTM data set was 5.2%. Respective heritability estimates of liability to clinical mastitis were 0.08 and 0.09 using the LTM, and 0.08 and 0.11 using the MTLM. When the TDTM was used, the estimated heritability was 0.15. Rank correlation between breeding values of the different data sets ranged between 0.40 and 0.97. Rank correlation between the LTM and MTLM were higher (0.78 to 0.97) than those between these 2 models and the TDTM (0.40 to 0.59).The MTLM combined the positive effects of both the LTM, with respect to the size of the data sets, and the TDTM, with respect to the lack of information.     

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.     

Short communication: Effect of preadjusting test-day yields for stage of pregnancy on variance component estimation in Canadian Ayrshires

Preadjustment of phenotypic records is an alternative to accounting for the effect of pregnancy within the genetic evaluation model. Variance components used in the Canadian Test-Day Model may need to be re-estimated after preadjusting for pregnancy. The objective of this study was to assess the effect of preadjusting test-day yields on variance components and estimated breeding values using a random regression test-day model in a random sample of Ayrshire cows. A random sample of 981 Canadian Ayrshire cows from 18 complete herds (average of 54.5 cows/herd) was analyzed. Two data sets were created using the same animals, one with unadjusted milk, fat, and protein yields, and one data set with test-day records adjusted for pregnancy effects. Pregnancy effect estimates from a previous study were used for additive preadjustment of records. Variance components were estimated using both data sets. Results were very similar between the 2 data sets for all estimated genetic parameters (heritabilities, genetic, and permanent environmental correlations). The relative squared differences were very small: 0.05% for heritabilities, 0.20% for genetic correlations, and 0.18% for permanent environmental correlations. Furthermore, paired Student's t-tests showed that the differences between the genetic parameters of data sets adjusted and unadjusted for pregnancy effect were not significantly different from 0. Results from this study show that preadjusting data for pregnancy did not yield changes in covariance component estimates, thus suggesting that preadjusting test-day records could be a feasible solution to account for pregnancy in the Canadian Test-Day Model without changing the current model. Estimated breeding values (EBV) were calculated for both data sets to observe the impact of preadjusting for pregnancy. Overall, the largest changes in EBV seen when preadjusting for pregnancy (compared with unadjusted records) occurred for nonpregnant elite cows, whose EBV declined. Preadjusting for pregnancy before genetic evaluations improves the estimation of breeding values by adding the negative impact of pregnancy back onto pregnant cow test-day records, causing an increase in their production EBV.     

Bayesian estimates of covariance components between lactation curve parameters and disease liability in Danish Holstein cows

In the present work, covariance components for milk yield and disease liability were estimated with bivariate random regression test-day sire models using a Bayesian approach and implemented via the Gibbs sampler. The data consist of 8075 first-parity Danish Holstein (DH) cows, from 1259 sires, performing in 57 herds from 1992 to 1997. Treatments associated with five different type of diseases were pooled into a single general disease liability for each cow. Two models were fitted to the data. First, using a bivariate model, milk yield is modeled via a random regression, and disease liability via a repeatablility model. Second, using a bivariate model, both milk yield and disease liability are modeled using random regressions. A comparison based on a Bayes factor provides very strong support for the bivariate random regression model. Posterior means of heritabilities for each of the traits were estimated for five different points in time throughout lactation. Across models, heritabilities for milk yield are lowest in the beginning of the lactation (0.19) and highest at the end of the lactation (0.35). Posterior means of heritabilities of disease liability range from 0.04 to 0.10 for test days, and is equal to 0.20 for the whole lactation. Heritability of persistency measures estimated from the two models are 0.20 and 0.21. Estimates of posterior means of genetic correlations between single test-day milk yield and single test-day disease liability are in the range of 0.31 to 0.57. The estimates of posterior mean and of the 95% posterior interval of the genetic correlation between persistency and (total) disease liability using the model with the highest posterior probability are -0.12 and (-0.44; 0.20), respectively. Even though the largest proportion of the posterior probability mass is spread along negative values of the correlation (indicating that individuals with a flatter lactation curve tend to have lower disease liability), a value of zero of the genetic correlation falls comfortably within the 95% posterior interval. Thus the prospects of reducing incidence of disease by manipulating persistency as defined in this work remain inconclusive.     

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 relationships of clinical mastitis,cystic ovaries,and lameness with milk yield and somatic cell score in first-lactation Canadian Holsteins

The objective of this study was to investigate the genetic relationships of the 3 most frequently reported dairy cattle diseases (clinical mastitis, cystic ovaries, and lameness) with test-day milk yield and somatic cell score (SCS) in first-lactation Canadian Holstein cows using random regression models. Health data recorded by producers were available from the National Dairy Cattle Health System in Canada. Disease traits were defined as binary traits (0 = healthy, 1 = affected) based on whether or not the cow had at least one disease case recorded within 305 d after calving. Mean frequencies of clinical mastitis, cystic ovaries, and lameness were 12.7, 8.2, and 9.1%, respectively. For genetic analyses, a Bayesian approach using Gibbs sampling was applied. Bivariate linear sire random regression model analyses were carried out between each of the 3 disease traits and test-day milk yield or SCS. Random regressions on second-degree Legendre polynomials were used to model the daily sire additive genetic and cow effects on test-day milk yield and SCS, whereas only the intercept term was fitted for disease traits. Estimated heritabilities were 0.03, 0.03, and 0.02 for clinical mastitis, cystic ovaries, and lameness, respectively. Average heritabilities for milk yield were between 0.41 and 0.49. Average heritabilities for SCS ranged from 0.10 to 0.12. The average genetic correlations between daily milk yield and clinical mastitis, cystic ovaries, and lameness were 0.40, 0.26, and 0.23, respectively; however, the last estimate was not statistically different from zero. Cows with a high genetic merit for milk yield during the lactation were more susceptible to clinical mastitis and cystic ovaries. Estimates of genetic correlations between daily milk yield and clinical mastitis were moderate throughout the lactation. The genetic correlations between daily milk yield and cystic ovaries were near zero at the beginning of lactation and were highest at mid and end lactation. The average genetic correlation between daily SCS and clinical mastitis was 0.59 and was consistent throughout the lactation. The average genetic correlation between daily SCS and cystic ovaries was near zero (−0.01), whereas a moderate, but nonsignificant, correlation of 0.27 was observed between SCS and lameness. Unfavorable genetic associations between milk yield and diseases imply that production and health traits should be considered simultaneously in genetic selection.     

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.     

Random regression test-day model for clinical mastitis: Genetic parameters,model comparison,and correlations with indicator traits

The objective was to study genetic (co)variance components for binary clinical mastitis (CM), test-day protein yield, and udder health indicator traits [test-day somatic cell score (SCS) and type traits of the udder composite] in the course of lactation with random regression models (RRM). The study used a data set from selected 15 large-scale contract herds including 26,651 Holstein cows. Test-day production and CM data were recorded from 2007 to 2012 and comprised parities 1 to 3. A longitudinal CM data structure was generated by assigning CM records to adjacent official test dates. Bivariate threshold-linear RRM were applied to estimate genetic (co)variance components between longitudinal binary CM (0 = healthy; 1 = diseased) and longitudinal Gaussian distributed protein yield and SCS test-day data. Heritabilities for liability to CM (heritability ~0.15 from 0 to 305 d after calving) were slightly higher than for SCS for corresponding days in milk (DIM) in the course of lactation. Daily genetic correlations between CM and SCS were moderate to high (genetic correlation ~0.70), but substantially decreased at the very end of lactation. Genetic correlations between CM at different test days were close to 1 for adjacent test days, but were close to zero for test days far apart. Daily genetic correlations between CM and protein yield were low to moderate. For identical DIM (e.g., DIM 20, 160, and 300), genetic correlations were −0.03, 0.11, and 0.18, respectively, and disproved pronounced genetic antagonisms between udder health and productivity. Correlations between estimated breeding values (EBV) for CM from the RRM and official EBV for linear type traits of the udder composite, including EBV from 74 influential sires (sires with >60 daughters), were −0.31 for front teat placement, −0.01 for rear teat placement, −0.31 for fore udder attachment, −0.32 for udder depth, and −0.08 for teat length. Estimated breeding values for CM from the RRM were compared with EBV from a multiple-trait model and with EBV from a repeatability model. For test days covering an identical time span and on a lactation level, correlations between EBV from RRM, multiple-trait model, and repeatability model were close to 1. Most relevant results suggest the routine application of threshold RRM to binary CM to (1) allow selection of genetically superior sires for distinct stages of lactation and (2) achieve higher selection response in CM compared with selection strategies based on indicator type traits or based on the indicator-trait SCS.     

Alternative somatic cell count traits to improve mastitis resistance in Canadian Holsteins

The objective of this study was to investigate whether alternative somatic cell count (SCC) traits are suitable as mastitis indicators in Canadian Holsteins. 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 one mastitis case in the period from calving to 305 d after calving. The analyzed alternative SCC traits included mean somatic cell score (SCS) from different time periods, maximum SCS, standard deviation of SCS, excessive test-day SCC, and a peak pattern of test-day records with suspicion of mastitis. Data of 53,626 first-lactation Holstein cows from 1,666 herds across Canada were analyzed using linear animal models. A heritability of 0.02 was obtained for mastitis. For both mean SCS in early and late lactation, a heritability of 0.11 was estimated. Heritabilities of various patterns of SCC ranged from 0.01 to 0.07. Estimated genetic correlations were 0.69 and 0.68 between mastitis and mean SCS in early and late lactation, respectively. Higher genetic correlations were found between mastitis and the different SCC patterns (0.82 to 0.91). Sires with high breeding values for mastitis resistance had consistently higher percentage of healthy daughters than sires with low breeding values for mastitis resistance. Breeding values for mean SCS in early lactation, standard deviation of SCS, and an excessive test-day SCC pattern (at least one SCC test-day above 500,000) were the best predictors of the breeding value for mastitis resistance and explained in total 41% of the variation in relative breeding values for mastitis resistance. The results demonstrated that patterns of SCC provide additional information for genetic evaluations of mastitis resistance that cannot be explained by mean SCS alone.     

Genetic analysis of somatic cell score in danish holsteins using a liability-normal mixture model

Mixture models are appealing for identifying hidden structures affecting somatic cell score (SCS) data, such as unrecorded cases of subclinical mastitis. Thus, liability-normal mixture (LNM) models were used for genetic analysis of SCS data, with the aim of predicting breeding values for such cases of mastitis. Here, putative mastitis statuses and breeding values for liability to putative mastitis were inferred solely from SCS observations. In total, there were 395,906 test-day records for SCS from 50,607 Danish Holstein cows. Four different statistical models were fitted: A) a classical (nonmixture) random regression model for test-day SCS; B1) an LNM test-day model assuming homogeneous (co)variance components for SCS from healthy (IMI-) and infected (IMI+) udders; B2) an LNM model identical to B1, but assuming heterogeneous residual variances for SCS from IMI- and IMI+ udders; and C) an LNM model assuming fully heterogeneous (co)variance components of SCS from IMI- and IMI+ udders. For the LNM models, parameters were estimated with Gibbs sampling. For model C, variance components for SCS were lower, and the corresponding heritabilities and repeatabilities were substantially greater for SCS from IMI- udders relative to SCS from IMI+ udders. Further, the genetic correlation between SCS of IMI- and SCS of IMI+ was 0.61, and heritability for liability to putative mastitis was 0.07. Models B2 and C allocated approximately 30% of SCS records to IMI+, but for model B1 this fraction was only 10%. The correlation between estimated breeding values for liability to putative mastitis based on the model (SCS for model A) and estimated breeding values for liability to clinical mastitis from the national evaluation was greatest for model B1, followed by models A, C, and B2. This may be explained by model B1 categorizing only the most extreme SCS observations as mastitic, and such cases of subclinical infections may be the most closely related to clinical (treated) mastitis.     

Genetic parameters across lactation for feed intake,fat- and protein-corrected milk,and liveweight in first-parity Holstein cattle

Breeding values for dry matter intake (DMI) are important to optimize dairy cattle breeding goals for feed efficiency. However, generally, only small data sets are available for feed intake, due to the cost and difficulty of measuring DMI, which makes understanding the genetic associations between traits across lactation difficult, let alone the possibility for selection of breeding animals. However, estimating national breeding values through cheaper and more easily measured correlated traits, such as milk yield and liveweight (LW), could be a first step to predict DMI. Combining DMI data across historical nutritional experiments might help to expand the data sets. Therefore, the objective was to estimate genetic parameters for DMI, fat- and protein-corrected milk (FPCM) yield, and LW across the entire first lactation using a relatively large data set combining experimental data across the Netherlands. A total of 30,483 weekly records for DMI, 49,977 for FPCM yield, and 31,956 for LW were available from 2,283 Dutch Holstein-Friesian first-parity cows between 1990 and 2011. Heritabilities, covariance components, and genetic correlations were estimated using a multivariate random regression model. The model included an effect for year-season of calving, and polynomials for age of cow at calving and days in milk (DIM). The random effects were experimental treatment, year-month of measurement, and the additive genetic, permanent environmental, and residual term. Additive genetic and permanent environmental effects were modeled using a third-order orthogonal polynomial. Estimated heritabilities ranged from 0.21 to 0.40 for DMI, from 0.20 to 0.43 for FPCM yield, and from 0.25 to 0.48 for LW across DIM. Genetic correlations between DMI at different DIM were relatively low during early and late lactation, compared with mid lactation. The genetic correlations between DMI and FPCM yield varied across DIM. This correlation was negative (up to −0.5) between FPCM yield in early lactation and DMI across the entire lactation, but highly positive (above 0.8) when both traits were in mid lactation. The correlation between DMI and LW was 0.6 during early lactation, but decreased to 0.4 during mid lactation. The highest correlations between FPCM yield and LW (0.3–0.5) were estimated during mid lactation. However, the genetic correlations between DMI and either FPCM yield or LW were not symmetric across DIM, and differed depending on which trait was measured first. The results of our study are useful to understand the genetic relationship of DMI, FPCM yield, and LW on specific days across lactation.     

Genetic parameters for lactose and its correlation with other milk production traits and fitness traits in pasture-based production systems

Lactose is a major component of milk (typically around 5% of composition) that is not usually directly considered in national genetic improvement programs of dairy cattle. Daily test-day lactose yields and percentage data from pasture-based seasonal calving herds in Australia were analyzed to assess if lactose content can be used for predicting fitness traits and if an additional benefit is achieved by including lactose yield in selecting for milk yield traits. Data on lactose percentage collected from 2007 to 2014, from about 600 herds, were used to estimated genetic parameters for lactose percentage and lactose yield and correlations with other milk yield traits, somatic cell count (SCC), calving interval (CIV), and survival. Daily test-day data were analyzed using bivariate random regression models. In addition, multi-trait models were also performed mainly to assess the value of lactose to predict fitness traits. The heritability of lactose percentage (0.25 to 0.37) was higher than lactose yield (0.11 to 0.20) in the first parity. Genetically, the correlation of lactose percentage with protein percentage varied from 0.3 at the beginning of lactation to ?0.24 at the end of the lactation in the first parity. Similar patterns in genetic correlations were also observed in the second and third parity. At all levels (i.e., genetic, permanent environmental, and residual), the correlation between milk yield and lactose yield was close to 1. The genetic and permanent environmental correlations between lactose percentage and SCC were stronger in the second and third parity and toward the end of the lactation (?0.35 to ?0.50) when SCC levels are at their maximum. The genetic correlation between lactose percentage in the first 120 d and CIV (?0.23) was similar to correlation of CIV with protein percentage (?0.28), another component trait with the potential to predict fertility. Furthermore, the correlations of estimated breeding values of lactose percentage and estimated breeding values of traits such as survival, fertility, SCC, and angularity suggest that the value of lactose percentage as a predictor of fitness traits is weak. The results also suggest that including lactose yield as a trait into the breeding objective is of limited value due to the high positive genetic correlation between lactose yield and protein yield, the trait highly emphasized in Australia. However, recording lactose percentage as part of the routine milk recording system will enable the Australian dairy industry to respond quickly to any future changes and market signals.     

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.     

Genetic evaluation of bulls and cows with single- and multiple-country test-day models

First-lactation milk yield test-day records on cows from Australia, Canada, Italy, and New Zealand were analyzed by single- and multiple-country random regression models. Models included fixed effects of herd-test day and breed composition-age at calving-season of calving by days in milk, and random regressions with Legendre polynomials of order four for animal genetic and permanent environmental effects. Milk yields in different countries were defined as genetically different traits for the purpose of multiple-trait model. Estimated breeding values of bulls and cows from single- and multiple-trait models were compared within and across countries for two traits: total milk yield in lactation and lactation persistency, defined as the linear coefficient of animal genetic curve. Correlations between single- and multiple-trait evaluations within country for total yield were higher than 0.95 for bulls and close to 1 for cows. Correlations for lactation persistency were lower than respective correlations for total yield. Between country correlations for lactation yield ranged from 0.93 to 0.96, indicating different ranking of bulls on different country scales under multiple-trait model. Lactation persistency had in general lower between-country correlations, with the highest values for Canada-Italy and Australia-New Zealand pairs, for both single- and multiple-country models. Although multiple-country random regression test-day model was computationally feasible for four countries, the same would not be true for routine international genetic evaluation in the near future.     

Relationships between milk yield and somatic cell score in Canadian Holsteins from simultaneous and recursive random regression models

Multiple-trait random regression animal models with simultaneous and recursive links between phenotypes for milk yield and somatic cell score (SCS) on the same test day were fitted to 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. Regressions were Legendre polynomials of order 4 on a scale from 5 to 305 d in milk (DIM). Bayesian methods via Gibbs sampling were used for the estimation of model parameters. Heterogeneity of structural coefficients was modeled across (the first 3 lactations) and within (4 DIM intervals) lactation. Model comparisons in terms of Bayes factors indicated the superiority of simultaneous models over the standard multiple-trait model and recursive parameterizations. A moderate heterogeneous (both across- and within-lactation) negative effect of SCS on milk yield (from −0.36 for 116 to 265 DIM in lactation 1 to −0.81 for 5 to 45 DIM in lactation 3) and a smaller positive reciprocal effect of SCS on milk yield (from 0.007 for 5 to 45 DIM in lactation 2 to 0.023 for 46 to 115 DIM in lactation 3) were estimated in the most plausible specification. No noticeable differences among models were detected for genetic and environmental variances and genetic parameters for the first 2 regression coefficients. The curves of genetic and permanent environmental variances, heritabilities, and genetic and phenotypic correlations between milk yield and SCS on a daily basis were different for different models. Rankings of bulls and cows for 305-d milk yield, average daily SCS, and milk lactation persistency remained the same among models. No apparent benefits are expected from fitting causal phenotypic relationships between milk yield and SCS on the same test day in the random regression test-day model for genetic evaluation purposes.     

Genetic parameters for first and second lactation milk yields of Polish black and white cattle with random regression test-day models

Single- and two-trait random regression models were applied to estimate variance components of test-day records of milk, fat, and protein yields in the first and second lactation of Polish Black and White cattle. The model included fixed herd test-day effect, three covariates to describe lactation curve nested within age-season classes, and random regressions for additive genetic and permanent environmental effects. In two-parity models, each parity was treated as a separate trait. For milk and the two-parity model, heritabilities were in the range of 0.14 to 0.19 throughout first lactation and 0.10 to 0.16 throughout second lactation. For fat, heritabilities were within 0.11 to 0.16 and 0.11 to 0.22 throughout first and second lactations, respectively. For protein in the two-parity model, heritabilities were within 0.10 to 0.15 throughout most of first lactation and within 0.06 to 0.15 throughout the most of second lactation. For milk, genetic correlations between the first and second parities were 0.6 at the beginning of the lactation, rising to 0.9 in the middle, and 0.8 at the end of the lactation. For fat, the corresponding correlations were 0.6, 0.8, and 0.7, respectively, and for protein were 0.6, 0.8, and 0.8, respectively. Heritability estimates for all traits were flatter for the two-parity model. Relatively smooth genetic and permanent environmental variances with the two-parity model indicated that large swings of heritabilities could be artifacts of single-trait random regression models. High correlations between most of test day records across lactations suggested that a repeatability model could be considered as an alternative to a multiple-trait model to analyze multiple parities.     

Use of repeated measures analysis for evaluation of genetic background of dairy cattle behavior in automatic milking systems

Milking frequencies measured at official test days were used with repeated measurement analysis to reveal the environmental and genetic impact on the milking frequency of cows in automatic milking systems. Repeated measurements were 3 test-day observations per cow within days in milk (DIM) classes, with 1,216 cows in DIM class 1 (d 0 to 99), from 1,112 cows in DIM class 2 (d 100 to 199), and from 1,004 cows in DIM class 3 (d 200 to 299) kept in 15 farms. Selection criteria for models analyzing repeated measurements were Akaike and Schwarz Bayesian values, which favored the autoregressive [AR(1)] covariance structure over the compound symmetry model. Results from the AR(1) model indicated a significant impact of fixed herd and parity effects. Milking frequencies decreased with increasing parities and were greatest for first-parity cows. High daily milk yield was associated with higher milking frequencies. Heritabilities for milking frequency were 0.16, 0.19, and 0.22 in DIM classes 1, 2, and 3, respectively, from the AR(1) model. Higher heritabilities in the later stage of lactation were due to a substantial reduction of the residual variance. Genetic correlations between test-day milk yield and daily milking frequency were in the range of 0.46 to 0.57 for all DIM classes and between milking frequency and somatic cell score were near zero. For verification of results, milking frequencies of the same cows obtained from herd management programs were averaged within DIM classes. Heritabilities were slightly above the values from the AR(1) model. In conclusion, heritabilities for milking frequency in automatic milking systems are moderate enough to incorporate this behavioral trait in a combined breeding goal. The inevitable improvement of labor efficiency in dairy cattle farming demands such cows going easily and voluntarily in automatic milking systems.     

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.     

Genetic and phenotypic relationships among milk yield and somatic cell count before and after clinical mastitis

This paper studies whether cows with originally lower somatic cell count (SCC) are more susceptible to clinical mastitis (CM) than cows with higher somatic cell count, and evaluates the correlations between CM, SCC, and milk yield. Data were extracted from the Finnish national milk-recording database and from the health recording system. First and second lactation records of 87,861 Ayrshire cows calving between January 1998 and December 2000 were included. Traits studied were incidence of CM, test-day SCC, and test-day milk yield before and following CM. Genetic parameters were estimated using multitrait REML with a sire model. Results did not indicate that cows with genetically low SCC would be more susceptible to CM. The genetic correlation between CM in the first and second lactation was reasonably high (0.73), suggesting that susceptibility to mastitis remains similar across lactations. The genetic correlation between CM and milk yield traits was positive (from 0.38 to 0.56), confirming the genetic antagonism between production and udder health traits. The genetic correlation between SCC and milk was positive in the first lactation, but negative, or near zero in the second lactation. This indicates that breeding for lower SCC might not affect milk production in later lactations. The results of this study support the use of SCC as an indicator of mastitis and a tool for selection for mastitis resistance.     

Genetic analysis of milk urea nitrogen and relationships with yield and fertility across lactation

The aim of this project was to investigate the relationship of milk urea nitrogen (MUN) with 3 milk production traits [milk yield (MY), fat yield (FY), protein yield (PY)] and 6 fertility measures (number of inseminations, calving interval, interval from calving to first insemination, interval from calving to last insemination, interval from first to last insemination, and pregnancy at first insemination). Data consisted of 635,289 test-day records of MY, FY, PY, and MUN on 76,959 first-lactation Swedish Holstein cows calving from 2001 to 2003, and corresponding lactation records for the fertility traits. Yields and MUN were analyzed with a random regression model followed by a multi-trait model in which the lactation was broken into 10 monthly periods. Heritability for MUN was stable across lactation (between 0.16 and 0.18), whereas MY, FY, and PY had low heritability at the beginning of lactation, which increased with time and stabilized after 100 d in milk, at 0.47, 0.36, and 0.44, respectively. Fertility traits had low heritabilities (0.02 to 0.05). Phenotypic correlations of MUN and milk production traits were between 0.13 (beginning of lactation) and 0.00 (end of lactation). Genetic correlations of MUN and MY, FY, and PY followed similar trends and were positive (0.22) at the beginning and negative (−0.15) at the end of lactation. Phenotypic correlations of MUN and fertility were close to zero. A surprising result was that genetic correlations of MUN and fertility traits suggest a positive relationship between the 2 traits for most of the lactation, indicating that animals with breeding values for increased MUN also had breeding values for improved fertility. This result was obtained with a random regression model as well as with a multi-trait model. The analyzed group of cows had a moderate level of MUN concentration. In such a population MUN concentration may increase slightly due to selection for improved fertility. Conversely, selection for increased MUN concentration may improve fertility slightly.