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.     

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.     

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.     

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 association between susceptibility to clinical mastitis and protein yield in norwegian dairy cattle

The objective of this study was to examine associations between susceptibility to clinical mastitis and protein yield in first-lactation Norwegian Dairy Cattle (NRF) cows. Records from 372,227 first-lactation daughters of 2411 NRF sires were analyzed bivariately, using a threshold-liability model for clinical mastitis and a linear Gaussian model for 305-d protein yield. The mean (SD) of the posterior distribution of heritability was 0.08 (0.004) for susceptibility to clinical mastitis and 0.19 (0.007) for 305-d protein yield. The posterior mean (SD) of the genetic correlation between susceptibility to clinical mastitis and 305-d protein yield was 0.43 (0.03). Posterior means of the correlations between herd-5-yr effects, and between model residuals were 0.19 and -0.008, respectively. Corresponding estimates of genetic, herd-5-yr, and residual correlations from a bivariate linear model analysis were 0.42, 0.18, and -0.008, respectively. An antagonistic genetic relationship between clinical mastitis and protein yield was corroborated.     

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.     

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.     

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.     

Genetic evaluation of susceptibility to clinical mastitis in Spanish Holstein cows

This study had 3 objectives: to estimate genetic parameters and predict sires’ transmitting abilities for clinical mastitis in a Spanish Holstein population, to propose a methodology for comparing models with different response variables by using a cost-based loss function, and to evaluate alternative genetic evaluation models by using this methodology. On-farm records for clinical mastitis from herds in 3 Spanish regions were analyzed as a binary trait (CM) and as number of episodes (NCM) per lactation. Linear and probit models were fitted for CM, whereas linear and Poisson models were used for NCM. Predictive ability of the models was evaluated by using the average predicted residual sum of squares from cross-validation and an alternative cost-based loss function. The loss function for model comparison was calculated by using average mastitis costs depending on the NCM and average cost per infected lactation. The average cost per infected lactation was $345.58, whereas the cost per lactation ranged from $204.86 to $985.44 for lactations with 1 to 5 cases, respectively. Management and hygiene practices on individual farms had a large impact on clinical mastitis because the herd-year variance was larger than that of other random effects considered. The sire variance was significantly different from zero, confirming that genetic variation exists for clinical mastitis. Estimates of heritability for CM using the linear and probit models were 0.07 and 0.10 on the underlying scale, respectively. For NCM, the estimate of heritability for the linear model was 0.10 and estimates for the Poisson model evaluated at the mean and the median of lambda on the underlying scale were 0.09 and 0.07, respectively. Regarding ranking of sires, the definition of response variable (CM or NCM) was of greater importance than the choice of statistical model. Cross-validation results indicated that models with the best fit for CM and NCM were the probit model and the linear model, respectively. However, a comparison across all models using the alternative cost-based loss function showed that using NCM as a response variable with a Poisson model provided the most accurate predictions of future costs associated with clinical mastitis.     

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.     

Comparison of different models for genetic analysis of clinical mastitis in Austrian Fleckvieh dual-purpose cows

The performance of different models for genetic analyses of clinical mastitis in Austrian Fleckvieh dual-purpose cows was evaluated. The main objective was to compare threshold sire models (probit and logit) with linear sire and linear animal models using REML algorithm. For comparison, data were also analyzed using a Bayesian threshold sire model. The models were evaluated with respect to ranking of sires and their predictive ability in cross-validation. Only minor differences were observed in estimated variance components and heritability from Bayesian and REML probit models. Heritabilities for probit and logit models were 0.06 and 0.08, respectively, whereas heritabilities for linear sire and linear animal models were lower (0.02). Correlations among ranking of sires from threshold and linear sire models were high (>0.99), whereas correlations between any sire model (threshold or linear) and the linear animal model were slightly lower (0.96). The worst sires were ranked very similar across all models, whereas for the best sires some reranking occurred. Further, models were evaluated based on their ability to predict future data, which is one of the main concerns of animal breeders. The predictive ability of each model was determined by using 2 criteria: mean squared error and Pearson correlation between predicted and observed value. Overall, the 5 models did not differ in predictive ability. In contrast to expectations, sire models had the same predictive ability as animal models. Linear models were found to be robust toward departures from normality and performed equally well as threshold models.     

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.     

Selection responses for clinical mastitis and protein yield in two Norwegian dairy cattle selection experiments

Inferences from two dairy cattle selection experiments, in which sires were selected from external sources, were drawn by using an animal model to analyze data from the entire population. The first selection experiment was carried out in the period from 1978 to 1989 and included groups selected for high milk production (HMP) and low milk production (LMP). Each year, the highest ranking proven sires for milk production, from the most recent group of Norwegian Dairy Cattle (NRF) test bulls, were selected and mated to the cows in the HMP group. A group of sires with low milk production indices from progeny testing in 1978 and 1979 were used as sires in the LMP group during the entire experiment. The second selection experiment, which started in 1989, included one high protein yield (HPY) group and one low clinical mastitis (LCM) group. The highest ranking proven NRF sires for protein yield and mastitis resistance were selected each year from the most recent group of progeny tested bulls and used as sires in the HPY and LCM groups, respectively. Genetic trends for protein yield were positive (as expected) for HMP and HPY cows, and negative for LMP and LCM cows. Estimates of annual genetic trends for clinical mastitis were +0.23, -0.02, +0.04, and -0.91% per year for HMP, LMP, HPY, and LCM cows, respectively. The difference in genetic trend of clinical mastitis between HMP and HPY groups, both selected for increased milk production, reflects the gradual change in the NRF breeding objective towards more weight on health relative to milk over the last 20 yr. After four cow generations, the genetic difference in mastitis between HMP and LMP group cows was 3.1% clinical mastitis, a correlated response to selection for increased milk production. The genetic difference between LCM and HPY cows of 8.6% clinical mastitis after three cow generations is mainly a result of direct selection against clinical mastitis in the LCM group. In the NRF population, an approximately flat genetic trend for clinical mastitis was found for cows born from 1976 to 1990, whereas cows born after 1990 showed a genetic improvement equivalent to a reduction of 0.19% clinical mastitis per year. The results show that it is possible to obtain considerable selection response for clinical mastitis, and that selection for increased milk production will result in an unfavorable correlated increase in mastitis incidence, if mastitis is ignored in the breeding program.     

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.     

Genetic evaluation of mastitis in dairy cattle using linear models, threshold models, and survival analysis: a simulation study

The objective was to study, by simulation, whether survival analysis results in a more precise genetic evaluation for mastitis in dairy cattle than cross-sectional linear models and threshold models by using observation periods for mastitis of 2 lengths (the first 150 d of lactation, and the full lactation, respectively). True breeding values for mastitis liability on the underlying scale were simulated for daughters of 400 sires (average daughter group size, 60 or 150), and the possible event of a mastitis case within lactation for each cow was created. For the linear models and the threshold models, mastitis was defined as a binary trait within either the first 150 d of lactation or the full lactation. For the survival analysis, mastitis was defined as the number of days from calving to either the first case of mastitis (uncensored record) or to the day of censoring (i.e., day of culling, lactation d 150 or day of next calving; censored record). Cows could be culled early in lactation (within 10 d after calving) for calving-related reasons or later on because of infertility. The correlation between sire true breeding values for mastitis liability and sire predicted breeding values was greater when using the full lactation data (0.76) than when using data from the first 150 d (0.70) with an average of 150 daughters per sire. The corresponding results were 0.60 and 0.53, respectively, with an average of 60 daughters per sire. Under these simulated conditions, the method used had no effect on accuracy. The higher accuracy of sire breeding values can be translated into a greater genetic gain, unless counteracted by a longer generation interval.     

Comparison between linear models and survival analysis for genetic evaluation of clinical mastitis in dairy cattle

Clinical mastitis was analyzed with mixed linear models (LM) and survival analysis (SA) using data from the first 3 lactations of >200,000 Swedish Holstein cows having their first calving between 1995 and 2000. The model for both methods included fixed effects of year-month and age at calving, fixed regressions of proportions of heterosis and North American Holstein genes, and random effects of herd-year at calving and sire. For the LM, clinical mastitis was defined as a binary trait measured from 10 d before to 150 d after calving. For the SA, clinical mastitis was defined either as the time period from 10 d before calving to the day of first treatment or culling because of mastitis (uncensored record) or from 10 d before to the day of next calving, culling for reasons other than mastitis, movement to a new herd, or to lactation d 240 (censored record). The heritability estimates from SA (0.03 to 0.04) were higher than those obtained with the LM (0.01 to 0.03). Consequently, the accuracies of estimated transmitting abilities were also higher for the trait analyzed with SA. The difference between estimates from the 2 methods was greater for later lactations. This study reveals the potential of analyzing clinical mastitis data with SA.     

A model for the genetic evaluation of number of clinical mastitis cases per lactation in Czech Holstein cows

Cases of mastitis from 9,550 lactations of 6,242 cows were recorded on 5 farms in the Czech Republic from 1996 to 2008. The number of clinical mastitis (CM) cases per cow adjusted to a lactation length of 305 d was analyzed with 4 linear single-trait animal models and one 3-trait model, which also included lactation mean somatic cell score (SCS) and 305-d milk yield. Factors included in the model of choice were parity, combined effect of herd and a 2-yr calving period, calving season, permanent environmental effect of the cow, and additive genetic effect of the cow. From both the single-trait and multiple-trait models, estimated heritability of number of CM cases was 0.11 (±0.015 for the multiple-trait model). Permanent environmental effects accounted for approximately one-third of the phenotypic variance. Heritability estimates for lactation mean SCS and 305-d milk yield were 0.17 ± 0.019 and 0.25 ± 0.011, respectively, and genetic correlations of these traits with number of CM cases were 0.80 ± 0.059 and 0.34 ± 0.079, respectively. Genetic evaluation of the number of CM cases in Czech Holsteins could be carried out including data from all parities using a 3-trait animal model with SCS and milk yield as additional traits.     

Genetic evaluation of mastitis resistance using a first-passage time model for wiener processes for analysis of time to first treatment

A Wiener process is a Brownian-motion process initiated in a certain state in a state space, and the first passage time is defined as the time of the process to reach a predefined absorbing state where the process stops. Time from 31 d prepartum to first treatment of clinical mastitis (CM) was modeled as first passage times of such Wiener processes. Two processes were used to allow for several risk factors, and for each process, initiation was at some arbitrary time point, in a certain health state with drift toward or away from absorption (disease). The drift parameter of each process was expressed as linear functions of covariates (year of calving and sire). First passage time was defined as the time from process initiation until the first health status process reached zero (absorption). The model was fitted to records for 36,178 first-lactation daughters of 245 Norwegian cattle sires using a Bayesian approach and Markov chain Monte Carlo methods. Genetic evaluation of sires was carried out by calculating the posterior probability of no CM (the value of the survival function) by d 331, i.e., 300 d after first calving. Alternatively, sire evaluation was based on the integrated area under the survival curve. These measures were highly correlated (0.999), which indicates a small degree of crossings of the sire-dependent survival curves. Hence, sire-specific hazards were close to proportional, resulting in a higher rank-correlation to sire evaluations from a survival model with proportional hazards than to the results from a multivariate threshold model.     

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.     

Efficacy of systemic ceftiofur as a therapy for severe clinical mastitis in dairy cattle

The objectives of this study were to determine the efficacy of intramuscular administration of ceftiofur to reduce the incidence of case-related death and culling following severe clinical mastitis in lactating dairy cattle. A total of 104 cows with severe clinical mastitis (systemic signs) were enrolled in the study and randomly assigned to one of two treatment groups. Immediately after detection of the case, one group was administered 2.2 mg/kg of ceftiofur intramuscularly, and the dose repeated at 24-h intervals for a total of five doses. The second group of cows did not receive systemic antibacterial therapy. Additionally, all cows in both treatment groups received intramammary pirlimycin (Pirsue) in the affected quarter every 24 h for a total of up to three doses. Also at the onset of the case, all cows on the trial were administered a supportive therapeutic regimen of fluids and anti-inflammatory agents that varied from farm to farm, but was standard within each herd at the discretion of the herd manager and veterinarian. Of all cases 14/104 (13.5%) resulted in a lost cow (died or culled). The proportion of cases that resulted in a lost cow and were treated with ceftiofur (4/51; 7.8%) did not statistically differ from cows that were not treated with ceftiofur (10/53; 18.9%). However, the proportion of cases that resulted in lost cows was higher for those cases that yielded a coliform organism on culture (14/56; 25.0%) than cases that did not yield coliforms (0/48; 0.0%; P < 0.001). Thus, among coliform cases, cows that were not treated with ceftiofur were more likely to be culled or die (10/27, 37.0%; P < 0.05) than cows treated with ceftiofur (4/29, 13.8%). We conclude that intramuscular administration of ceftiofur did not affect the outcome of severe clinical mastitis when all etiologic agents are included in the analysis. However, for severe clinical mastitis cases caused by coliform organisms, ceftiofur therapy reduced the proportion of cases that resulted in cow death or culling. This benefit may be realized because of the amelioration of bacteremic-related pathogenesis.