Relationships among severity and duration of clinical mastitis and sire transmitting abilities for somatic cell score,udder type traits,productive life,and protein yield

The objective of this study was to determine the relationships among severity and duration of clinical mastitis during first and second lactation and sire transmitting abilities for somatic cell score, udder type traits, productive life, and protein yield. Recording of clinical episodes began at first parturition for 1704 Holstein cows (in six Pennsylvania herds and one Nebraska herd) and continued into second lactation for 1055 of these cows. A total of 456 cows (sired by 168 bulls) had at least one clinical episode during first lactation, and 230 cows (sired by 100 bulls) had at least one clinical episode during second lactation. A severity code from 1 (normal milk) to 5 (acute systemic mastitis) was assigned daily (for up to 30 d after detection) to all quarters that had clinical mastitis. Only the severity codes for the first clinical episode to occur during first and second lactation are considered here. The initial and maximum severity codes, as well as the natural logarithms of both the sum of severity codes that were above normal (> 1) and the total days severity codes were above normal were regressed on herd (a classification variable), age at first calving, days in milk at clinical detection, and sire transmitting abilities taken one at a time. Linear and nonlinear effects were estimated for sire transmitting abilities. Separate analyses were conducted on dependent variables that considered severity and duration of clinical mastitis from: all organisms, coagulase-negative staphylococci, coliform species, streptococci other than Streptococcus agalactiae, and the most common environmental organisms (coliform species and streptococci other than Streptococcus agalactiae). Daughters of sires that transmit the lowest somatic cell score had the least severe and shortest clinical episodes from environmental organisms during first lactation. Selection for lower somatic cell score may reduce the severity and duration of clinical episodes from environmental organisms during first lactation.     

Heritability of intramammary infections at first parturition and relationships with sire transmitting abilities for somatic cell score,udder type traits,productive life,and protein yield

The objective of this study was to determine the relationships among daughter intramammary infections at first parturition and sire transmitting abilities for somatic cell score, udder type traits, productive life, and protein yield. Quarter milk samples from 958 daughters (in eight Pennsylvania herds and one Nebraska herd) of 182 Holstein sires were collected within a few days of first calving and cultured to determine intramammary infection status. A total of 446 cows had intramammary infections in 835 quarters at first parturition. Incidence of intramammary infections at first parturition and the proportion of quarters infected per cow were regressed on age at first calving, days in milk at sample collection, herd-season of calving (a classification variable), and sire transmitting abilities taken one at a time. Linear effects, non-linear effects, and odds ratios were estimated for sire transmitting abilities. Separate, preplanned analyses were conducted on data from one herd that gave all heifers an intramammary antibiotic infusion in each quarter 30 d prior to the expected calving date. Separate analyses were also conducted on dependent variables that considered intramammary infections at first parturition from: all organisms, coagulase-negative staphylococci, coliform species, streptococci other than Streptococcus agalactiae, and the most common environmental organisms (coliform species and streptococci other than Streptococcus agalactiae). Daughters of sires that transmit the lowest somatic cell score had the fewest intramammary infections at first parturition. Daughters of sires that transmit longer productive life, shorter teats, and closely spaced front teats had fewer intramammary infections at first parturition. Selection for lower somatic cell score, longer productive life, shorter teats, or closely spaced front teats may reduce the incidence of intramammary infections at first parturition.     

Incidence of clinical mastitis in a herd of Jersey cattle.

Incidence of clinical mastitis in 1278 lactations of 390 Jersey cows was studied for effects of lactation number, quarter of udder, month of calving, sire, and milk yield. Results for quarter did not conflict with the usual finding that incidence is higher in rear quarters. A mastitis index based on stage of lactation at which infection occurred had less variation, greater variation among sires, and a continuous distribution, in contrast to the traits porportion infected and number of cases. Mastitis increased with advancing lactation number subsequent to second lactations. Fall calvers may have less mastitis since they would be dry or in late lactation during summer. Incidence of mastitis increased at a decreasing rate as total milk yield in the lactation affected increased.     

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.     

Predictive abilities of different statistical models for analysis of survival data in dairy cattle

The objective of this study was to compare alternative trait definitions and statistical models for genetic evaluation of survival in dairy cattle. Data from the first 5 lactations of 808,750 first-crop daughters of 3,064 Norwegian Red sires were analyzed. Seven sire models were used for genetic analyses: linear and threshold cross-sectional models for binary survival scores from first lactation; a linear multi-trait model for survival scores from the first 3 lactations; linear and threshold repeatability models for survival scores from the first 5 lactations; a Weibull frailty model for herd life in first lactation; and a Weibull frailty model for herd life in the first 5 lactations. The models were compared to assess predictive ability of sire estimated breeding values with respect to average survival 365 d after first calving for second-crop daughters (not included in calculation of predicted transmitting abilities) of 375 elite sires. Generally, the linear multi-trait model analyzing survival in the first 3 lactations as correlated traits gave more-accurate predicted sire breeding values compared with both linear and Weibull frailty models using data from first lactation only, even when the latter models were extended to include data up to the sixth lactation. The Weibull frailty models did not improve predictive ability of sire estimated breeding values over what was obtained using a simple cross-sectional linear model for binary survival in first lactation.     

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.     

Durability of Traits: Nonlinear Association between Initial and Subsequent Measures

Subjective linearized scores were recorded for milking speed, fore udder smoothness, shoulder looseness, and udder depth on 7357 and 3730 Holstein cows during first and second lactations. Random sire effects in threshold models were estimated for each trait and lactation. There were 95 sires that had estimated effects for all the traits in both lactations. For each trait, sire effects for first and second lactations were used as independent and dependent variables, respectively, in quadratic regression. Sire effects corresponding to milking speed in second lactation had linear relationship to sire effects corresponding to milking speed in first lactation. Similar relationships for udder smoothness, shoulder looseness, and udder depth appeared nonlinear. The quadratic terms associated with prediction equations for shoulder looseness and udder depth were significant. Nonlinear associations between genetic evaluations in first and second lactations may have resulted from aging.     

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 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.     

Clinical mastitis in primiparous Holsteins: comparisons of bovine leukocyte adhesion deficiency carriers and noncarriers

The objective of this study was to determine the impact of bovine leukocyte adhesion deficiency on clinical mastitis incidence, severity, and duration in Holstein cows. Genomic DNA from milk of 847 Holstein cows in six Pennsylvania herds was used to determine bovine leukocyte adhesion deficiency genotypes (82 or 9.7% carriers). Data on clinical mastitis incidence, severity, duration, and pathogen involved were collected during first lactation for the project cows. One hundred ninety-four cows had one or more clinical mastitis episodes; milk samples from each quarter with clinical mastitis were collected at discovery of the episode and were cultured following National Mastitis Council recommendations. The overall incidence of clinical mastitis was significantly affected by sire and herd-year-season of calving. In addition, incidence of clinical mastitis tended to increase with age at first calving. Severity and duration of clinical mastitis were impacted by the pathogen involved. Incidence of clinical mastitis from all pathogens, from coagulase-negative staphylococci, and from coliform bacteria was not significantly related to bovine leukocyte adhesion deficiency status. Carriers tended to have lower rates of mastitis from streptococci other than Streptococcus agalactiae when compared with noncarriers, but this result should be interpreted with caution because of the low frequency of mastitis from the streptococci. Bovine leukocyte adhesion deficiency status was unrelated to severity or duration of clinical episodes. Bovine leukocyte adhesion deficiency carriers are probably similar to noncarriers in resistance to clinical mastitis.     

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.     

Genetic improvement of mastitis resistance: validation of somatic cell score and clinical mastitis as selection criteria

Mean daughter deviations for clinical mastitis among second-crop daughters were regressed on predicted transmitting abilities for clinical mastitis and lactation mean somatic cell score in first-crop daughters to validate the predictive ability of these traits as selection criteria for reduced incidence of clinical mastitis. A total of 321 sires had 684,897 second-crop daughters, while predicted transmitting abilities were calculated for 2159 sires, based on 495,681 records of first-crop daughters. Predictive ability, as a measure of efficiency of selection, was 23 to 43% higher for clinical mastitis than for lactation mean somatic cell score. Compared to single-trait selection, predictive ability improved 8 to 13% from utilizing information on both traits. The relative weight that should be assigned to standardized predicted transmitting abilities from univariate genetic analyses were 60 to 67% for clinical mastitis and 33 to 40% for lactation mean somatic cell score. No significant nonlinear genetic relationship between the two traits was found.     

Comparison between a Weibull proportional hazards model and a linear model for predicting the genetic merit of US Jersey sires for daughter longevity

Predicted transmitting abilities (PTA) of US Jersey sires for daughter longevity were calculated using a Weibull proportional hazards sire model and compared with predictions from a conventional linear animal model. Culling data from 268,008 Jersey cows with first calving from 1981 to 2000 were used. The proportional hazards model included time-dependent effects of herd-year-season contemporary group and parity by stage of lactation interaction, as well as time-independent effects of sire and age at first calving. Sire variances and parameters of the Weibull distribution were estimated, providing heritability estimates of 4.7% on the log scale and 18.0% on the original scale. The PTA of each sire was expressed as the expected risk of culling relative to daughters of an average sire. Risk ratios (RR) ranged from 0.7 to 1.3, indicating that the risk of culling for daughters of the best sires was 30% lower than for daughters of average sires and nearly 50% lower than than for daughters of the poorest sires. Sire PTA from the proportional hazards model were compared with PTA from a linear model similar to that used for routine national genetic evaluation of length of productive life (PL) using cross-validation in independent samples of herds. Models were compared using logistic regression of daughters' stayability to second, third, fourth, or fifth lactation on their sires' PTA values, with alternative approaches for weighting the contribution of each sire. Models were also compared using logistic regression of daughters' stayability to 36, 48, 60, 72, and 84 mo of life. The proportional hazards model generally yielded more accurate predictions according to these criteria, but differences in predictive ability between methods were smaller when using a Kullback-Leibler distance than with other approaches. Results of this study suggest that survival analysis methodology may provide more accurate predictions of genetic merit for longevity than conventional linear models.     

Genetic parameters for clinical mastitis, somatic cell score, and production in the first three lactations of Swedish holstein cows

Using a mixed linear animal model, genetic parameters were estimated for clinical mastitis (MAST), lactation average somatic cell score (LSCS), and milk production traits in the first 3 lactations of more than 200,000 Swedish Holstein cows with first calving from 1995 to 2000. Heritability estimates for MAST (0.01 to 0.03) were distinctly lower than those for LSCS (0.10 to 0.14) and production traits (0.23 to 0.36). The genetic correlation between MAST and LSCS was high for all lactations (mean 0.70), implying that selection for low LSCS will reduce the incidence of mastitis. Undesirable genetic relationships with production were found for both MAST and LSCS with genetic correlations ranging from 0.01 to 0.45. This emphasizes the need for including udder health traits in the breeding goal. Genetic correlations across lactations for the same trait were positive and high for both MAST (>0.7), LSCS (>0.8), and production traits (>0.9), with the strongest correlations between second and third parity for all traits (>0.9 for udder health traits and close to unity for production traits).     

Heritabilities of teat end shape and teat diameter and their relationships with somatic cell score.

Teat end shapes were categorized for 1740 Holstein cows with 2261 lactations in nine herds. Frequencies of teat end shapes were pointed, 7%; pointed disk, 1%; round, 43%; round ring, 16%; round flat, 5%; round disk, 11%; flat, 6%; disk, 10%; and inverted, 0.8%. Teat diameters were measured 1.5 cm from the end of the teat. Teat end lesions were visually classified into four categories: no lesion, rough ring, very rough, and ulcerated, raw appearance. Repeatability estimates for teat end shape and teat diameter were 0.75 and 0.36, respectively. Heritability estimates of teat end shape for first, second, and all lactations combined were 0.53, 0.44, and 0.56, respectively. Teat diameter heritabilities were 0.23, 0.27, and 0.35, respectively. The genetic correlation between teat end shape and teat diameter was 0.64. Linear somatic cell scores (SCS) averaged across lactation and adjusted for days in milk and for month and age at calving were available for single lactations of 1506 cows. Least squares means of SCS for categorically scored teat end shapes were computed from a model that included herd date, parity, days in milk, lesion, and teat diameter. Teat end shape and teat end lesion did not significantly affect SCS. Wider teat diameters were associated with higher SCS. Predicted transmitting abilities for SCS and udder composite index scores were available for 113 sires that had five or more daughters with teat end scores. Predicted transmitting abilities for SCS were significantly associated with udder composite index but not with sire solutions for teat end shape.     

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.     

Clinical mastitis in two California dairy herds participating in contagious mastitis control programs

The occurrence of clinical mastitis in two large California dairy herds over a 3-yr period is described. Herds had been participating for 15 or 22 yr in mastitis control programs against Streptococcus agalactiae and Staphylococcus aureus, had low bulk tank SCC, and had maintained good standards of hygiene and husbandry, but clinical mastitis remained a serious problem. A total of 1654 clinical mastitis cases were detected; the annual incidence in each herd was 49%. Coliform bacteria and environmental streptococci were etiological agents in 60% of the total clinical mastitis cases; coliforms produced 1.6 times more clinical mastitis than environmental streptococci. A higher susceptibility to clinical mastitis, primarily from coliform bacteria and environmental streptococci, was found in the first months of lactation. Clinical mastitis incidence peaked for cows in lactations 4 and 5 and was lowest during the first lactation. Highest incidence of clinical mastitis due to coliform bacteria and environmental streptococci at each dairy occurred during the rainy season (late fall and winter).     

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

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

Heritabilities for Lactation Average of Somatic Cell Counts in First,Second, and Third or Later Parities

Heritabilities were estimated for lactation average log, base 2, somatic cell count from cows with four or more tests in each lactation. Estimates were for first, second, and third or later parities (defined by age at calving) individually and for mixed parities. Estimates were from sire components of variance with numbers of sires and daughters of 406 and 22,140; 337 and 8,659; 311 and 6,122; and 310 and 10,217 for mixed, first, second, and third or later parities, respectively.Both sire and error components of variance increased with parity. Heritabilities were .18, .09, .10, and .29, for mixed, first, second, and third or later parities.     

Relationships of sire predicted transmitting ability for somatic cell score with measures of daughter performance.

The relationship between sire predicted transmitting ability (PTA) for somatic cell score (SCS) and occurrence of mastitis in daughters was characterized with 304 Holsteins first freshening since 1991 in the Virginia Tech dairy herd. No direct sire selection for PTA SCS was practiced in the herd. Linear regressions of first lactation average SCS (1.3), number of cases of mastitis (0.80), days clinical (7.0), and number of treatments for mastitis (2.0) on PTA SCS were significant. Linear regression coefficients for second and third lactations were generally positive, but like quadratic and cubic coefficients in this study, were not significant. Relationship of sire PTA SCS and measures of lifetime (84 mo opportunity) performance were determined for 2,494,195 Holsteins born between 1979 and 1987. Linear coefficients from regression on PTA SCS for number of lactations (-0.31), days of productive life (-87.0), total days in milk (-72.2), lifetime milk (-1609.1), fat (-80.7), and protein (-48.2) production, relative net income adjusted for opportunity cost for fluid markets (+13.47), first lactation average SCS (+1.00), and first lactation mature equivalent milk (+429.9) were different from zero. Partial regressions holding PTA milk or PTA protein constant were substantially larger than linear coefficients. When PTA productive life was held constant, the relationship between PTA SCS and measures of herd life and lifetime yield became positive, and relative net income adjusted for opportunity cost variables became moderately positive. One of the major expenses associated with higher susceptibility (higher PTA SCS) may be shorter herd life.