Prevention of clinical coliform mastitis in dairy cows by a mutant Escherichia coli vaccine.

A prospective cohort study was undertaken in two commercial California dairies. The treatment group, 246 cows, received three doses of a whole cell bacterin of J5 Escherichia coli (mutant of E. coli O111:B4) plus Freund's incomplete adjuvant vaccine (two in the dry period and one after calving) while 240 unvaccinated cows served as controls. Thirty-five cases of clinical coliform mastitis were diagnosed, six in vaccinated cows and 29 in unvaccinated cows. Bacteria isolated from the clinical cases included 15 E. coli five Klebsiella pneumoniae, three K. oxytoca, three K. ozaenae, five Enterobacter aerogenes, three Serratia marcescens and one Serratia spp. Four control cows were culled, three of them because of chronic coliform mastitis and one because of postcoliform infection agalactia. Incidence rate of clinical gram-negative mastitis was 2.57% in vaccinated cows and 12.77% in unvaccinated cows. The estimated risk ratio, the measure of risk of having clinical gram-negative mastitis for vaccinated cows to unvaccinated cows, was 0.20 (p less than 0.005), indicating a strong relationship between vaccination and lack of clinical gram-negative mastitis. The results of this trial indicate that the administration of the E. coli J5 vaccine is protective against natural challenge to gram-negative bacteria, and reduces the incidence of clinical gram-negative mastitis in dairy cows during the first three months of lactation.     

Partial budget analysis of vaccinating dairy cattle against coliform mastitis with an Escherichia coli J5 vaccine

Partial budget analysis of clinical coliform mastitis prevention supported vaccination of dairy cows with an Escherichia coli J5 vaccine. Increased profits of $57/cow lactation were predicted using a computer spreadsheet derived partial budget with generalized herd input data. Herd vaccination programs were predicted to be profitable when greater than 1% of cow lactations resulted in clinical coliform mastitis. Herd vaccination programs were predicted to be profitable at all herd milk production levels.     

Quarter-milking-, quarter-, udder- and lactation-level risk factors and indicators for clinical mastitis during lactation in pasture-fed dairy cows managed in an automatic milking system

Objectives To identify risk factors and indicators at quarter‐milking and other levels for clinical mastitis during lactation in pasture‐fed cows managed in an automatic milking system. Design A retrospective nested case–control study using data collected over a 31‐month period. A total of 803,948 quarter‐milkings from 249 cows were available for analysis, of which 245 were selected as clinical mastitis quarter‐milking cases and 2450 unaffected quarter‐milkings were selected as controls. Most of the diagnoses of clinical mastitis had been made after clinical assessments of quarters following automated alerts by the milking system. Potential risk factors and indicators were assessed using univariable and multivariable multilevel logistic models. Results Quarters that are milked infrequently and have low yield, fast peak milk flow rates, blood in the milk and/or elevated milk conductivity are at increased risk of clinical mastitis. Quarters were also at increased risk between days 10 and 29 of lactation, and during higher parity lactations. Milk fat and protein concentrations and the fat : protein ratio were not significantly associated with the development of clinical mastitis. Neither quarter position (fore or rear) nor side (left or right) was associated with clinical mastitis occurrence. Quarters that had been clinically affected more than 30 days previous in the current lactation were not at increased risk of redeveloping clinical mastitis. Conclusions Under the study conditions, the risk of clinical mastitis increased for quarter‐milkings in quarters that were milked less frequently in the previous 7 days, were low‐yielding, had fast peak milk flow rates and had more milkings in which blood was detected in milk and/or the milk conductivity was elevated. Risk was also increased in days 10–29 of lactation and in higher parity lactations.     

Coliform mastitis

Gram-negative bacteria that commonly cause bovine mastitis are classified as environmental pathogens. The point sources of coliform bacteria that cause infections include bedding materials, soil, manure and other organic matter in the environment of cows. Rates of coliform mastitis increase during climatic periods that maximize populations in the environment. The portal of entry into the mammary gland for Gram-negative bacteria is the teat canal. Once in the gland, bacteria must utilize available substrates in the mammary secretion to replicate and evade host defenses. Rates of coliform mastitis are greater during the transitional phases of the non- lactating period than during lactation. The ability to infect the non-lactating gland is directly related to the ability of bacteria to acquire iron from the mammary secretion. The primary host defense against coliform mastitis during lactation is the elimination of bacteria by neutrophils migrating into the gland in response to inflammation. Damage to the host is mediated by the release of endotoxin. The severity and duration of clinical signs associated with coliform mastitis are reduced by the use of core-antigen bacterins.     

Assessing individual sow risk factors for coliform mastitis: a case-control study

In order to investigate sow-specific risk factors associated with coliform mastitis, a case-control study was performed over the course of 28 months. Data of three farms were collected under production conditions. Sows suffering from coliform mastitis after farrowing served as cases, and healthy half- or full-sib sows from the same farm served as controls. Individual sow characteristics and the seasonal influence were analysed by conditional logistic regression. The final multivariate model identified four risk factors: the risk of suffering from coliform mastitis increased with a higher number of piglets born alive and stillborn piglets. Gilts had an increased risk for the disease, and birth intervention was also associated with a higher prevalence of mastitis. Birth induction and season had no significant influence on the occurrence of coliform mastitis. The time during and soon after farrowing is a very sensitive period in pig production demanding great attention by the farmer. With respect to the economic losses, monitoring of potentially endangered sows as well as detailed documentation and selection of disease cases are of particular importance when coping with coliform mastitis.     

Costs associated with selected preventive practices and with episodes of clinical mastitis in nine herds with low somatic cell counts

Nine dairy herds (mean size, 149 cows) with bulk-tank milk somatic cell counts of less than 300,000 cells/ml and greater than 80% of cows with Dairy Herd Improvement Association linear somatic cell counts less than or equal to 4 were selected for study. Each herd was monitored for 12 consecutive months. Duplicate quarter-milk specimens were collected from each cow for bacteriologic culturing at beginning of lactation, cessation of lactation, and at the time of each clinical episode of mastitis. Streptococcus agalactiae was never isolated and Staphylococcus aureus was isolated from less than 1% of all quarters. There were 554 episodes of clinical mastitis. During the year of study, the incidence rate of clinical mastitis varied from 15.6 to 63.7% of cows among the 9 herds. Mean costs per cow per year in herd for mastitis prevention were: $10 for paper towels, $3 for nonlactating cow treatment, and $10 for teat disinfectants. Mean cost associated with clinical mastitis was $107/episode. Approximately 84% ($90) of the costs attributed to a clinical episode were associated with decreased milk production and nonsalable milk. Costs of medication and professional veterinary fees per clinical episode varied significantly among the 9 herds. Three of the herds did not have a veterinarian treat a clinical episode of mastitis during the year of study even though 2 of these herds had the first and third highest incidence rates of clinical mastitis. When calculated on a per cow in herd basis, mean costs of $40/cow/year were attributed to clinical mastitis.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of veterinary-treated clinical mastitis and pregnancy status on culling in Swedish dairy cows

The interaction of the effects of pregnancy status and veterinary-treated clinical mastitis on culling in Swedish dairy cattle was analyzed with survival analysis. The data were from 978,780 cows with first calvings between 1988 and 1996. Four breeds (Swedish Red and White (SRB), Swedish Friesian (SLB), Swedish Polled Breed and Jersey) were included in the analysis, together with the SRB x SLB crossbreds. Length of productive life was defined as the number of days between first calving and culling or censoring (end of data collection). The model (Weibull proportional hazard) included the interaction of parity by pregnancy status by veterinary-treated clinical mastitis, peak test-day milk-yield deviation within herd-year-parity, age at first calving, year by season, region, breed, herd production level, and the random effect of herd. The effects of pregnancy status and veterinary-treated clinical mastitis were modeled as time-dependent covariates. The lactation was divided into five stages during which a veterinary-treated clinical mastitis and culling might occur and in which the pregnancy status was assumed to be known and culling could occur. Open cows had a pronounced effect on culling: they had a very high risk of being culled in all lactations, and it was even higher if they were treated for mastitis in early lactation. For pregnant cows, the later they got pregnant during the lactation, the greater their risk to be culled. The risk associated with cases of veterinary-treated clinical mastitis remained important throughout the lactation.     

Immune response of sows and their offspring to pseudorabies virus: serum neutralization response to vaccination and field virus challenge.

One month prior to breeding, sows were vaccinated with an attenuated pseudorabies virus vaccine or challenged with a field strain of pseudorabies virus. A third group of sows were not vaccinated or challenged before breeding. Pigs from these sows were vaccinated at 3, 6, or 12 weeks of age and challenged with virulent virus three weeks later. One pig from each litter served as an unvaccinated, unchallenged control. Serum neutralization titers of these pigs were monitored from birth until 22 weeks of age. Titers of the sows were monitored through breeding, gestation and farrowing. The maximum prefarrowing anti-pseudorabies virus titer in the field virus challenged sows occurred four weeks following challenge. A significant decline in titers occurred at farrowing. Titers rose from one week postfarrowing and then declined. Titers in the field virus infected sows were consistently two to threefold greater than those of the vaccinated sows. The maximum prefarrowing anti-pseudorabies virus titer in the vaccinated sows occurred six weeks following vaccination. The geometric mean titer in these sow's then decreased and increased for two weeks after farrowing. The results in the pigs can be summarized as follows: Pigs from control sows had a greater serological response following field virus challenge than following vaccination with a modified live virus. Pigs from control sows responded serologically to vaccination at 3, 6 and 12 weeks of age. Pigs from control sows which were challenged at 6, 9 and 15 weeks of age had similar antibody responses. Pigs from vaccinated sows had no increase in titer following vaccination at three and six weeks of age. Titers increased when these pigs were vaccinated at 12 weeks of age. There was no significant increase in mean titers of pigs from challenged sows following vaccination at 3, 6 and 12 weeks of age. Vaccinated pigs from control and vaccinated sows had a secondary response following challenge three weeks after vaccination.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictive variables for the occurrence of early clinical mastitis in primiparous Holstein cows under field conditions in France

Holstein heifers from 47 dairy herds in France were enrolled in a field study to determine predictors for clinical mastitis within the first month of lactation. Precalving and calving variables (biochemical, hematological, hygienic, and disease indicators) were collected. Early clinical mastitis (ECM) predictive variables were analyzed by using a multiple logistic regression model (99 cows with ECM vs. 571 without clinical mastitis throughout the first lactation). Two variables were associated with a higher risk of ECM: a) difficult calving and b) medium and high white blood cell (WBC) counts in late gestation. Two prepartum indicators were associated with a lower ECM risk: a) medium and high serum concentrations of immunoglobulin G1 (IgG1) and b) high percentage of eosinophils among white blood cells. Calving difficulty and certain biological blood parameters (IgG1, eosinophils) could represent predictors that would merit further experimental studies, with the aim of designing programs for reducing the risk of clinical mastitis in the first lactation.     

Management factors associated with the incidence of clinical mastitis over the non-lactation period and bulk tank somatic cell count during the subsequent lactation

Aim: To evaluate associations between management decisions related to the control of mastitis, including the infusion of antibiotics at the end of lactation (dry-cow therapy; DCT), on the incidence of clinical mastitis over the non-lactating period and the bulk tank somatic cell count (BTSCC) in the subsequent lactation. Methods: Dairy herd owners (n=158) provided information via a retrospective survey about (a) the proportion of their herds treated with DCT; (b) DCT management, including: number of occasions on which cows were dried off; manipulation of feed and water intake around drying off; infusion technique (partial vs full depth insertion of cannula); and hygiene before and after DCT infusion; (c) occurrence of mastitis and frequency of occurrence following drying off and in the subsequent lactation; (d) number of cows culled for mastitis-related conditions; (e) reasons for culling; (f) incidence of clinical mastitis; and (g) stock purchase policy with regard to mastitis. The BTSCC for each vat of milk supplied for the 1999/2000 and 2000/2001 seasons, and records of antibiotic purchases were collated for each herd. The probability that >2% of cows within a herd were diagnosed with clinical mastitis over the dry period was initially examined using univariate analysis (i.e. chi2 or logistic regression) and associated factors (p<0.2) were offered to a reverse stepwise logistic regression model. Factors hypothesised as being associated with the average lactation log10 BTSCC for the 2000/2001 season were initially examined using univariate analysis (i.e. ANOVA or linear regression analysis) and associated factors (p<0.2) were then tested using a forward manual model-building approach. Results: Increasing the percentage of the herd treated with DCT at the end of lactation was associated with reduced probability that >2% of a herd would be diagnosed with clinical mastitis over the non-lactating period and with a lower BTSCC in the subsequent lactation (p<0.01). A lower BTSCC was associated with small herds (<150 cows; p<0.05), not reducing feed intake around drying off (p<0.05), checking for clinical mastitis over the dry period in the milking parlour rather than at pasture (p<0.05), partial insertion of the DCT cannula (p<0.01), and use of 'change in udder shape' during lactation as a diagnostic criterion for mastitis (p<0.05). The incidence of clinical mastitis over the dry period was positively associated with reduced feeding around drying off (p=0.05) and the estimated volume of milk being produced at the time of drying off (p=0.014). Conclusions: Use of dry cow therapy was associated with fewer cases of clinical mastitis over the non-lactating period and reduced BTSCC over the subsequent lactation. Reduced BTSCC was also associated with smaller herds, use of partial (compared with full depth) insertion of the DCT cannula, not reducing feed intake at the time of drying off, checking for clinical mastitis over the dry (non-lactation) period in the milking parlour, and use of udder shape for diagnosis during lactation. Control of clinical mastitis and BTSCC involves a range of management practices that need to be used in conjunction with DCT. Keywords: Dairy cows, mastitis, dry-cow therapy, somatic cell count, management practices.     

An epidemiologic study of disease in 32 registered Holstein dairy herds in British Columbia.

Data recorded in a herd health management system were obtained from 32 registered Holstein dairy herds from British Columbia. Frequencies of disease were described, and the effect of herd, age, year, season, and the interrelationships between diseases within a lactation on the occurrence of disease were evaluated. Lactational incidence rates were computed for diseases with a short period of risk (ie, udder edema, milk fever, retained placenta, metritis, displaced abomasum, and ketosis), whereas for diseases with a longer period of risk (ie, cystic ovaries, mastitis and stable footrot), incidence densities were calculated. Overall, the disease incidence was low and showed an increase in frequency by year, which we attributed to more observing and complete recording by the owner, rather than an actual increase in disease incidence. Most diseases occurred early in lactation and their frequency increased with lactation number; the exception was udder edema, which occurred mainly during the first 2 lactations. An informal path model of disease interrelationships was made conditional on herd. Based on the results we inferred 2 independent pathways: one started by udder edema, and the other by milk fever. Udder edema was directly associated with mastitis occurrence from 0 to 30 d in lactation, metritis, and cystic ovaries. Mastitis from 0-30 d in lactation increased the risk of both mastitis from 31-150 d in lactation and cystic ovaries. Both of these increased the risk of late lactation mastitis. Milk fever was directly related with displaced abomasum, which increased the risk of footrot. In general, diseases that occurred in early lactation tended to increase the risk of other diseases later in lactation.     

Growth inhibition of Escherichia coli and Klebsiella pneumoniae during involution of the bovine mammary gland: relation to secretion composition

Mammary secretions from 12 Holstein dairy cows were collected to evaluate growth inhibition of Escherichia coli and Klebsiella pneumoniae during involution and during physiologic transitions of the mammary gland. Mammary secretions obtained during late lactation poorly inhibited growth of E coli and K pneumoniae. However, as involution progressed, mammary secretions increasingly inhibited growth of both coliform mastitis pathogens. Greatest inhibition of E coli and K pneumoniae growth was observed when mammary glands were fully involuted. Growth inhibition remained high until 7 days before parturition, and then it decreased significantly (P less than 0.05) to that observed during late lactation. Inhibition of coliform mastitis pathogen growth was associated with high concentrations of lactoferrin and immunoglobulin G, decreased citrate concentration, and a low citrate to lactoferrin molar ratio. These data suggested that differences in susceptibility or resistance to new intramammary infection with coliform mastitis pathogens during the nonlactating period may be attributable, in part, to marked changes in mammary secretion composition that develop during physiologic transitions of the mammary gland. Resistance of the fully involuted mammary gland to coliform infection may be associated with high concentrations of natural protective factors.     

The association between serological evidence of mycoplasma infection and respiratory disease in feedlot calves.

Calves from five Ontario feedlots were bled on arrival and approximately 28 days later. Calves treated during this interval for undifferentiated respiratory disease were classified as cases and untreated calves were classified as controls. Serum was titrated blindly for antibodies to Mycoplasma bovis and Mycoplasma dispar. Indirect hemagglutination titers of 1:20 or more were assumed to reflect recent or current exposure, whereas 1:10 or less were not. The titers to M. bovis increased in all feedlots indicating active infection. The initial titers to M. dispar were higher than the titers against M. bovis, yet they increased in all feedlots except one, suggesting widespread infection with this organism. There was an increased risk (although not statistically significant) of being treated if the titer against M. bovis rose during the period. Calves with low M. dispar titers on arrival were at increased risk of being treated and titer increases were strongly associated with treatment (statistically significant). Thus, the serological results indicate high prevalence of M. bovis and M. dispar in the feedlot calves and that calves with increasing titers in particular to M. dispar are at increased risk of being treated for respiratory disease.     

中国荷斯坦牛乳房炎风险评估模型建立及预测分析

实验旨在探究奶牛乳房炎的风险因素,建立奶牛乳房炎风险评估模型,预测奶牛乳房炎患病风险。本研究利用北京地区1998—2016年196万余条奶牛群体改良(Dairy Herd Improvement,DHI)测定记录,将具有统计学意义的因素进行多因素Logistic回归分析,分析其中的风险因素,并建立奶牛乳房炎风险评估模型,通过大量DHI记录进行奶牛乳房炎患病风险预测研究。多因素Logistic回归分析结果发现,场规模越大,奶牛患乳房炎的概率相对越小;胎次越高,奶牛患乳房炎的概率越大;夏季奶牛患乳房炎的概率比其他季节的概率高;泌乳天数高于300 d的奶牛患乳房炎风险约为泌乳天数低于100 d奶牛的2倍。使用北京地区DHI记录进行Logistic回归分析得出,奶牛隐性乳房炎风险评估模型和奶牛临床乳房炎风险评估模型预测价值分别为0.721和0.825,认为可以应用于实际牛群。综上,本研究中确定的奶牛场规模、胎次、DHI测定季节、泌乳阶段等风险因素可用于奶牛乳房炎预测,并构建了奶牛隐性乳房炎、临床乳房炎的风险评估模型,以减少奶牛群的乳房炎发生概率。     

关中奶山羊乳房炎灭活菌苗的制备及其免疫效果测定

对自制乳房炎疫苗免疫后的抗体效价进行评估.用甲醛37℃过夜灭活大肠埃希菌、葡萄球菌,分别制备蜂胶灭活疫苗、转移因子灭活苗及无佐剂疫苗,接种泌乳期奶山羊后,分别在不同时间采集免疫羊的血清和乳汁,ELISA测定血清大肠埃希菌和葡萄球菌的抗体效价.研究结果显示,大肠埃希菌和葡萄球菌经甲醛灭活彻底;与免疫前相比,血清和乳汁中的...     

Effect of hyperimmunization with an Escherichia coli J5 bacterin in adult lactating dairy cows

OBJECTIVE: To determine the effect of hyperimmunization with an Escherichia coli J5 bacterin on serum IgG2 concentration, incidence of clinical mastitis, and rate of survival to the end of the lactation period (ie, day 305) in adult lactating dairy cattle. DESIGN: Randomized controlled trial. ANIMALS: 1,012 Holstein cows in their second lactation and greater. PROCEDURES: All cows were given 3 doses of the J5 bacterin; cows in the hyperimmunization group were given an additional 3 doses during the first 3 months of lactation. Blood was collected from a small sample of cows to determine anti-J5 IgG2 concentrations. RESULTS: Cows in the hyperimmunization group had higher mean serum anti-J5 IgG2 concentrations than did control cows 28 days after administration of the fourth, fifth, and sixth doses of the J5 bacterin. However, mean serum anti-J5 concentrations during the subsequent lactation were not significantly different between groups. The proportions of cows that developed clinical mastitis were not significantly different between groups. However, control cows were more likely to have severe clinical mastitis than were cows in the hyperimmunization group. The percentage of control cows that remained in the herd to day 305 was significantly lower than the percentage of cows in the hyperimmunization group that did. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that hyperimmunization of mature lactating dairy cattle was associated with increased serum anti-J5 IgG2 concentrations and decreased incidence of severe clinical mastitis, but did not alter survival rate of cows that developed severe clinical mastitis.     

Management of dairy heifers and its relationships with the incidence of clinical mastitis

AIM: To describe aspects of management of dairy heifers before calving and determine risk factors for clinical mastitis postpartum in heifers, at the herd level, under pasture-based management systems in the Waikato and Taranaki regions of New Zealand. METHODS: Dairy herdowners (n=578) provided information via a prospective survey about their practices for rearing heifers and management of mastitis. A proportion of herdowners (n=250) subsequently provided data on the cases of clinical mastitis in their herds, including the date, cow identification, age and quarter affected from cases occurring in the 4 months after the planned start of calving (PSC) in the subsequent lactation. The relationship between management factors and the proportion of heifers diagnosed with clinical mastitis within a herd was examined using bivariate and multivariate analyses. RESULTS: The herd average percentage of heifers with clinical mastitis was 13.6 (95% confidence interval (CI)=12.3-14.9)%, and multiparous cows with clinical mastitis was 9.0 (95% CI=8.2-9.8)% in the first 4 months of lactation. There were positive relationships between the proportion of heifers with clinical mastitis and average milk production per cow (kg milksolids/ lactation; p<0.001), number of cows milked per labour unit (p=0.003), stocking rate (<> 3.30 cows/ha; p=0.002), and incidence of clinical mastitis in multiparous cows (%/120 days; p<0.04), in the final multivariate model. The proportion of heifers with clinical mastitis per herd was lower in herds that milked their lactating cows in multiple groups (p=0.02). CONCLUSIONS: The risk of clinical mastitis in heifers was significantly associated with management practices. It may be possible to reduce the incidence of clinical mastitis in heifers by modification of management practices at the herd level, and further studies are required to investigate this.     

Prevalence of clinical mastitis in 38 Waikato dairy herds in early lactation

AIM: To determine the prevalence of clinical mastitis in spring-calving dairy herds in the Waikato Region of New Zealand and to identify factors associated with variation in the prevalence of clinical mastitis between herds. METHOD: A total of 799 quarters from 595 dairy cows from 38 dairy herds were diagnosed by herd owners as having clinical mastitis between 8 July and 21 August 1997. Quarters diagnosed with clinical mastitis were sampled for bacterial culture and somatic cell count, and the presence of clots in the milk and the presence of udder oedema were assessed by a technician or veterinarian. RESULTS: Clinical mastitis was diagnosed in an average (+/-s.e.m.) of 9.9% (+/-0.8%, range 0.9-21.4%) of calved cows within the herds. Bacteria were not cultured from an average of 12.4 % (+/- 2.0%, range 0.0-45.5%) of cows and 22.3% (+/- 2.4%, range 0.0-54.0%) of quarters diagnosed as having clinical mastitis. There were significant differences between herds in the proportion of cows diagnosed with mastitis and in the proportion of clinical mastitis cases from which bacteria were not cultured. A decreased prevalence of clinical mastitis (p<0.001) was associated with an increased percentage of the herd treated with dry cow antibiotics. An increased prevalence of clinical mastitis (p<0.0001) was associated with both an increased percentage of cows treated in the previous season with lactating cow antibiotics and an increased percentage of heifers in the herd. Herds that were fed supplements before or during lactation had a higher prevalence of clinical mastitis than herds that were not fed supplements (p<0.001). An increased proportion of quarters diagnosed with clinical mastitis that did not culture bacteria was associated with an increased prevalence of clinical mastitis (p<0.001). The proportion of quarters that the technician or veterinarian found with evidence of clinical mastitis (i.e. a somatic cell count >500,000 cells/ml and the presence of either clots or udder oedema) within a herd was inversely related to the proportion of quarters within a herd from which no bacteria were isolated. CONCLUSION: There was a large variation in the prevalence of clinical mastitis and in the proportion of clinical quarters from which no bacteria were grown between herds. Management factors such as the use of dry cow therapy, feeding regimes and heifer replacement rates all affected the prevalence of clinical mastitis. Herd owners appear to differ in the sensitivity and specificity of their diagnosis of clinical mastitis, with bacteria not isolated from up to 50% of quarters diagnosed with clinical mastitis in some herds. Improvements in the specificity of herd owner diagnosis of clinical mastitis may reduce the use of antibiotics for mastitis during lactation and hence may reduce the risk of antibiotic contamination of milk supplied for human consumption.