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PubMed2004

Somatic cell count distributions during lactation predict clinical mastitis.

This research investigated somatic cell count (SCC) records during lactation, with the purpose of identifying distribution characteristics (mean and measures of variation) that were most closely associated with clinical mastitis. Three separate data sets were used, one containing quarter SCC (n = 1444) and two containing cow SCC (n = 933 and 11,825). Clinical mastitis was defined as a binary outcome, present or absent, for each lactation, and SCC were log (base 10) transformed. A generalized linear mixed model within a Bayesian framework was used for analysis. Parameters were estimated using Markov Chain Monte Carlo with Gibbs sampling. Results from the 3 data sets were similar. Increased maximum and standard deviation log SCC during lactation, rather than increased geometric mean, were the best overall indicators of clinical mastitis. Distributions of SCC were also investigated separately for different mastitis pathogens. Increased maximum log SCC was associated with clinical mastitis caused by all pathogen types. Increased standard deviation log SCC was associated with Staphylococcus aureus, and Streptococcus uberis clinical mastitis and increased coefficient of variation log SCC (standard deviation divided by mean) was associated with Escherichia coli clinical mastitis. Increased geometric mean lactation SCC was associated with an increased risk of Staph. aureus clinical mastitis but a reduced risk of E. coli clinical mastitis. Our results suggest that using measures of variation and maximum cow SCC would enhance the accuracy of predicting clinical mastitis, compared with geometric mean SCC, and therefore improve genetic programs that aim to select for clinical mastitis resistance. The results are also consistent with low SCC increasing susceptibility to some mastitis pathogens.

Animals↗
PubMed2006

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.

Analysis of Variance↗
PubMed1993

Interrelationships of somatic cell count, mastitis, and milk yield in a low somatic cell count herd.

In a high yielding low SCC herd, changes in milk yield associated with SCC and occurrence of clinical mastitis and differences in SCC with parity, clinical mastitis, and DIM were investigated. Milk yield data were obtained at every milking, and SCC was measured once every 48 h in 117 cows during the first 119 d postpartum. Effects of SCC and clinical mastitis on cumulative milk yield in the first 119 d postpartum were evaluated with least squares linear regression. Repeated measures ANOVA was used to detect changes in SCC. The SCC was highest at lactation onset, and cows with clinical mastitis had significantly higher SCC. During the 10 d prior to onset of clinical mastitis, SCC was higher in affected cows than in matched unaffected controls and surged just prior to diagnosis. During the 10-d period following a mastitis treatment, SCC differences between treated and control cows remained significant but became smaller with time and returned to the premastitis differences. Occurrence of clinical mastitis was associated with 5% milk yield loss. Cows with mean SCC > 245,000 cells/ml over the 119 d showed 6.2% yield loss compared with cows with SCC < or = 90,000 cells/ml. Cows with clinical mastitis had higher SCC prior to and following the end of treatment for mastitis than did controls. Clinical mastitis and SCC were associated with significant yield loss. Milk yield loss attributed to clinical mastitis was greater than that associated with elevated SCC (> 245,000 cells/ml) because a greater percentage of cows (26%) had clinical mastitis than elevated SCC (12.5%).

Animals↗
PubMed1999

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.

Aging↗
PubMed1998

Clinical mastitis in dairy cattle in Ontario: frequency of occurrence and bacteriological isolates.

The objective of this study was to describe the frequency of occurrence of clinical mastitis in dairy herds in Ontario. The study group consisted of 65 dairy farms involved in a 2-year observational study, which included recording all clinical mastitis cases and milk sampling of quarters with clinical mastitis. Lactational incidence risks of 9.8% for abnormal milk only, 8.2% for abnormal milk with a hard or swollen udder, and 4.4% for abnormal milk plus systemic signs of illness related to mastitis were calculated for 2840 cows and heifers. Overall, 19.8% of cows experienced one or more cases of clinical mastitis during location. Teat injuries occurred in 2.1% of lactations. Standard bacteriology was performed on pretreatment milk samples from 834 cows with clinical mastitis. The bacteria isolated were Staphylococcus aureus (6.7%), Streptococcus agalactiae (0.7%), other Streptococcus spp. (14.1%), coliforms (17.2%), gram-positive bacilli (5.5%), Corynebacterium bovis (1.7%), and other Staphylococcus spp. (28.7%). There was no growth in 17.7% of samples, and 8.3% of samples were contaminated. Clinical mastitis is a common disease in dairy cows in Ontario; approximately 1 in 5 cow lactations have at lease one episode of clinical mastitis. There is, however, considerable variation in the incidence of clinical mastitis among farms. The majority of 1st cases of clinical mastitis occur early in lactation, and the risk of clinical mastitis increases with increasing parity. Environmental, contagious, and minor pathogens were all associated with cases of clinical mastitis.

Animals↗
PubMed2025

Multivariate Effects of SNPs on Environmental Streptococcal Mastitis Evaluated With an NGS-Based Association Study Using Targeted Resequencing in the Bovine MHC Region.

Mastitis is an inflammatory reaction caused by bacterial infection of the teat, and a relationship between its onset and cattle major histocompatibility complex (BoLA) region has been reported. However, no comprehensive genetic analysis of mastitis caused by environmental streptococci has been reported. Here, we resequenced the BoLA region using a hybridisation capture target next-generation sequencing (NGS) method to identify disease susceptibility markers mapped to the BoLA region in environmental streptococcal mastitis. This study examined 75 cows with mastitis caused by environmental streptococci selected from 1641 cows with mastitis and 222 healthy cows without mastitis in Japan. Targeted sequences obtained from MiSeq NGS were aligned to the bovine reference genome (ARS-UCD1.2/bosTau9), and 2,920,355 variants were detected within the BoLA region of the 297 Holstein cattle. In an association study using 2264 variants after quality control, the top 20 variants with the lowest P values were selected and assigned to the 18 surrounding candidate genes, and a gene network analysis of these genes resulted in the narrowing down of five candidate genes POU5F1, IER3, GNL1, ABCF1, and PRR3. Multivariate effect analysis of all 6 SNPs associated with these 5 genes revealed that they were significantly correlated with mastitis, indicating that they were useful for classification of mastitis-resistant and mastitis-susceptible cattle. This is the first report to identify SNPs associated with environmental streptococcal mastitis with an NGS-based association study using targeted resequencing in the BoLA region, and understanding host factors may provide important clues for mastitis control.

Animals↗
PubMed1997

Patterns of clinical mastitis manifestations in Danish organic dairy herds.

Danish organic dairy production is characterized by a low input of antibiotics for udder treatment and a high input of other mastitis control procedures. A study was conducted in 14 organic dairy herds with the objectives of obtaining a comprehensive description of clinical mastitis cases and identifying characteristic patterns in these results. Clinical signs, inflammatory reactions and microbiological identifications were obtained from 367 cases of clinical mastitis occurring over 18 months. Cow characteristics and preincident values such as milk yield and somatic cell count were obtained for each cow. Signs of previous udder inflammation were present in two-thirds of the clinical mastitis cases. Severe local inflammatory reactions were found in 21% of the cases and some indication of generalized signs such as fever and reduced appetite were found in 35% of the cases. Logistic regression analyses were performed based on the results of an initial (exploratory) multiple correspondence analysis. Coliform mastitis (6% of the cases) was rarely preceded by pathogen isolation or inflammatory reactions in the same quarter. Coliform mastitis cases usually occurred in one quarter only. Escherichia coli infections were typically (truly) acute cases. Bacteriologically negative mastitis (20% of the cases) showed strong similarities with clinical coliform mastitis. Staphylococcus aureus cases (18% of the cases) occurred most frequently in late lactation or around drying-off. Prior isolation of Staph. aureus and slight decreases in milk yield were two factors that interacted but both were strongly and positively related to clinical Staph. aureus. Staph. aureus mastitis typically had a subclinical debut, and increasing degrees and duration of inflammation decreased shedding of this pathogen. Streptococcus dysgalactiae (9% of the cases) mastitis was typically persistent virulent and manifest in periods of lower cow resistance. More patterns of subclinical and clinical Str. uberis mastitis (23% of the cases) seemed to be present.

Animals↗
PubMed2002

Lactation mastitis: occurrence and medical management among 946 breastfeeding women in the United States.

In 1994-1998, the authors followed 946 breastfeeding women from Michigan and Nebraska for the first 3 months postpartum or until they stopped breastfeeding to describe mastitis incidence, mastitis treatment, and any associations between mastitis occurrence and hypothesized host characteristics and behaviors. Participants were interviewed by telephone at 3, 6, 9, and 12 weeks postpartum or until they ceased breastfeeding. A total of 9.5% reported provider-diagnosed lactation mastitis at least once during the 12-week period, with 64% diagnosed via telephone. After adjustment in a logistic regression model, history of mastitis with a previous child (odds ratio (OR) = 4.0, 95% confidence interval (CI): 2.64, 6.11), cracks and nipple sores in the same week as mastitis (OR = 3.4, 95% CI: 2.04, 5.51), using an antifungal nipple cream (presumably for nipple thrush) in the same 3-week interval as mastitis (OR = 3.4, 95% CI: 1.37, 8.54), and (for women with no prior mastitis history) using a manual breast pump (OR = 3.3, 95% CI: 1.92, 5.62) strongly predicted mastitis. Feeding fewer than 10 times per day was protective regardless of whether or not feeding frequency in the same week or the week before mastitis was included in the model (for the same week: 7-9 times: OR = 0.6, 95% CI: 0.41, 1.01; < or =6 times: OR = 0.4, 95% CI: 0.19, 0.82). Duration of feeding was not associated with mastitis risk.

Adult↗
PubMed1975

A large scale mastitis control programme in Somerset.

The results of a mastitis control programme operated in south west England for three years are given. Farmers participating in the full mastitis control group agreed to treat each cow at drying off with 500 mg benzathine cloxacillin in each quarter, to have their milking machines tested and to correct any faults, and to practise teat dipping. Data covering cell counts, milk production, milk quality and clinical mastitis, were assessed from herds taking part in the programme. Cell counts were analysed from all 507 herds taking part in the programme. Milk production records for the full mastitis control group (188 herds) over a three year period are discussed, and these results compared with milk production figures from Milk Marketing Board records from herds in the south west of England which were carrying out no specific mastitis control programme. The milk quality data compare the findings in 159 herds in the full mastitis control programme with those in 247 herds in the partial and no mastitis control groups. Cases of clinical mastitis during the three year period were recorded in 73 herds in the full mastitis control group. The problems of applying the control routines are presented with observations on clinical mastitis, bulk milk cell count, milk production and milk quality. After three years, herds in the programme had on average increased milk production by 75 gallons a cow, achieved a 14.6 per cent reduction in the incidence of clinical mastitis, and improved the milk total solids percentage by one milk quality payment class.

Animals↗
PubMedDate not supplied

Genetic analysis for mastitis resistance and milk somatic cell score in French Lacaune dairy sheep.

Genetic analysis for mastitis resistance was studied from two data sets. Firstly, risk factors for different mastitis traits, i.e. culling due to clinical or chronic mastitis and subclinical mastitis predicted from somatic cell count (SCC), were explored using data from 957 first lactation Lacaune ewes of an experimental INRA flock composed of two divergent lines for milk yield. Secondly, genetic parameters for SCC were estimated from 5 272 first lactation Lacaune ewes recorded among 38 flocks, using an animal model. In the experimental flock, the frequency of culling due to clinical mastitis (5% ) was lower than that of subclinical mastitis (10% ) predicted from SCC. Predicted subclinical mastitis was unfavourably associated with the milk yield level. Such an antagonism was not detected for clinical mastitis, which could result, to some extent, from its low frequency or from the limited amount of data. In practice, however, selection for mastitis resistance could be limited in a first approach to selection against subclinical mastitis using SCC. The heritability estimate of SCC was 0.15 for the lactation mean trait and varied from 0.04 to 0.12 from the first to the fifth test-day. The genetic correlation between lactation SCC and milk yield was slightly positive (0.15) but showed a strong evolution during lactation, i.e. from favourable (-0.48) to antagonistic (0.27). On a lactation basis, our results suggest that selection for mastitis resistance based on SCC is feasible. Patterns for genetic parameters within first lactation, however, require further confirmation and investigation.

Animals↗
PubMed2002

Genetic parameters of dairy character, protein yield, clinical mastitis, and other diseases in the Danish Holstein cattle.

The primary aim of this study was to estimate genetic correlations between dairy character, protein yield, clinical mastitis, and other diseases. Data consisted of first lactation records of Danish Holstein cows calving from 1990 to 1999. After editing, the data included records on 934,639 cows, of which 101,853 were assessed for dairy character, 472,421 for diseases, and 834,993 for protein yield. The disease traits were defined as binary traits in the period from 10 d before to 50 d after calving for clinical mastitis, and from 10 d before to 100 d after calving for diseases other than mastitis. Data were analyzed with a linear sire model using the method of AI-REML. Heritabilities were estimated to be 0.265 for protein yield, 0.261 for dairy character, 0.035 for clinical mastitis, and 0.020 for diseases other than mastitis. Estimates of genetic correlations between protein yield and dairy character, protein yield and clinical mastitis, and protein yield and diseases other than mastitis were 0.38, 0.33, and 0.14. Between the two disease traits, the genetic correlation was 0.24. The genetic correlation between dairy character and clinical mastitis was 0.24. Between dairy character and diseases other than mastitis the genetic correlation was 0.41. Thus, cows with high score for dairy character were more prone to diseases. The genetic correlation between dairy character and the disease traits, when both traits were adjusted for protein yield, was 0.13 for clinical mastitis and 0.39 for diseases other than mastitis. These findings suggest that, dairy character should be given a negative rather than a positive weight in the breeding goal.

Animals↗
PubMed2002

Influence of dry period bacterial intramammary infection on clinical mastitis in dairy cows.

Milk samples were taken from 1920 quarters (480 cows, six herds) on four occasions to examine the relationship between quarter level intramammary infection (IMI) during the dry period and clinical mastitis in the next lactation. All quarters were sampled at drying off and within 1 wk of calving, and two quarters from each cow were sampled both 0 to 7 and 8 to 14 d before calving. Milk samples were collected from all cases of clinical mastitis during the following lactation. Logistic regression models were developed to investigate the associations between IMI present during the sampling period and clinical mastitis. The probability of a quarter succumbing to clinical mastitis increased when Streptococcus dysgalactiae, Streptococcus faecalis, Escherichia coli, or Enterobacter spp. were cultured at drying off and when Escherichia coli, coagulase-positive staphylococcus, Serratia spp., or Streptococcus faecalis were cultured in two out of three late dry and post-calving samples. Quarters from which Corynebacterium spp. were isolated at drying off were at an increased risk of clinical mastitis, whereas the presence of Corynebacterium spp. in the late dry and post-calving samples was associated with a reduction in the risk of clinical mastitis. The risk of mastitis for specific pathogens increased if the same species of bacteria that had caused mastitis was isolated at least twice in the late dry and post-calving samples. Kaplan-Meier survival plots indicated that clinical mastitis associated with dry period infections was more likely to occur earlier in lactation than clinical mastitis not associated with dry period infections. There was evidence of quarter susceptibility to IMI or the possibility that infection with one organism led to clinical mastitis with another.

Animals↗
PubMed2004

Association of CXCR2 polymorphisms with subclinical and clinical mastitis in dairy cattle.

The ability to identify objectively cows that are more or less susceptible to mastitis has been a long-standing goal. Genetic markers associated with inflammatory responses during mastitis could aid in selection of these cattle. One potential marker is CXCR2, a chemokine receptor required for neutrophil migration to infection sites, which contains single nucleotide polymorphisms (SNP) within the gene. The objective of this experiment was to evaluate the association of CXCR2 SNP genotypes with subclinical and clinical mastitis. Thirty-seven Holstein and 42 Jersey cows that completed at least 2 full lactations were used. Quarter foremilk samples were collected for bacteriological examination quarterly and when cows exhibited clinical mastitis. Subclinical mastitis was defined as the presence of the same pathogen in the same quarter in at least 2 of 3 consecutive samples. A significant association was detected between CXCR2 SNP +777 genotype and percentages of subclinical mastitis cases in Holsteins. Holsteins expressing genotype GG had decreased percentages of subclinical mastitis, but genotype CC cows had increased percentages of subclinical mastitis. Significant differences in clinical mastitis incidence were not detected between genotypes for either breed. This approach of genetically identifying mastitis resistant cows may represent an effective means of marker-assisted selection for mastitis and other inflammatory diseases involving neutrophils.

Animals↗
PubMed2006

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.

Animals↗
PubMed1990

Risk factors for clinical mastitis in herds with a low bulk milk somatic cell count. 1. Data and risk factors for all cases.

The incidence rate of clinical mastitis in 125 herds with a low annual bulk milk SCC (less than 150,000 cells/ml) was modeled using a Poisson regression model. The rate of clinical mastitis was significantly associated with some variables that increased the exposure to environmental microorganisms: poor cubicle cleanliness increased the mastitis rate; rubber mats in cubicles were associated with a higher incidence; and drinking water from sources other than public water also increased the rate of mastitis. Other variables may be associated with host resistance: an increasing percentage of cows leaking milk increased the rate of mastitis; postmilking teat disinfection was associated with a higher incidence of clinical mastitis; and a high frequency of cubicle disinfection was also associated with more mastitis. Three other variables were associated with the rate of mastitis: breed (Holstein-Friesian had a lower incidence than the Meuse-Rhine-Yssel breed); use of sugar beet pulp in the ration increased the mastitis rate; and in herds with high milk production a higher incidence of mastitis was observed. These items are discussed in respect to their causal relation to clinical mastitis.

Animals↗
PubMed1989

[Escherichia coli mastitis in cattle. I. Clinical diagnosis and epidemiological aspects].

The diagnostic aspects, incidence, risk factors and prevention of coliform mastitis are reviewed in the present paper. It is concluded that it is not possible to establish an accurate diagnosis of coliform mastitis, which is based on a specific clinical symptom differentiating it from other forms of mastitis. Not any single symptom or combination of symptoms is specific for coliform mastitis. The importance of coliform mastitis in dairy cattle showed a marked increase during the last few decades. Successful programmes for the prevention of mastitis reduced the importance of contagious organisms, but the overall incidence of mastitis has remained unchanged; therefore, the proportion of cases of coliform mastitis increased. The observation that coliform micro-organisms are common bacteria causing mastitis in herds with low bulk milk somatic cell counts implies that the future of the dairy industry will be associated with particular risks. Factors involving the risk of coliform mastitis are divided into cow level factors and herd level factors. The most important cow level factors were: leaking milk in between milkings, lesions of the teats and a reduced capacity of the immune system. Risk factors on the herd level include: the bedding material, the design of cubicles, exposure to daylight in summer-time, exposure to dirt and the use of dry-cow therapy. The possible role of antibiotic dry-cow treatment and teat dipping in colonisation resistance is discussed. Preventive programmes designed to reduce the incidence of coliform mastitis have not been very successful so far.

Animals↗
PubMed1981

[Organizing mastitis control (author's transl)].

In view of the considerable losses caused by clinical, though particularly subclinical, mastitis, organized mastitis control is justified. Cell counts of herd milk samples are the most effective method so far available in detecting herds in which mastitis is a problem. Cell counts are primarily made to determine the quality of the milk delivered; secondly, cell counts are used in mastitis control. Using the same cell count in determining the quality and in detecting herds affected with mastitis is a difficult matter. Herds in which mastitis is a problem, are systematically detected in a limited number of provinces in the Netherlands. In mastitis control on a farm, particular attention is paid to: (1) hygiene on the farm (2) the house climate (3) special arrangements for maintenance of the milking plant (4) the procedure adopted in milking (5) teat dipping (6) dry cow therapy (7) culling chronically infected cattle. Because of mastitis in the cows, there may be an increase in bacterial counts due to streptococci causing mastitis in addition to cell counts in herd samples. These streptococci are perceptible in the form of small punctate colonies, so-called pin-points, in bacterial counts. Bacteria other than streptococci causing mastitis may also produce these pin-points. In recent years, the cell counts of herd milk samples showed a marked decrease in the southern Netherlands. This decrease was due in part to the large number of improvements in the milking apparatus. Moreover, intensive education by lectures, excursions and counselling of factories has also stimulated this favourable development. However, these effects are hard to measure. The continued reduction of the cell count in herd samples imparts confidence in the results of this mastitis control.

Animals↗
PubMed1999

Vaccines and diagnostic methods for bovine mastitis: fact and fiction.

A number of problems are uniquely associated with vaccination of dairy cows for mastitis. One of these is that the number of mastitis pathogens is numerous and heterogeneous. Vaccine efforts have concentrated mainly on the major mastitis pathogens. While at least one S. aureus bacterin has been commercially available for a number of years, no large-scale, independent field trials have been published in refereed journals which support the efficacy of this vaccine. Experimental vaccines for S. aureus composed of pseudocapsule-enriched bacterins supplemented with alpha- and/or beta-toxoids appear promising, but none of these has been commercialized. With S. uberis, some protection against homologous strain challenges was reported recently with a live strain and a bacterin, but other data from the same laboratory showed this vaccine would not protect against heterologous challenge strains. At this time there is only one highly effective vaccine for mastitis, the core-antigen vaccine for coliform mastitis. All of the commercially available vaccines for this indication are bacterins of rough mutants of E. coli strain J5 or Salmonella spp. Preliminary success with an experimental vaccine based on the plasminogen activator of S. uberis is a very different approach for a mastitis vaccine. Little success has been reported with vaccination against other mastitis pathogens. For diagnostic methods, the high somatic cell count, as measured by direct count or indirect assays, remains the cornerstone of mastitis diagnosis. However, for subclinical mastitis, bacterial cell culture is a reliable diagnostic method. Pathogen identification may rely on older biochemical testing methods or newer commercial identification systems, depending on the laboratory budget. ELISA assays also have been used to assess herd infection status. Epidemiologic studies have used DNA fingerprinting and ribotyping, but none of these methods has yet produced an easily utilized commercial format. Within the next decade, additional efficacious vaccines for several of the most common agents for bovine mastitis are likely. A review written at that time then can be more fact than fiction.

Animals↗