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

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

Animals↗

Effect of carprofen treatment following experimentally induced Escherichia coli mastitis in primiparous cows.

Acute Escherichia coli mastitis is one of the major sources of economic loss in the dairy industry due to reduced milk production, treatment costs, discarded milk, and occasional fatal disease. Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used as adjunctive therapy to antibiotics. The objective of the current study was to evaluate the effect of carprofen treatment following infusion of Escherichia coli into the mammary glands of primiparous cows during the periparturient period. Severity of mastitis was scored based on the average milk production in the uninfected quarters on d +2 postinoculation and a clinical severity score. Carprofen was administered intravenously at 9 h postchallenge, when clinical signs of mastitis appeared. In previous work, efficacy of NSAIDs was mainly evaluated using clinical symptoms. In the present study, the effect of carprofen on innate immune response was also assessed by quantification of inflammatory mediators. All primiparous cows reacted as moderate responders throughout the experimental period. Primiparous cows were intramammarily inoculated with 1 x 10(4) cfu of E. coli P4:O32 in 2 left quarters. Analysis of blood and milk parameters, including IL-8, complement component C5a, lipopolysaccharide-binding protein (LBP), soluble CD14, prostaglandin E2, and thromboxane B2 was performed from d 0 to d +6 relative to intramammary inoculation. Rectal temperature in carprofen-treated animals was lower than in control animals at 3 and 6 h posttreatment. Treatment also restored the decreased reticulorumen motility that occurs during E. coli mastitis to preinfection levels faster than in control animals. Carprofen treatment resulted in an earlier normalization of the clinical severity score. Eicosanoid (prostaglandin E2 and thromboxane B2) production in milk tended to be inhibited by carprofen. No significant differences in the kinetic patterns of somatic cell count, IL-8, complement component C5a, LBP, and soluble CD14 were observed. In conclusion, carprofen treatment improved general clinical condition by effective antipyrexia and restoration of reticulorumen motility but did not significantly inhibit eicosanoid production. Carprofen treatment did not result in a significant decrease of chemotactic inflammatory mediators, IL-8 and C5a, and early innate immune molecules, sCD14 and LBP. Therefore, major modulatory effects from NSAID administration were not observed in this mastitis model, although a larger study might confirm some apparent trends obtained in the present results.

Animals↗

Effects of induced clinical mastitis during preovulation on endocrine and follicular function.

The objective of the study was to determine if experimentally induced clinical mastitis before ovulation resulted in alterations of endocrine function, follicular growth, or ovulation. On d 8 (estrus = d 0), cows were challenged (TRT; n = 19) with Streptococcus uberis or were not challenged (control; n = 14). Forty-eight hours after induction of luteal regression on d 12, blood samples were collected to determine estradiol-17beta, LH pulse frequency, and occurrence of the LH surge. Ovaries were scanned to monitor follicular growth and ovulation. Cows with clinical mastitis (n = 12) had elevated rectal temperatures, somatic cell counts, and mammary scores. Estrus and ovulation occurred in 4 of 12 clinically infected cows and in all control cows. Cows that were challenged but did not develop clinical mastitis (n = 5) displayed estrus and ovulated. Due to differences in expression of estrus, cows were further subdivided for analyses into 4 groups: control, TRT-EST (infected cows that displayed estrus; n = 4), TRT-NOEST (infected cows that did not display estrus; n = 8), and NOMAS (cows that were inoculated but did not develop mastitis; n = 4). Ovulation rate was 100% for CON, NOMAS, and TRT-EST compared with 0% for TRT-NOEST cows. Size of the ovulatory follicle ("presumed" ovulatory follicle in TRT-NOEST cows) was similar for all groups. Frequency of LH pulses was decreased in TRT-NOEST compared with CON, TRT-EST, and NO-MAS. Estradiol-17beta increased over time in CON, NO-MAS, and TRT-EST cows, but did not increase in TRT-NOEST cows. Cows with clinical mastitis may exhibit estrus and ovulate normally or have disruptions in normal physiology including decreased LH pulsatility, absence of an LH surge and estrous behavior, suppressed estradiol-17beta, and failure to ovulate.

Animals↗

Cross-infection between cats and cows: origin and control of Streptococcus canis mastitis in a dairy herd.

Group G streptococci in animals usually belong to the species Streptococcus canis and are most commonly found in dogs and cats. Occasionally, Strep. canis is detected in milk from dairy cows. An outbreak of Strep. canis mastitis in a dairy herd is described. Based on results from bacterial culture and ribotyping, a cat with chronic sinusitis was the most likely source of the outbreak. Subsequent cow-to-cow transmission of Strep. canis was facilitated by poor udder health management, including use of a common udder cloth and failure to use postmilking teat disinfection. Infected cows had macroscopically normal udders and milk, but significantly higher somatic cell counts than Strep. canis-negative herd mates. The outbreak was controlled through antibiotic treatment of lactating cows, early dry-off with dry cow therapy, culling of infected animals, and implementation of standard mastitis prevention measures. Cure was significantly more likely in dry-treated cows (87.5%) and cows treated during lactation (67%) than in untreated cows (9%). Whereas mastitis due to group G streptococci or Strep. canis in dairy cows is usually limited to sporadic cases of environmental (canine or feline) origin, this case study shows that crossing of the host species barrier by Strep. canis may result in an outbreak of mastitis if management conditions are conducive to contagious transmission. In such a situation, measures that are successful in control of Strep. agalactiae can also be used to control Strep. canis mastitis.

Animals↗

Escherichia coli isolates' serotypes, genotypes, and virulence genes and clinical coliform mastitis severity.

Dairy cattle with clinical mastitis caused by Escherichia coli exhibit a wide range of disease severity, from mild, with only local inflammatory changes of the mammary gland, to severe, with significant systemic derangement. The present study was designed to examine the relationship between serotype and virulence genes of E. coli mastitis isolates, different levels of systemic disease severity, and farm from which the E. coli strain was obtained. One hundred twenty-three E. coli milk isolates were obtained from cows with clinical mastitis of varying systemic disease severity from 6 different farms. No predominant serotype was identified by farm or by systemic disease severity; however, the most frequent serotype, O158:NM (n = 3), was isolated from cows in the moderate severity group. Virulence genes evaluated were identified infrequently and were not associated with systemic disease severity. Evaluation of genetic similarity showed no clustering assigned by farm or mastitis severity based on systemic disease signs. We concluded that a high degree of genotypic variability is characteristic of E. coli strains causing clinical mastitis within and between different farms and systemic severity groups, and that specific cow factors probably play a more important role in determining systemic disease severity.

Animals↗

Prolactin-induced activation of nuclear factor kappaB in bovine mammary epithelial cells: role in chronic mastitis.

We sought to determine whether prolactin (PRL) could influence the neutrophilic inflammation that characterizes chronic mastitis. Most of the genes encoding inflammatory proteins depend on the nuclear factor kappaB (NF-kappaB) for their expression. We addressed the hypothesis that immunomodulatory activities of PRL might arise from an increase in NF-kappaB activity. MAC-T cells, a bovine mammary epithelial cell line, were stimulated with increasing concentrations of bovine PRL (1, 5, 25, 125, and 1,000 ng/mL). Level of NF-kappaB binding activity was measured and mRNA was evaluated for IL-1beta, IL-6, IL-8, granulocyte-macrophage colony-stimulating factor (GMCSF), IFN-gamma, and tumor necrosis factor (TNF)-alpha, cytokines known to require NF-kappaB for their maximal transcription. Prolactin activated NF-kappaB; maximal NF-kappaB activation was weaker with PRL than with TNF-alpha at 30 or 180 min poststimulation. In addition, PRL significantly amplified, in a dose-dependent manner, mRNA expression of IL-1beta, IL-6, IL-8, GMCSF, and TNF-alpha. We measured PRL concentrations in blood and milk from healthy and chronic mastitis-infected cows, and studied the relationship between the PRL concentration and the degree of inflammation in the mammary gland as indirectly assessed by somatic cell counts (SCC). Plasma PRL did not differ significantly between healthy and chronic mastitis-affected cows (63.7 and 67.5 ng/mL, respectively). Milk PRL concentration was significantly increased in chronic mastitis-affected quarters with the highest SCC, and had a positive significant correlation between SCC, as well as between the number of neutrophils present in milk samples. The present findings show that PRL promotes an inflammatory response in bovine mammary epithelial cells via NF-kappaB activation, and suggest a role for PRL in the pathogenesis of chronic mastitis.

Animals↗

Relationship between antimicrobial drug usage and antimicrobial susceptibility of gram-positive mastitis pathogens.

The objective of this study was to analyze relationships between usage of antimicrobial drugs on dairy farms and results of antimicrobial susceptibility testing of mastitis pathogens. Exposure to selected antimicrobial drugs (n = 10) was standardized by calculation of the number of defined daily doses used per cow. Farms (n = 40) were categorized based on amount of antimicrobial exposure: organic (no usage); conventional-low usage (conventional farms not using or using less than or equal to the first quartile of use of each compound); and conventional-high usage (conventional farms using more than the first quartile of a particular compound). The minimum inhibitory concentration (MIC) of selected antimicrobial drugs was determined using a commercial microbroth dilution system for isolates of Staphylococcus aureus (n = 137), coagulase-negative staphylococci (CNS, n = 294), and Streptococcus spp. (n = 95) obtained from subclinical mastitis infections. Most isolates were inhibited at the lowest dilution tested of most antimicrobial drugs. Survival curves for Staph. aureus and CNS demonstrated heterogeneity in MIC based on the amount of exposure to penicillin and pirlimycin. For CNS, farm type was associated with the MIC of ampicillin and tetracycline. For Streptococcus spp., farm type was associated with MIC of pirlimycin and tetracycline. For all mastitis pathogens studied, the MIC of pirlimycin increased with increasing exposure to defined daily doses of pirlimycin. The level of exposure to most other antimicrobial drugs was not associated with MIC of mastitis pathogens. A dose-response effect between antimicrobial exposure and susceptibility was observed for some pathogen-antimicrobial combinations, but exposure to other antimicrobial drugs commonly used for prevention and treatment of mastitis was not associated with resistance.

Animals↗

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.

Animals↗

Relationship between vitamin A and beta-carotene in blood plasma and milk and mastitis in Holsteins.

Blood and milk were sampled and quarter California Mastitis Test scores were taken during four 2-wk periods from 45 lactating cows. Vitamin A and beta-carotene in plasma and milk were analyzed within 48 h after collection. Total vitamin A equivalent (2 X amount of beta-carotene plus amount of vitamin A) also was calculated. Additionally, the total amount of vitamin A and beta-carotene excreted in milk was calculated from concentrations of vitamin A and beta-carotene in milk and milk weights recorded on sampling day. Independent effects of lactation number, period of collection, days in lactation, and California Mastitis Test Scores (the highest test score of four quarters used in the analysis) were examined by least-squares procedures using each blood and milk measure as the dependent variable. Results showed a highly significant independent effect of California Mastitis Test Scores for concentrations of plasma vitamin A, beta-carotene, and total vitamin A equivalent. Cows with lower plasma vitamin A, beta-carotene, and total vitamin A equivalent had higher test scores than cows with higher vitamin A and beta-carotene. Similar comparisons for amount of milk vitamin A, beta-carotene, and total vitamin A equivalent and total amount of each component excreted in milk showed no significant independent effects attributed to California Mastitis Test. Therefore, low concentrations of vitamin A and beta-carotene in plasma were associated with severity of mastitis in cows.

Animals↗

Associations between dry cow therapy, clinical mastitis, and somatic cell count score with milk and fat production in ten New Zealand dairy herds.

Cows in each of 10 dairy herds were assigned to two similar groups on age, breed, production, and previous mastitis history. Only cows in one group received dry cow therapy at the end of their 1977-1978 lactations. Production of all cows was tested at bi-monthly intervals during their 1978-1979 lactations. The composite evening and morning sample for milk fat measurement also was used for somatic cell counting. In the therapy group, 15.4% of cows had clinical mastitis detected by the herd owners during post-treatment lactations compared to a 9% incidence among untreated herd mates. Lactational average milk somatic cell count was higher in cows detected with clinical mastitis but lower in the therapy group. Untreated cows subsequently produced less milk (3706 versus 3966 liters) with this effect most pronounced among untreated cows with higher average cell count scores. Similarly, the depressive effects of detected clinical mastitis on production were most apparent among those cows in which clinical infection was associated with high lactational cell count score. Clinical mastitis depressed production more in Jersey cows than in Friesian-Jersey crossbreds. In these herds selective dry cow therapy may have been preferable to whole herd therapy.

Age Factors↗

Milk antitrypsin as a marker of bovine mastitis--correlation with bacteriology.

Milk antitrypsin reflects leakage of protein of blood plasma into milk. Mastitis detection can be based on measurement of the trypsin-inhibitor capacity in milk; the "Eflab Mastitis Test" procedure is based on this principle. The procedure was developed to screen for subclinical mastitis; high capacity and sensitivity permits whole herds to be analyzed on a quarter basis to identify inflamed quarters during a single sampling. Milk antitrypsin was measured on 2174 quarter milk samples by a colorimetric procedure. The Multiskan MC reader was hooked to desk computer to interpolate antitrypsin from the standard curve and to analyze results. The analysis of inflammation was based on antitrypsin as well as computerized interquarter evaluation. These measures were compared with bacteriologic study of milk to set criteria for automatic identification of mastitis in individual quarters. The comparison against the lowest teat antitrypsin gave better indication of infection than antitrypsin as such. By strict criteria that identified inflammations caused by major pathogens, 18.8% of uninfected quarters were identified as false positive. The explanation is that a single bacteriological culture is not reliable for detecting mastitis, because there are temporary causes of tissue irritation other than bacteria that may be identified during standard bacteriologic examination.

Animals↗

Preinfection chemotactic response of blood polymorphonuclear leukocytes to predict severity of Escherichia coli mastitis.

Experimental mastitis was induced by inoculating rear right quarters of 10 healthy cows with 10(3) cfu of Escherichia coli. The chemotactic responses of peripheral blood polymorphonuclear leukocytes at d-6, -5, -2, -1, and immediately prior to inoculation were measured. Chemiluminescence of polymorphonuclear leukocytes was measured immediately prior to inoculation. Severity of the experimental mastitis was assessed by bacterial growth in the inoculated quarters. Results of this study indicated that severity of the experimental mastitis may be predicted by the chemotactic response in vitro of polymorphonuclear leukocytes isolated from the peripheral blood at d 2, d 1, and immediately prior to inoculation. The number of circulating polymorphonuclear leukocytes immediately prior to inoculation also showed a negative relationship with the severity of mastitis. No relationship existed between preinfection chemiluminescence of polymorphonuclear leukocytes and the severity of the experimental mastitis.

Animals↗

Severity of experimental Escherichia coli mastitis in ketonemic and nonketonemic dairy cows.

The severity of experimental Escherichia coli mastitis in relation to in vitro chemotaxis of polymorphonuclear leukocytes was investigated in cows during negative energy balance. The negative energy balance was induced by feed restriction. Cows were classified into two groups, ketonemic and nonketonemic, based on the beta-hydroxybutyrate concentration in the peripheral blood at the moment of inoculation. Bacterial growth in the inoculated quarter was used as a parameter to indicate the severity of experimental mastitis. In the nonketonemic cows, experimental mastitis ranged from moderate to severe. Severity of experimental mastitis was negatively related to preinfection chemotactic response of polymorphonuclear leukocytes. In contrast, the course of experimental mastitis in the ketonemic group was relatively severe in all cows, regardless of preinfection chemotactic response.

3-Hydroxybutyric Acid↗

Distribution of clinical mastitis among quarters of the bovine udder.

Clinical mastitis episodes occurring from 1962 through 1991 in the Louisiana State University Dairy Research Herd were studied to determine the distribution of clinical mastitis among quarters of the udder. Data were detailed records of all mastitis episodes that occurred during 1630 Holstein lactations. Incidence of episodes, categorized according to which quarters within a cow were clinical for a given case, were compared with mathematical expectations based upon the assumption that quarters were independent. Results indicated that quarters within a cow were more alike with respect to clinical mastitis than would be expected if quarters were independent. More episodes occurred in which either no quarters or all four quarters were clinical. Deviation of observed frequencies from expectation could have resulted from generalized cow differences, such as cow milk yield, immune competency, mammary type characteristics, and general health. Front quarters had less clinical mastitis than rear quarters when all episodes were considered. No difference was observed in incidence between front and rear quarters when only first episodes in first lactations were considered. No difference was observed between incidence in left and right quarters. Diagonal pairs occurred less often than expected and at about half the frequency of other pairs. Dependence between quarters should be taken into consideration when experiments are designed and analyzed.

Animals↗

Effect of somatotropin on changes in milk production and composition during coliform mastitis in periparturient cows.

The potential protective and therapeutic effects of bST during coliform mastitis in periparturient cows were evaluated. In a first study, 19 cows, classified as moderate or severe responders based on the respiratory burst activity of blood neutrophils, were treated with recombinant bST or vehicle 48 h after intramammary inoculation of Escherichia coli. Clinical status and changes in milk production and composition were compared in the four groups. In a second study, 8 cows received bST or vehicle 7 d before bacterial challenge. During mastitis, losses in milk production and compositional changes were most pronounced in infected glands and in severe responders. Milk production of bST cows recovered better than that of placebo cows. Recovery of milk components was accelerated in severe responders treated with bST, but not in moderate responders. Pretreatment of severe responders with bST enhanced milk production before infection, protected the mammary glands from excessive loss of milk during the subsequently induced coliform mastitis, and accelerated normalization of milk composition. In conclusion, the beneficial effects of bST upon normalization of milk production and composition in periparturient cows suffering from coliform mastitis seem to be restricted to the severe responders. In severe responders that had been treated with bST, changes observed during mastitis resembled those in moderate responders treated with the placebo.

Animals↗

Selection on somatic cell score to improve resistance to mastitis in the United States.

Increased genetic susceptibility to mastitis has accompanied the rapid genetic increase in milk yield, and genetic selection for mastitis resistance should be considered. Somatic cell score is recommended as an indicator trait to achieve genetic improvement for mastitis resistance. Heritability of somatic cell score is around 10%, and genetic correlation between somatic cell score and clinical mastitis is around .6 to .8. Selection for lower somatic cell score is consistent with the goal of maximizing genetic improvement for total economic merit and should be included in breeding programs. National genetic evaluations for somatic cells scores will use the same animal models and methods as are currently used for milk yield traits. Reliabilities of PTA for somatic cell scores will be smaller than for yield traits because of lower heritability and availability of records from fewer cows. Several forms are proposed for reporting genetic evaluations of somatic cells to producers, and advantages and disadvantages are discussed. Using somatic cell scores for breeding decisions would marginally decrease genetic gain for milk yield and increase total economic merit. Optimal selection indexes would slow the rate of increase in mastitis, rather than decrease its incidence.

Animal Husbandry↗

A decision support system for evaluating mastitis information.

A data-driven decision support system, MAST, was developed to summarize systematically the DHI data related to mastitis. MAST determines weaknesses and problems of a mastitis control strategy by pinpointing problem areas, highlighting the scope of the mastitis problem, providing reference values for comparison, offering potential solutions to problem areas, and monitoring changes in the control strategy. Advantages of a DHI data-driven system include accuracy of input data, fast execution speeds, access to untapped information available in DHI data, and a consistent analysis of data. An on-farm decision support system allows the evaluation of the mastitis control strategy at any time, which in turn increases the value of DHI information. The sequence of the graphical results allows users to understand intuitively the overall mastitis problems, find the potential origins, and assess their impact on the herd. Color-coded graphs with supplementary text allow for a rapid analysis of level and trends over time, as well as comparisons among parities, lactation stages, and active and culled cows.

Animals↗

A knowledge-based system for diagnosis of mastitis problems at the herd level. 1. Concepts.

Much specialized knowledge is involved in the diagnosis of a mastitis problem at the herd level. Because of their problem-solving capacities, knowledge-based systems can be very useful to support the diagnosis of mastitis problems in the herd. Conditional causal models with multiple layers are used as a representation scheme for the development of a knowledge-based system for diagnosing mastitis problems. Construction of models requires extensive cooperation between the knowledge engineer and the domain expert. The first layer consists of three overview models: the general overview conditional causal model, the contagious overview conditional causal model, and the environmental overview conditional causal model, giving a causal description of the pathways through which mastitis problems can occur. The conditional causal model for primary udder defense and the conditional causal model for host defense are attached to the overview models at the second layer, and the conditional causal model for deep primary udder defense is attached to the conditional causal model for the primary udder defense at the third layer. Based on quantitative user input, the system determines the qualitative values of the nodes that are used for reasoning. The developed models showed that conditional causal models are a good method for modeling the mechanisms involved in a mastitis problem. The system needs to be extended in order to be useful in practical circumstances.

Animals↗