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At least 217 records · Page 12Linked to original sources
PubMed2000

Endocrine profiles of dairy cows following experimentally induced clinical mastitis during early lactation.

Concentrations of LH, cortisol, estradiol-17beta (E(2)), prolactin and 13,14-dihydro-15-keto-prostaglandin F(2alpha) (PGFM) were determined in cows with experimentally induced clinical mastitis during early lactation. Cows free of intramammary infection (IMI) and in the luteal phase of the estrous cycle were balanced by lactation number and days in milk and assigned to either control (n=5) or treatment (n=5) groups. Treated cows were infected experimentally (day 0), in two mammary quarters, with Streptococcus uberis and developed clinical mastitis within 60 h after inoculation as evidenced by increased mastitis scores, elevated rectal temperatures, mammary swelling and isolation of S. uberis pathogen. Four days following bacterial challenge, blood samples were collected every 20 min for 8 h for determination of PGFM and LH following administration of oxytocin and GnRH, respectively. Blood samples were also collected on days 0, 4 and 7 of the experiment to determine concentrations of E(2), prolactin and cortisol. Four days after bacterial challenge, concentrations of cortisol were higher (P=0.04) in experimentally infected cows than controls. Experimentally challenged cows had increased (P=0.02) concentrations of cortisol on days 4 and 7 compared with day 0. Control cows had no significant increase in blood cortisol during the experimental period. Baseline concentrations of PGFM did not differ between groups; however, peak concentrations of PGFM following oxytocin challenge were elevated (P=0.006) in cows with clinical mastitis compared with control animals. Prolactin, E(2) and LH did not differ between cows with clinical mastitis or controls. Experimentally induced mastitis during early lactation elevated concentrations of cortisol during the luteal phase of the estrous cycle. Furthermore, mastitic cows demonstrated an increased PGFM response following oxytocin administration. Altered reproductive efficiency in cows with clinical mastitis caused by Gram-positive pathogens may be the result of increased uterine sensitivity to prostaglandin F(2alpha) (PGF(2alpha)).

Animals↗
PubMed2003

Mycoplasmal mastitis in dairy herds.

Mycoplasmal bovine mastitis is potentially a highly contagious disease that can cause severe economic problems in affected herds. The purchase of replacement heifers and cows are frequently the origin of mycoplasmal mastitis outbreaks in previously Mycoplasma-free herds. Purchased cows and heifers should be quarantined and tested for mycoplasmal mastitis before admission to the regular herd. Detection of Mycoplasma-infected cows by culture of milk is straightforward, although there are problems of sensitivity for its detection in milk samples that are inherent to the nature of the disease and laboratory procedures. After detection of infected cows, the best way to protect the herd is to culture all cows in the herd, cows with clinical mastitis, and all heifers and cows after calving and before entering the milking herd. Control of mycoplasmal mastitis requires test and culling from the herd of Mycoplasma-positive cows if possible. When a large number of cows are infected, strict segregation with adequate management is an option; however, animals in this group should never re-enter the Mycoplama-free herd. The functioning of the milking equipment and milking procedures should be evaluated carefully and any flaws corrected. There is no treatment for mycoplasmal mastitis, and vaccination has not proven to be efficacious to prevent, decrease the incidence, or ameliorate the clinical signs of mycoplasmal mastitis. Waste milk should not be fed to calves without pasteurization. M bovis may cause several other pathologies in animals of different ages on a farm, including pneumonia, arthritis, and ear infections. The survival of mycoplasmas in different farm microenvironments needs to be further investigated for its impact on the epidemiology of the disease.

Animals↗
PubMed1993

Immunization and immunotherapy for mastitis.

Immunization and immunotherapy for mastitis are active areas of investigation. The past decade has seen development of effective and economical R-mutant vaccines for gram-negative mastitis. These vaccines doubtless will prove beneficial on well managed dairies that have eradicated contagious mastitis pathogens. Development of vaccines for other mastitis pathogens has been noticeably slower. A commercially available Staphylococcus aureus vaccine appears to reduce the frequency and severity of clinical episodes, but probably has minimal impact on the incidence or prevalence of infection. This product has not been extensively studied. The recent recognition of virulence factors produced in vivo by Staphylococcus aureus may provide a breakthrough in the development and production of Staphylococcus aureus vaccines. Bacterins employing this principle presently are not commercially available, however. In the case of all contagious mastitis pathogens (Streptococcus agalactiae, Staphylococcus aureus, and Mycoplasma spp.), traditional control and eradication efforts (teat dip, dry cow therapy, culling programs) likely will prove preferable to long-term immunization. Ongoing research may provide more efficacious vaccines for these mastitis syndromes. Immunostimulants are an active area of research. Although leukopoietic factors appear promising as immunostimulants, no compound has clearly demonstrated efficacy in either the prevention or treatment of bovine mastitis.

Animals↗
PubMed1990

A method for assessing loss in milk yield due to subclinical mastitis.

A method for assessing the loss in quarter milk yield due to subclinical mastitis is proposed. It is based upon two indices calculated from quarter milk yields and results from the assessment of mastitis obtained by measurement of the electrical conductivity of milk. The results were obtained from the cows through repeated quarter-milkings during several months of lactation. The grade of abnormality of a quarter with subclinical mastitis was expressed by the first index, the mean quarter difference of electrical conductivity of milk produced by the quarter (mQdEC, 25 degrees C). The reduction in milk yield of a quarter presumed to be due to subclinical mastitis was expressed by another index, the quarter yield ratio, R, which is that percentage of normal milk yield produced by a quarter with mastitis. Examination of the relationship between these two indices showed that subclinical mastitis caused a reduction in milk yield in the affected quarters. From the linear regression, it was found that approximately 3% reduction in quarter milk yield occurred for every 1 X 10(-4)S/cm increase in the mQdEC of the quarter with presumed subclinical mastitis.

Animals↗
PubMed2003

Bovine mastitis in selected areas of southern Ethiopia.

A study on bovine mastitis, designed to determine the causal agents, prevalence of infection and impact of risk factors in three cattle breeds, was conducted in selected areas of southern Ethiopia. A total of 307 lactating and non-lactating cows, of which 162 were indigenous Zebu, 85 Jersey and 60 Holstein-Friesian. were examined by clinical examination and the California mastitis (CMT) test. Of these, 40.4% were positive by CMT and bacteriology for clinical or subclinical mastitis, with prevalence rates of 37.1% and 62.9%, respectively. Out of 1133 quarters examined, 212 (18.7%) were found to be infected, 83 (39.21%) clinically and 129 (60.8%) subclinically. The prevalence of mastitis was significantly higher in Holstein-Friesian than in indigenous Zebu, in non-lactating cows than in lactating cows, in the early lactation stage than in the mid-lactation stage, in cows with lesions and/or tick infestation on skin of udder and/or teats than in cows without this factor, and in the wet season than in the dry season. Mastitis increased with parity number (R = 0.9). Of 248 CMT and clinically positive udder quarter samples analysed microbiologically, 212 were culturally positive for known mastitis pathogens and 36 were negative. Of the 199 positive samples. Staphylococcus accounted for 39.2%. Streptococcus for 23.6%, coliforms for 14.1%, Micrococcus and Bacillus species for 8.0% each and Actinomyces or Arcanobacterium (Corynebacterium) for 7.0%. It was concluded that there was a high prevalence of clinical and subclinical mastitis, mainly caused by Staphylococcus aureus, Streptococcus agalactiae and Escherichia coli, in this study area.

Animal Husbandry↗
PubMedDate not supplied

Genetics of resistance to mastitis in dairy cattle.

Genetic variability of mastitis resistance is well established in dairy cattle. Many studies focused on polygenic variation of the trait, by estimating heritabilities and genetic correlation among phenotypic traits related to mastitis such as somatic cell counts and clinical cases. The role of Major Histocompatibility Complex in the susceptibility or resistance to intrammamary infection is also well documented. Finally, development from molecular genome mapping led to accumulating information of quantitative trait loci (QTL) related to mastitis resistance and better understanding of the genetic determinism of the trait. From economic and genetic analyses, and according to welfare and food safety considerations and to breeders and consumer's concern, there is more and more evidence that mastitis should be included in breeding objective of dairy cattle breeds. Many countries have implemented selection for mastitis resistance based on linear decrease of somatic cell counts. Given biological questioning, potential unfavourable consequences for very low cell counts cows are regularly investigated. Improvement of selection accuracy for mastitis resistance is ongoing and includes: advances in modelling, optimal combination of mastitis related traits and associated predictors, such as udder morphology, definition of global breeding objective including production and functional traits, and inclusion of molecular information that is now available from QTL experiments.

Animals↗
PubMed1999

Streptococcus uberis: a permanent barrier to the control of bovine mastitis?

The prevalence of bovine mastitis has been reduced over the past 25 years due to the implementation of a five-point control plan aimed at reducing exposure, duration and transmission of intramammary infections by bacteria. This has markedly reduced the incidence of bovine mastitis caused by bacteria which show a contagious route of transmission, but has had little effect on the incidence of mastitis due to bacteria which infect the gland from an environmental reservoir. Streptococcus uberis is one such bacterium which is responsible for a significant proportion of clinical mastitis worldwide. The inadequacies of the current methods of mastitis control have led to the search for additional measures, particularly vaccines to prevent intramammary infection by this bacterium. Such an approach requires detailed knowledge of the pathogenesis of intramammary infection. Our understanding of this area has grown in recent years but a lack of information still hampers disease control. Both live vaccines and, recently, crude sub-unit vaccines have shown promise against bovine mastitis due to S. uberis. Vaccines against mastitis must, however, be able to control infection without the participation of a marked inflammatory response. This review provides an overview of the recent advances which have been made in our understanding of host-pathogen interactions which promote infection and disease and highlights areas for strategic research aimed at controlling this bacterial infection.

Animals↗
PubMed2006

Mastitis pathogens present in bulk tank milk from seven dairy herds in the Waikato region, New Zealand.

AIM: To identify and enumerate colony forming units (cfu) of mastitis pathogens in bulk tank milk (BTM) from pasture-fed New Zealand dairy cows in the Waikato region. METHODS: BTM samples from seven seasonal-calving dairy herds in the Waikato region were collected monthly from August to December 2004 (cows calved during July-September). Milk samples were cultured on blood aesculin and MacConkey agar plates for 24 h, and the number of mastitis pathogens identified and counted. RESULTS: Colonies identified in BTM included aesculin-positive streptococci, Staphylococcus aureus, coagulase-negative staphylococci (CNS), and coliforms; counts ranged from zero to >1,000 cfu/ml. Counts>1,000 cfu/ml for total aesculin-positive streptococci, CNS and coliforms were present in 48%, 51% and 11% of BTM samples, respectively. Counts of Staph. aureus ranged from zero to 1,000 cfu/ml, but first appeared in BTM samples only in October. Staphylococcus aureus was repeatedly isolated in BTM from 4/7 farms during the testing period. CONCLUSIONS: Counts of mastitis pathogens in this study appeared high relative to interpretive criteria set by other workers, which may indicate a high prevalence of mastitis risk factors on these farms. Interpretation of results is difficult as aesculin-positive streptococci, CNS and coliforms can be isolated from the environment as well as from cows with clinical or subclinical mastitis. Furthermore, Staph. aureus is inconsistently excreted from infected bovine mammary glands. More extensive study of this method is required in New Zealand to attempt to further validate the interpretation of results of bacterial culture of BTM. CLINICAL RELEVANCE: This method may be used to monitor challenge from mastitis pathogens over time as part of milk quality control programmes. The technique may be of use as a screening test to provide information to veterinarians, affording them the opportunity to have an input into mastitis control on dairy farms in New Zealand.

Animals↗
PubMed1997

The effect of discontinuation of postmilking teat disinfection in low somatic cell count herds. I. Incidence of clinical mastitis.

Results are described of a split-udder trial on the effect of discontinuation of postmilking teat disinfection on the incidence of clinical mastitis in seven dairy herds with a low bulk milk somatic cell count and a high incidence of clinical mastitis. Overall incidence of clinical mastitis was non-significantly lower (18%), whereas the incidence of the most prevalent pathogen associated with clinical mastitis, Escherichia coli, was significantly lower in quarters for which postmilking teat disinfection was discontinued. We concluded that discontinuation of postmilking teat disinfection may decrease the incidence of clinical Escherichia coli mastitis in herds for which standard mastitis prevention measures are executed adequately, bulk milk somatic cell count is low, and incidence of clinical mastitis is high. However, because an increase in intramammary infections with contagious pathogens may occur, care is recommended when advising discontinuation of postmilking teat disinfection.

Animals↗
PubMed2001

Aetiology of clinical mastitis in six Somerset dairy herds.

Clinical mastitis was monitored in six Somerset dairy herds for one year. The herds all had three-month geometric mean bulk milk somatic cell counts of less than 250,000 cells/ml. Escherichia coli was the predominant pathogen isolated on all the farms and in all months of the year. Environmental pathogens accounted for 61.4 per cent of all cases of clinical mastitis and for 79.3 per cent of the mastitis cases in which an aetiological agent was identified. The mean annual incidence was 41.6 cases per 100 cows (range 14 to 75). Affected cows suffered a mean of 1.5 cases and 16.4 per cent of quarters suffered at least one repeat case. Mastitis due to E. coli was more severe than mastitis due to other causes and it tended to be more severe in early lactation and during the housing period. Mastitis was significantly more severe (grades 2 and 3) in the herd with the lowest bulk milk somatic cell count and in the herd which was kept indoors throughout the year than in the other four herds. Mastitis was fatal in 2.2 per cent of cases and resulted in the death of 0.6 per cent of the lactating cows.

Animals↗
PubMed2002

Study of clinical mastitis in British dairy herds with bulk milk somatic cell counts less than 150,000 cells/ml.

A 12-month prospective study of clinical mastitis was conducted in 482 British dairy herds with a bulk milk somatic cell count (BMSCC) of less than 150,000 cells/ml. The mean proportion of cows in the herd with clinical mastitis was 23.1 per cent (range 0 to 80), with a mean of 1.50 quarter cases per cow. The mean incidence rate of clinical mastitis was 36.7 quarter cases per 100 cow years (range 0 to 208.2). Twelve per cent of the quarter cases showed systemic signs, including inappetence and severe lethargy. Over 22 per cent of quarter cases occurred in the first seven days of lactation and over 50 per cent occurred in the first 90 days of lactation. Cluster analysis indicated that the main difference between herds with a low and average incidence of mastitis was the proportion of clinical cases occurring in the first seven days of lactation, 14 per cent compared with 44 per cent, respectively. The risk of severe clinical mastitis compared with mild clinical mastitis decreased significantly as the individual cow somatic cell count (SCC) in the month before clinical mastitis was diagnosed increased.

Animals↗
PubMed1990

A descriptive study of lactation mastitis in long-term breastfeeding women.

This descriptive retrospective study surveyed women attending two lactation/breastfeeding conferences about their experiences with mastitis. One-third of the sample reported having mastitis while breastfeeding their last child. Episodes of mastitis occurred most often in the first three months postpartum; however, one-third occurred after six months and nearly one-quarter occurred after one year of breastfeeding. The outer upper quadrants of both breasts were found to be the most frequent sites of infection. The incidence of mastitis in the left and right breasts did not differ. More than one-third of the respondents did not contact their physician when they developed mastitis and and nearly half never used antibiotics for the infection. All respondents reported continuing to breastfeed through the infection. Mothers reported that the following factors (in order of importance) preceded their mastitis: fatigue, stress, plugged duct, change in the number of feedings, engorgement/stasis, an infection in the family, breast trauma and poor diet. Study findings indicate that the most important teaching areas for preventing mastitis are management and control of stress and fatigue.

Adult↗
PubMed2004

Cumulative risk of bovine mastitis treatments in Denmark, Finland, Norway and Sweden.

Data from the national dairy cow recording systems during 1997 were used to calculate lactation-specific cumulative risk of mastitis treatments and cumulative risk of removal from the herds in Denmark, Finland Norway and Sweden. Sweden had the lowest risk of recorded mastitis treatments during 305 days of lactation and Norway had the highest risk. The incidence risk of recorded mastitis treatments during 305 days of lactation in Denmark, Finland, Norway and Sweden was 0.177, 0.139, 0.215 and 0.127 for first parity cows and 0.228, 0.215, 0.358 and 0.204 for parities higher than three, respectively. The risk of a first parity cow being treated for mastitis was almost 3 times higher at calving in Norway than in Sweden. The period with the highest risk for mastitis treatments was from 2 days before calving until 14 days after calving and the highest risk for removal was from calving to 10 days after calving in all countries. The study clearly demonstrated differences in bovine mastitis treatment patterns among the Nordic countries. The most important findings were the differences in treatment risks during different lactations within each country, as well as differences in strategies with respect to the time during lactation mastitis was treated.

Animals↗
PubMed2003

Energy imbalance related predisposition to mastitis in group-fed high-producing postpartum dairy cows.

The energy imbalance related predisposition to mastitis was studied in group-fed postpartum dairy cows (n = 333) kept in 4 large-scale units and producing milk of low somatic cell count (SCC). Blood samples were taken on Days 1-3 after calving for assaying some metabolites and hormones related to the negative energy balance (NEB). If mastitis was diagnosed later, aseptic milk samples were taken to identify the pathogens. Considering pathogen types [contagious pathogens: Staphylococcus (S.) aureus, Gram-positive (GP) environmental pathogens, and Gram-negative (GN) environmental pathogens + mastitis with no detectable pathogens (NDP)] separately, stepwise logistic regression was used to analyse the relation between the potential prognostic value of hormones and metabolites and mastitis outbreak. Only the elevated (> or = 1.00 mmol/l) serum beta-hydroxybutyrate (BHB) levels predisposed the cows to mastitis in the subsequent 4 weeks. This prognostic value of BHB was significant only in GN + NDP mastitis and in cases caused by GP environmental pathogens, but not in S. aureus mastitis (odds ratio: 5.333, 3.600 and 1.333, respectively).

3-Hydroxybutyric Acid↗
PubMed2003

Increased nuclear factor kappaB activity in milk cells of mastitis-affected cows.

Bacterial mastitis is accompanied by a drastic increase in milk somatic cell count (SCC), with neutrophils being the predominant cell type found in the infected quarters. Accumulation and activation of neutrophils at the site of infection require local expression of many inflammatory genes encoding adhesion molecules, chemokines and cytokines. Most of the inflammatory genes contain binding sites for the nuclear factor kappaB (NF-kappaB) within their promoter and therefore partly depend on NF-kappaB for their expression. We thus hypothesized that an increase in NF-kappaB activity in the mammary gland could contribute to development of the neutrophilic inflammation that characterizes mastitis. In an attempt to verify this hypothesis, we first assessed milk cells from healthy and acute and chronic mastitis-affected cows for NF-kappaB activity using electrophoretic mobility shift assays. We next studied the relationships between the intensity of NF-kappaB activity in these cells and the degree of udder inflammation. Active NF-kappaB complexes were undetectable in milk cells from healthy cows, whereas high levels of NF-kappaB activity were always found in cells from cows with acute mastitis. In milk cells obtained from chronic mastitis-affected cows, NF-kappaB activity varied from low to high. Finally, the level of NF-kappaB activity measured in milk cells from chronic mastitis-affected cows was not correlated to SCC or to the proportion of neutrophils present in milk samples, but was highly correlated with the expression level of interleukin-8 and granulocyte/macrophage colony-stimulating factor, two NF-kappaB-dependent cytokines crucially involved in initiation and perpetuation of neutrophilic inflammation. These results suggest that NF-kappaB might play a role in mastitis pathogenesis.

Animals↗
PubMed2003

Genetic analysis of longitudinal trajectory of clinical mastitis in first-lactation Norwegian cattle.

Clinical mastitis records for 36,178 first-lactation daughters of 245 Norwegian Cattle (NRF) sires were analyzed with a Bayesian longitudinal threshold model. For each cow, the period going from 30 d before calving to 300 d after calving was divided into 11 intervals of 30 d length each. Absence or presence of clinical mastitis within each interval was scored as "0" or "1", respectively. A Bayesian threshold model consisting of a set of explanatory variables plus Legendre polynomials on time of order four was used to describe the trajectory of liability to clinical mastitis. Heritability ranged between 0.07 and 0.13 before calving, from 0.04 to 0.15 during the first 270 d after calving, and increased sharply thereafter, as a consequence of the form of the polynomial. Genetic correlations between adjacent days were close to 1, and decreased when days were further apart. Most genetic correlations were moderate to high. A measure of probability of future daughters contracting clinical mastitis during lactation was computed for each sire. A typical curve had a peak near calving followed by a decrease thereafter. The best sires had a low peak around calving and a low expected probability of mastitis among daughters throughout lactation. Expected fraction of days without mastitis was derived from the probability curves and used for ranking of sires. Rank correlations with genetic evaluations of sires obtained from cross-sectional models were high. However, sire selection was affected markedly, especially at high selection intensity. An advantage of the longitudinal model for clinical mastitis is its ability to take multiple treatments and time aspects into account.

Animals↗
PubMed2006

Short communication: genetic correlation between test-day electrical conductivity of milk and mastitis.

Electrical conductivity (EC) of milk is an indicator of mastitis. If EC shows genetic variation and is genetically correlated to mastitis, it could be used in a breeding program that includes selection for improved mastitis resistance. In this study, daily records of EC and mastitis from about 1,500 Holstein cows were analyzed. A bivariate animal model was used for estimation of (co)variance components, including fixed effects of age of calving, herd-test-day, and days in milk, in addition to random additive genetic effects and permanent environmental effects. For EC, the estimated heritability was moderate (0.22 to 0.39), whereas for mastitis, the heritability was low (0.013). The genetic correlation between EC and mastitis was estimated to be 0.75, and genetic improvement of mastitis resistance should be feasible through selection for reduced EC.

Analysis of Variance↗
PubMed1985

Udder and teat morphology related to mastitis resistance: a review.

Annual losses by mastitis are estimated to be in excess of two billion dollars in the United States. Udder and teat morphologies have been associated with incidences of mastitis without clear conclusion on the closeness. Streak canal diameter was correlated with udder health, but it is difficult to measure. Udder depth and teat-end shape have been associated with udder health. Selection to reduce frequencies of cows with deep udders and flat, disk, or inverted teat ends may reduce mastitis incidence. Heritabilities of udder morphology are moderate to high, and a single score during the lifetime of a cow may be adequate for selection. There is no concensus in the literature on relationships between mastitis and teat size, general teat shape, teat-end lesions, teat pigmentation, or milk flow rate. Different breeds, milking procedures, measures of mastitis, and statistical procedures may account for different conclusions. Genetic approaches to improve mastitis resistance of dairy cattle seem warranted. This paper attempts to summarize evidence dealing with possible physical bases for genetic variation associated with mastitis in dairy cattle.

Animals↗