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At least 703 records · Page 39Linked to original sources
PubMed1999

Effect of antibiotic induced bacterial clearance in the udder on L-selectin shedding of blood neutrophils in cows with Escherichia coli mastitis.

Bacterial clearance, L-selectin adhesion receptor expression and neutrophil recruitment during experimentally induced Escherichia coli mastitis were investigated. Acute mastitis was induced by injection of 10(4) cfu E. coli into both left quarters of 12 clinically healthy lactating cows, 2-6 weeks after parturition. Half the cows were treated intravenously 10 h after infection, and subcutaneously 30 h after infection with enrofloxacin. In both groups, bacterial count, milk serum albumin, milk somatic cell count, circulating leukocyte count and L-selectin expression on neutrophils were determined. Both groups responded to challenge with udder inflammation and fever. Treatment with enrofloxacin affected the elimination rate of bacteria at hours +14, +18, +24, +48, and +72 after challenge, but not the bacteriological cure rate (five out of six for treated and three out of six for nontreated cows). The drop in L-selectin expression found following challenge did not differ between groups throughout the study. No effect of treatment was found on SCC. Based on these findings, it may be concluded that when treatment is administered 10 h after infection, the number of bacteria in milk is not correlated with L-selectin expression on circulating PMN during experimentally induced E. coli mastitis. The initial bacterial load probably dictates the extent of the decrease in L-selectin expression and milk somatic cells.

Animals↗
PubMed2001

Detection model for mastitis in cows milked in an automatic milking system.

Automated detection of diseases (such as mastitis) in dairy cows might be an alternative for detection by observation during milking - especially when using an automatic milking system (AMS). An outline of a detection model is given. This detection model includes time-series models for two variables (milk yield and electrical conductivity of milk), with interpolation on previous values. The model is flexible in the number of variables actually used. Parameter values and the residual variances are updated by linear regression after each milking. Alerts for mastitis are given when the residuals fall outside given confidence intervals. A data set with 111 cows for 16 months (on average, 58 lactating cows per day) was used to test the model. Depending on the chosen confidence interval, 42-44 out of 48 cases of clinical mastitis were detected; the remaining cases were not detected because not all data needed were available. These results were better than the results obtained with the model usually used on the farm. The number of false-positive alerts depended on the chosen confidence interval and was higher than the number found with the model usually used.

Animals↗
PubMed1998

Biological predictors for early clinical mastitis occurrence in Holstein cows under field conditions in France.

Individual risk factors for clinical mastitis within the first month of lactation (early clinical mastitis, ECM) were analyzed in 695 Holstein multiparous cows (561 ECM- and 134 ECM+) which were clinical mastitis-free during the previous lactation. They belonged to 44 herds from the French Brittany region and were surveyed for 4 years. Individual biological parameter levels during the last 2 months of gestation, production of the preceding lactation and calving conditions and health were the available explanatory variables. The construction and explanation model used multiple logistic regression run with herd as a fixed effect. High precalving plasma ceruloplasmin oxidase (p < 0.01) and low glutamate dehydrogenase (p < 0.05) activities, high 305-day previous-lactation milk yield (p < 0.001) and milk protein content at the last milk-test day before drying-off (p < 0.01) were the significant risk factors for ECM occurrence. Intensive production and unsatisfactory dietary conditions (energy and antioxidants) would increase ECM risk in the dairy cow. Further studies should be conducted to determine if metabolic and/or genetic factors could explain the relationship between ceruloplasmin and subsequent ECM occurrence.

Animals↗
PubMed1998

Loss in milk yield and related composition changes resulting from clinical mastitis in dairy cows.

Relationships between clinical mastitis and milk yield and composition in dairy cows were reviewed. Requirements for inclusion were: data had to be collected after 1975; dependent variables for milk yield and milk composition had to be defined at the cow level; mastitis cases had to be defined by clinical signs, and at least 250 lactations had to be considered. Twenty studies dealing with milk-yield loss and, for four of them, also with related composition changes were selected. Study populations, design of data collection, and analysis methods differed widely between studies. As expected from these differences--but also due to structural-variation factors such as type of pathogen, animal and production level--estimates for milk-yield losses differed in average magnitude and pattern. Literature data regarding changes in milk-fat % and total-protein % changes were contradictory. Critiques of materials and methods allowed us to propose some final recommendations for values to be used as basic inputs in economic calculations of losses caused by mastitis.

Animals↗
PubMed1984

Mycoplasma mastitis.

Recognition of Mycoplasma-induced mastitis is on the increase. Although Mycoplasma bovis is identified as the causative agent in more than 50 per cent of the mastitis cases, seven other Mycoplasma species have also been isolated. The mycoplasmas are commonly found in the microflora of the respiratory and urogenital tracts of normal cattle, where precipitating factors can initiate their role as pathogens. Most udder infections are spread from cow to cow by physical contact and are precipitated through deficiencies in procedures in milking, equipment maintenance, sanitation, and udder infusion. Generally, the reaction in the udder is severe and persistent, and recovered animals remain shedders and potential carriers. Extensive therapy with antibiotics has not proven effective in altering the course of the disease. Control procedures in epizootics of mycoplasmal mastitis are based either on elimination of the infected animals by culling or through the co-existence on the dairy of known carrier animals segregated and milked separately from the uninfected animals. Adequate sanitation, proper udder infusion, and good milking principles are requisites to preventing mycoplasmal infections.

Animals↗
PubMed1984

The importance of hygienic procedures in controlling mastitis.

Properly designed and instituted sanitation will improve milk quality and reduce mastitis. The majority of mammary infections occur during milking. Since the populations of pathogenic organisms on the teat are directly correlated to the incidence of udder infections, hygienic practices in the milking parlor are of major importance to accomplish effective mastitis control. The organisms causing mastitis have two general sources. The contagious pathogens originating from infected udders are passed from cow to cow. The environmental agents are ubiquitous, gaining entrance to the mammary gland from external sources; they do not rely on intramammary infection for survival in the dairy environment. Cow hygiene in the milking parlor consists of three separate steps: premilking cleansing, sanitation of the milking unit between cows, and covering the teats with a germicide after milking. Each step has separate requirements in terms of product selection, concentration of germicide, time commitment, and mechanical assistance. Premilking sanitation is most effective against coliform-like infections as well as the other environmentals. Unit flushing and teat dipping are the greater deterrents to infection from the contagious pathogens, Staphylococcus aureus, Streptococcus agalactiae, and the Mycoplasma species. Extra care needs to be given to hygiene measures when infusing the mammary gland with antibiotics. Dipping the teats in an effective germicide both before and after infusion is highly effective in reducing mammary infections. Fresh cows and sick cows are both highly susceptible to infection. Only minimal sanitation of these animals while milking is generally practiced. Dipping prior to milking and leaving the germicide in contact with the teat while milking can be recommended as an additional procedure to reduce pathogens. All products used during milking should bear the label for product safety in food environments, and judicious use should not threaten product safety through potential residues.

Animals↗
PubMed2003

The influence of mastitis on antibody transfer to infants through breast milk.

Clinical and subclinical mastitis are common among lactating women but their potential influence on programmes to improve infant health through maternal vaccination has not previously been addressed. Maternal antibodies, acquired either through natural infection or through vaccination, enter milk through two main pathways: by transcytosis or paracellularly. Transfer through both pathways is likely to be increased during mastitis, mediated by inflammatory cytokines. The increases are of similar order of magnitude to the variation in milk antibody concentrations between women within a population or between women in developing and developed countries. Thus, the effects of mastitis on vaccination programmes can be subsumed under the larger question of how breastfeeding in general affects these.

Animals↗
PubMed1997

Further studies on the efficacy of a live vaccine against mastitis caused by Streptococcus uberis.

Three groups of dairy cows were immunized by subcutaneous (s.c.) administration of a preparation of live Streptococcus uberis (strain 0140J) and an intramammary infusion of a soluble surface extract derived from same the bacteria. Animals in Groups 1 and 2 received two s.c. vaccinations plus an intramammary inoculation. Animals in Group 3 received two s.c. vaccinations but did not receive the intramammary infusion. In addition to the vaccinated animals, each group also contained two non-vaccinated (control) animals. All animals were challenged experimentally by intramammary infusion (in two quarters per animal) of ca 100 c.f.u. of S. uberis (strain 0140J or C221) and monitored for clinical signs of disease, bacterial numbers in milk, somatic cell count in milk, and daily milk yield for the following 10 days. Animals in Group I were challenged with strain 0140J. Only one out of six challenged quarters of three vaccinated cows developed clinical disease compared to all (four out of four) quarters of non-vaccinated cows. Animals in Group 2 were challenged with strain C221. All challenged quarters of three vaccinated (six out of six) and two non-vaccinated (four out of four) cows developed clinical mastitis. Animals in Group 3 were challenged with strain 0140J. Five out of eight quarters on four vaccinated cows developed clinical mastitis but the onset was delayed in comparison with that in both non-vaccinated cows in which four out of four challenged quarters developed clinical mastitis. These results indicated that vaccination with live S. uberis protects against challenge with the homologous strain but was less effective against a heterologous strain. Reduced protection was also seen when the intramammary booster was omitted.

Animals↗
PubMed2002

Geographical variation in the presence of genes encoding superantigenic exotoxins and beta-hemolysin among Staphylococcus aureus isolated from bovine mastitis in Europe and USA.

The object was to examine the geographical variation in the presence of superantigenic exotoxins and beta-hemolysin among epidemiologically independent Staphylococcus aureus isolates from bovine mastitis. A total of 462 S. aureus isolates from nine European countries and USA were examined for the presence of genes encoding staphylococcal enterotoxins A-E, and H, toxic shock toxin-1 (TSST-1), and beta-hemolysin, and 128 of these were examined for exfoliative toxins A and B. The detection was done by PCR. Phenotypic methods were used to confirm the PCR-results. None of the 128 isolates carried the genes for exfoliative toxin A or B. The total proportion of isolates in which superantigenic exotoxins were detected varied from 2% (one isolate) of the Danish isolates to 65% (32 isolates) of the Norwegian isolates. This marked and highly significant geographical variation was also present for the individual exotoxins. The genes encoding enterotoxin C, TSST-1, and enterotoxin D were the most common superantigens. The present and earlier studies demonstrate that the superantigenic exotoxins that were investigated in this study, do not play a role in the pathogenesis of bovine S. aureus mastitis. In contrast to the geographical variation among superantigenic exotoxins, 97% of the isolates were PCR-positive for and/or produced beta-hemolysin on 5% calf blood agar. Except for three isolates, the Norwegian isolates were PCR-negative, but positive on 5% calf blood agar. Sequence variation in the primer regions in the beta-hemolysin encoding gene of the Norwegian isolates is suggested, and should be investigated further. The consistent presence of beta-hemolysin suggests that this factor, or a co-existing gene correlated to beta-hemolysin, may be an active virulence factor in the pathogenesis of bovine S. aureus mastitis.

Animals↗
PubMed2002

Virulence factors of Escherichia coli isolated from bovine clinical mastitis.

Escherichia coli isolates from bovine mastitis were examined for a selection of virulence factors. The strains originated from Finland and Israel, which have differences in the proportion of mastitis caused by E. coli, clinical pictures of coliform mastitis, environmental conditions and herd management. The genes of nine virulence factors were detected by polymerase chain reaction. Presence of K1 and K5 capsules was assessed by use of specific bacteriophages. Serum resistance was tested by a turbidimetric assay. Out of 160 Finnish isolates, 37% had traT, 14% cnf2, 8% cnf1, 11% aer, 9% f17, 8% sfa, 7% pap, 1% afa8D and 1% afa8E. Out of 113 Israeli isolates, 41% had traT, 4% aer, 3% cnf2, 1% cnf1, 1% sfa and 1% f17. Some of the genes were distributed among two major pathotype groups, with either f17 family or sfa, pap and cnf1 as major determinants. Genes for F17a, CS31A, Afa7D and Afa7E were not detected. Altogether 49% of Finnish and 42% of Israeli isolates had at least one virulence gene, but genes other than traT were present in only 24% of Finnish and 5% of Israeli isolates. Serum resistance was more common among Finnish (94/160) than Israeli isolates (19/113). K1 and K5 capsules were not detected.

Animals↗
PubMed2003

The epidemiology of Staphylococcus aureus infections from subclinical mastitis in dairy cows during a control programme.

The objective was to investigate the spread of S. aureus in seven dairy herds. Milk samples were taken to determine mastitis pathogens and somatic cell count. An approved hygiene programme was established to control the spread of S. aureus from quarter to quarter. S. aureus isolates were differentiated by geno- and phenotyping to trace their spread within a herd. In two herds S. aureus showed a high prevalence, but were eliminated from the herds by the control programme. In these herds and a third herd typing results identified a particular type that was found much more frequently than all other types. The frequent types were repeatedly detectable during the study. In three other herds with a lower S. aureus prevalence and also in one herd with a long history of S. aureus and high prevalence subclinical mastitis was caused by several distinguishable S. aureus types. These types occurred simultaneously in the particular herd and showed little or no tendency to spread from quarter to quarter. They seemed to circumvent the control procedures resulting in a relatively high rate of new infected animals and therefore were hardly eliminated. The typing results and the clinical observations indicated that strains differed in their tendency to spread and their ability to infect udder quarters. In three herds typing methods identified a predominant type with the common epidemiological features of a contagious mastitis pathogen, while in the other herds the S. aureus type patterns were similar to that of environmental pathogens.

Animals↗
PubMed1998

Potential virulence factors of Streptococcus dysgalactiae associated with bovine mastitis.

Mastitis caused by environmental pathogens is a major problem that affects many well-managed dairy herds. Among the environmental pathogens, Streptococcus dysgalactiae is isolated frequently from intramammary infections during lactation and during the nonlactating period. In spite of its high prevalence, little is known about factors that contribute to the virulence of S. dysgalactiae. During the last decade, several cell-associated and extracellular factors of S. dysgalactiae have been identified; yet, the relative importance of these factors in the transmission and pathogenesis of mastitis caused by S. dysgalactiae has not been defined. Streptococcus dysgalactiae can interact with several plasma and extracellular host-derived proteins such as immunoglobulin G, albumin, fibronectin, fibrinogen, collagen, vitronectin, plasminogen, and alpha 2-macroglobulin. These interactions are mediated by bacterial surface proteins. This organism also produces hyaluronidase and fibrinolysin which may be involved in promoting dissemination of the organism into host tissue. Streptococcus dysgalactiae adheres to and is internalized by bovine mammary epithelial cells in vitro. Involvement of host cell kinases, intact microfilaments and de novo eukaryotic protein synthesis are required for internalization of S. dysgalactiae into bovine mammary epithelial cells; a process that appeared to occur by a receptor-mediated endocytosis mechanism. However, de novo bacterial protein synthesis was not required for epithelial cell internalization. Furthermore, S. dysgalactiae survived within mammary epithelial cells for extended periods of time without losing viability or damaging the eukaryotic cell. Further research on characterization of host-pathogen interactions that take place during the early stages of mammary gland infection will enhance our understanding of pathogenesis of intramammary infection which may contribute to development of methods to minimize production losses due to mastitis.

Animals↗
PubMed2003

Mastitis therapy and pharmacology.

Mastitis remains the most frequent cause of antibacterial use on dairy farms and contributes to a substantial portion of total drug and veterinary costs incurred by the dairy industry. Ultimately, the best outcome of mastitis therapy is a positive effect on the amount of marketed milk harvested and long-term survival of the cow. This article describes the strategies of therapy for bovine mastitis, with an emphasis on antibacterial and anti-inflammatory therapy.

Animals↗
PubMed2003

The management and treatment of environmental streptococcal mastitis.

Environmental streptococci are responsible for at least one third of all cases of clinical mastitis, with the proportion varying widely between herds. Each dairy farmer should know the etiology of mastitis in the herd to allow for appropriate management. Control requires lowering the prevalence of infection, and includes shortening the duration of and preventing new infections. Prompt and aggressive treatment of clinical cases may achieve a high clinical and bactriologic rate of cure. Dry-cow treatment remains highly effective in eliminating infection. Prophylactic dry-cow treatment remains of substantial benefit in preventing new intramammary infections and clinical mastitis. An internal teat sealant has shown a comparable effect in uninfected cows in field studies. Management of exposure to environmental streptococci is essential and requires assessment of the risk of exposure (especially in bedding and other lying areas), reduction of teat-end contamination, and good hygienic milking practices. The key is in the quality of application of management.

Animals↗
PubMed2003

Vaccination strategies for reducing clinical severity of coliform mastitis.

Brief history and extensive published field efficacy data of the two rough ("R") bacterial mutants utilized in commercial preparations of the core antigen bacterins Escherichia coli O111:B4 (strain J5) and Salmonella typhimurium Re-17 are summarized. Particular dosage schedules and routes of administration of coliform mastitis bacterins are compared for their associated ecacy. Practical concerns in employing a coliform mastitis vaccination program are discussed. Characteristics of farms using coliform mastitis vaccination and suggested guidelines for whether individual dairy herds should adopt this practice are presented for consideration.

Animals↗
PubMed2001

Mastitis of sheep and goats.

This article presents an overview of the recent research into ovine and caprine mastitis. The common clinical presentations of mastitis in these species are reviewed, as are the important etiologic agents and their significance. The interpretation of somatic cell counts and surrogate tests, factors that affect somatic cell count levels, and association of somatic cell count levels with productivity are reviewed. Investigations into the treatment and prevention of mastitis and milking equipment function are discussed, and comments are made on the public health implications of extra label drug use and the consumption of unpasteurized milk.

Animals↗
PubMed1993

Procedures for mastitis diagnosis and control.

Procedures for mastitis diagnosis and control include culturing individual cow and bulk tank milk samples, antibiotic susceptibility testing, and evaluation of somatic cell count reports and clinical mastitis treatment records. Integrated use of such procedures is necessary for effective mastitis diagnosis and control.

Animals↗
PubMed1993

Nutrition and mastitis.

Increasing evidence presents a relationship between nutrition and mammary resistance to infection. The role of nutrition in mammary resistance has been best defined for antioxidants. To optimize this interaction, rations should be balanced and formulated for lactational stage. Although supplementation of nutrients with antioxidant function may enhance immune resistance against infections, therapeutic roles for nutritional management of clinical mastitis, as yet, are not well documented. The need to monitor herd antioxidant status as part of a mastitis control program is critical because (1) antioxidant supplementation improves mammary resistance to infectious disease during the most critical period for enhanced resistance, the dry and early postpartum periods; and (2) dry cows and heifers often are on a marginal plane of Se supplementation, particularly during periods of risk for mastitis and reproductive disorders. In areas where forages contain less than 0.1 ppm Se (dry matter) because of low soil availability, herds should be tested for Se status and, if found to be below optimum levels, increased dietary supplementation or sustained-release Se boluses should be considered. Similarly, vitamins A (or beta-carotene) and E status should be monitored in herds, especially confined herds receiving a large proportion of ensiled forages.

Animal Feed↗