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Temporal patterns of lost milk production following clinical mastitis in a large Michigan Holstein herd.

Cows with three hundred and sixteen cases of clinical mastitis were sampled by microbiologic culture during a 6-mo period on a 1700-cow Michigan Holstein dairy farm. Daily milk weights were obtained on all cows before clinical onset and for 60 d after onset. Predicted post-mastitis production, projected on the basis of premastitis production and the lactation curves of contemporary non-mastitic herdmates, was compared with actual daily milk production during the 60 d following clinical onset. Cows experiencing clinical mastitis produced approximately 341 kg less salable milk during the 60 d after clinical onset compared with projected production. This milk loss included both decreased production and milk withheld from market following antibiotic treatment. Pluriparous cows lost 2.06 times as much milk as first lactation cows, and cows with mastitis occurring before 150 d in lactation lost 1.40 times as much milk when compared with other cows. Cows with mastitis occurring in the winter showed a milk loss 1.37 times greater than cows with mastitis in summer. The identity of the mastitis agent isolated from the clinical case was not strongly associated with the drop in milk production in the 60 d following clinical onset.

Animals↗

Blood polymorphonuclear leukocyte chemotaxis during experimental Escherichia coli bovine mastitis.

The relationship between the severity of experimental Escherichia coli mastitis and the chemotactic response of blood polymorphonuclear leukocytes was investigated before and during mastitis. Experimental E. coli mastitis was induced in 10 healthy cows by inoculation of the rear right quarters with 10(3) cfu of E. coli. Cows were classified into two groups based on the severity of the mastitis. Bacterial growth in the inoculated quarter was used as parameter that indicated severity. Before and during experimental mastitis, the chemotactic response and the number of circulating polymorphonuclear leukocytes were greater for the moderately diseased cows than for the severely diseased cows. During the first 24 h of the experimental mastitis, the chemotactic response of polymorphonuclear leukocytes decreased in both groups. Recovery of the chemotactic response of white blood cells was more rapid in moderately diseased cows than in severely diseased cows. Possibly, the larger proportion of band neutrophils (the less chemotactically active band neutrophils) partially accounts for the lower chemotactic response of the circulating polymorphonuclear leukocytes during experimental mastitis in the severely diseased cows.

Animals↗

Effect of Re-17 mutant Salmonella typhimurium bacterin toxoid on clinical coliform mastitis.

The objective of this study was to test the hypothesis that the incidence and severity of clinical coliform mastitis could be decreased by Re-17 mutant Salmonella typhimurium bacterin toxoid. Holstein-Friesian cows from two Arizona dairies were selected for this study based on July through November projected calving dates; peak lactation occurred during the period of highest rainfall and peak environmental stress. The cows were randomly assigned to either a vaccinate or a control group, and 1292 cows were paired by herd, parity, calving date, and milk yield. The 646 vaccinates were injected twice during the third trimester of pregnancy with an Re-17 mutant S. typhimurium bacterin toxoid, and the 646 controls were not vaccinated. Vaccinated cows had significantly fewer clinical cases of coliform mastitis with positive coliform cultures and had lower culling rate from coliform mastitis than control cows during the first 5 mo of lactation. During the same period, the mortality rate from clinical coliform mastitis was 75% less in the vaccinated clinical coliform mastitic group than in the control group. Incidence of mastitis increased with advancing parity. The Re-17 mutant Salmonella typhimurium bacterin toxoid provided cross-protection against coliform mastitis; incidence and severity of clinical coliform mastitis were significantly lowered during the first 5 mo of lactation.

Animals↗

Comparison of analysis techniques for on-line detection of clinical mastitis.

Three techniques were compared for analysis of automatically collected data from the milking parlor. Mammary quarters showing signs of clinical mastitis were compared with randomly selected healthy quarters. Automatic data were analyzed from the milking on which the milkers observed clinical mastitis as well as data from the two prior milkings. Electrical conductivity of milk was not corrected for individual cows. Milking parlor data were preprocessed so that information on the electrical conductivity pattern during a milking was retained. Principal component analysis was used to verify whether variation in the data was caused by mastitis. Performance of logistic regression models for detection of clinical mastitis was compared with that of backpropagation neural networks. Variation in the quarter data was caused by mastitis. Automatic data from infected quarters did not always differ from data from healthy quarters, especially from the two prior milkings. The detection performance of the logistic regression model was similar to that of the neural networks. When both models were tested on the development data, sensitivity was approximately 75%, and specificity was approximately 90% at the milking of mastitis observation. Detection results were lower for the prior milkings. Therefore, not all incidences of clinical mastitis cases could be detected before clinical signs occurred.

Animals↗

Recombinant bovine somatotropin and clinical mastitis: incidence, discarded milk following therapy, and culling.

Holstein cows (n = 555) from four Michigan dairy farms were randomly assigned to receive bovine somatotropin (bST) or to serve as untreated controls. Bovine somatotropin (500 mg) was administered every 14 d beginning at 63 to 69 d of lactation and continuing until approximately 21 d prior to dry-off or until the cow was removed from the herd. Trial objectives were to determine the effect of bST on the incidence of clinical mastitis, number of days that milk was discarded because of therapy for clinical mastitis, and culling for mastitis. A total of 127 (22.9%) cases of clinical mastitis occurred during lactation. In the pretrial period (before 63 to 69 d of lactation), 42 (33.1%) cases occurred, and 85 (66.9%) cases occurred during the trial. Of the 42 pretrial cases, 57.1% occurred in control cows, and 42.9% occurred in treated cows. Of the 85 trial cases 47.1% occurred in control cows, and 52.9% occurred in treated cows. Using logistic regression, the odds ratio for the occurrence of clinical mastitis in treated cows was 1.06 (95% confidence interval = 0.62 to 1.81). The number of days that milk was discarded following therapy for clinical mastitis and the culling rate for mastitis did not differ between study groups.

Animals↗

Partial budget of the discounted annual benefit of mastitis control strategies.

The objective of this study was to rank the benefits associated with various mastitis control strategies in simulated herds with intramammary infections caused by Streptococcus agalactiae, Streptococcus spp. other than Strep. agalactiae, Staphylococcus aureus, coagulase-negative staphylococci, and Escherichia coli. The control strategies tested were prevention, vaccination for E. coli, lactation therapy, and dry cow antibiotic therapy. Partial budgets were based on changes caused by mastitis control strategies from the mean values for milk, fat, and protein yields of the control herd and the number of cows that were culled under a fixed mastitis culling criterion. Each annual benefit (dollars per cow per year) of a mastitis control strategy was compared with the revenue for the control herd and was calculated under two different milk pricing plans (3.5% milk fat and multiple-component pricing), three net replacement costs, and three prevalences of pathogen-specific intramammary infection. Twenty replicates of each control strategy were run with SIMMAST (a dynamic discrete event stochastic simulation model) for 5 simulated yr. Rankings of discounted annual benefits differed only slightly according to milk pricing plans within a pathogen group but differed among the pathogen groups. Differences in net replacement costs for cows culled because of mastitis did not change the ranking of control strategies within a pathogen group. Both prevention and dry cow therapy were important mastitis control strategies. For herds primarily infected with environmental pathogens, strategies that included vaccination for mastitis caused by E. coli dominated strategies that did not include vaccination against this microorganism.

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Prevalence of coagulase-negative staphylococci in bovine mastitis in Zimbabwe.

This study was carried out to determine the prevalence of coagulase-negative staphylococci in clinical and subclinical mastitis in commercial and small-scale farms in Zimbabwe. Thirty five quarter milk samples from clinical mastitis cases and 371 quarter milk samples from cows with subclinical mastitis were cultured for bacterial pathogens. The most frequent pathogens isolated in clinical mastitis were the enteric bacteria (31.4%), followed by coagulase negative staphylococci (22.9%) and then Staphylococcus aureus (17.1%), whereas in subclinical mastitis S. aureus (34.2%) and coagulase-negative staphylococci were (33.2%) the most common. Bacillus species were only isolated in milk samples from subclinical mastitis. Coagulase-negative staphylococci were observed in mixed infections with other bacteria in only 2.2 of the 406 milk samples from clinical and subclinical mastitis where they were isolated together with Bacillus species in 6 of the 9 mixed infection cases. About 95% of the milk samples from which 131 coagulase-negative staphylococci were isolated had correspondingly high somatic cell counts. The coagulase-negative staphylococci isolated most frequently were S. chromogenes (7.9%), S. epidermidis (7.4%) and S. hominis (5.9%). They were all associated with high somatic cell counts. All the coagulase-negative staphylococci isolates were susceptible to cloxacillin and erythromycin, and more than 90% of the isolates were susceptible to neomycin, penicillin and streptomycin. The highest resistance was to tetracycline (17.6%), followed by lincomycin (13.7%). About 8% of the isolates were resistant to both penicillin and streptomycin.

Animals↗

[Treatment of mastitis in general practice].

BACKGROUND: This article presents an update on causes and management of mastitis in general practice. MATERIAL AND METHODS: Published articles on the causes and management of mastitis were identified by Medline and Embase searches, and reviewed. In addition, clinical experience from The National Breast-Feeding Centre in Norway is included. RESULTS AND INTERPRETATION: Most studies report an incidence of mastitis of less than 20% though major methodological limitations make estimates difficult. Common symptoms of mastitis is a swollen, red, hot and painful breast, and systemic symptoms as fever occur frequently. Mastitis may be inflammatory or caused by microorganisms, and often secondary to milk stasis. Effective milk removal is a most essential part of the treatment and may make antibiotics superfluous. In most cases bacterial mastitis is caused by Staphylococcus aureus resistant to beta-lactamase sensitive antibiotics. Culture of the milk is necessary to determine the infecting organism and its antibiotic sensitivity. When antibiotics are warranted, dicloxacillin or cloxacillin are suggested as first-line drugs. The transfer of dicloxacillin/cloxacillin to breast milk is minimal. In most cases women with mastitis can continue to breast-feed also from the affected breast during treatment.

Anti-Infective Agents↗

Effects of endotoxin-induced mastitis on the pharmacokinetic properties of aditoprim in dairy cows.

Plasma disposition of aditoprim, a new dihydrofolate reductase inhibitor, was studied in healthy cows and cows with endotoxin-induced mastitis. A single dose of 5 mg of aditoprim/kg of body weight was administered IV to 5 healthy cows and to the same cows 3 weeks later at 2 hours after intramammary infusion of 0.1 mg of endotoxin into the rear quarters. Mastitis developed in all endotoxin-infused quarters and cows had systemic signs of disease (fever, tachycardia, depression) from 2 to 10 hours after infusion of endotoxin. Pharmacokinetic characteristics of aditoprim in healthy cows were a large volume of distribution (6.28 L/kg), a systemic clearance of 0.82 L/h/kg, and an elimination half-life of 7.26 hours. In cows with mastitis, plasma concentrations of aditoprim were lower between 5 and 26 hours after injection. The systemic clearance (1.00 L/h/kg) and the volume of distribution (12.25 L/kg) were significantly higher in cows with mastitis, but elimination half-life was not significantly different. The lower plasma concentrations of aditoprim between 5 and 26 hours after injection in cows with mastitis are explained by fluid compartment shifts and/or blood flow changes induced by mastitis, although increased elimination of aditoprim in cows with mastitis cannot completely be ruled out. The antibacterial activity of aditoprim is nearly the same as that of trimethoprim. The longer elimination half-life time of aditoprim, however, indicates that it may have a practical pharmacotherapeutic advantage over trimethoprim.

Animals↗

Enzootic mycoplasmal mastitis in a large dairy during an eight-year period.

During an 8-year period, a study was conducted in a large dairy in the Sacramento Valley of California, to define factors associated with the introduction and spread of mycoplasmal mastitis. To identify cows in which mycoplasmal infection appeared in 22 of 25 (88%) periods of new infection, milk samples were collected weekly from freshened cows and from hospitalized cows with clinical mastitis. The disease first appeared in freshened cows in at least 36% of the periods of new cases of mycoplasmal mastitis, which indicated that special attention must be paid to freshening cows in an attempt to control spread of the disease. New cases of mycoplasmal mastitis were recorded more often in January through April than during the rest of the year. Rates of mastitis infection caused by other pathogens (contagious and environmental organisms) increased during months when new cases of mycoplasmal mastitis were recorded. Sanitation on the farm during udder infusion and milking was a major factor in controlling the introduction and spread of mycoplasmal mastitis.

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[Finding of the staphyloccoi and streptococci of mastitis on the udder after various ways and means of cleaning].

The presence of mastitis staphylococci and streptococci on the udder's surface of 400 cows was studied following application of various ways and means of cleaning. The presence of agents causing mastitis was determined before and after cleaning the udder. On uncleaned udder surfaces presence of mastitis staphylococci was observed in 52.5% and of mastitis streptococci--39.5% of udders studied. After washing with water mastitis staphylococci--on 12-20% of the udders. Following udder cleaning with solutions of antigerm 50 (0.04%) or yozan CCT (4%), mastitis staphylococci were found on 4% and 6% of the udders, respectively, while mastitis staphylococci--on 2% and 6%, respectively. Udder surface staphylococci belong in 2.2% to II phagous group, in 46.6%--to the III group, and in 37.7% -- to mixed groups. The most frequently encountered phagous types were 6 and 42D.

Animals↗

Fatal mastitis of dairy cows: a retrospective study.

The necropsy records of dairy cows with mastitis were reviewed from the provincial veterinary laboratory in Guelph (44 cases of mastitis in nine years) and from the Ontario Veterinary College (168 cases in 14 years). Mastitis was considered to be the primary cause of death in 167 of 212 cows (79%). Of these 167 cases of mastitis, Escherichia coli was involved in 107 (64%), Klebsiella sp. in 12 (7%) and Staphylococcus aureus in 11 (7%). Bacteriology was not reported in 22 cases. Coliform mastitis, the most commonly identified type of fatal mastitis, was characterized histologically by the presence of infarcted areas in affected glands and by the lack of demonstrable bacteria, and was thus easily identified from fatal mastitis caused by S. aureus.

Animals↗

Field observations on the incidence of bovine clinical mastitis and teat diseases.

The incidence of bovine clinical mastitis, thelitis and teat wounds was investigated in 283 herds over a period of eight years (about 2590 cows per year). The incidence of clinical mastitis treated on farm visits was 0.102 cases per cow per year and the total incidence with cases treated by phone orders was about 0.26. The incidence of mastitis increased 6% per year. Mastitis occurred more frequently in March-April. The peak of seasonal variation of thelitis (incidence 0.032) was in April-May and that of teat wounds (incidence 0.008) in June-September. The size of herd and participating in milk recording affected the incidence of mastitis. The type of housing affected the incidence of teat diseases but not that of mastitis. Herds with a high incidence of mastitis also had a high incidence of thelitis, r = 0.41.

Animals↗

Epidemiological study of clinical mastitis in dairy cattle.

The incidence rate of clinical mastitis in primiparous Swedish Friesian cows was 15%. The risk of mastitis was greater for calving in July and August and increased with age at calving. Calving disorders and ketosis increased the risk of mastitis 1.8 and 2 fold, while tramped teats and udder injuries increased it 6 and 3 fold, respectively. Herds accounted for 13% of the variation in incidence of mastitis and the risk of mastitis was 1.4 and 1.25 fold greater in high and average producing herds relative to low producing herds. High production predisposed cows for mastitis. Cows with clinical mastitis produced 260 kg less milk and were 2.8 fold more likely to be culled.

Age Factors↗

Mastitis today: incidence, prevention and treatment.

The study concerned 664 women of South-West Finland, and they were studied 5-12 weeks after delivery. The total frequency of mastitis in this population was much higher than generally reported in literature, 24% as opposed to 3%. The frequency of mastitis was similar among nulli- and multiparous women. The diagnosis was based on the judgement of midwives of physicians. If a multiparous woman has had mastitis during a previous puerperium, the probability of mastitis during a subsequent puerperium is threefold. The type of skin, its reaction of the sun, allergies, rashes, getting cold and oxytocin medication during delivery did nto affect the incidence of mastitis. Mothers under 21 and over 35 years of age had a decreased incidence (P = 0.034) of mastitis. If the women had sore nipples, the frequency increased (P = 0.003). Prophylaxis, by means of physical training, neither decreased nor increased the frequency of puerperal mastitis. The treatment advised by midwives and physicians was primarily conservative, but 38% received antibiotics; some of the antibiotics were not effective against staphylococcal infection.

Adolescent↗

Economic analysis of a mastitis monitoring and control program in four dairy herds.

Mastitis monitoring and control programs were instituted in 4 Illinois dairy herds for 12 months. Two herds had high mean monthly bulk tank somatic cell counts (> 490,000 cells/ml) and 2 had low mean monthly bulk tank somatic cell counts (< 260,000 cells/ml) at the start of the study. The mastitis monitoring and control programs included mandatory mastitis control measures, as well as individualized control measures that were based on results of bacterial cultures of milk, bulk tank milk analyses, milking machine and milking procedure evaluations, and environmental inspections in each herd. Changes in mastitis prevalence, clinical mastitis incidence, milk yield, and individual cow somatic cell counts were evaluated, and an economic analysis was performed for each herd. Mastitis-associated economic losses during the study period ranged from $161.79 to $344.16/lactating cow in the 4 herds. Gross economic benefits resulted when mastitis-associated losses were lower with the monitoring and control program than predicted without it. There were no gross economic benefits in the herds with low somatic cell counts, and, when the marginal costs of the programs were added, there were large net losses ($84.06 and $113.01/lactating cow) in those herds. Gross economic benefits resulted in both of the herds with high somatic cell counts. However, in 1 of the herds, the marginal costs of the program exceeded the benefits, resulting in a net loss of $12.96/lactating cow. The net loss was attributed primarily to poor producer compliance with recommendations. There was a net economic benefit of $19.11/lactating cow in the other herd with high somatic cell counts, in which producer compliance was better.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Epidemiological characteristics of bovine clinical mastitis caused by Staphylococcus aureus and Escherichia coli studied by DNA fingerprinting.

OBJECTIVE: To study the epidemiology of clinical mastitis caused by Escherichia coli and Staphylococcus aureus by differentiating isolates with DNA fingerprinting techniques, using polymerase chain reaction. DESIGN: Milk samples were collected from cases of clinical mastitis in dairy cows. Escherichia coli and S aureus isolates from these cases were compared within and between cows and herds. SAMPLE POPULATION: Seven dairy herds with an average bulk milk somatic cell count < 150,000/ml, and incidence of cows with clinical mastitis of > 25%/y. PROCEDURE: Chromosomal DNA was isolated from E coli and S aureus strains isolated from cases of clinical mastitis, and amplified by polymerase chain reaction, using enterobacterial repetitive intergenic consensus primers for E coli and a random amplified polymorphic DNA primer for S aureus. Escherichia coli and S aureus strains were identified and differentiated, using their DNA polymorphism pattern. RESULTS: Multiple E coli genotypes were found in each of the herds. Persistent infections with E coli were sporadic. Only a limited number of different S aureus genotypes was found in each of the herds studied. Recurrent cases of S aureus mastitis were found in 25% of quarters with clinical S aureus mastitis. Comparing S aureus isolates from different herds indicated that 1 S aureus genotype was most prevalent. CONCLUSIONS: Because different quarters were infected with different genotypes, it was concluded that E coli is an environmental pathogen, and does not generally spread from quarter to quarter. The hypothesis that S aureus mastitis is a contagious disease, spreading from infected to uninfected quarters, could not be rejected.

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[Comparative studies of total milk protein and protein fractions in various forms of bovine mastitis].

The content of total protein was assessed in 112 milk samples and of protein fractions--in 106 samples taken from cows suffering from clinical mastitis, subclinical mastitis, secretory disturbances, latent infection, and normal milk. Total protein increased along with the rise of cell content. It increased considerably also in the secretion of cows suffering from clinical mastitis, but the rise in the milk of cows with subclinical mastitis, secretory mastitis and laten infection was insignificant. In all mastitis forms the content of serum albumins and gamma-globulin rose significantly, while alpha-lactoalbumins and beta-lactoglobulin were reduced. These changes in the protein fractions of milk can be used with certainty in the diagnosis of all forms of mastitis.

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