Survey of the incidence and aetiology of mastitis on dairy farms in England and Wales

A survey of clinical and subclinical mastitis was carried out on 97 dairy farms in England and Wales, selected at random from members of a national milk recording scheme. The farmers were asked to collect aseptic milk samples from five consecutive cases of clinical mastitis and from five quarters with high somatic cell counts using a defined protocol, and they completed a questionnaire that included information on the cows sampled, the herd and the history of mastitis in the herd. The samples were collected throughout the year. The mean incidence of clinical mastitis was 47 cases per 100 cows per year (estimated from historic farm records) and 71 cases per 100 cows per year (estimated from the samples collected). Streptococcus uberis and Escherichia coli were isolated in pure culture from 23.5 per cent and 19.8 per cent, respectively, of the clinical samples; 26.5 per cent of the clinical samples produced no growth. The most common isolates from the samples with high cell counts were coagulase-negative staphylococci (15 per cent), S uberis (14 per cent) and Corynebacterium species (10 per cent). Staphylococcus aureus and coagulase-positive staphylococci together accounted for 10 per cent of the samples with high somatic cell counts; 39 per cent produced no bacterial growth.     

Incidence of clinical mastitis on farms with low somatic cell counts in bulk milk

A total of 1140 clinical cases of mastitis, with at least one inflamed quarter, were reported on 125 farms with somatic cell counts in bulk milk less than 150,000/ml. The average annual incidence was 17.9 cases per 100 cows and ranged from none to 80 cases per 100 cows. The microorganisms most frequently isolated were Escherichia coli (16.2 per cent), coagulase negative staphylococci (13.0 per cent), Staphylococcus aureus (9.6 per cent) and Streptococcus uberis (8.0 per cent). Only two cases of Streptococcus agalactiae were found. As the incidence of clinical mastitis increased, the proportion of S aureus also increased, while the proportions of E coli, S uberis and Streptococcus dysgalactiae remained about the same. Most of the clinical cases of mastitis occurred in early lactation, in November, December and January. However, after correction for the number of calvings per month, the incidence of mastitis was highest in the early summer months.     

Observations on the incidence of clinical bovine mastitis in non-lactating cows in England and Wales

Epidemiological features of clinical mastitis in dry cows from a three year prospective study are described. Two hundred and seventy-three herds in England and Wales participated in the first year (1980) and 209 and 159 of them continued in the study in the subsequent two years. Clinical mastitis was recorded in 1.5 per cent of cows during the dry period in each of the three years. These cases represented between 3.6 and 4.2 per cent of samples from all clinical cases examined. The incidence of clinical mastitis in dry cows increased during the winter housing period (October to March), a peak occurring at the end of this period. A secondary peak in incidence was recorded in August. Streptococcus uberis was the predominant pathogen. Variations in the monthly incidences of cases associated with the major mastitis pathogens were observed. A greater proportion of cases which occurred during the dry period exhibited systemic signs than of cases which occurred during lactation, with the exception of cases associated with Escherichia coli. The risk of clinical mastitis was apparently higher during the last 30 days of the dry period than during the earlier stages of the dry period.     

Mastitis in a large, zero-grazed dairy herd

A zero-grazed herd of approximately 400 cows had a significant mastitis problem associated with Escherichia coli and Streptococcus uberis during a study over three and a half years. Dry cow therapy and post-milk teat dipping effectively controlled staphylococci and the bulk milk cell count averaged less than 400 X 10(3) cells/ml, but over 1800 clinical cases of mastitis occurred over this period, 32 per cent of which were associated with E coli and 25 per cent with Str uberis. Only 8 per cent of the cases associated with E coli showed obvious systemic disturbance and 75 per cent were cured following penicillin and streptomycin treatment. The incidence was highest during spring and summer when the housed cows were dirtiest. Gross teat-end contamination came mainly from sources other than cubicle bedding, and changing the bedding from sawdust to sand did not alter the incidence of clinical mastitis. It was not possible to maintain adequate cleanliness either inside or outside the parlour, nor maintain a trouble-free milking apparatus. The costs of mastitis in this herd during one year are calculated.     

Within herd comparison of teat dipping and dry cow therapy with only selective dry cow therapy in six herds

A within herd comparison of teat dipping and dry cow therapy (full treatment) with only selective dry cow therapy (partial treatment) was carried out in six commercial dairy herds for a two year period. In four herds, the incidence of clinical mastitis was 2 to 12 per cent higher in the partial treatment group. In another herd, in which the pattern of clinical mastitis isolates was unusual in that minor pathogens were isolated from 30 per cent of mastitis cases, the incidence was 43 per cent higher in the partial treatment group. In the remaining herd the incidence was 10 percent higher in the full treatment group. Streptococcus uberis mastitis was more common in the partial treatment groups of five herds; coliform mastitis was more common in the full treatment groups of two herds and similar in both groups in the other herds. High rates of coliform mastitis were associated with poor herd environmental conditions but this was not true for Strep uberis mastitis. Rates of staphylococcus aureus and Strep dysgalactiae mastitis were low in all herds. The level of major pathogen infection in cows completing the trial in all herds increased in the partial treatment group from 5 per cent of quarters at the start to 12 per cent at the finish of the trial. In the full treatment group, however, there was only a small increase in this level. In contrast, levels of Corynebacterium bovis infection increased by 17 per cent in both treatment groups. Continued use of teat dipping and dry cow therapy was associated with a higher rate of coliform mastitis in two of the three herds where there were poor standards of hygiene and husbandry.     

Effects of a mastitis control programme on the incidence of clinical mastitis

Summary

The results of a mastitis control field experiment in Utrecht over three and a half years, including sevens herds with a total of 225 lactating cows are presented. Every case of clinical mastitis was examined bacteriologically. Quarter samples were taken routinely at an average interval of five weeks.

The incidence of clinical mastitis in each herd at the start of the experiment varied from 10 to 104 quarter cases per 100 cows per year. The majority of cases of clinical mastitis (33.1 per cent) occurred during the first month of lactation.

In 74.4 per cent of the lactations marked by clinical mastitis only a single case was observed during that lactation period. If the animals were on pasture during the first month of lactation, the incidence of clinical mastitis was significantly lower during this month, compared with the first month when they were housed. Str. dysgalactiae was the most common isolate from clinical cases (21.5 per cent). A total proportion of 40.3 per cent of the clinical cases were caused by cocci, 20.3 per cent by Gram‐negative bacteria and 16.0 per cent were bacteriologically negative. Of the clinical cases caused by streptococci and staphylococci, 33.3 per cent were preceded by subclinical infection, compared with 11.8 per cent of the clinical cases due to E. coli. The overall incidence of clinical mastitis in this experiment decreased from 47 to 31 per 100 cows per year.     

Heifer teats sprayed in the dry period with an iodine teat sanitizer have reduced Streptococcus uberis teat-end contamination and less Streptococcus uberis intra-mammary infections at calving

Heifers managed under pastoral conditions are at risk from Streptococcus uberis mastitis infections at calving. A total of 397 heifers from six farms around New Zealand were enrolled in a study to identify and enumerate S. uberis on teat-ends of heifers in the peri-partum period, and to understand the effect of teat-spraying in the pre-calving period on the prevalence and incidence of S. uberis mastitis post-calving. Heifers were randomly assigned to Control or Sprayed groups. Sprayed heifers were teat-sprayed once, three times a week (Monday, Wednesday and Friday) with a commercial iodine-based teat sanitizer, starting at 3 weeks prior to calving and ending at day of calving. Across three farms, all glands of cows in both groups were sampled at calving to determine S. uberis intra-mammary infection (IMI) prevalence. For all farms, clinical mastitis (CM) cases detected during the week after calving were sampled and submitted for bacteriological analysis. Swabbing of teat-ends of 54 heifers from one farm showed that heifers had a pre-existing S. uberis contamination averaging 610 colony-forming units per swab (cfu/swab), at 3 weeks prior to calving. At calving, teat-end contamination was 560 cfu/swab for Sprayed heifers and 1775 cfu/swab for Control heifers. Two weeks after calving, teat-end contamination was similar between both groups, at 30 cfu/swab. The prevalence of S. uberis IMI was significantly lower in the Sprayed (3.5% glands) vs. the Control (7.4%) heifers in the first week after calving. There was a trend for Sprayed heifers (3.6% heifers) to have a lower incidence of S. uberis CM compared with Control heifers (7.4% heifers). It is concluded that teat-spraying in the dry period is a management option that could contribute to controlling heifer S. uberis mastitis in the transition period.     

Occurrence of clinical and sub-clinical mastitis in dairy herds in the West Littoral Region in Uruguay

Twenty-nine dairy farms were selected to determine the incidence of clinical mastitis, prevalence of sub-clinical mastitis and bacterial aetiology in the West Littoral Region of Uruguay. In samples taken by the owner and frozen at -20 degrees C during a week the incidence rate of clinical mastitis was determined as 1.2 cases per 100 cow-months at risk. Staphylococcus aureus was the most common isolated pathogen in 37.5% of 40 milk samples from clinical cases obtained in 1 month. No bacteria grew in the 32.5% of the total samples. A sub-sample including 1077 dairy cows from randomly selected farms was used to determine the prevalence of sub-clinical mastitis. These samples were taken on one visit to each farm. The prevalence was 52.4% on a cow basis and 26.7% on an udder quarter basis. In 55.1% of the quarters of the selected animals with more than 300,000 cells/ml there was no growth. The isolated pathogens from sub-clinical cases and their relative frequencies were: Staphylococcus aureus 62.8%, Streptococcus agalactiae 11.3%, Enterococcus sp. 8%, coagulase-negative staphylococci 7.4%, Streptococus uberis 6.4%, Streptococcus dysgalactiae 1.8%, Escherichia coli 1.5% and Staphylococcus hyicus coagulase-positive 0.6%.     

Intramammary infections and risk factors for clinical mastitis in herds with low somatic cell counts in bulk milk

Ten herds with low somatic cell counts in bulk milk had an incidence of clinical mastitis of only 2.2 per 100 cows whereas 10 other herds with similarly low cell counts had an incidence of 53.6 per 100 cows. The major pathogens in the herds with a high incidence were Escherichia coli, Streptococcus uberis, Staphylococcus aureus and the coagulase-negative staphylococci. The percentage of uninfected quarters in the herds with a high incidence of clinical mastitis was 21.4 per cent compared with 12.2 per cent in the herds with a low incidence of clinical mastitis. The prevalence of coagulase-negative staphylococci, Corynebacterium bovis and Micrococcus species was higher in the herds with a low incidence of clinical mastitis. There was a significant linear relationship between the percentage of uninfected quarters and the incidence of clinical mastitis in the herds with a high incidence of clinical mastitis. In herds with a low incidence of clinical mastitis significantly less teat disinfection after milking was practised. The results suggest that infections with minor pathogens tend to protect cows against mastitis, and that teat disinfection after milking may increase the percentage of uninfected quarters and lead to an increased risk of clinical mastitis in herds with low somatic cell counts in bulk milk.     

National intervention study of mastitis control in dairy herds in England and Wales

An intervention study was carried out on 52 dairy farms in England and Wales to determine whether the implementation of a well-specified mastitis control plan in herds with an incidence of clinical mastitis of more than 35 cases per 100 cows per year would reduce the incidence of clinical mastitis, and also reduce the incidence of increases in the somatic cell counts of individual cows. A clearly defined plan for the diagnosis and control of mastitis was developed by two veterinary specialists from the research literature. The herds were randomly allocated to receive the plan either at the start of the study (intervention herds) or after one year (control herds). Data on mastitis management and the farm environment were collected during farm visits. After one year there was a significant 22 per cent reduction in the proportion of cows affected with clinical mastitis on the intervention farms compared with the control farms. There were also significant reductions of approximately 20 per cent in the incidence of clinical mastitis and in the occurrence of increases in the somatic cell counts of individual cows from below, to above 200,000 cells/ml.     

Treatment of persistent intramammary infections with Streptococcus uberis in dairy cows

A survey was conducted of the prevalence of environmental pathogens, especially Streptococcus uberis, as causes of clinical mastitis in dairy cows. The response of intramammary infections with S uberis to conventional treatment was monitored by taking milk samples for bacteriology and somatic cell counting seven, 14 and 21 days after the treatment. The results showed that 51 per cent of the infections failed to respond, and the odds of cases failing to respond was significantly increased when the individual quarter somatic cell count seven days after the treatment was greater than 201,000 cells/ml. Ninety-six per cent of the suspected S uberis isolates identified by culture were confirmed as S uberis by using the api 20 Strep system. Restriction endonuclease fingerprinting was used to type the strains of S uberis isolated from 75 milk samples from 32 cows. Analysis showed that 96 per cent of the cases of S uberis that failed to respond to conventional treatment were persistent infections with one strain rather than reinfections with different strains. The persistent cases of S uberis were treated further with an extended course of intramammary preparations containing either procaine penicillin with dihydrostreptomycin or cefquinome. There was no significant difference between the cure rates achieved by the two preparations, and 55 per cent of the cases that had failed to respond to conventional treatment responded to the additional treatment.     

Field trial of a staphylococcal mastitis vaccine in dairy herds: clinical, subclinical and microbiological assessments

Objective To assess the efficacy of a new staphylococcal mastitis vaccine under commercial dairying conditions.
Design A field trial involving 1819 cows and heifers conducted on seven dairy herds in Victoria. The trial was done 'blind'; approximately half the animals were vaccinated and the remainder were untreated controls.
Procedure The vaccine was given twice during the last 10 weeks of pregnancy. Effects of vaccination were assessed, during the ensuing lactation, on the basis of clinical and sub-clinical mastitis and microbiological investigations of the milk.
Results A total of 273 cases of clinical mastitis were recorded. Staphylococcus aureus was isolated from 112 of these, 45 cases in vaccinates and 67 cases in controls; the difference was not statistically significant. One herd was notable in having a high incidence of clinical staphylococcal mastitis. This herd accounted for 15.8% of the animals in the field trial but 54.5% of cases of clinical staphylococcal mastitis. For this herd, vaccinated animals had significantly lower incidence of clinical staphylococcal mastitis and prevalence of subclinical mastitis, relative to controls. An unexpected feature of the trial as a whole was the low incidence of clinical mastitis from which S aureus was isolated in pure culture (26.3% of cases) and the high incidence of clinical Streptococcus uberis mastitis (22.7% of cases).
Conclusions The trial showed that the vaccine was efficacious in reducing the incidence of clinical mastitis and prevalence of subclinical mastitis in a herd that had a serious staphylococcal mastitis problem.     

Simultaneous intramammary and intranasal inoculation of lactating cows with bovine herpesvirus 4 induce subclinical mastitis

In this study, we examined whether an experimental bovine herpesvirus 4 (BHV4) infection can induce bovine mastitis, or can enhance bovine mastitis induced by Streptococcus uberis (S. uberis). Four lactating cows were inoculated intramammarily and intranasally with BHV4, and four lactating control cows were mock-inoculated. After 14 days, two of four cows from each group were inoculated intramammarily with S. uberis. No clinical signs were recorded in cows inoculated only with BHV4, and their milk samples showed no abnormal morphology, despite the fact that BHV4 replicated in inoculated quarters. Somatic cell count increased significantly in milk from three of six BHV4-inoculated quarters, compared to the non-inoculated quarters of the same cows (within-cow) and the quarters of mock-inoculated cows (control group) on days 8, 9 and 11 post-inoculation (pi). BHV4 was isolated from nasal swabs between days 2 and 9 pi. Clinical mastitis was observed in all four cows intramammarily inoculated with S. uberis. A preceding BHV4 infection did not exacerbate the clinical mastitis induced by S. uberis. S. uberis infections appeared to trigger BHV4 replication. From one quarter of each of two cows inoculated with BHV4 and S. uberis, BHV4 was isolated, and not from quarters inoculated with BHV4 only. In conclusion, BHV4 did not induce bovine clinical mastitis after simultaneous intranasal and intramammary inoculation. However, the BHV4 infection did induce subclinical mastitis in 50% of the cows and the quarters.     

Costs associated with selected preventive practices and with episodes of clinical mastitis in nine herds with low somatic cell counts

Nine dairy herds (mean size, 149 cows) with bulk-tank milk somatic cell counts of less than 300,000 cells/ml and greater than 80% of cows with Dairy Herd Improvement Association linear somatic cell counts less than or equal to 4 were selected for study. Each herd was monitored for 12 consecutive months. Duplicate quarter-milk specimens were collected from each cow for bacteriologic culturing at beginning of lactation, cessation of lactation, and at the time of each clinical episode of mastitis. Streptococcus agalactiae was never isolated and Staphylococcus aureus was isolated from less than 1% of all quarters. There were 554 episodes of clinical mastitis. During the year of study, the incidence rate of clinical mastitis varied from 15.6 to 63.7% of cows among the 9 herds. Mean costs per cow per year in herd for mastitis prevention were: $10 for paper towels, $3 for nonlactating cow treatment, and $10 for teat disinfectants. Mean cost associated with clinical mastitis was $107/episode. Approximately 84% ($90) of the costs attributed to a clinical episode were associated with decreased milk production and nonsalable milk. Costs of medication and professional veterinary fees per clinical episode varied significantly among the 9 herds. Three of the herds did not have a veterinarian treat a clinical episode of mastitis during the year of study even though 2 of these herds had the first and third highest incidence rates of clinical mastitis. When calculated on a per cow in herd basis, mean costs of $40/cow/year were attributed to clinical mastitis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Protective effect of previous intramammary infection with Streptococcus uberis against subsequent clinical mastitis in the cow

Following challenge of 23 quarters of 17 lactating cows with 10(3) colony forming units of Streptococcus uberis 0140J, 20 (87 per cent) developed clinical mastitis. Once the disease had resolved each animal was rechallenged in two quarters, one previously challenged and one additional quarter. Of the 34 secondary quarter challenges 11 (32.2 per cent) led to clinical mastitis, a highly significant reduction over the primary challenges.     

Use of an inhibitor typing scheme to study the epidemiology of Streptococcus uberis mastitis

An inhibitor typing scheme, based on the production of and sensitivity to bacteriocin-like inhibitor substances was used to identify strains of Streptococcus uberis obtained from skin swabs and milk samples of dairy cows. Thirty-nine isolates from one herd were compared, with one isolate examined per site for any sampling day. Eighteen different inhibitor profiles were observed from these isolates. When several isolates were obtained from various skin sites on a cow on the same day, the inhibitor profiles were all different. In three cases, Str. uberis was simultaneously isolated from milk sample and teat surface of the same quarter, but similar inhibitor profiles were only observed for one pair of isolates. Furthermore, when several isolates were obtained by repeated swabbing of a single skin site on a cow on the same day, differences in the inhibitor profiles were again seen. It is likely that numerous strains of Str. uberis are capable of producing clinical mastitis since a comparison of ten isolates obtained from cases of clinical mastitis revealed eight different inhibitor profiles. Monthly sampling (April-November) of eleven cows revealed that Str. uberis could be isolated from the skin of the abdominal wall, medial thigh, udder and teats, but was not isolated from the rectum of any of the cows. Str. uberis was more frequently isolated from the skin and milk samples during the winter when the cows had been dried off, than during the spring and autumn.     

THE NEW SOUTH WALES MASTITIS CONTROL PROGRAM

SUMMARY A mastitis control program based on teat dipping and dry cow therapy was evaluated in 35 herds over a 3 year period. The incidence of subclinical mastitis as detected by the Rapid Mastitis Test (RMT) fell from 34% to 12% quarters positive, a reduction of 65%. Clinical mastitis was reduced from 37 clinical cases per 100 cows in the first 3 month period to 12 clinical cases per 100 cows in the last 3 month period, a reduction of 68%. Variations in response to the program in the reduction of subclinical and clinical mastitis are discussed and the results compared with similar trials conducted overseas. The Modified Whiteside Test was used on bulk milk samples from the control herds and these results were significantly correlated with the prevalence of subclinical mastitis assessed by RMT individual quarters.     

Incidence and economics of clinical mastitis in five Holstein herds in the Czech Republic

Data on clinical mastitis (CM) collected between 1996 and 2003 on five Holstein dairy farms in the Czech Republic were analyzed. Lactational incidences of CM, averaged across farms and calculated only from cows with complete lactations, were 0.35, 0.45 and 0.57 for the first, second and third plus subsequent lactations, respectively. The mean numbers of CM cases per cow and lactation were 0.63, 0.94 and 1.22, and the incidence of CM cases per cow-year at risk were 0.68, 1.00 and 1.27 for the first, second and third plus subsequent lactations, respectively. Longitudinal analysis of CM prevalence based on daily records showed the highest proportion of infected cows in the first 10 days of lactation. The within-farm incidence of CM cases per cow per year, averaged over lactations, ranged from 0.53 to 1.56 with a mean value of 0.94 in the whole data set. Direct financial losses from CM per cow per year within farm ranged from 43.63 to 84.84 euros. They included losses from discarded milk, cost for drugs, veterinary service, herdsman's time, cost for an extra milking machine and cost for antibiotic drying of cows. The economic value of CM incidence (change in direct losses per cow per year when increasing CM incidence by one case above the average value) ranged from 58.3 to 80.1 euros per CM case per cow per year with the mean value of 62.6 euros per CM case per cow per year in the total data set. Daily prevalence rate of CM was shown to be the best among various indicators of CM susceptibility, because it accounted for the censored character of the data and for repeated cases of CM within lactations. In order to reduce the incidence of clinical mastitis for dairy cattle in the Czech Republic, we recommend that it should be included as a goal in the breeding program.     

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.     

Experimental infection of lactating bovine mammary glands with Streptococcus uberis in quarters colonized by Corynebacterium bovis

Twenty-seven quarters of 18 lactating dairy cows were inoculated intramammarily with 3.6 X 10(4) colony-forming units (CFU) of a strain of Streptococcus uberis isolated from a cow with clinical mastitis. Before quarters were inoculated, 22 were considered as naturally colonized with Corynebacterium bovis, and 5 were considered bacteriologically negative. Streptococcus uberis was isolated from all quarters within 2 days after inoculation, and all quarters developed clinical mastitis by 3 days after inoculation. Mastitis was acute, and most cows had increased rectal temperatures. The number of somatic cells increased significantly (P less than 0.05), and milk production decreased significantly. In many cows, rectal temperatures remained increased, and Str uberis was isolated from infected glands after intramammary and systemic antimicrobial treatments were given. A decreased number (110 CFU) of the same strain of Str uberis caused equally severe mastitis in 3 quarters colonized with C bovis and in 1 bacteriologically negative quarter in 2 cows. Streptococcus uberis was isolated from all inoculated quarters, and all quarters developed clinical mastitis by 2 days after inoculation. Two quarters colonized with C bovis and 2 bacteriologically negative quarters were inoculated once with 25 CFU and once with 240 CFU of a different strain of Str uberis (ATCC 27958). Streptococcus uberis was never isolated from inoculated quarters, and changes in milk yield or number of somatic cells were not observed.