Mycoplasmal mastitis in a dairy herd

In October 1985, mycoplasmas were isolated from bulk tank milk samples in a large Florida dairy (greater than 1,400 lactating cows). At that time, measures to isolate and control the spread of infection were instituted. In an initial screening test, Mycoplasma bovis was isolated from 21 of 153 milking string samples (milk from all quarters of 10 cows/string). Composite quarter milk samples from all quarters of every individual lactating cow in the herd were obtained for culture in November 1985 and December 1985. In October, 88 of 1,535 (5.7%) cows were identified as Mycoplasma-positive. An additional 31 Mycoplasma-infected cows were identified in December. The dairy elected to maintain the infected cows in a separate Mycoplasma-positive subherd, which would be milked at the end of each milking session. Seven additional Mycoplasma-positive cows were identified at initiation of lactation. All newly identified infected cows were transferred to the Mycoplasma-positive subherd. After segregation of Mycoplasma-positive cows, bulk tank milk samples obtained routinely from the main herd remained culture negative throughout the study. From February 1986 to October 1986, quarter milk samples were obtained monthly from cows in the Mycoplasma-positive subherd. Any cow that developed clinical mastitis or substantial decrease in milk production was, at the discretion of the herdsman, culled. Of the 126 cows in the subherd, 22 (17.5%) were culled for mastitis, 35 (27.8%) were culled for low production, and 9 (7.1%) were culled for other reasons. Of the remaining 60 cows, 16 (12.7% of the 126 cows) were Mycoplasma-positive on the basis of results from one or more samples obtained after February 1986.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serratia liquefaciens mastitis in a dairy herd

Serratia liquefaciens mastitis was detected and investigated in a 41-cow Holstein herd. Twenty cows were treated for mastitis over a 3-month period. Serratia liquefaciens was isolated from milk samples obtained from 8 of 12 cows tested during the epizootic. Results of an epidemiologic investigation suggested that extensive frostbite of the teats decreased the udder defense. Poor milking technique and hygiene were responsible for increased exposure of the damaged teats to potential udder pathogens. Treatment of each cow resulted in initial clinical improvement, but exacerbations occurred in 75% of the cows with documented S liquefaciens infections.     

An outbreak of Streptococcus canis mastitis in a dairy herd in Israel

CASE HISTORY: An increase in the bulk somatic cell count (BSCC) of up to 1,000 × 10³ cells/ml occurred in a dairy herd in Israel at the end of 2001 and beginning of 2002.

CLINICAL FINDINGS: Bacteriological examination of milk from 69 cows revealed a high prevalence of Streptococcus group G bacteria, identified as S. canis, affecting 38% of cows and 20% of all quarters. Isolates were sensitive to cephalothin and moderately sensitive to penicillin G. Infected cows were separated from the herd, treated with intramammary antibiotics, milked last, and strict hygiene practices were introduced to the milking routine. The pathogen was cleared from the herd and BSCC decreased to 250-350 × 103 cells/ml after 6 months.

DIAGNOSIS: Streptococcus canis mastitis.

CLINICAL RELEVANCE: Streptococcus canis infection may cause subclinical mastitis and high bulk SCC in dairy herds and be resolved by treatment with intramammary antibiotics and the introduction of strict hygiene practices.     

An outbreak of Streptococcus canis mastitis in a dairy herd in Israel

CASE HISTORY: An increase in the bulk somatic cell count (BSCC) of up to 1,000 x 103 cells/ml occurred in a dairy herd in Israel at the end of 2001 and beginning of 2002. CLINICAL FINDINGS: Bacteriological examination of milk from 69 cows revealed a high prevalence of Streptococcus group G bacteria, identified as S. canis, affecting 38% of cows and 20% of all quarters. Isolates were sensitive to cephalothin and moderately sensitive to penicillin G. Infected cows were separated from the herd, treated with intramammary antibiotics, milked last, and strict hygiene practices were introduced to the milking routine. The pathogen was cleared from the herd and BSCC decreased to 250-350 x 103 cells/ml after 6 months. DIAGNOSIS: Streptococcus canis mastitis. CLINICAL RELEVANCE: Streptococcus canis infection may cause subclinical mastitis and high bulk SCC in dairy herds and be resolved by treatment with intramammary antibiotics and the introduction of strict hygiene practices.     

Nonclinical Pseudomonas aeruginosa mastitis in a dairy herd

Atypical Pseudomonas aeruginosa mastitis in a dairy herd was characterized by nonclinical mastitis that responded to antibiotic treatment, but only for the cows to become reinfected because of a persisting source of contamination in the milking parlor wash water. At least 36% of the cows were infected during a 37-month period. The source of infection was contaminated water, wash hoses, and spray nozzles in the parlor. After the source of infection was removed and long-term control measures were instituted, the nonclinical infections became less severe and shorter in duration and they occurred for a lesser percentage of the lactation period.     

Epidemiology of Streptococcus uberis intramammary infections in a dairy herd.

From 1987 to 1991, almost 36,000 quarter samples of mammary secretion representing 1790 lactations of 510 dairy cows from a research herd were collected for bacteriological examination. The percentage of cows infected with Streptococcus uberis ranged from 12 to 16% of cows/year. S. uberis was isolated from 14.2% of lactations over the 5-year period. The prevalence of S. uberis intramammary infection (IMI) was significantly higher in cows with > or = 4 lactations than in cows with 3 or fewer lactations. Regardless of lactation number, the prevalence of S. uberis was highest before parturition, during early lactation and near drying off. The prevalence of S. uberis infected quarters ranged from 1.3 to 2.3% of quarters/year; the prevalence rate for the 5-year period was 2% of quarters. The quarter prevalence of S. uberis was lowest in cows with < or = 3 lactations, increased significantly with lactation number and was highest in cows with > or = 6 lactations. The percentage of quarters infected with S. uberis varied significantly by year. The majority (95%) of S. uberis IMI were subclinical. The ratio of subclinical IMI to clinical IMI was lowest during early lactation, and increased with days in milk, and with lactation age except for cows in their 5th and 6th lactations. Results of this epidemiological investigation suggest that opportunities exist where suitable control measures could be applied to reduce the impact of S. uberis infections in the dairy herd.     

Prototheca zopfii mastitis in a herd of dairy cows

Mastitis caused by the colourless alga Prototheca zopfii was diagnosed in 17 of 120 cows in a dairy herd. Infection occurred in animals varying from 3-14 years old and was present in one to four quarters of each cow. Nine cases were associated with clinical mastitis characterised by the presence in milk of flakes or small clots. Somatic cell counts consistent with subclinical mastitis (>500 x 10(3) cells/ml) were recorded in five of the eight remaining cows. Histological examination of udder tissue showed the presence of granulomatous lesions associated with the presence of Prototheca. The problem was identified and controlled by repeated microbiological examination of milk samples from all lactating cows and immediate culling of infected animals. P. zopfii was also recovered from environmental water samples on this farm. It is suggested that infection may have occurred as a result of teat sores caused by trauma from a milking machine, and the tendency for cows to lay down on a race, the surface of which was sometimes flooded by drain water in which Prototheca were present.     

Prototheca zopfii mastitis in a herd of dairy cows

Mastitis caused by the colourless alga Prototheca zopfii was diagnosed in 17 of 120 cows in a dairy herd. Infection occurred in animals varying from 3–14 years old and was present in one to four quarters of each cow.

Nine cases were associated with clinical mastitis characterised by the presence in milk of flakes or small clots. Somatic cell counts consistent with subclinical mastitis (>500 × 10³ cells/ml) were recorded in five of the eight remaining cows.

Histological examination of udder tissue showed the presence of granulomatous lesions associated with the presence of Prototheca.

The problem was identified and controlled by repeated microbiological examination of milk samples from all lactating cows and immediate culling of infected animals.

P. zopfii was also recovered from environmental water samples on this farm. It is suggested that infection may have occurred as a result of teat sores caused by trauma from a milking machine, and the tendency for cows to lay down on a race, the surface of which was sometimes flooded by drain water in which Prototheca were present.     

An economic justification of "blitz" therapy to eradicate Streptococcus agalactiae from a dairy herd

Streptococcus agalactiae was identified as the cause of mastitis in a 240-cow dairy herd. Forty-five per cent of the herd had cell counts over 500,000/ml, and 28 per cent had cell counts over 1,000,000/ml. Dry cow therapy was used regularly but teat dipping had not been used for three years. The procedures at milking were modified, teat dipping was introduced, and the herd was divided into two according to cell count. The 120 cows with higher cell counts were treated with 300 mg erythromycin (Erythrocin intramammary; Sanofi Animal Health) preparation per quarter at two consecutive milkings. Towards the end of lactation, all the 90 lactating cows in the herd were again treated with erythromycin. Milk samples were collected from all the cows in the herd 12 months after the initial treatment, and S agalactiae was isolated from only one replacement heifer which had been purchased after the treatments with erythromycin. The butterfat and protein levels in the milk were compared with those of a similar, but untreated, herd for 12 months before and after therapy. The butterfat levels rose sharply after treatment, and financial assessment showed a 41 per cent return on investment in the 12 months following the treatment.     

Microbiologic investigation of an epizootic of mastitis caused by Serratia marcescens in a dairy herd.

An epizootic of subclinical and clinical mastitis caused by Serratia marcescens was investigated in a 1,000-cow dairy farm in California. Serratia marcescens was isolated from 13 to 18% of composite milk samples obtained from lactating dairy cows. During monthly milk sampling performed during a 4-month period, S marcescens was isolated from 38.8 to 62.3% of composite milk samples obtained from cows from which S marcescens was previously isolated. Few cows infected with S marcescens had evidence of clinical mastitis. Somatic cell count value was associated with isolation of S marcescens. Cows with somatic cell counts greater than 500,000 were 5.48 times as likely to have intramammary infections with S marcescens, compared with cows with somatic cell count less than or equal to 500,000. Lactation number also was associated with S marcescens intramammary infection. After adjusting for the effect of lactation number, cows with high somatic cell count values were 2.98 times as likely to have intramammary infection with S marcescens, compared with cows with low somatic cell counts. Infection with S marcescens was independent of days in lactation, production string, and daily milk production. Eleven months after the beginning of the epizootic, S marcescens was isolated from organic bedding samples obtained from the dairy. Despite numerous attempts, other sources of S marcescens could not be identified on this dairy.     

A three-month study of environmental mastitis in a dairy herd.

During the autumn/winter of 1976, a study was made of a severe mastitis outbreak which occurred in a herd of 96 cows. Forty-four cows and 61 quarters were clinically infected with new infections between September and mid-December. Escherichia coli was isolated in 84 per cent of clinical samples submitted for bacteriological examination.     

奶牛乳房炎无乳链球菌的分离与鉴定

利用THB固体培养基和色素培养基初步筛选出奶牛乳房炎中无乳链球菌，以分离的12株疑似菌的基因组DNA为模板进行PCR扩增，对扩增产物进行分析，结合选择培养的生理生化特性对分离菌进行鉴定。结果表明，12株疑似菌中有8株为无乳链球菌.     

Outbreak of subclinical mastitis due to beta hemolytic group L streptococci (S. dysgalactiae ssp. equisimilis) in an Austrian dairy herd

This study is reporting an outbreak of subclinical mastitis due to beta-hemolytic group L streptococci in an Austrian dairy herd with a history of high somatic cell count. At the first survey 16 of 33 lactating cows (28 quarters of 132) were cultured positive for beta-hemolytic, CAMP and esculin negative cocci that grew on Columbia blood agar with small grey catalase negative colonies. With the commercial API 20 Strep system (bioMerieux, F) isolates were classified as members of streptococci group L. All tested strains (eight of 28) produced acid from ribose, lactose, trehalose, amidon and glycogen; they hydrolysed hippurate and showed beta-glucuronidase, beta-galactosidase, alkaline phosphatase, leucinaminopeptidase and arginindehydrolase activity. Isolates were sensitive to bacitracin but resistant to tetracycline. Using phenotypic characterisation as well as sequence analysis of the 16S-23S intergenic spacer region of a representative strain, recovered isolates were identified as Streptococcus (S.) dysgalactiae ssp. equisimilis. Mastitis was characterized by normal milk secretions and absence of clinical abnormalities but high elevations of somatic cell count. Based on the characteristics of the strains and on the observations during the first herd survey, contagious transmission during milking as a result of poor milking hygiene was assumed. The mastitis was controlled through implementation of a strict hygiene protocol including use of single-use udder towels, post milking teat desinfection and cluster disinfection between milking cows in combination with antibiotic treatment of infected udders.     

Milk protein profiles in response to Streptococcus agalactiae subclinical mastitis in dairy cows

The objective of this study was to investigate the milk protein profiles of normal milk and those of milk during the course of subclinical mastitis, caused by natural Streptococcus agalactiae infection. Two‐dimensional gel electrophoresis and liquid chromatography mass spectrometry were used to assess protein profiles and to identify the proteins. The results showed that S. agalactiae subclinical mastitis altered the protein profiles of milk. Following Mascot database matching, 11 and 12 protein types were identified in the milk collected from healthy and S. agalactiae subclinical mastitic udders, respectively. The distinct presence of the antibacterial protein cathelicidin‐1 was detected in infected milk samples, which in turn was highly correlated to the severity of subclinical mastitis as represented by the milk somatic cell count (r = 0.616), but not the bacterial count. The protein profile of milk reveals changes in the host response to S. agalactiae intramammary infection; cathelicidin‐1 could therefore serve as a biomarker for the detection of subclinical mastitis in dairy cows.