We assessed the incidence of enterobacterial infection of the mammary glands of 629 cows, from six commercial herds in Somerset, during the nonlactating period; samples were collected from all clinical quarters of these cows during the subsequent lactation. A rise in the incidence of intramammary enterobacterial infection was detected between drying off and before calving. Quarters infected with an enterobacterial organism during the dry period were more likely to develop mastitis due to that pathogen than were uninfected quarters. Of all enterobacterial mastitis occurring in the first 100 d of lactation, 52.6% arose in quarters previously infected, during the dry period, with the same strain of bacteria, as identified by DNA fingerprinting using enterobacterial repetitive intergenic consensus primers. When compared with unsampled controls, quarters sampled during the dry period did not show a higher incidence of infection at calving or of subsequent clinical mastitis. These findings suggest that chronic infections are important in the epidemiology of enterobacterial mastitis and that environmental management during the dry period may greatly impact the incidence of enterobacterial mastitis in the subsequent lactation.

Clinical mastitis in six Somerset dairy herds was monitored over a 12-month period.Escherichia coliwas implicated in 34.7% of all clinical cases. Forty-one percent of all clinicalE. colimastitis cases occurred in just 2.2% of the population. A total of 23.9% of clinicalE. colicases occurred in quarters suffering recurrent cases ofE. colimastitis. The genotypes of strains involved in recurrent cases of clinicalE. colimastitis were compared by DNA fingerprinting with enterobacterial repetitive intergenic consensus primers. In 85.7% of cases of recurrent quarterE. colimastitis, the same genotype was implicated as the cause of disease, suggesting persistence of the organism within the mammary environment. The same genotype as that in the original case was also implicated in 8.5% of recurrent cases occurring in different quarters of the same cow, suggesting spread between quarters. These findings challenge our current understanding of the epidemiology ofE. colimastitis and suggest that pathogen adaptation and host susceptibility may be playing a part in the changing pattern of clinical mastitis experienced in the modern dairy herd.

The efficacy of an intramammary antibiotic dry cow preparation with significant gram-negative spectrum (product A; Leo Red Dry Cow, Leo Animal Health, UK) was compared with a product with no gram-negative efficacy (product B; Orbenin Extra DC, Pfizer Ltd, UK) as assessed by control of coliform mastitis in the first 100 d of the lactation. The efficacy of both products was also compared for control of noncoliform mastitis and for the ability to control existing and new intramammary infections as measured by individual cow somatic cell counts. Cows treated with product A were significantly less likely to develop clinical Escherichia coli or coliform mastitis during the dry period or the first 100 d of lactation than cows treated with product B. Cows treated with product A were no more likely to develop clinical mastitis due to a noncoliform organism than were cows treated with product B. There was no significant difference between the two groups as measured by individual cow somatic cell count changes across the dry period. This study is the first to have demonstrated the clinical efficacy of an intramammary antibiotic dry cow preparation, as measured by reduction in gram-negative clinical mastitis in the subsequent lactation. These findings demonstrate that selection of a dry cow intramammary preparation with a significant gram-negative spectrum can influence the incidence of clinical coliform mastitis in the subsequent lactation. This finding should be one of the factors taken into account when selecting products.