Prevalence of clinical mastitis in 38 Waikato dairy herds in early lactation.

AIM: To determine the prevalence of clinical mastitis in spring-calving dairy herds in the Waikato Region of New Zealand and to identify factors associated with variation in the prevalence of clinical mastitis between herds.
METHOD: A total of 799 quarters from 595 dairy cows from 38 dairy herds were diagnosed by herd owners as having clinical mastitis between 8 July and 21 August 1997. Quarters diagnosed with clinical mastitis were sampled for bacterial culture and somatic cell count, and the presence of clots in the milk and the presence of udder oedema were assessed by a technician or veterinarian.
RESULTS: Clinical mastitis was diagnosed in an average (+/-s.e.m.) of 9.9% (+/-0.8%, range 0.9-21.4%) of calved cows within the herds. Bacteria were not cultured from an average of 12.4 % (+/- 2.0%, range 0.0-45.5%) of cows and 22.3% (+/- 2.4%, range 0.0-54.0%) of quarters diagnosed as having clinical mastitis. There were significant differences between herds in the proportion of cows diagnosed with mastitis and in the proportion of clinical mastitis cases from which bacteria were not cultured. A decreased prevalence of clinical mastitis (p<0.001) was associated with an increased percentage of the herd treated with dry cow antibiotics. An increased prevalence of clinical mastitis (p<0.0001) was associated with both an increased percentage of cows treated in the previous season with lactating cow antibiotics and an increased percentage of heifers in the herd. Herds that were fed supplements before or during lactation had a higher prevalence of clinical mastitis than herds that were not fed supplements (p<0.001). An increased proportion of quarters diagnosed with clinical mastitis that did not culture bacteria was associated with an increased prevalence of clinical mastitis (p<0.001). The proportion of quarters that the technician or veterinarian found with evidence of clinical mastitis (i.e. a somatic cell count >500,000 cells/ml and the presence of either clots or udder oedema) within a herd was inversely related to the proportion of quarters within a herd from which no bacteria were isolated.
CONCLUSION: There was a large variation in the prevalence of clinical mastitis and in the proportion of clinical quarters from which no bacteria were grown between herds. Management factors such as the use of dry cow therapy, feeding regimes and heifer replacement rates all affected the prevalence of clinical mastitis. Herd owners appear to differ in the sensitivity and specificity of their diagnosis of clinical mastitis, with bacteria not isolated from up to 50% of quarters diagnosed with clinical mastitis in some herds. Improvements in the specificity of herd owner diagnosis of clinical mastitis may reduce the use of antibiotics for mastitis during lactation and hence may reduce the risk of antibiotic contamination of milk supplied for human consumption.