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1 Institute for Animal Science and Health, ID-Lelystad, P.O. Box 65, 8200 AB Lelystad, The Netherlands
2 Department of Health Management, Atlantic Veterinary College, University of Prince Edward Island, 550 University Avenue, Charlottetown, Prince Edward Island, Canada C1A 4P3
Data from 274 Dutch herds recording clinical mastitis (CM) over an 18-mo period were used to investigate the effect of pathogen-specific CM on the lactation curve for somatic cell count (SCC). Analyzed pathogens were Staphylococcus aureus, coagulase-negative staphylococci,Escherichia coli, Streptococcus dysgalactiae, Streptococcus uberis, other streptococci, and the culture-negative samples. The dataset contained 178,754 test-day records on SCC, recorded in 26,411 lactations of 21,525 cows of different parities. In lactations without both clinical and subclinical mastitis, SCC was high shortly after parturition, decreased to a minimum at 50 days in milk (DIM), and increased slowly toward the end of the lactation. Effects of CM on lactation curves for SCC differed among the pathogens isolated. Before a case of clinical E. coli mastitis occurred, SCC was close to the SCC of lactations without both clinical and subclinical mastitis, and after the case of CM had occurred, SCC returned rather quickly to a low level again. Similar curves were found for lactations with cases of CM associated with culture-negative samples. Before a case of clinical Staph. aureus mastitis occurred, average SCC was already high, and it remained high after the occurrence. Effects of CM associated with Strep. dysgalactiae, Strep. uberis, and other streptococci on the lactation curve for SCC were comparable. They showed a continuous increase in SCC until the case of pathogen-specific CM occurred, and afterwards SCC stayed at a higher level. Using SCC test-day records, these typical characteristics of each pathogen may be used to find more effective indicators of CM.
Key Words: somatic cell count • lactation curve • clinical mastitis • pathogen
Submitted on October 24, 2001
Accepted on December 19, 2001
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