Abstract

A single prolonged milking interval (PMI), such as might be associated with technical failures in automatic milking systems, leads to a subsequent somatic cell count (SCC) peak in bulk tank milk. Increased SCC indicates mastitis in cows. It is generally correlated with reduced milk yield and quality, and is often used as a criterion for milk payment. Whether the transient SCC peak after a single PMI affects yield and quality is not known. The short duration of the inflammatory reaction after a PMI and its nonpathological history raise questions about the underlying immunological mechanisms and possible role of immunocompetent natural milk components. It is important to learn more about this kind of physiological inflammation to improve the interpretation of SCC and the general understanding of udder immunology. This thesis investigated the inflammatory reaction after a single PMI of 24 h at both the cow and the quarter level, and how it influences milk yield and quality. The PMI appeared to induce temporarily impaired epithelial integrity but no epithelial damage. Even so,milk yield per cow was reduced with 0.75 kg/day after the PMI, notably for up to the 10 days studied. Thus, based on the long-lasting reduction in yield and a possibly reduced milk payment due to the SCC peak, a PMI is of significant economic concern for the farmer although milk quality itself was shown not to be afflicted. The PMI caused a two-fold increase in the SCC, which then remained elevated for 2 days and was associated with an increased proportion of polymorphonuclear leukocytes (PMN) in milk. The most pronounced SCC reaction after the PMI was not seen until the udder had been emptied once. The initiation of inflammation occurred first during the PMI and elicited a systemic acute phase response of serum amyloid A (SAA), observed in blood prior to its appearance in milk. The milk showed consistently high chemotactic activity in vitro, although no increased content of the cytokines IL-1β and IL-8 was detected. The PMI induced significant alterations in the content of α-lactalbumin (ALA) and prolactin (PRL), in relation to the PMN reaction. ALA inhibited and PRL stimulated PMN migration, when tested in vitro. Based on the findings in this thesis, it is probable that SAA played a significant role in the inflammatory reaction after a PMI but it cannot be excluded that ALA and PRL might also have been contributing factors.