Endocrine aspects in pathogenesis of mastitis in postpartum dairy cows.

Abstract

In well-managed dairy herds some environmental pathogens including Gram-negative (GN) strains (E. coli and others) have been recognized recently as the predominant causative microbes of mastitis in the peri-parturient period. In early weeks of lactation hyperketonaemia may predispose the high-producing cows for GN mastitis. In GN mastitis cytokines, eicosanoids and oxygen radicals are released, which are responsible for the local and systemic symptoms. Experimental administration of endotoxin induces a complex endocrine cascade. Similar changes in plasma levels of cortisol, insulin, insulin-like growth factor-I and thyroid hormones are seen also in severe cases of GN mastitis. However, leptin is not responsible for the anorexia associated with severe mastitis in ruminants. Mastitis can postpone the resumption of ovarian cyclic activity in dairy cows when its outbreak occurs between days 15 and 28 after calving (at the expected time of first ovulation). In cyclic cows severe cases of GN mastitis can induce premature luteolysis or prolong the follicular phase.