Review/Oorsig Volume 22, Issue 03 - Page 13

Volume 22 • Issue 03 • 2018 the outcome (Palmer, 1932, Paisley et al., 1986, Bolinder et al., 1988). Risco et al. (1994) observed that cows with RFM, dystocia or both, which were left untreated, had similar reproductive outcomes to untreated cows which had not suffered from these disorders. Treatment of cows with RFM with GnRH, F2α or oxytocin is not beneficial in terms of placental release or future reproductive performance (Risco et al., 1994). Similarly, oral administration of calcium chloride gel had no effect of subsequent metritis, days to first insemination or pregnancy to first insemination (Hernandez et al., 1999). Many practitioners in different parts of the world still rely on intrauterine infusion of antibiotics as a treatment for RFM, despite a lack of evidence for its efficacy. Note that antibiotic therapy, especially with tetracyclines, which have the ability to inhibit matrix metalloproteinases (zinc-dependent extracellular proteinases), may actually prolong retention of fetal membranes. Benign neglect, without attempts at manual removal, and systemic administration of antibiotics only to cows showing fever or other signs of metritis is our current recommendation. (Drillich et al., 2003, Drillich et al., 2006a, Drillich et al., 2006b) The most effective strategy for prevention of RFM is to ensure that cows have continued access to feed during the prepartum period, to avoid regrouping and other forms of social stress during this period and to ensure that dietary selenium and vitamin E are adequate. Nutritional strategies to prevent hypocalcemia are likely to be beneficial in limiting incidence of RFM. Routine treatment of cows at calving with either prostaglandin F2α or oxytocin is not effective in preventing RFM (Stevens and Dinsmore, 1997). Feeding of monensin has been reported to decrease incidence of RFM in multiparous cows (Melendez et al., 2006), although this effect was not noticed in another (smaller) trial (Beckett et al., 1998). Supplementation with beta- carotene may reduce incidence of retained fetal membranes in multiparous cows (Oliveira et al., 2015). Puerperal Metritis Acute puerperal metritis usually occurs in the first 10 days postpartum and is characterized by an enlarged, flaccid uterus, a fetid, watery red-brown discharge and, usually, fever (Gilbert and Schwark, 1992, Sheldon et al., 2006) and other signs of systemic illness such as depression or decreased milk yield and feed intake. Fever may follow development of other signs by a day or two (Lima et al., 2014) and is sometimes not detected (Benzaquen et al., 2007, Lima et al., 2014). Risk of metritis is increased by RFM, obstetric complications and twin birth. It is more common in cows that are over or underconditioned. Feeding urea to dry cows has been implicated as a cause of postpartum uterine infection (Barnouin and Chacomac, 1992). The condition is more prevalent in dairy cows than in beef animals and occurs with higher frequency in primiparous cows. The lactation incidence rate of metritis is about 15-20%, but may be much higher in some herds. Milk yield of affected cows is reduced (Galvão et al., 2010, Dubuc et al., 2011a, Wittrock et al., 2011, Giuliodori et al., 2013). Metritis contributes to delayed conception and increased risk of culling (Wittrock et al., 2011, Giuliodori et al., 2013). Costs of acute metritis are associated with treatment costs, increased culling, and impaired fertility. Cows with metritis are at increased risk for other postpartum complications such as displaced abomasum and for endometritis. Cows that have diminished food intake during the late dry period have increased risk of puerperal metritis (Huzzey et al., 2007); these cows frequently show elevated beta-hydroybutyrate or non-esterified fatty acid concentrations in peripheral blood. They have impaired immune function, partially mediated by low intracellular glycogen content of neutrophils. Circulating cortisol and estradiol concentrations tend to be increased immediately postpartum in affected cows (Galvão et al., 2010). Milk yield is depressed, particularly in affected first lactation animals (Galvão et al., 2010). Bacteria commonly involved in puerperal metritis are Escherichia coli, and the gram negative anaerobes Prevatella melaninogenica and Fusobacterium necrophorum (Santos et al., 2011, Machado et al., 2012c, Santos and Bicalho, 2012). Specific strains of E. coli expressing specific virulence factors seem to be implicated; E. coli are the earliest invaders and their presence increases the risk for subsequent invasion of the uterus by other pathogens (Santos et al., 2008, Sheldon et al., 2010). Of several viru lence factors expressed by metritis-causing E. coli the most important appears to be FimH, a pili adhesive protein enabling the bacteria to adhere to and colonize epithelial surfaces (Bicalho et al., 2010a). FimH adhesion is mediated by mannose, and in vitro mannose is capable of preventing adhesion to cultured uterine epithelial cells (Sheldon et al., 2010). However, intrauterine administration of mannose was ineffective in preventing metritis (Machado et al., 2012a). Cows with FimH- 13