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