Definition: Failure to expel the foetal membranes within 12 to 24 h after calving.Incidence: Varies from 4.0-16.1%, but can be much higher in problem herds.It depend on farm status.
Recent knowledge on pathogenesis of placental retention in cattle (Davies at al., 2004)
The key element in the pathogenesis of retained placenta in cattle is a failure of timely breakdown of the cotyledon-caruncle attachment after delivering the calf.
Mechanism of normal placental separation
Maternal immunological recognition of foetal MHC class I proteins expressed by trophoblast cells triggers an immune/inflammatory response that contributes to placental separation at parturition.
Mechanism of placental retentionChemotactic factor for leukocytes is found in placentomes of cows with normal placental separation. It is absent in placentomes from cows with retained placentas. Blood leukocytes and neutrophils of cows with retained placenta are less reactive to chemotactic stimuli than in cows with normal placental separation.
Research presented by LeBlanc et al. (2004) points out that cows with a greater degree of negative energy balance prepartum and higher non-esterified fatty acid (NEFA) concentrations were 80% more likely to suffer from retained placenta. Similarly these authors found higher risk for retained foetal membranes in cows with lower circulating vitamin E concentration.
The recent data indicate that lack of uterine motility plays little or no role in the occurrence of retained placenta. Moreover cows with retained placenta have normal or increased uterine activity in the days after calving (Frazer 2005).
Consequences of retained foetal membranes in cattle
Delayed placental separation predisposes cows to acute puerperium metritis and endometritis post partum through:
- increased bacterial multiplication in the uterus
- impairment of immune function of endometrial macrophages and neutrophiles by bacterial endotoxins