Bovine retained placenta: aetiology, pathogenesis and economic loss

Abstract

The literature on the effects and causes of retained placenta in the cow is reviewed. On a herd basis the condition can adversely affect milk yield and fertility, but on an individual cow basis the effects are unpredictable. The aetiology of retained placenta has been extensively studied and many causal factors have been implicated, but little is known of how many of them cause the condition. As a result its prevention and prediction is uncertain, primarily because of the lack of knowledge of the normal process of placental release. Vascular changes and uterine contractions play a role in placental release, but current opinion suggests that the primary cause of retained placenta is the retention of the feto-maternal union. Release only occurs after a process of maturation, which involves hormonal and structural changes. The factors which are thought to influence these changes, and thus cause the condition, are discussed.

The role of placental MHC class I expression in immune-assisted separation of the fetal membranes in cattle

“…The maternal and fetal epithelia are largely intact following separation of the fetal membranes (Laven and Peters, 1996;Williams et al, 1987), indicating that the loss of fetal adherence is not a destructive process. Therefore, known, but appears to be related to the recognition of fetal MHC class I and could potentially be caused by non-classical MHC class I induced FAS receptor mediated apoptosis of activated CD8 T cells in incompatible pregnancies (Fournel et al, 2000).…”

“…IL-1β, IL-6, TNF-α) (Chazaud, 2014). In cattle the mRNA expression levels of the pro-inflammatory cytokines IL-1β, IL-6 Placental maturation is characterized by increased apoptosis of trophoblasts and maternal endothelium (Boos et al, 2003) and is one of the processes believed to be involved in the loss of fetal-maternal adherence (Boos et al, 2003;Laven and Peters, 1996). Uterine macrophages produce TNF-α (Davies et al, 2004), which can induce apoptosis in cells and as such may influence placental maturation.…”

“…Retained fetal membranes (RFM), persistence of the adherence between the fetal membranes and the maternal placenta after parturition, is a frequently occurring postpartum disorder in cattle (Laven and Peters, 1996;van Werven et al, 1992) and is associated with reduced reproductive performance (Joosten et al, 1988;van Werven et al, 1992) and economic losses (Joosten et al, 1988).…”

“…The loss of fetalmaternal adherence in cattle is believed to involve several processes: i) Collapse of the fetal-placental circulation, leading to shrinking of the placentomal villi (Laven and Peters, 1996) ii) Placental-maturation, characterized by a decrease in the number and the height of maternal epithelial cells (Boos et al, 2003;Laven and Peters, 1996) and a drop in BNC numbers (Gross et al, 1991;Williams et al, 1987) iii) Breakdown of the extracellular matrix linking the fetal and maternal epithelium (Beagley et al, 2010). The first indications for the involvement of the maternal immune system in the loss of fetal-maternal adherence and the occurrence of RFM were provided by Gunnink (Gunnink, 1984a;Gunnink, 1984b).…”

Effect of microorganisms collected from uterus of Hanwoo cattle with low conception rate on the development of IVF-derived embryos

“…소 수정란이식의 성공률을 향상시키 기 위하여 수란우의 발정 유무 (Nelson and Nelson, 1985), 발정유기 방법 (Walton et al, 1986), 자궁각의 위치 (Wright, 1981), 이식 부위 (Boland et al, 1976), 수란우 의 발정동기화 (Sreenan, 1983) 및 혈중 progesterone 농 도 (Sreenan and Diskin, 1987), 영양상태 (Broadbent et al, 1991), 산차 (Sreenan and Diskin, 1987) 및 황체등급 (Donaldson, 1985) (Laven and Peters, 1996;Mellado and Reyes, 1994). 그러나 정상적인 자궁은 분만 후 박테리아 침입에 대한 방어기구를 가지고 있는데 (Jainudeen et al, 1993), polymorphonuclear inflammatory cells (PMNs)이 질이나 자궁강으로 유입되어 자궁 내부를 감염시 키는 미생물들을 탐식함으로써 방어적인 기능을 한다고 알 려져 있다 (Hussain and Daniel, 1992) (Announ et al, 2004), 수막염 (Leighton et al, 1986) …”