Periparturient stress and immune suppression as a potential cause of retained placenta in highly productive dairy cows: examples of prevention

Abstract

The immune system during the periparturient period is impaired. At this time the most important factor causing immune-suppression in highly productive cows is metabolic stress resulting from hormonal and metabolic fluctuations, a negative energy balance, shortage of proteins, minerals and vitamins which are required to meet the demands of the fetus as well as the onset of lactation. This stress can activate the hypothalamic-pituitary-adrenocortical axis (HPA), which results in increase plasma corticosteroids. As a result, the cortisol concentration during the periparturient period increases by several folds particularly on the day of calving. Cortisol is a powerful immune-suppressive agent. During stress, this hormone causes depression of the leukocyte proliferation and their functions. Decreased phagocytosis of neutrophils, decreased cytotoxic ability of lymphocytes, as well as depressed activity of their cytokines, make it impossible for the normal, efficient maternal immune recognition and rejection of fetal membranes (as a foreign, allogeneic tissue expressed fetal antigens—MHC class I proteins by trophoblast cells) and finally results in their retention in cows. The metabolic periparturient stress also activates production of catecholamines, especially adrenalin. Adrenalin activates adrenoreceptors of the myometrium and then causes hypotony or atony of the uterus. Thus, cortisol and adrenalin inhibit rejection and expulsion of fetal membranes and cause their retention. These mechanisms of retained placenta (RP) often have a metabolic etiology and occur in herds, where important infectious diseases causing placentitis are absent or prevented. The aim of this article is to show the fundamental mechanisms occurring during periparturient stress and the accompanied immune-suppression in cows, as well as their consequences in relation to RP. The paper also gives examples of the symptomatic prevention of RP in cows caused by metabolic and immune suppressive factors. The prevention of RP was carried out using drugs which inhibit the activity of cortisol or adrenalin in dairy cows during calving.

Trophoblast of domestic and companion nimals: basic and applied clinical perspectives

“…It is interesting to note that in these situations there is a clear adaptation of the immune system for a function distinct from protection against pathogens. In summary, as pointed out in recent reviews (McNaughton and Murray, 2009;Benedictus et al, 2015;Mordak and Stewart, 2015;Attupuram et al, 2016), MHC compatibility and expression of MHC class 1 antigen by the trophoblasts has significant molecular consequences in controlling the expulsion the incidence of retention of fetal membranes. Addressing and remedying this particular issue scientifically can reduce the economic loss in production animals due to this condition and may help to address this issue in companion animals wherein it is a life threatening issue, if veterinary treatment is not provided.…”

Physiological changes in the adenosine deaminase activity, antioxidant and inflammatory parameters in pregnant cows and at post‐partum

“…These authors observed a gradual decrease on seric IL‐6 until the parturition day, but they did not observed an increase on seric IL‐6 after calving. It is important to emphasize that calving is a stressor condition linked to immune suppression (Mordak & Anthony, ), and the elevated seric levels of proinflammatory cytokine IL‐6 can be associated with a stress response, as several studies have linked the stress and physiological perturbations with augmentation of IL‐6 levels (Bob et al., ; Rohleder, Aringer, & Boentert, ).…”

Efeito De Diferentes Momentos De Inseminação Artificial Laparoscópica Em Programas Comerciais De Múltipla Ovulação E Transferência De Embriões Em Ovinos

“…horas (Werven, 1992;Perumal et al, 2013;Paisley;Mickelsen;Anderson, 1986;Zobel;Tkalčić, 2013). É provocada por falha na separação das vilosidades da placenta fetal (cotilédones) e criptas maternas (carúnculas) (Werven, 1992;Mordak;Anthony, 2015).…”