**2. Physiology of parturition: low state systemic inflammation involved (PDS)**

Nest building and the phases of farrowing are orchestrated by responding changes in reproductive hormones. It is well established that decline in progesterone and peak in prostaglandin F2alpha triggers nest building behavior while oxytocin rise at the beginning of expulsion phase marks the session of nest building [9]. Prostaglandin F2alpha peak also induces CL regression with a concomitant decline in progesterone, making uterine contractions and parturition possible. Oxytocin is mainly in charge of uterine contractions during the expulsion phase of parturition and letdown of colostrum and milk, while prolactin will promote mammary gland development to the extent that initiation of milk production after parturition will become possible [10–12].

It has also been described in the literature and also shown by our group that allowing the sow to build up a nest prior to farrowing will increase oxytocin release and shorten the duration of farrowing [5, 13]. Other ways of shortening the duration of farrowing include increasing fiber in the feedstuff and encouraging water intake [5, 14]. However, even applying most good management interventions prior

**61**

early lactation.

*Troubled Process of Parturition of the Domestic Pig DOI: http://dx.doi.org/10.5772/intechopen.94547*

those markers described above [15].

the udder [27] or both of them.

however, remains less explored [31].

to farrowing, duration of farrowing of modern hyperprolific sows is extended four – to five hold as described [2, 15, 16]. Prolonged duration of farrowing will mean reduced quality and quantity of colostrum intake by piglets, increased degree of intrapartum hypoxia of fetuses [17], increased rate of retained placentae [18], increased rate of uterine inflammation and post partum dysglactia (PDS) [19] and

likely, reduced development of next generation of follicles fertility [3, 17].

Moreover, during the periparturient period, biological mechanisms coordinate the mobilization of body reserves in order to support fetal growth and milk production; insulin concentrations are reduced and the response of hormone-sensitive lipase in adipose tissue (e.g., low insulin, high growth hormone and catecholamines, or high glucocorticoid concentrations) is greater to facilitate lipid mobilization. This periparturient period is also characterized by a low state of inflammation encompassing an increase in hepatic production of positive acute-phase proteins (APP), and a decrease in the production of negative APP [15, 20]. It has been rather well described in the literature that these responses are mediated by the pro-inflammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α) [15]. Additionally, evidence in the dairy cow indicates that oxidative stress also occurs during this period and is driven by the imbalance between the production of reactive oxygen metabolites (ROM), reactive nitrogen species (RNS), and the neutralizing capacity of antioxidant mechanisms in tissues and blood [21]. The extent and duration of the inflammatory process will determine whether or not the condition is ending up as a clinical disease. However, it is noteworthy, that in the hyper prolific sows lines as those typical of Denmark and Belgium, the incidence of sows contracting a systemic disease postpartum is as high as >30% [15, 22, 23]. Moreover, it is obvious that even in those sows staying healthy as far as clinical symptoms, the inflammatory process is heavily present as indicated by means of

Typically, within two to three days post partum, the process of inflammation may develop into endotoxemia, which involves the release of the inflammation markers described. Endotoxemia is associated with clinical symptoms indicating a systemic response to infectious agents such as coliform bacteria – and PDS [24–26]. The condition comes with acute general symptoms such as inappetite, lethargy and fever [25], followed by local symptoms that usually affect either the uterus [19] or

After parturition, concomitant with the process of inflammation, the sow undergoes metabolic stress due to loss of body reserves in favor of milk produced for large litters. This change rate is highest during the first 10 days of lactation. One of major mediators of metabolic stress is IGF-1, which is also seen as an indicator for fertility. Low IGF-1 levels indicate inflammation, metabolic stress present and fertility. IGF-1 is also regarded as one of the most important factors driving follicle development [28–30]. The role of extracellular vesicles, although proposed as being key players in follicle development and the cross talk between the mother and the embryo, in this inflammatory process and its effect on follicle development,

In conclusion, in hyperprolific sows, the physiological process of farrowing is prolonged, making the system vulnerable in terms of increased rate of inflammation and emerging infectious uterine and mammary disease. In fact, recent evidence now shows that even in sows staying without symptoms, there seems to be considerable degree of "silent inflammation" in the body. In an increased proportion of sows, however, post partum disease PDS is detected and hopefully treated. The consequences of inflammation, regardless of clinical symptoms, include reduced quantity and quality of piglet colostrum intake and milk intake during

#### *Troubled Process of Parturition of the Domestic Pig DOI: http://dx.doi.org/10.5772/intechopen.94547*

*Animal Reproduction in Veterinary Medicine*

increased competition for teats and reduced birth weight. This all may show up later

*Relationship between litter size and the duration of farrowing in 20 studies from 1992 to 2018 (adapted from* 

The metabolic challenge related to hyper-prolific sow production model begins in the growing phase of gilts and goes beyond farrowing and lactation. The sow is supposed to eat enough to meet the requirement of growing litters prior to farrowing, which may cause some of the problems seen at around farrowing [5, 6]. In the early part of lactation, sows with large litters loose more energy while producing milk than what they can consume in their feed, ending up in a negative energy

The growing litter size and intensity of production as such appear as items for welfare concern for the public. This seems to happen regardless of whether those concerns would be warranted or not. However, this review will tackle those items relating to welfare of the hyper-prolific sow model that we know, based on scientific

**2. Physiology of parturition: low state systemic inflammation involved** 

Nest building and the phases of farrowing are orchestrated by responding changes in reproductive hormones. It is well established that decline in progesterone and peak in prostaglandin F2alpha triggers nest building behavior while oxytocin rise at the beginning of expulsion phase marks the session of nest building [9]. Prostaglandin F2alpha peak also induces CL regression with a concomitant decline in progesterone, making uterine contractions and parturition possible. Oxytocin is mainly in charge of uterine contractions during the expulsion phase of parturition and letdown of colostrum and milk, while prolactin will promote mammary gland development to the extent that initiation of milk production after parturition will

It has also been described in the literature and also shown by our group that allowing the sow to build up a nest prior to farrowing will increase oxytocin release and shorten the duration of farrowing [5, 13]. Other ways of shortening the duration of farrowing include increasing fiber in the feedstuff and encouraging water intake [5, 14]. However, even applying most good management interventions prior

in emergence of diseases in the growing phase of piglets/fattening pigs.

*Oliviero et al. 2019, reproduction in domestic animals, Wiley-Blackwell).*

**60**

balance (NEB) [7, 8].

**Figure 1.**

**(PDS)**

become possible [10–12].

literature, as having reasons to be addressed.

to farrowing, duration of farrowing of modern hyperprolific sows is extended four – to five hold as described [2, 15, 16]. Prolonged duration of farrowing will mean reduced quality and quantity of colostrum intake by piglets, increased degree of intrapartum hypoxia of fetuses [17], increased rate of retained placentae [18], increased rate of uterine inflammation and post partum dysglactia (PDS) [19] and likely, reduced development of next generation of follicles fertility [3, 17].

Moreover, during the periparturient period, biological mechanisms coordinate the mobilization of body reserves in order to support fetal growth and milk production; insulin concentrations are reduced and the response of hormone-sensitive lipase in adipose tissue (e.g., low insulin, high growth hormone and catecholamines, or high glucocorticoid concentrations) is greater to facilitate lipid mobilization. This periparturient period is also characterized by a low state of inflammation encompassing an increase in hepatic production of positive acute-phase proteins (APP), and a decrease in the production of negative APP [15, 20]. It has been rather well described in the literature that these responses are mediated by the pro-inflammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α) [15]. Additionally, evidence in the dairy cow indicates that oxidative stress also occurs during this period and is driven by the imbalance between the production of reactive oxygen metabolites (ROM), reactive nitrogen species (RNS), and the neutralizing capacity of antioxidant mechanisms in tissues and blood [21]. The extent and duration of the inflammatory process will determine whether or not the condition is ending up as a clinical disease. However, it is noteworthy, that in the hyper prolific sows lines as those typical of Denmark and Belgium, the incidence of sows contracting a systemic disease postpartum is as high as >30% [15, 22, 23]. Moreover, it is obvious that even in those sows staying healthy as far as clinical symptoms, the inflammatory process is heavily present as indicated by means of those markers described above [15].

Typically, within two to three days post partum, the process of inflammation may develop into endotoxemia, which involves the release of the inflammation markers described. Endotoxemia is associated with clinical symptoms indicating a systemic response to infectious agents such as coliform bacteria – and PDS [24–26]. The condition comes with acute general symptoms such as inappetite, lethargy and fever [25], followed by local symptoms that usually affect either the uterus [19] or the udder [27] or both of them.

After parturition, concomitant with the process of inflammation, the sow undergoes metabolic stress due to loss of body reserves in favor of milk produced for large litters. This change rate is highest during the first 10 days of lactation. One of major mediators of metabolic stress is IGF-1, which is also seen as an indicator for fertility. Low IGF-1 levels indicate inflammation, metabolic stress present and fertility. IGF-1 is also regarded as one of the most important factors driving follicle development [28–30]. The role of extracellular vesicles, although proposed as being key players in follicle development and the cross talk between the mother and the embryo, in this inflammatory process and its effect on follicle development, however, remains less explored [31].

In conclusion, in hyperprolific sows, the physiological process of farrowing is prolonged, making the system vulnerable in terms of increased rate of inflammation and emerging infectious uterine and mammary disease. In fact, recent evidence now shows that even in sows staying without symptoms, there seems to be considerable degree of "silent inflammation" in the body. In an increased proportion of sows, however, post partum disease PDS is detected and hopefully treated. The consequences of inflammation, regardless of clinical symptoms, include reduced quantity and quality of piglet colostrum intake and milk intake during early lactation.
