Improved health, welfare and viability in young pigs: general information and legislation

This factsheet provides an overview of EU organic regulations that aim to ensure piglet health in organic pigs. Additionally, it presents the results of the Core Organic Cofund project POWER on the impact of improvement of health and reduction of mortality in piglets on animal welfare and the environment

Improved health, welfare and viability in young pigs: oral iron supply in neonatal piglets to avoid anaemia

This factsheet evaluates strategies of iron supplementation to avoid anaemia and reduce piglet mortality and health problems. Additionally, it presents the results of the Core Organic Cofund project POWER on iron supplementation’s relevance for animal welfare and its environmental impact

Evaluation of the potential benefits of iron supplementation in organic pig farming

Background: Iron from the stock acquired during foetal life and the ingestion of milk is not sufficient to cover the needs of the piglets during their first weeks of life. In organic farming, systematic supplementation with iron is problematic due to a strong limitation in pharmaceutic treatments. Methods: Erythroid parameters around weaning were measured in piglets from organic outdoor and indoor farms, and related to indicators of the inflammatory status. Blood samples were collected from 28.9±2.6 piglets/herd at 42.0±3.2 days of age and 11.9±3.0 kg live weight (mean ± SD) in 21 farms from the west part of France. Among the 11 outdoor farms, only one had supplemented piglets with 200 mg iron while among the 10 indoor farms, only one had not supplemented piglets, one had supplemented them with 100 mg, 8 with 200 mg and one with 400 mg. Results: Compared to outdoor piglets without supplementation, piglets kept indoors and receiving 200 mg iron had lower haemoglobin concentration (105 vs 118±2 g/l, mean ± SE) and red blood cell volume (56 vs 60±1 fl) (P<0.005). The reduction in haemoglobin concentration and red blood cell volume was more pronounced in indoor piglets supplemented with 100 mg of iron and even more when they had not received iron. The plasma concentration of haptoglobin was lower in outdoor than in indoor piglets (0.51±0.06 vs 0.78±0.09 g/l) whereas no effect of housing was observed for markers of oxidative stress (dROM, BAP). In the 14 farms where sow parity was known, the haemoglobin concentration was lower in piglets from primiparous than from multiparous sows (109 versus 114±2 g/l, P < 0.001). Conclusion: With the exception of soils where the content of bioavailable iron is very low, piglets from outdoor farms do not require iron supplementation, unlike those raised indoors

The cortisol response to ACTH in pigs, heritability and influence of corticosteroid-binding globulin

In the search for biological basis of robustness, this study aimed (i) at the determination of the heritability of the cortisol response to ACTH in juvenile pigs, using restricted maximum likelihood methodology applied to a multiple trait animal model, and (ii) at the study of the relationships between basal and stimulated cortisol levels with corticosteroid-binding globulin (CBG), IGF-I and haptoglobin, all important players in glucose metabolism and production traits. At 6 weeks of age, 298 intact male and female piglets from 30 litters (30 dams and 30 boars) were injected with 250 µg ACTH(1–24) (Synacthen). Blood was taken before ACTH injection to measure basal levels of cortisol, glucose, CBG, IGF-I and haptoglobin, and 60 min later to measure stimulated cortisol levels and glucose. Cortisol increased 2.8-fold after ACTH injection, with a high correlation between basal and stimulated levels (phenotypic correlation, rp=0.539; genetic correlation, rg=0.938). Post-ACTH cortisol levels were highly heritable (h2=0.684) and could therefore be used for genetic selection of animals with a more reactive hypothalamic–pituitary–adrenocortical axis. CBG binding capacity correlated with cortisol levels measured in basal conditions in males only. No correlation was found between CBG binding capacity and post-ACTH cortisol levels. Basal IGF-I concentration was positively correlated with BW at birth and weaning, and showed a high correlation with CBG binding capacity with a strong sexual dimorphism, the correlation being much higher in males than in females. Basal haptoglobin concentrations were negatively correlated with CBG binding capacity and IGF-I concentrations. Complex relationships were also found between circulating glucose levels and these different variables that have been shown to be related to glucose resistance in humans. These data are therefore valuable for the genetic selection of animals to explore the consequences on production and robustness traits, but also point at pigs as a relevant model to explore the underlying mechanisms of the metabolic syndrome including the contribution of genetic factors

Review. Divergent selection for residual feed intake in the growing pig

To view supplementary material for this article, please visit https:/doi.org/10.1017/S175173111600286XThis review summarizes the results from the INRA (Institut National de la Recherche Agronomique) divergent selection experiment on residual feed intake (RFI) in growing Large White pigs during nine generations of selection. It discusses the remaining challenges and perspectives for the improvement of feed efficiency in growing pigs. The impacts on growing pigs raised under standard conditions and in alternative situations such as heat stress, inflammatory challenges or lactation have been studied. After nine generations of selection, the divergent selection for RFI led to highly significant ( P<0.001) line differences for RFI (−165 g/day in the low RFI (LRFI) line compared with high RFI line) and daily feed intake (−270 g/day). Low responses wereobserved on growth rate (−12.8 g/day, P <0.05) and body composition (+0.9mm backfat thickness, P = 0.57; −2.64% lean meat content, P<0.001) with a marked response on feed conversion ratio (−0.32 kg feed/kg gain, P<0.001). Reduced ultimate pH and increased lightness of the meat ( P<0.001) were observed in LRFI pigs with minor impact on the sensory quality of the meat. These changes in meat quality were associated with changes of the muscular energy metabolism. Reduced maintenance energy requirements (−10% after five generations of selection) and activity (−21% of time standing after six generations of selection) of LRFI pigs greatly contributed to the gain in energy efficiency. However, the impact of selection for RFI on the protein metabolism of the pig remains unclear. Digestibility of energy and nutrients was not affected by selection, neither for pigs fed conventional diets nor for pigs fed high-fibre diets. A significant improvement of digestive efficiency could likely be achieved by selecting pigs on fibre diets. No convincing genetic or blood biomarker has been identified for explaining the differences in RFI, suggesting that pigs have various ways to achieve an efficient use of feed. No deleterious impact of the selection on the sow reproduction performance was observed. The resource allocation theory states that low RFI may reduce the ability to cope with stressors,via the reduction of a buffer compartment dedicated to responses to stress. None of the experiments focussed on the response of pigs to stress or challenges could confirm this theory. Understanding the relationships between RFI and responses to stress and energy demanding processes, as such immunity and lactation, remains a major challenge for a better understanding of the underlying biological mechanisms of the trait and to reconcile the experimental results with the resource allocation theory

Dynamics of serum antibodies to and load of porcine circovirus type 2 (PCV2) in pigs in three finishing herds, affected or not by postweaning multisystemic wasting syndrome

Background: Despite that PMWS commonly affects pigs aged eight to sixteen weeks; most studies of PMWS have been conducted during the period before transfer to finishing herds. This study focused on PCV2 load and antibody dynamics in finishing herds with different PMWS status. Methods: Sequentially collected blood samples from 40 pigs in each of two Swedish (A and B) and one Norwegian (C) finishing herds were analysed for serum PCV2-load and -antibodies and saliva cortisol. The two Swedish herds differed in PMWS status, despite receiving animals from the same sow pool (multi-site production). However, the PMWS-deemed herd (A) had previously also received pigs from the spot market. ResultsThe initial serum PCV2 load was similar in the two Swedish herds. In herd A, it peaked after two weeks in the finishing herd and a high number of the pigs had serum PCV2 levels above 10(7) per ml. The antibody titres increased continually with exception for the pigs that developed PMWS, that had initially low and then declining antibody levels. Pigs in the healthy herd B also expressed high titres of antibodies to PCV2 on arrival but remained at that level throughout the study whereas the viral load steadily decreased. No PCV2 antibodies and only low amounts of PCV2 DNA were detected in serum collected during the first five weeks in the PMWS-free herd C. Thereafter a peak in serum PCV2 load accompanied by an antibody response was recorded. PCV2 from the two Swedish herds grouped into genotype PCV2b whereas the Norwegian isolate grouped into PCV2a. Cortisol levels were lower in herd C than in herds A and B. Conclusions: The most obvious difference between the Swedish finishing herds and the Norwegian herd was the time of infection with PCV2 in relation to the time of allocation, as well as the genotype of PCV2. Clinical PMWS was preceded by low levels of serum antibodies and a high load of PCV2 but did not develop in all such animals. It is notable that herd A became affected by PMWS after errors in management routine, emphasising the importance of proper hygiene and general disease-preventing measures

Modulation de la production de cytokines par l'environnement social et susceptibilité aux infections

The immune consequences of environmental stress are complex and difficult to predict. Stress affects the immune system either at the level of innate immunity, through the alteration of inflammatory reactivity, or at the level of acquired immunity, through the modulation of Th1 and Th2 cytokines. In social species, social environment contributes to the development and expression of diseases. The social position in a group modulates susceptibility to infections. However, the endocrine and immune mechanisms involved in these differences are not known. Instability in the social organization generates a severe stress of which immune consequences are still controversial. The purposes of this thesis are (1) to describe the influence of social status on the endocrine and immune systems, (2) to specify the effects of social stress on cytokine production and susceptibility to infections and (3) to look for possible sources of variability in the immune consequences of social stress. Mixing piglets after weaning transiently increases salivary cortisol and modifies behavior but does not affect blood lymphocyte reactivity. The following experiments used a procedure of chronic social defeat in mice. Results show an influence of social status. In the absence of stress, dominants show higher basal corticosterone levels and specific response to tuberculin than subordinates. After social defeat, dominants are more affected. Social defeat increases inflammatory reactivity but does not clearly modify the balance between Th1 and Th2 cytokines production and does not affect the development of specific immunity against a mycobacterial infection. Immune effects of social defeat can be observed only when the stress involves significant fights and injuries. Our work shows that the response to stress depends on individual social experience, in particular on social status. Furthermore the immune consequences of stress depend on recent immune experience. Indeed a systemic inflammatory challenge inhibits the release of plasma inflammatory cytokines in response to a subsequent psychological stress.Les conséquences immunitaires d'un stress d'origine environnementale sont complexes et encore difficilement prévisibles. Le stress affecte le système immunitaire soit en agissant sur l'immunité innée, en altérant la réactivité inflammatoire, soit en agissant sur l'immunité acquise, en modulant la production de cytokines dites Th1 et Th2. L'environnement social contribue largement au développement et à l'expression de maladies. Dans les espèces sociales, la position sociale occupée dans le groupe module la susceptibilité aux infections mais les supports endocriniens et immunitaires de ces différences de susceptibilité sont ignorés. La remise en cause de l'organisation sociale engendre un stress important dont les conséquences immunitaires sont encore sujettes à controverse. Ce travail de thèse a pour objectifs (1) de décrire l'influence du statut social sur le fonctionnement des systèmes endocrinien et immunitaire, (2) de préciser les effets du stress social sur la production de cytokines et la susceptibilité aux infections et (3) de rechercher des facteurs à l'origine de la variabilité des conséquences immunitaires du stress social. Chez le porcelet, un regroupement après le sevrage élève transitoirement le cortisol salivaire et altère le comportement mais n'affecte pas la réactivité des lymphocytes sanguins. La suite des travaux a utilisé une procédure de défaite sociale chronique chez la souris. Les résultats obtenus mettent en évidence une influence du statut social. En absence de stress, les dominants présentent des niveaux de base de corticostérone et une réponse spécifique à la tuberculine supérieurs aux dominés. Suite à une défaite sociale, les dominants sont plus affectés que les dominés. La défaite sociale augmente la réactivité inflammatoire mais ne modifie pas de façon nette l'équilibre de la production de cytokines de type Th1 et Th2 et n'affecte pas l'immunité spécifique développée contre une infection mycobactérienne. Les conséquences immunitaires de la défaite sociale ne sont observées que lorsque le stress est associé à des combats et à des blessures. Ces travaux montrent que la réponse au stress dépend de l'histoire sociale de l'individu, en particulier de son statut social. De plus, les répercussions immunitaires du stress dépendent aussi de l'histoire immunitaire récente. En effet, une réaction inflammatoire systémique inhibe la libération plasmatique de cytokines inflammatoires en réponse à un stress psychologique ultérieur

Conséquences du stress sur la fonction immunitaire chez les animaux d'élevage

National audienceThis article shows how situations of acute (transport, mixing animals) or chronic (poor housing conditions) stress affect the immune function of farm animals. The stress response implies the release of corticotrope axis hormones that inhibit leakocyte activity, but also of numerous other immunoactive or immunosuppressive hormones and neuropeptides (growth hormone, prolactin, enkephalins...). The increase in the blood neutophfl to lymphocyte ratio and the inhibition of the ability of lymphocyte to proliferate are markers of a stress response. Other tests bring more functional information because they measure the effect of stress on precise immune functions. Functions related to the innate immune system, which is the first line of defence of the organism, are sensitive to stress. Natural killer cell cytotoxicity is inhibited and data from rodent studies indicate that the inflammatory response can be dramatically disturbed. Some stressors enhance the production of inflammatory cytokines and increase the susceptibility to septic choc, whereas other stressors inhibit leukocyte migration to the infection site, thereby limiting the inflammatory response and delaying wound healing. Lymphocytes form the second line of defence, which is the acquired immunity. Stress can inhibit the development of lymphocyte response to antigens, for example the response to a vaccine. It decreases specific cellular responses but does not affect or even sometimes stimulates antibody production. Alteration of innate and acquired functions decreases resistance of animals to viral or bacterial infections.Cet article présente comment des situations de stress aigu (un transport, un regroupement) ou chronique (conditions de logement contraignantes) affectent la fonction immunitaire chez les animaux d’élevage. La réponse de stress est caractérisée par l’activation de l’axe corticotrope, dont les hormones inhibent l’activité des leucocytes, et la libération de nombreuses autres hormones et neuromédiateurs immunoactifs et immunosuppresseurs (hormone de croissance, prolactine, enképhalines…). Ainsi, l’augmentation transitoire du ratio neutrophiles / lymphocytes dans le sang et l’inhibition de la capacité des lymphocytes sanguins à proliférer sont des indicateurs d’une réponse de stress. D’autres tests sont plus informatifs car ils mesurent les effets du stress sur des fonctions immunitaires précises. Des fonctions relevant de l’immunité innée, première ligne de défense de l’organisme, sont sensibles au stress. Ainsi, la cytotoxicité des cellules tueuses naturelles sanguines est inhibée et des données chez les rongeurs montrent que la réponse inflammatoire peut être fortement déréglée. Certains facteurs de stress favorisent la production de cytokines inflammatoires et augmentent la sensibilité de l’organisme aux chocs septiques, tandis que d’autres inhibent la migration des polynucléaires vers un site d’infection, limitant ainsi la réponse inflammatoire et retardant le phénomène de cicatrisation. Les lymphocytes, vecteurs de l’immunité acquise, constituent la seconde ligne de défense. Le stress peut inhiber le développement de la réponse lymphocytaire à un antigène, par exemple une réponse vaccinale. Il inhibe les réponses de type cellulaire mais affecte peu, voire même parfois stimule, la production d’anticorps. L’altération des réponses innées et acquises diminue la résistance des animaux aux infections virales ou bactériennes

Modulation de la production de cytokines par l'environnement

The immune consequences of environmental stress are complex and difficult to predict. Stress affects the immune system either at the level of innate immunity, through the alterationof inflammatory reactivity, or at the level of acquired immunity, through the modulation of Th1 and Th2 cytokines. In social species, social environment contributes to the developmentand expression of diseases. The social position in a group modulates susceptibility to infections. However, the endocrine and immune mechanisms involved in these differences arenot known. Instability in the social organization generates a severe stress of which immune consequences are still controversial.The purposes of this thesis are (1) to describe the influence of social status on the endocrine and immune systems, (2) to specify the effects of social stress on cytokine production and susceptibility to infections and (3) to look for possible sources of variability in the immune consequences of social stressLes conséquences immunitaires d'un stress d'origine environnementale sont complexes et encore difficilement prévisibles. Le stress affecte le système immunitaire soit en agissant sur l'immunité innée, en altérant la réactivité inflammatoire, soit en agissant sur l'immunité acquise, en modulant la production de cytokines dites Th1 et Th2. L'environnement socialcontribue largement au développement et à l'expression de maladies. Dans les espèces sociales, la position sociale occupée dans le groupe module la susceptibilité aux infections mais les supports endocriniens et immunitaires de ces différences de susceptibilité sont ignorés. La remise en cause de l'organisation sociale engendre un stress important dont les conséquences immunitaires sont encore sujettes à controverse.Ce travail de thèse a pour objectifs (1) de décrire l'influence du statut social sur le fonctionnement des systèmes endocrinien et immunitaire, (2) de préciser les effets du stresssocial sur la production de cytokines et la susceptibilité aux infections et (3) de rechercher des facteurs à l'origine de la variabilité des conséquences immunitaires du stress social.Chez le porcelet, un regroupement après le sevrage élève transitoirement le cortisol salivaire et altère le comportement mais n'affecte pas la réactivité des lymphocytes sanguins.La suite des travaux a utilisé une procédure de défaite sociale chronique chez la souris. Les résultats obtenus mettent en évidence une influence du statut social. En absence de stress, lesdominants présentent des niveaux de base de corticostérone et une réponse spécifique à la tuberculine supérieurs aux dominés. Suite à une défaite sociale, les dominants sont plus affectés que les dominés. La défaite sociale augmente la réactivité inflammatoire mais ne modifie pas de façon nette l'équilibre de la production de cytokines de type Th1 et Th2 et n'affecte pas l'immunité spécifique développée contre une infection mycobactérienne. Les conséquences immunitaires de la défaite sociale ne sont observées que lorsque le stress est associé à des combats et à des blessures. Ces travaux montrent que la réponse au stress dépend de l'histoire sociale de l'individu, en particulier de son statut social. De plus, lesrépercussions immunitaires du stress dépendent aussi de l'histoire immunitaire récente. En effet, une réaction inflammatoire systémique inhibe la libération plasmatique de cytokinesinflammatoires en réponse à un stress psychologique ultérieur

Conséquences du stress sur la fonction immunitaire chez les animaux d'élevage

Cet article présente comment des situations de stress aigu (un transport, un regroupement) ou chronique (conditions de logement contraignantes) affectent la fonction immunitaire chez les animaux d’élevage. La réponse de stress est caractérisée par l’activation de l’axe corticotrope, dont les hormones inhibent l’activité des leucocytes, et la libération de nombreuses autres hormones et neuromédiateurs immunoactifs et immunosuppresseurs (hormone de croissance, prolactine, enképhalines…). Ainsi, l’augmentation transitoire du ratio neutrophiles / lymphocytes dans le sang et l’inhibition de la capacité des lymphocytes sanguins à proliférer sont des indicateurs d’une réponse de stress. D’autres tests sont plus informatifs car ils mesurent les effets du stress sur des fonctions immunitaires précises. Des fonctions relevant de l’immunité innée, première ligne de défense de l’organisme, sont sensibles au stress. Ainsi, la cytotoxicité des cellules tueuses naturelles sanguines est inhibée et des données chez les rongeurs montrent que la réponse inflammatoire peut être fortement déréglée. Certains facteurs de stress favorisent la production de cytokines inflammatoires et augmentent la sensibilité de l’organisme aux chocs septiques, tandis que d’autres inhibent la migration des polynucléaires vers un site d’infection, limitant ainsi la réponse inflammatoire et retardant le phénomène de cicatrisation. Les lymphocytes, vecteurs de l’immunité acquise, constituent la seconde ligne de défense. Le stress peut inhiber le développement de la réponse lymphocytaire à un antigène, par exemple une réponse vaccinale. Il inhibe les réponses de type cellulaire mais affecte peu, voire même parfois stimule, la production d’anticorps. L’altération des réponses innées et acquises diminue la résistance des animaux aux infections virales ou bactériennes.This article shows how situations of acute (transport, mixing animals) or chronic (poor housing conditions) stress affect the immune function of farm animals. The stress response implies the release of corticotrope axis hormones that inhibit leakocyte activity, but also of numerous other immunoactive or immunosuppressive hormones and neuropeptides (growth hormone, prolactin, enkephalins...). The increase in the blood neutophfl to lymphocyte ratio and the inhibition of the ability of lymphocyte to proliferate are markers of a stress response. Other tests bring more functional information because they measure the effect of stress on precise immune functions. Functions related to the innate immune system, which is the first line of defence of the organism, are sensitive to stress. Natural killer cell cytotoxicity is inhibited and data from rodent studies indicate that the inflammatory response can be dramatically disturbed. Some stressors enhance the production of inflammatory cytokines and increase the susceptibility to septic choc, whereas other stressors inhibit leukocyte migration to the infection site, thereby limiting the inflammatory response and delaying wound healing. Lymphocytes form the second line of defence, which is the acquired immunity. Stress can inhibit the development of lymphocyte response to antigens, for example the response to a vaccine. It decreases specific cellular responses but does not affect or even sometimes stimulates antibody production. Alteration of innate and acquired functions decreases resistance of animals to viral or bacterial infections