What exactly is early embryonic death?
Early embryonic death
Early embryonic death
Embryonic death is one of the important factors affecting the reproductive rate of livestock. The embryonic mortality rate of livestock is approximately 25%-40%. Pigs are polytocous livestock, and embryonic death is relatively common, and embryos can die at any stage of development, especially before the embryo implants into the uterine endometrium or during the implantation process, which is the most critical period for pregnancy recognition. When sows are in a poor environment, lacking nutrition, or suffering from disease, embryonic death is even more severe. The first peak of embryonic death in sows is at 9-16 days after zygote implantation, when embryos are susceptible to various factors, with a mortality rate of about 40%-50%; the second peak is at the 3rd week after mating, with a mortality rate of about 30%-40%. However, under general circumstances, the death of a small number of embryos will not affect the normal progression of pregnancy.
1 Genetic factors Inbreeding is one of the important causes of embryonic death in livestock. The smaller the degree of difference between male and female animals of the same species, the greater the embryonic death. This is because inbreeding can lead to low fertilization compatibility and weak embryonic vitality. Genetics research has proven that chromosomal abnormalities such as triploidy are related to embryonic death. Structural chromosomal variations such as translocation (boar 38, XYt) and deletion can also cause early embryonic death. Individuals with genotypes composed of deleterious genes, that is, embryos with genetic defects, also undergo embryonic death in early pregnancy.
2 Nutritional factors Under general circumstances, long-term low nutritional levels or deficiency of certain nutrients will not only reduce ovulation number and fertilization rate, but also lead to embryonic death.
Embryonic death in sows is most severe 1-3 days after mating. Within 7 days after mating, appropriate restricted feeding (feed intake controlled at 50%-60% of ad libitum intake) can reduce embryonic death. However, restricted feeding will cause pregnant sows to suffer from hunger pain, and also prolong the retention time of digestive tract contents in the intestines, and the harmful gases produced (such as H2S) are absorbed into the blood circulation and cause embryonic death (Lyu Jianwei, 2000). Severe nutritional deficiency in early pregnancy will also reduce the embryonic survival rate (Speer, 1990), mainly because some embryos die due to lack of nutrition.
High nutritional level feeding in early pregnancy can reduce the embryonic survival rate by 5% (Hughs, 1989). Toplis confirmed that increasing feed intake in early pregnancy for primiparous sows can reduce the embryonic survival rate. This is because within 3 weeks after mating, the formation of embryos from fertilized eggs requires almost no additional nutrition, so sows are given a low-level ration (DE<3．OMJ／kg，CP<13％），喂量约2．0g／d（Boyb妊娠头21饲喂水平应为维持需要的1．5倍以下），即能维持正常的繁殖需要。相反摄入过高营养水平的日，配种后最初24～48小时机体代谢旺盛，促使肾上腺激素分泌增加，从而影响孕激素的分泌，进而降低循环血液中黄体酮水平和极为重要的子宫特异性蛋白质的分泌，从而造成胚胎死亡（Jindal等，1996）。母猪的养分需要量随妊娠时间的推移而增加，与胚胎的发育相一致(等，1985)。
The body condition of the sow determines the effect of feed intake on embryonic survival rate. For sows in good body condition, high feed intake will increase embryonic death; but for thin sows in poor body condition, feeding more feed will actually increase the embryonic survival rate (Bob Thaler, 2000). Therefore, the feed intake in early pregnancy should be adjusted according to the body condition of each sow.
Sows with low feed intake during lactation and high feed intake in early pregnancy have more embryos and a higher embryonic survival rate. Sows with both low feed intake during gestation and lactation have the fewest embryos and the highest mortality rate (Baidoo et al., 1992).
If primiparous sows lose a relatively large amount of body weight or experience a relatively large decline in body condition during lactation, the re-mating interval will be prolonged, and both the conception rate and embryonic survival rate will decrease (Mulla, 1996).
Vitamin A (retinoic acid-binding protein RBP) is one of the important vitamins necessary for pig reproduction. Vitamin A is necessary for the maintenance and development of epithelial tissues in pregnant sows and for the secretion of specific uterine proteins. Deficiency of vitamin A not only makes RNA metabolism and transferrin synthesis abnormal, but may also lead to embryonic death or resorption. Brief pointed out that the embryonic survival rate within the first 4 weeks after mating is positively correlated with the progesterone level in the blood, while vitamin A deficiency reduces iron absorption and serum progesterone levels, thereby increasing the embryonic mortality rate; at the same time, vitamin A deficiency increases the variability of embryonic diameter, reduces the uniformity of embryonic size and the synchrony of development, and promotes embryonic death.
Vitamin E is a highly effective biological antioxidant present in all cell membranes and organelles. High doses (Che recommended 66 IU/kg feed) of vitamin E can not only improve immune function before and after stress (Li Xiaolin, 1996), but are also necessary for embryonic development in pregnant sows. Deficiency of vitamin E will lead to reproductive dysfunction, damage the placenta and embryonic blood vessels of sows, and cause embryonic death.
Folic acid may play an important role in maintaining the reproductive function of sows and early embryonic development. Adding coenzyme-form folic acid to sow diets is relatively effective. Research by FilChS et al. (1996) showed that dietary supplementation of folic acid (suitable dose 10 mg/kg, Matte et al.) can increase the embryonic survival rate in early pregnancy, especially in sows with a relatively large number of ovulations (such as those treated with pregnant mare serum gonadotropin). Matte (1993) confirmed that as the folic acid level in sow diets increases, embryonic folate levels increase linearly, and sow folic acid may be transported to embryos through an active transport mechanism in the uterus. Folic acid deficiency not only limits DNA synthesis, but also causes DNA defects, thereby leading to embryonic death and fetal malformations.
In addition, severe deficiency of mineral elements such as Se, Cr, and Zn, as well as toxic substances in moldy, rotten, deteriorated, and frozen feed (such as gossypol in cottonseed cake, aflatoxin in peanut cake, ergot toxin, decomposition products of glucosinolates in rapeseed cake, zearalenone in corn, etc.) can all cause embryonic death.
Some forages such as red clover and subterranean clover contain large amounts of estrogen-like substances (such as isoflavone phytoestrogens) that are similar in chemical structure to estradiol and can bind to estrogen receptors (ESR), causing endocrine system disruption and ultimately resulting in embryonic death.
3 Environmental factors
Environmental influences come from two aspects: the maternal internal environment (the direct environment of the embryo) and the maternal external environment. The number of embryos is crucial to whether embryos can survive. Each embryo can only develop normally in a certain amount of space. An increase in the number of embryos will reduce the blood supply to each embryo implantation site, thereby limiting the development of the fetal membranes and ultimately leading to embryonic death. In pigs, death due to embryo crowding is common when the number of embryos in the sow is too large. If the number of embryos is too small, it is insufficient to maintain pregnancy, because the hormones produced by the embryos are insufficient, maternal pregnancy recognition is impaired, and the luteolytic substances in the uterus then cause corpus luteum regression, ultimately leading to embryonic death. Although the maternal external environment has only an indirect effect on embryos, high temperature, changing pens, long-distance transport, cramped barns, crowded herds, intimidation, chasing and beating, and work use can also cause embryonic death by adversely affecting the physiological state of the mother. Sows are most sensitive to high-temperature stress. High-temperature stress (above 30 degrees C) causes a relatively high embryonic mortality rate. Research shows that from 3 days to two weeks after mating, especially at 11-12 days after mating, even staying in a 32 degrees C-39 degrees C environment for 24 hours can cause embryonic death, while the survival rate is reduced by 35%-40%. In multiparous sows during the high-temperature season from June to September, 32.5%-42% of embryonic development is inhibited, while in other months only 8.2%-20.7% (Japanese data). This is mainly because the environmental temperature is too high, and the pig body cannot maintain body heat balance by relying solely on physical regulation for heat dissipation, so it must use chemical regulation for heat dissipation, thereby causing a series of changes in the body's endocrine system. Harmful gases in the barn (CO, HS, H3, etc.) can significantly increase the embryonic mortality rate of sows in the first two weeks of pregnancy. Whether the sow has disease at the time of embryo implantation or whether sows fight with each other during the 10-20 days after mating can all affect the embryonic mortality rate. About 25%-30% of embryonic deaths are caused by the external environment. If the sow must be moved to a different pen after mating, it should be done within the first 72 hours after mating or at 28 days after mating; otherwise it will cause stress before embryo implantation or during mixing, leading to embryonic death.
4 Lactation factors Sows will not come into estrus or conceive during lactation, but if early weaning is carried out on the 7th day of lactation and then mating is performed, embryonic death will be severe at 9-20 days of pregnancy. Research shows that the embryonic survival rate decreases as the lactation period is shortened. Therefore, sows with a lactation period of less than 21 days have a lower embryonic survival rate. The harmful effect of lactation on embryonic development may lie in hindering embryo implantation, and may also be related to the recovery of the endometrium.
5 Endocrine factors Within 21 days after mating, the endocrine system of the sow is in a state of adjustment. If the pig is affected by stress factors at this time, it will interfere with the secretion of endocrine hormones, thereby affecting embryo implantation and increasing embryonic death. Hormone secretion and the dynamic balance among hormones play an important role in embryonic survival. In early pregnancy, embryonic estrogen will not only lead to uneven embryonic development and increase early embryonic death, but the secretion of estrogen by dominant embryos also leads to the death and resorption of weaker embryos (Jiang Jinhu, 1995). At the same time, after a sow is mated and conceives, if estrogen and progesterone secretion is disordered and the ratio is imbalanced, it will lead to corpus luteum regression, affect normal embryo implantation, and then cause embryonic death. For underdeveloped embryos, their endocrine function is insufficient to counter the luteolytic effect of uterine luteolytic substances, resulting in decreased progesterone levels, termination of pregnancy, and embryonic death.
6 Boar factors Some of the causes of embryonic death come from the boar. The genetic material carried by sperm, sperm quality, and possible incompatibility between sperm and egg as well as between embryo and mother can all affect embryonic vitality and development.
Timely mating is an important guarantee for improving the embryonic survival rate. Delayed mating, however, causes the embryonic survival rate to decrease rapidly. Research shows that when mating was performed 6 hours before ovulation and 14 hours after ovulation, the embryonic survival rates were 88% and 32%, respectively. If the timing of the 2 matings is controlled relatively well, it is best not to mate each sow more than 2 times. Mating in the later part of the standing reflex period will cause embryonic death. Mating sows immediately after abortion will cause early embryonic death; instead, mating should wait until the next estrous cycle. Mating stimulation and seminal plasma can affect early embryonic development. Four days after mating, the degree of embryonic development in naturally mated sows is higher than in those artificially inseminated. If boar semen is preserved at room temperature for more than 3 days for artificial insemination, it will also cause early death of fertilized embryos. Delayed ovulation time can reduce embryo uniformity, increase embryonic mortality, and decrease litter size. Abnormal sperm or abnormal fertilization, such as polyspermic fertilization or monospermic fertilization of eggs containing two female pronuclei, can both cause early embryonic death.
7 Immunological factors Immune incompatibility can affect embryonic development. Experiments have shown that after pregnant sows are sensitized by allogeneic antigens of plasma proteins, the placental barrier will be damaged, and macromolecular substances such as antigens and antibodies can pass through and enter each other's bodies, which will inevitably cause immune rejection and lead to embryonic death. In pigs, it has been proven that certain blood types and uterine transferrin in the blood are related to embryonic death. The effect of immunization on embryos is also very obvious. Under general circumstances, sows are prohibited from being injected with vaccines in the first 4 weeks of pregnancy. If immunization is needed, it should be supplemented after 4 weeks; otherwise it will cause embryonic death.
8 Sow age and body weight Primiparous sows and sows that have farrowed more than 5 times have a relatively high embryonic mortality rate. At the same time, sows with a relatively high body weight at first mating (above 150 kg) have a reduced conception rate and severe embryonic death; while sows with a relatively low body weight (120 kg) not only have a low embryonic mortality rate, but also lose less body weight during lactation.
9 Disease factors Infantile and malformed reproductive organs, uterine diseases, and infectious diseases that endanger reproductive capacity can all directly or indirectly affect embryos to varying degrees. Microorganisms are an important cause of impaired reproductive capacity in sows. When pregnant sows are infected with certain viruses and bacteria, it will cause symptoms such as elevated body temperature (40 degrees C-41 degrees C), reduced appetite, or complete loss of appetite, thereby causing embryonic death. Pseudorabies virus (PRV), classical swine fever virus (HCV), Japanese encephalitis virus (JEV), porcine parvovirus (PPV), porcine reproductive and respiratory syndrome virus (PRRSV), etc. can all cause embryonic death and mummification. Leptospira, Staphylococcus, Pasteurella, and Brucella can cause embryonic death.
--------------------------------------
It is also possible that the mycotoxin content in the feed exceeds the standard. Among these, zearalenone can cause abortion and embryonic death in sows.
Embryonic death is one of the important factors affecting the reproductive rate of livestock. The embryonic mortality rate of livestock is approximately 25%-40%. Pigs are polytocous livestock, and embryonic death is relatively common, and embryos can die at any stage of development, especially before the embryo implants into the uterine endometrium or during the implantation process, which is the most critical period for pregnancy recognition. When sows are in a poor environment, lacking nutrition, or suffering from disease, embryonic death is even more severe. The first peak of embryonic death in sows is at 9-16 days after zygote implantation, when embryos are susceptible to various factors, with a mortality rate of about 40%-50%; the second peak is at the 3rd week after mating, with a mortality rate of about 30%-40%. However, under general circumstances, the death of a small number of embryos will not affect the normal progression of pregnancy.
1 Genetic factors Inbreeding is one of the important causes of embryonic death in livestock. The smaller the degree of difference between male and female animals of the same species, the greater the embryonic death. This is because inbreeding can lead to low fertilization compatibility and weak embryonic vitality. Genetics research has proven that chromosomal abnormalities such as triploidy are related to embryonic death. Structural chromosomal variations such as translocation (boar 38, XYt) and deletion can also cause early embryonic death. Individuals with genotypes composed of deleterious genes, that is, embryos with genetic defects, also undergo embryonic death in early pregnancy.
2 Nutritional factors Under general circumstances, long-term low nutritional levels or deficiency of certain nutrients will not only reduce ovulation number and fertilization rate, but also lead to embryonic death.
Embryonic death in sows is most severe 1-3 days after mating. Within 7 days after mating, appropriate restricted feeding (feed intake controlled at 50%-60% of ad libitum intake) can reduce embryonic death. However, restricted feeding will cause pregnant sows to suffer from hunger pain, and also prolong the retention time of digestive tract contents in the intestines, and the harmful gases produced (such as H2S) are absorbed into the blood circulation and cause embryonic death (Lyu Jianwei, 2000). Severe nutritional deficiency in early pregnancy will also reduce the embryonic survival rate (Speer, 1990), mainly because some embryos die due to lack of nutrition.
High nutritional level feeding in early pregnancy can reduce the embryonic survival rate by 5% (Hughs, 1989). Toplis confirmed that increasing feed intake in early pregnancy for primiparous sows can reduce the embryonic survival rate. This is because within 3 weeks after mating, the formation of embryos from fertilized eggs requires almost no additional nutrition, so sows are given a low-level ration (DE<3．OMJ／kg，CP<13％），喂量约2．0g／d（Boyb妊娠头21饲喂水平应为维持需要的1．5倍以下），即能维持正常的繁殖需要。相反摄入过高营养水平的日，配种后最初24～48小时机体代谢旺盛，促使肾上腺激素分泌增加，从而影响孕激素的分泌，进而降低循环血液中黄体酮水平和极为重要的子宫特异性蛋白质的分泌，从而造成胚胎死亡（Jindal等，1996）。母猪的养分需要量随妊娠时间的推移而增加，与胚胎的发育相一致(等，1985)。
The body condition of the sow determines the effect of feed intake on embryonic survival rate. For sows in good body condition, high feed intake will increase embryonic death; but for thin sows in poor body condition, feeding more feed will actually increase the embryonic survival rate (Bob Thaler, 2000). Therefore, the feed intake in early pregnancy should be adjusted according to the body condition of each sow.
Sows with low feed intake during lactation and high feed intake in early pregnancy have more embryos and a higher embryonic survival rate. Sows with both low feed intake during gestation and lactation have the fewest embryos and the highest mortality rate (Baidoo et al., 1992).
If primiparous sows lose a relatively large amount of body weight or experience a relatively large decline in body condition during lactation, the re-mating interval will be prolonged, and both the conception rate and embryonic survival rate will decrease (Mulla, 1996).
Vitamin A (retinoic acid-binding protein RBP) is one of the important vitamins necessary for pig reproduction. Vitamin A is necessary for the maintenance and development of epithelial tissues in pregnant sows and for the secretion of specific uterine proteins. Deficiency of vitamin A not only makes RNA metabolism and transferrin synthesis abnormal, but may also lead to embryonic death or resorption. Brief pointed out that the embryonic survival rate within the first 4 weeks after mating is positively correlated with the progesterone level in the blood, while vitamin A deficiency reduces iron absorption and serum progesterone levels, thereby increasing the embryonic mortality rate; at the same time, vitamin A deficiency increases the variability of embryonic diameter, reduces the uniformity of embryonic size and the synchrony of development, and promotes embryonic death.
Vitamin E is a highly effective biological antioxidant present in all cell membranes and organelles. High doses (Che recommended 66 IU/kg feed) of vitamin E can not only improve immune function before and after stress (Li Xiaolin, 1996), but are also necessary for embryonic development in pregnant sows. Deficiency of vitamin E will lead to reproductive dysfunction, damage the placenta and embryonic blood vessels of sows, and cause embryonic death.
Folic acid may play an important role in maintaining the reproductive function of sows and early embryonic development. Adding coenzyme-form folic acid to sow diets is relatively effective. Research by FilChS et al. (1996) showed that dietary supplementation of folic acid (suitable dose 10 mg/kg, Matte et al.) can increase the embryonic survival rate in early pregnancy, especially in sows with a relatively large number of ovulations (such as those treated with pregnant mare serum gonadotropin). Matte (1993) confirmed that as the folic acid level in sow diets increases, embryonic folate levels increase linearly, and sow folic acid may be transported to embryos through an active transport mechanism in the uterus. Folic acid deficiency not only limits DNA synthesis, but also causes DNA defects, thereby leading to embryonic death and fetal malformations.
In addition, severe deficiency of mineral elements such as Se, Cr, and Zn, as well as toxic substances in moldy, rotten, deteriorated, and frozen feed (such as gossypol in cottonseed cake, aflatoxin in peanut cake, ergot toxin, decomposition products of glucosinolates in rapeseed cake, zearalenone in corn, etc.) can all cause embryonic death.
Some forages such as red clover and subterranean clover contain large amounts of estrogen-like substances (such as isoflavone phytoestrogens) that are similar in chemical structure to estradiol and can bind to estrogen receptors (ESR), causing endocrine system disruption and ultimately resulting in embryonic death.
3 Environmental factors
Environmental influences come from two aspects: the maternal internal environment (the direct environment of the embryo) and the maternal external environment. The number of embryos is crucial to whether embryos can survive. Each embryo can only develop normally in a certain amount of space. An increase in the number of embryos will reduce the blood supply to each embryo implantation site, thereby limiting the development of the fetal membranes and ultimately leading to embryonic death. In pigs, death due to embryo crowding is common when the number of embryos in the sow is too large. If the number of embryos is too small, it is insufficient to maintain pregnancy, because the hormones produced by the embryos are insufficient, maternal pregnancy recognition is impaired, and the luteolytic substances in the uterus then cause corpus luteum regression, ultimately leading to embryonic death. Although the maternal external environment has only an indirect effect on embryos, high temperature, changing pens, long-distance transport, cramped barns, crowded herds, intimidation, chasing and beating, and work use can also cause embryonic death by adversely affecting the physiological state of the mother. Sows are most sensitive to high-temperature stress. High-temperature stress (above 30 degrees C) causes a relatively high embryonic mortality rate. Research shows that from 3 days to two weeks after mating, especially at 11-12 days after mating, even staying in a 32 degrees C-39 degrees C environment for 24 hours can cause embryonic death, while the survival rate is reduced by 35%-40%. In multiparous sows during the high-temperature season from June to September, 32.5%-42% of embryonic development is inhibited, while in other months only 8.2%-20.7% (Japanese data). This is mainly because the environmental temperature is too high, and the pig body cannot maintain body heat balance by relying solely on physical regulation for heat dissipation, so it must use chemical regulation for heat dissipation, thereby causing a series of changes in the body's endocrine system. Harmful gases in the barn (CO, HS, H3, etc.) can significantly increase the embryonic mortality rate of sows in the first two weeks of pregnancy. Whether the sow has disease at the time of embryo implantation or whether sows fight with each other during the 10-20 days after mating can all affect the embryonic mortality rate. About 25%-30% of embryonic deaths are caused by the external environment. If the sow must be moved to a different pen after mating, it should be done within the first 72 hours after mating or at 28 days after mating; otherwise it will cause stress before embryo implantation or during mixing, leading to embryonic death.
4 Lactation factors Sows will not come into estrus or conceive during lactation, but if early weaning is carried out on the 7th day of lactation and then mating is performed, embryonic death will be severe at 9-20 days of pregnancy. Research shows that the embryonic survival rate decreases as the lactation period is shortened. Therefore, sows with a lactation period of less than 21 days have a lower embryonic survival rate. The harmful effect of lactation on embryonic development may lie in hindering embryo implantation, and may also be related to the recovery of the endometrium.
5 Endocrine factors Within 21 days after mating, the endocrine system of the sow is in a state of adjustment. If the pig is affected by stress factors at this time, it will interfere with the secretion of endocrine hormones, thereby affecting embryo implantation and increasing embryonic death. Hormone secretion and the dynamic balance among hormones play an important role in embryonic survival. In early pregnancy, embryonic estrogen will not only lead to uneven embryonic development and increase early embryonic death, but the secretion of estrogen by dominant embryos also leads to the death and resorption of weaker embryos (Jiang Jinhu, 1995). At the same time, after a sow is mated and conceives, if estrogen and progesterone secretion is disordered and the ratio is imbalanced, it will lead to corpus luteum regression, affect normal embryo implantation, and then cause embryonic death. For underdeveloped embryos, their endocrine function is insufficient to counter the luteolytic effect of uterine luteolytic substances, resulting in decreased progesterone levels, termination of pregnancy, and embryonic death.
6 Boar factors Some of the causes of embryonic death come from the boar. The genetic material carried by sperm, sperm quality, and possible incompatibility between sperm and egg as well as between embryo and mother can all affect embryonic vitality and development.
Timely mating is an important guarantee for improving the embryonic survival rate. Delayed mating, however, causes the embryonic survival rate to decrease rapidly. Research shows that when mating was performed 6 hours before ovulation and 14 hours after ovulation, the embryonic survival rates were 88% and 32%, respectively. If the timing of the 2 matings is controlled relatively well, it is best not to mate each sow more than 2 times. Mating in the later part of the standing reflex period will cause embryonic death. Mating sows immediately after abortion will cause early embryonic death; instead, mating should wait until the next estrous cycle. Mating stimulation and seminal plasma can affect early embryonic development. Four days after mating, the degree of embryonic development in naturally mated sows is higher than in those artificially inseminated. If boar semen is preserved at room temperature for more than 3 days for artificial insemination, it will also cause early death of fertilized embryos. Delayed ovulation time can reduce embryo uniformity, increase embryonic mortality, and decrease litter size. Abnormal sperm or abnormal fertilization, such as polyspermic fertilization or monospermic fertilization of eggs containing two female pronuclei, can both cause early embryonic death.
7 Immunological factors Immune incompatibility can affect embryonic development. Experiments have shown that after pregnant sows are sensitized by allogeneic antigens of plasma proteins, the placental barrier will be damaged, and macromolecular substances such as antigens and antibodies can pass through and enter each other's bodies, which will inevitably cause immune rejection and lead to embryonic death. In pigs, it has been proven that certain blood types and uterine transferrin in the blood are related to embryonic death. The effect of immunization on embryos is also very obvious. Under general circumstances, sows are prohibited from being injected with vaccines in the first 4 weeks of pregnancy. If immunization is needed, it should be supplemented after 4 weeks; otherwise it will cause embryonic death.
8 Sow age and body weight Primiparous sows and sows that have farrowed more than 5 times have a relatively high embryonic mortality rate. At the same time, sows with a relatively high body weight at first mating (above 150 kg) have a reduced conception rate and severe embryonic death; while sows with a relatively low body weight (120 kg) not only have a low embryonic mortality rate, but also lose less body weight during lactation.
9 Disease factors Infantile and malformed reproductive organs, uterine diseases, and infectious diseases that endanger reproductive capacity can all directly or indirectly affect embryos to varying degrees. Microorganisms are an important cause of impaired reproductive capacity in sows. When pregnant sows are infected with certain viruses and bacteria, it will cause symptoms such as elevated body temperature (40 degrees C-41 degrees C), reduced appetite, or complete loss of appetite, thereby causing embryonic death. Pseudorabies virus (PRV), classical swine fever virus (HCV), Japanese encephalitis virus (JEV), porcine parvovirus (PPV), porcine reproductive and respiratory syndrome virus (PRRSV), etc. can all cause embryonic death and mummification. Leptospira, Staphylococcus, Pasteurella, and Brucella can cause embryonic death.
--------------------------------------
It is also possible that the mycotoxin content in the feed exceeds the standard. Among these, zearalenone can cause abortion and embryonic death in sows.