In dairy cattle, service dates are normally known; hence the date of anticipated parturition is calculated and recorded once pregnancy is confirmed. In beef cattle, in which cows often run with a bull, exact calving dates are not known but individual pregnant cows are expected to calve within a recognized calving season. Individual animals that have not calved at the anticipated time are checked to confirm that they are still pregnant and that their pregnancy appears to be normal.
In sheep, the exact lambing date is seldom known unless ewes were served in hand or by artificial insemination. In most flocks the ewes run with rams and, when served, receive a raddle crayon mark on their rumps to indicate that service has occurred. Crayon color is changed at 14- to 17-day intervals, and following later pregnancy confirmation, a lambing date within a 14- to 17-day period is calculated. Individual ewes that fail to lamb are culled or further evaluated for pregnancy.
In many cases, prolonged gestation is incorrectly diagnosed because of human error. Miscalculation of the prospective calving or lambing date, failure to record a subsequent service, faulty pregnancy diagnosis, and incorrect identification of animals may lead to a diagnosis of prolonged gestation in an animal that has a normal pregnancy. True prolonged gestation is relatively uncommon; the common denominator is a defective hypothalamic-pituitary-adrenal axis. Suspected cases should be investigated and examined with care. In some cases, the fetus is dead or severely deformed and is of little economic value. The life of the dam may be at risk if prolonged gestation is allowed to continue, and termination of the abnormal pregnancy is recommended.
Prolonged Gestation Associated with Fetal Death
Fetal death may be followed by abortion, fetal maceration, or fetal mummification. In cases of abortion and fetal maceration, the hormonal support of pregnancy is lost. The animal normally shows signs that pregnancy has terminated. An aborted fetus may be found, the dam may show an abnormal vaginal discharge, and she may return to estrus. Fetal bones may be trapped in the uterus.
In cases of fetal mummification, fetal death is often not immediately apparent. In such cases, the corpus luteum persists in the ovary and there is no vaginal discharge. The abnormal pregnancy in such animals continues indefinitely. Affected animals are normally identified when owners notice that external signs of late pregnancy including abdominal enlargement are less obvious than in other members of a group. Clinical examination reveals that the fetus is dead although the dam is pregnant. Rectal examination reveals an irregularly shaped, contracted uterus with a fetal mass but no fetal fluid within it. There is no fremitus in the uterine artery. Ultrasonographic examination of accessible parts of the uterus per rectum confirms the diagnosis. The abnormal pregnancy can be terminated by a single IM injection of prostaglandin F2α. The fetus is expelled from the uterus and can be manually removed from the vagina 48 hr later.
In sheep, fetal mummification may be diagnosed by abdominal palpation supported by a transabdominal ultrasonographic scan. Affected animals are normally culled on economic grounds.
Prolonged Gestation Associated with Fetal Deformity
These cases usually occur as the result of some compromise of the pituitary-adrenal axis of the fetus, which is no longer able to initiate parturition. The affected fetus may either die and be aborted or live on indefinitely in the uterus. Genetic, infectious, toxic, and unknown causes have been associated with this problem.
In Holstein-Friesian cows, genetically determined prolonged gestation is caused by an autosomal recessive gene of the fetus. The fetal adrenal glands fail to produce corticosteroids at term, in response to fetal ACTH. As a result, the fetus continues to grow until it outgrows its blood supply. Induction with dexamethasone does not induce normal labor and parturition due to insufficient preparation of the birth canal. A cesarean section will save the dam, but the fetus invariably dies due to adrenal insufficiency.
Three genetic abnormalities associated with prolonged gestation in various breeds of cattle involve fetal pituitary abnormalities. In one condition, severe fetal oversize (fetal giantism) is present. In the second, the calf has severe craniofacial defects and is much smaller than normal. In the third condition, multiple skeletal abnormalities are present. In a fourth condition, genetic abnormalities may occur as a result of cloning.
Prolonged gestation and fetal giantism has been reported in Holstein, Ayrshire, and Swedish breeds of cattle. Gestation is prolonged by 21–150 days. Pronounced abdominal enlargement is seen in some cases. There is no attempted parturition unless the fetus dies first after having outgrown its blood supply. Cervical relaxation is poor and dystocia invariably results. The calf weighs 48–80 kg at birth and shows signs of postmaturity. The coat and hooves are longer than normal and prominent loose teeth are present in the gums. Breathing is difficult as a result of failure of surfactant release, and the calf may die from hypoglycemia. At necropsy, hypoplasia of the anterior pituitary and adrenal glands is seen.
Prolonged gestation with craniofacial defects in the fetus has been reported in Ayrshire, Guernsey, and Jersey breeds of cattle and is thought to be caused by a recessive gene. Affected fetuses cease to grow at 7 mo gestation. There is no spontaneous parturition in affected Guernsey cattle due to the nonfunctional pituitary gland in the fetus. Calves are usually dead when delivered. Some may show evidence of severe abnormalities of the cranium and face.
Prolonged gestation associated with multiple skeletal abnormalities has been reported in Hereford cattle. Affected calves show evidence of pituitary aplasia or hypoplasia. Arthrogryposis, torticollis, kyphosis, and scoliosis are present, and some calves have cleft palates.
Prolonged gestation associated with cloning has been reported in both fetal calves and lambs produced by somatic cell nuclear cloning. Early placental abnormalities have been detected in a high proportion of such animals and placentomegaly may be observed in later pregnancy. The abnormality may result in fetal death or, if the fetus survives, in the large offspring syndrome. Spontaneous birth may not occur, and prolonged gestation results. Fetal lung and maternal mammary development is retarded and can compromise fetal survival.
Although bovine viral diarrhea virus can cause abortion in cattle, it can also produce congenital defects in the fetus. These include cerebellar hypoplasia, anencephaly, and hydrocephaly. Affected calves may be born with severe defects of the CNS, but prolonged gestation occasionally occurs if pituitary function is compromised. The related pestivirus border disease virus (see Congenital and Inherited Anomalies: Border Disease) can produce severe brain and coat abnormalities in fetal lambs. Pituitary compromise in such lambs can lead to prolonged gestation.
Akabane virus (see Congenital and Inherited Anomalies: Akabane Virus Infection), which is found in Africa, Australia, the Middle East, and the Far East, can be transmitted by insects to both pregnant cattle and sheep. Bovine fetuses exposed to the virus at 76–104 days gestation may develop hydranencephaly (fluid-filled cavitation of the brain). Exposure to the virus at 105–174 days of pregnancy may cause both hydranencephaly and arthrogryposis. Affected fetuses may have severe brain damage. The cerebral cortex may be absent and the cranial cavity filled with fluid. Cerebellar hypoplasia may be present, and the brain stem is smaller than normal. Compromise of pituitary function in the affected fetus can lead to prolonged gestation.
Bluetongue virus (see Bluetongue), which is found in Africa, Australia, North and South America, and in parts of Europe, is also transmitted by insects; infection can occasionally cause prolonged gestation. The fetuses of cows exposed to the virus at 60–120 days of pregnancy developed hydranencephaly, while fetuses exposed later in pregnancy developed less severe CNS defects.
Gestation lengths >200 days have been recorded in ewes vaccinated during pregnancy with Rift Valley fever attenuated viral vaccine. Affected lambs developed severe brain defects and skeletal abnormalities. Some ewes developed hydrops amnion by the fourth month of gestation. Ewes in which pregnancy was not terminated developed ketosis.
Several plant toxins cause fetal deformity and prolonged gestation when eaten accidentally or fed experimentally. When fed to sheep in early pregnancy, Veratrum californicum (skunk cabbage) produces fetal deformities, giantism, and prolonged gestation. Cranial defects and brain and eye abnormalities were seen in fetuses of ewes fed this plant at 14 days of gestation; pregnancy length in some cases was >230 days. The plant contains the amine cyclopamine, which is believed to be responsible for the fetal abnormalities. This plant also contains a number of toxic alkaloids that cause GI disturbance, dyspnea, and convulsions in sheep. Veratrum album has similarly caused prolonged gestation and fetal abnormalities in Holstein-Friesian cows in Japan.
An unidentified toxin in the plant Salsola tuberculatiformis (cauliflower saltwort) is thought to cause prolonged gestation in sheep. Pregnancy was extended >220 days, and affected lambs showed atrophy of the pituitary, adrenal, and thyroid glands. Fetuses appear to be most susceptible to the toxin in the first and third trimesters of pregnancy. Amniotic fluid continues to increase in volume in cases of prolonged gestation associated with this plant. Physical abnormalities such as cleft palate prevent normal swallowing of amniotic fluid in affected fetuses. Excessive fetal weight and the weight of accumulated fetal fluids may lead to rupture of the prepubic tendon in ewes.
When a number of cases of prolonged gestation occur in a herd or flock, a full investigation should be mounted in an attempt to identify the cause and possibly a preventive program. A genetic abnormality may be determined by a study of pedigrees or by finding an abnormal karyotype in affected fetuses. Possible exposure to toxic plants and viral infection should be investigated. Tests for evidence of pathogenic viruses or serologic evidence of exposure to them may lead to clear evidence of virus involvement. In some cases, the cause of prolonged gestation remains unknown. Evidence of pituitary hypoplasia or compromise may be found, but the underlying cause remains elusive.
In a case of suspected prolonged gestation, the patient's breeding records, if available, should be checked to ensure that parturition really is overdue. Treatment of a case in which gestation is not genuinely prolonged may result in the delivery of a premature fetus that is unlikely to survive. Once the true length of gestation is established, a full clinical examination of the dam should be conducted.
In cattle, rectal examination of the uterus and its contents is an important diagnostic aid. Fetal parts may be palpable and in some cases it is possible to detect an abnormal cranium. An ultrasonographic scan may confirm the presence of fetal abnormalities including a thin-walled, fluid-filled cranium. The weight of an overdue fetus may cause it to pass under the rumen while still within the uterus, so that it cannot be palpated.
In some animals, prolonged gestation is accompanied by the development of excessive amounts of fetal fluid. The origin of excessive fetal fluid can be assessed by analysis of sodium and chloride levels in an aspirated sample. Amniotic fluid contains approximately 120 mmol/L of sodium and 90 mmol/L of chloride. Allantoic fluid contains 50 mmol/L of sodium and 20 mmol/L of chloride. The correlation between hydrops amnii and hydrops allantois and prolonged gestation is tenuous, however. Most fetal giants suffer from oligoamnios.
In true prolonged gestation, the fetus is unlikely to be of any economic value. Treatment should be aimed at fetal delivery with minimal damage to the dam. In cases of fetal giantism, the dam may be distressed by the weight of her fetus and its associated fluids. Painful edema in front of the udder may indicate rupture or impending rupture of the prepubic tendon. A canvas sling support can be placed around the abdomen to prevent further damage until the pregnancy is terminated. General health of the dam should be assessed and economic considerations discussed with the owner before treatment is attempted.
Successful induction of parturition requires an intact hypothalamic-pituitary-adrenal axis. Pregnancy is maintained in cases of prolonged gestation chiefly by continued production of progesterone by the corpus luteum. Spontaneous induction of birth in cases of prolonged gestation fails as a result of insufficient production of fetal cortisol and the failure of luteolysis to occur. Birth in both cows and sheep can be successfully induced by administering both prostaglandin F2α (or its synthetic analog cloprostenol) and the corticosteroid dexamethasone by IM injection. Luteolysis is induced by the prostaglandin, and the maternal hormone cascade that precedes parturition is initiated by the corticosteroid. In cows, 500 μg cloprostenol and 20 mg dexamethasone are given; in sheep 125 μg cloprostenol and 16 mg dexamethasone are recommended. A single dose of these 2 drugs is normally effective. Parturition should begin in 24–72 hr.
Induced parturition should be monitored carefully. Assistance may be required if there is evidence of uterine inertia or damage to the abdominal wall, either of which might make expulsive efforts ineffective. Fetal malposition requiring obstetric assistance may occur once birth commences. If the fetus is very large, dystocia due to fetal-pelvic disproportion may occur, and assisted delivery by careful traction may be attempted. If this is not possible, cesarean section may be required. If the dam is seriously ill, an elective cesarean without an attempt at vaginal delivery may be considered if the patient is considered well enough to withstand surgery. Fetal dysmaturity can be a problem, especially in very valuable cloned offspring, and intensive care facilities may be needed.
After fetal delivery, uterine involution may be encouraged by administration of oxytocin. Retention of fetal membranes is managed in the usual way (see Retained Fetal Membranes in Large Animals). Fluid therapy, antibiotics, and treatment with NSAID such as flunixin meglumine may aid recovery.
Last full review/revision July 2011 by Peter G. G. Jackson, MA, BVM&S, DVM&S, FRCVS