Pregnancy Toxemia in Sheep and Goats

The primary predisposing cause of pregnancy toxemia in sheep and goats is inadequate nutrition during late gestation, usually because of insufficient energy density of the ration and decreased rumen capacity as a result of fetal growth.

In the last 4 weeks of gestation, metabolizable energy requirements rise dramatically. For example, the energy requirement of a 70-kg ewe carrying a single lamb is 2.8 Mcal/day in early gestation, compared with 3.45 Mcal/day in late gestation (ie, a 23% increase). This change is more dramatic in ewes bearing twins, with an energy requirement of 3.22 Mcal/day in early gestation and 4.37 Mcal/day in late gestation (36% increase), and in ewes bearing triplets, with an energy requirement of 3.49 Mcal/day in early gestation and 4.95 Mcal/day in late gestation (42% increase). Dairy goats have similar changes in energy requirements.

In late gestation, the liver increases gluconeogenesis to facilitate glucose availability to the fetuses. Each fetus requires 30–40 g of glucose/day in late gestation, which represents a substantial percentage of the ewe’s glucose production and which is preferentially directed to supporting the fetuses rather than the ewe. Mobilization of fat stores is increased in late gestation as a way to assure adequate energy for the increased demands of the developing fetuses and impending lactation. However, in the circumstance of negative energy balance, this increased mobilization may overwhelm the liver’s capacity and result in hepatic lipidosis, with subsequent impairment of function. Additionally, twin-bearing ewes appear to have more difficulty producing glucose and clearing ketone bodies, thus increasing their susceptibility to pregnancy toxemia.

Females with a poor body condition score (BCS ≤2/5) or that are overconditioned (BCS ≥4/5) and carrying more than one fetus are most at risk of developing pregnancy toxemia, although the condition can occur even in ideally conditioned ewes on an adequate ration.

Susceptible, thin ewes or does develop ketosis because a chronically inadequate ration is offered or because other diseases (eg, lameness or dental disease) limit intake. With increasingly insufficient energy to meet increasing fetal demands, the ewe or doe mobilizes more body fat, with resultant ketone body production and hepatic lipidosis.

Overconditioned animals may have decreased appetites, and adipose mobilization quickly overwhelms the liver’s capacity, resulting in hepatic lipidosis. In addition, there may be a population of animals less responsive to insulin production when nutritional intake is inadequate. Ewes fitting these criteria may quickly shift from subclinical ketosis to clinical pregnancy toxemia if feed intake is acutely curtailed by such events as adverse weather, transport, handling for shearing or preventive medication, or other concomitant disease (footrot, pneumonia, etc).

These variants of pregnancy toxemia have been termed primary pregnancy toxemia (thin ewes and inadequate nutrition), estate ketosis (overconditioned ewes), and secondary pregnancy toxemia (ewes suffering from other disease). Dairy does often experience ketosis after kidding (serum beta-hydroxybutyrate [BHB] >1.7 mmol/L), which may or may not be connected with pregnancy ketosis before kidding. Ketosis after kidding appears to be more common in herds fed a complete pelleted ration.

Early clinical signs of pregnancy toxemia can be detected by an observant producer. Most cases develop 1–3 weeks before parturition. Onset earlier than day 140 of gestation is associated with more severe disease and increased risk of death. Selective anorexia or decreased drive to eat at feeding, particularly with grain consumption, indicates a problem. Animals will spend more time recumbent and have more frequent bouts of lying than their healthy herdmates. As the disease advances, ewes or does may also develop clinical signs of listlessness, aimless walking, muscle twitching or fine muscle tremors, opisthotonos, and grinding of the teeth. This progresses (generally over 2–4 days) to blindness, ataxia, and finally sternal recumbency, coma, and death. Cerebral hypoglycemia coupled with ketosis, ketoacidosis, and reduced hepatic and renal function lead to clinical signs and fetal death. Blood glucose concentration may return to normal or even become high terminally, possibly indicating fetal death. Septicemia develops in the ewe or doe after fetal death.

• Clinical signs of selective anorexia in late gestation

• Definitive diagnosis via laboratory tests

Pregnancy toxemia may be suspected based on history and clinical signs, particularly selective anorexia in late gestation.

Laboratory findings of pregnancy toxemia in individual patients may include hypoglycemia (often < 2 mmol/L), increased urine ketone concentrations (evaluated by commercial qualitative test strips), increased serum BHB concentrations (normal < 0.8 mmol/L, subclinical ketosis ≥0.8 mmol/L, and clinical disease >3 mmol/L), and occasionally hypocalcemia. Hypoglycemia is not a consistent finding, with up to 40% of cases having normal glucose concentrations and up to 20% having hyperglycemia. If the diagnosis needs further confirmation, cerebrospinal fluid glucose concentrations may be more accurate than blood glucose concentrations; they remain low even when serum glucose concentration rebounds in advanced cases after fetal death. Concentration of BHB is a more reliable indicator of disease severity than are blood glucose concentrations. Nonesterified fatty acids concentration can also be increased above 0.4 mmol/L, indicating likely hepatic lipidosis, resulting in impaired hepatic function.

Although hypocalcemia is common in cases of pregnancy toxemia, it should also be considered when formulating hypotheses regarding recumbent late gestational sheep and goats. This is similarly true with hypomagnesemia, which is a common finding in cases of pregnancy toxemia; however, it should also be considered as a differential diagnosis for periparturient CNS disease. Other CNS diseases to be considered include polioencephalomalacia, pulpy kidney disease (enterotoxemia), rabies, scrapie, maedi-visna and ovine progressive pneumonia, lead toxicosis, chronic copper toxicosis, and listeriosis. These can be differentiated based on clinical and laboratory findings or during postmortem examination.

• Administration of energy sources and removal of factors causing reduced energy availability

• Increased care of the newborn offspring

Ewes or does in the early stages of pregnancy toxemia (ie, ambulatory, decreased appetite for grain, and few CNS clinical signs) can often be treated successfully with propylene glycol (60 mL, PO, every 12 hours, for 3 days, or 100 mL/day). Adding oral supplementation with calcium (12.5 g calcium lactate) and potassium (7.5 g KCl) and administration of protamine zinc insulin (0.4 U/kg, SC, every 24 hours) increases survival rates. Commercial calf electrolyte solutions containing glucose may also be given by stomach tube at a dose of 3–4 L, every 6 hours, or drenched as a concentrated solution.

It may also be prudent to induce parturition or abortion if the ewe or doe is also thin or overconditioned and cannot manage fetal demands late in pregnancy. This can be done by administering dexamethasone (20 mg, IV or IM). Parturition is expected within 24–72 hours, with most animals giving birth within 36 hours. Does may also benefit by the addition of prostaglandin F2alpha (dinoprost [10 mg, IM] or cloprostenol [75 mcg/45 kg]). Contributing factors (eg, nutrition, housing, illness, and other stressors) should be corrected for the group, and feeding management assessed (eg, adequate feeder space, feeding frequency, and protection from adverse weather).

Treatment of advanced cases of pregnancy toxemia is frequently unrewarding. If a ewe or doe is already comatose, euthanasia is warranted, and treatment should focus on the rest of the flock. However, if the female is valuable and the owner wishes to pursue treatment despite the poor prognosis, then aggressive treatment should be directed against the ketoacidosis and hypoglycemia. Before starting treatment, it should be determined whether the fetuses are alive (eg, via real-time or Doppler ultrasonographic examination). If the fetuses are alive and within 3 days of a calculated due date (gestation length, 147 days), then an emergency cesarean section may be considered if economically viable. If the fetuses are dead or too premature to survive a cesarean section, it is less stressful to the ewe or doe to induce early parturition with dexamethasone. Antimicrobial therapy (usually procaine penicillin G at 20,000 U/kg, IM, every 24 hours for up to 5 days) is appropriate if the fetuses are thought to be dead.

Hypoglycemia can be treated by a single injection of 50% dextrose (60–100 mL, IV), followed by fluid therapy with balanced electrolyte solution with 5% dextrose. Intravenous drips and lower dextrose concentrations in solution might cause less of a diuretic effect; however, this is often impractical in a field setting. Repeated IV boluses of glucose should be avoided because they may result in a refractory insulin response. Protamine zinc insulin can be administered (20–40 U, IM, every other day). Calcium (50–100 mL of a commercial calcium gluconate or borogluconate solution, SC) can be administered safely without serum biochemistry data. If serum biochemical analysis demonstrates hypocalcemia, ~50 mL of a commercial calcium solution can be administered by slow IV injection while monitoring the heart rate and rhythm. Oral administration of potassium chloride (KCl) is also indicated because serum potassium concentrations are often decreased. Administration of flunixin meglumine at 2.5 mg/kg improves survival rate of ewes and their lambs, although the mechanism is unknown. Although aggressive treatment and intensive nursing care may be successful, it is not unusual to see case fatality rates >40%. Given the cost, it is prudent to share the guarded prognosis with owners before undertaking treatment.

A sample of late-gestation ewes or does can be tested for serum BHB concentrations to determine the extent of the risk in the rest of the flock. Generally, 10–20 animals in late gestation should be sampled (3%–20% of the pregnant flock). The risk of the flock can be determined based on the mean value of these results: normal (low risk), 0–0.7 mmol/L; moderate underfeeding (moderate risk), 0.8–1.6 mmol/L; and severe underfeeding (high risk), 1.7–3.0 mmol/L. Other diseases (eg, footrot) should be treated; administration of anthelmintics, to cover a broad spectrum against trematode and nematode parasites, might also be beneficial. Females off feed should be separated from the group and hand fed. For their comfort, they should be able to see the group.

Ewes or does should not enter the last 6 weeks of gestation with a BCS < 2.5/5; this can be prevented by good feeding management (eg, adequate feeder space for pregnant animals, sorting [based on body condition, fetal numbers, and animal size], forage analysis [for energy, digestible fiber, and protein]), and ration formulation). During the last 6 weeks of gestation, grain is required as a source of carbohydrates in the ration to maintain the health of multiple-bearing females. Amount varies depending on forage quality, adult body weight and condition score, and number of fetuses; however, protein must also be balanced for rumen microbes to make optimal use of available carbohydrates.

Producers should ideally assess body condition at breeding and midgestation, usually at the time of ultrasonographic pregnancy evaluation, so that thin animals can be fed as a separate group. It takes ~6 weeks to raise BCS by 1 point, so early intervention is important to avoid problems in late gestation.

If real-time ultrasonographic examination allows for fetal number determination, then animals should also be managed based on fetal numbers. With prolific breeds, triplet-bearing ewes and thin, twin-bearing ewes can be fed together. Because of the added energy young animals need for growth, producers may find it convenient to feed pregnant ewe-lambs or doelings along with twin-bearing females and thin, single-bearing females.

Overconditioned females (ie, BCS ≥4/5) are not as common but may be seen in small hobby flocks. Overweight and obese females are much less responsive to treatment, and owners should be advised on how to avoid the problem via proper feeding management. However, late pregnancy is not the time to decrease body condition in overconditioned females. Serum BHB concentration can be used as a flock screening test to detect flocks at risk of pregnancy toxemia. If the number of fetuses in the pregnancy has not been determined, a concentration of 0.8 mmol/L should be considered to distinguish animals at higher risk to develop the disease. Otherwise, if the number of fetuses has been determined, BHB concentration in blood should be measured only in animals with multiple fetuses; in this case, the cutoff to be used for identifying animals at risk is 1.1 mmol/L.

Effective anthelmintic treatment, especially in farms with high parasitic burdens, would further contribute to prevention of the disease.

• LeValley S. Fact Sheet No. 1.630: Pregnancy Toxemia (Ketosis) in Ewes and Does. Colorado State University Extension, 2010.