Parturient paresis in pregnant and lactating sheep and goats is a metabolic disturbance characterized by acute-onset hypocalcemia and rapid development of hyperexcitability, altered gait, weakness, tremors, and ataxia, progressing to depression, recumbency, coma, and death. It can occur any time from 6 weeks before parturition to 10 weeks after parturition. When prepartum, it is typically due to high calcium demands associated with fetal skeletal mineralization and often co-occurs with energy or macromineral deficiencies. Postpartum parturient paresis in high-producing dairy goats is due to calcium loss associated with milk production. Diagnosis is based on clinical signs of recumbency and response to treatment with IV or subcutaneous calcium. Prevention includes adequate pre- and postpartum nutrition and stress reduction.
Parturient paresis in pregnant and lactating sheep and goats is a metabolic disturbance characterized by acute-onset hypocalcemia and rapid development of hyperexcitability and ataxia, progressing to depression, recumbency, coma, and death. Unlike parturient paresis in dairy cows, which primarily occurs within a few days of calving, the condition in ewes and does can occur up to 6 weeks before lambing; however, high-producing dairy does often succumb in the weeks after kidding. This condition may be underdiagnosed in some situations.
Etiology of Parturient Paresis in Sheep and Goats
Parturient paresis in sheep and goats is due to decreased calcium intake under conditions of increased calcium requirements, usually during late gestation. This combination of factors results in low serum calcium concentration, particularly in animals pregnant with multiple fetuses. Some cases are complicated by concurrent pregnancy toxemia, hypomagnesemia, or hypophosphatemia. Ewes that are both hypocalcemic and ketotic may not be able to produce endogenous glucose as readily as ewes that are only ketotic; therefore, the risk for developing more severe pregnancy toxemia is greater when both conditions are present.
Parturient paresis can occur any time from 6 weeks before parturition to 10 weeks after parturition; however, the greatest demand for calcium in nondairy animals occurs 3–4 weeks before parturition, because of fetal skeletal mineralization, particularly when multiple fetuses are present in utero. In high-producing dairy goats, parturient paresis typically occurs 1–4 weeks after parturition, as a result of calcium loss through milk production.
Whenever an abrupt decrease in calcium intake occurs, the body requires 24–72 hours to activate the metabolic mechanisms necessary to mobilize stored calcium. Mobilization of stored calcium can be inadequate to meet an animal’s needs, especially in older ewes and does, animals with chronic calcium deficiency, and animals fed calcium-deficient diets.
Examples of forages with low calcium content include cereal hays or pasture, poor-quality grassy hays and pasture, and corn silage. Most grains also contain minimal calcium; in addition, they have a high phosphorus content, which can lead to an inverse dietary calcium:phosphorus ratio, increasing dietary risk. Vitamin D deficiency, which occurs in housed ruminants during winter months, also depresses calcium absorption from the GI tract.
Clinical Findings and Diagnosis of Parturient Paresis in Sheep and Goats
Timing (late gestation or the postpartum period) coupled with altered gait, tremors, recumbency
Positive response to calcium administration
Low calcium concentration in blood (< 1.2 mmol/L [5.0 mg/dL])
Typically, parturient paresis in sheep and goats occurs in outbreaks; however, it is not uncommon for individual animals to be affected. Usually, < 5% of animals are affected; however, severe outbreaks may involve up to 30% of the flock.
In most cases, parturient paresis occurs in the last few weeks of gestation. Onset is sudden and often follows—within 24 hours—an abrupt change of feed, a sudden change in weather, or short periods of fasting imposed by circumstances such as shearing or transportation (also see Transport Tetany in Ruminants).
In early parturient paresis in ewes, the most common clinical signsare the following:
stiff gait
ataxia
salivation
constipation
depressed rumen motility, progressing to bloat
In addition, tachycardia may be present in affected ewes; heart sounds are quieter than normal. Often, when recumbent, ewes are in a sternal froglike position, with the hindlegs extended caudally.
Goats have a similar presentation; however, muscle tremors are more common in does than in ewes.
A working diagnosis of parturient paresis in sheep and goats is based on history and clinical signs. In outbreaks occurring before parturition, pregnancy toxemia is the main differential diagnosis. These two diseases may also occur concurrently. A tentative diagnosis of acute hypocalcemia is supported by an immediate, dramatic, and usually lasting response to slow IV administration of calcium.
Diagnosis can be confirmed by testing serum calcium concentration before treatment. Urine ketone concentration or serum beta-hydroxybutyrate concentration should always be evaluated at the same time as serum calcium concentration.
Clinical hypocalcemia (parturient paresis) in sheep and goats is often defined as a total serum calcium concentration < 1.2 mmol/L (5.0 mg/dL). Normal values for total serum calcium concentrations are 2.9–3.2 mmol/L (11.5–12.8 mg/dL) for sheep and 2.2–2.9 mmol/L (8.9–11.7 mg/dL) for goats (1).
Animals with low serum albumin concentration, as occurs with Johne's diseaseand clinical severe GI parasitism, may have low total serum calcium and normal ionized calcium concentrations.
Treatment and Prevention of Parturient Paresis in Sheep and Goats
IV or SC calcium administration
Provision of adequate dietary calcium throughout gestation
Treatment of parturient paresis in sheep and goats should begin immediately. Standard treatment is usually one of the following (2, 3):
calcium borogluconate, IV (50–100 mL of a 23% solution, once)
calcium borogluconate, SC (30–60 mL of a 23% solution, once) if venous access is not available
IV administration must be performed slowly, over 5–7 minutes, whereas subcutaneous calcium can be administered quickly.
Given that hypocalcemia in sheep and goats is also concurrent with other macromineral or energy deficiencies, calcium-containing products that also contain phosphorus and magnesium, as well as dextrose, might have additional therapeutic value; however, solutions containing dextrose should not be administered subcutaneously, because they can irritate tissue. Oral or subcutaneous administration of a calcium solution helps to prevent relapse; however, dosage and administration frequency have not been well studied.
During treatment with IV calcium, the heart should be monitored, and treatment should be stopped if arrhythmias occur.
For ease of IV administration, it may be preferable to increase the volume of the product by adding 50–100 mL of a 23% calcium borogluconate or gluconate solution to 1 L of a 5% dextrose solution and administer this volume over 10 minutes.
Calcium solutions are irritating, so when administration is subcutaneous, the total volume should be divided into two or three equal quantities and administered to different parts of the body.
Calcium administration (subcutaneous or IV) can be repeated after 24 hours.
Dietary modifications to increase the dietary calcium:phosphorus ratio (> 1.5:1) and to ensure that the total amount of dietary calcium (and vitamin D) meets National Research Council requirements may help prevent further cases in pregnant animals. (Also see Nutritional Requirements of Sheep and Nutritional Requirements of Goats.) Sudden dietary changes or other stressors should be avoided during late gestation, and risk factors for pregnancy toxemia should be investigated.
Key Points
Parturient paresis in sheep and goats is a metabolic disease occurring mostly around the time of parturition.
Diagnostic confirmation is via rapid response to calcium administration in recumbent parturient animals.
IV calcium administration is effective but should be performed with appropriate caution.
Prevention is based on proper nutrition during gestation and early lactation.
References
Smith BP, Van Metre DC, Pusterla N, eds. Large Animal Internal Medicine. 6th ed. Elsevier Mosby; 2020.
Smith MC, Sherman DM. Nutrition and metabolic diseases. Goat Medicine. 3rd ed. Wiley-Blackwell; 2022:chap 19.
Pugh DG, Baird AN. Feeding and nutrition. Sheep, Goat, and Cervid Medicine. 3rd ed. Elsevier; 2020:chap 2.
