Parturient paresis in pregnant and lactating ewes and does is a disturbance of metabolism characterized by acute hypocalcemia and rapid development of hyperexcitability and muscle tremors, which then progress to paresis, depression, recumbency, coma, and death. Unlike parturient paresis in dairy cattle, which primarily occurs on the day of calving, the disease in ewes and does occurs before and after parturition, with few cases occurring on the day of parturition.
The cause is a sudden decrease in calcium intake under conditions of increased calcium requirements. This results in a low serum calcium concentration, particularly in animals with multiple fetuses or those that are heavily lactating. Some cases are complicated by concurrent hypophosphatemia and hyper- or hypomagnesemia. The disease can occur at any time from 6 wk before to 10 wk after parturition; however, due to the rate of calcification of fetal bones, the greatest demand for calcium for sheep and goats occurs 1–3 wk prepartum, particularly when 2 or more fetuses are present in utero. Whenever an abrupt decrease in calcium intake occurs, the body requires 24–72 hr to activate the metabolic machinery necessary to mobilize stored calcium. Mobilization of stored calcium can be inadequate to meet the animal's needs in older ewes and does, and in animals with chronic calcium deficiency, such as animals on prolonged grain feeding during times of drought.
Clinical Findings and Diagnosis
Characteristically, the disease occurs in outbreaks with most cases in late gestation. The incidence is usually <5%, but in severe outbreaks, 30% of the flock may be affected at one time. The onset is sudden and almost invariably follows—within 24 hr—an abrupt change of feed, a sudden change in weather, or short periods of fasting imposed by circumstances such as shearing, crutching, or transportation (also see Transport Tetany in Ruminants). In early hypocalcemia, a stiff gait or muscle tremors, constipation, and depressed rumen motility may be evident. As the disease progresses, clinical signs include an increased heart rate (but a decrease in the intensity of the heart sounds), bloat, depression, recumbency, and eventually, if untreated, death.
Diagnosis is based on the history and clinical signs, particularly weakness, depression, ruminal hypomotility or atony, and decreased intensity of heart sounds on thoracic auscultation. In outbreaks occurring before lambing, pregnancy toxemia (see Hepatic Lipidosis: Pregnancy Toxemia in Ewes) is the main differential diagnosis. These diseases may also occur concurrently. A tentative diagnosis of acute hypocalcemia can be confirmed readily by a dramatic and usually lasting response to slow IV administration of calcium.
Treatment and Prevention
Treatment should be initiated immediately, usually as IV calcium borogluconate (50–150 mL of a 23% solution). Oral administration of a calcium gel or the SC administration of calcium solutions helps prevent relapse. During treatment, the heart should be monitored, and therapy slowed or stopped if arrhythmias occur. An alternative mode of therapy would be to add 50–150 mL of a 23% calcium borogluconate or gluconate solution to 1 L of a 5% dextrose solution. Dietary modifications useful for the prevention of milk fever in dairy cattle may be of value in dairy sheep and goats. Therefore, reducing or eliminating diets rich in cations (alfalfa), clovers, or supplemental calcium and phosphorus in the late dry period may aid in prevention. Immediately after parturition, the calcium levels in the diet should be increased. Movement, periods of inadequate dietary intake, heavy parasite burdens, or other forms of stress should be minimized in sheep during the final 8 wk of gestation.
Last full review/revision July 2011 by Peter D. Constable