Parturient paresis in pregnant and lactating ewes and does/MILK FEVER

Parturient paresis in pregnant and lactating ewes and does is a disturbance of metabolism characterized by acute hypocalcemia and rapid development of hyperexcitability, ataxia, paresis, coma, and death.

Etiology:

The exact cause is unknown, but the conditions under which field outbreaks occur are fairly well defined. Low concentrations of serum calcium are found in heavily lactating animals or those with multiple fetuses. Some cases are also complicated by hypophosphatemia and hyper- or hypomagnesemia. The disease occurs at any time from 6 wk before parturition to 10 wk after. Due to calcification of fetal bones, the greatest demand for calcium for nondairy animals occurs 3-4 wk prepartum, particularly if >1 fetus is present in utero. Whenever an abrupt calcium demand occurs, the body requires 24-72 hr to activate the metabolic machinery necessary to mobilize stored calcium. High intake of calcium, phosphorus, or some cations (potassium, sodium) may decrease the production of parathyroid hormones. During decreased parathyroid function, less 1,25-dihydroxycholecalciferol is produced, resulting in lowered absorption and mobilization of calcium from the intestines and bones, respectively.

Clinical Findings and Diagnosis:

Characteristically, the disease occurs in outbreaks with more 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.  In early hypocalcemia, a stiff gait or ataxia, tremors, tetany, constipation, and/or depressed rumen motility are seen. As the disease progresses, signs include increased heart and respiratory rates, regurgitation of rumen contents, bloat, depression, and eventually, if untreated, opisthotonos and/or death. Diagnosis is based on the history and clinical signs. In outbreaks occurring before lambing, pregnancy toxemia ( 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 calcium therapy.

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. The more hypocalcemic an animal is (ie, the worse the clinical signs are), the more cardiotoxic the intravenously administered calcium becomes. 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.