Pregnancy Disease

W. A. ANDERSON AND C. L. DAVIS.

PREGNANCY disease is a highly fatal metabolic disorder of ewes. It occurs during the fourth or fifth (last) month of pregnancy and is associated with an inadequate supply of carbohydrates.

It affects older ewes, particularly those carrying twins or triplets, but occasionally an animal bearing a single large fetus will succumb. The disease occurs wherever sheep are raised. It has been reported from all parts of the United States and in Australia, South Africa, Canada, Great Britain, and Europe. In this country it is primarily a disease of small farm flocks; large bands of range sheep are seriously affected less often.

Symptoms include lambing paralysis, hypoglycemia, preparturient paresis of ewes, staggers, and old ewe disease. Ketosis is probably the most satisfactory term that has been suggested, because the condition in ewes bears a physiological similarity to that disease in cattle.

Death losses are severe. It is estimated that 90 percent of the animals showing visible symptoms die. O. H. Muth and J. N. Shaw, of the Oregon Agricultural Experiment Station, have reported that losses reached 10 percent and sometimes 20 percent in bands of ewes in that State. To the loss from the death of a ewe must be added the potential value of the unborn lambs and the disruption of management practices that follows a lamb crop smaller than expected. Thus the overall economic loss involved makes this disease one of the outstanding hazards of the sheep industry.

It was formerly believed that pregnancy disease chiefly involved fat ewes, but further experience has shown that animals in poor condition also are frequently affected. The disease is definitely associated with an insufficient or unbalanced diet. This may be complicated by lack of exercise, the effects of parasitism, or exposure.

The essential cause of pregnancy disease is an insufficient intake of carbohydrates. The conditions under which that may occur are fairly well understood. A particular blood-sugar level necessary to meet the normal metabolic requirements is supplied primarily by the carbohydrates and to a lesser extent by fats and proteins.

In late pregnancy, the nutritional demands of the fetus upon the pregnant animal are extremely high and are increased by the added requirements of twins or triplets. When for any reason carbohydrates in the diet become inadequate, the blood-sugar level is lowered, and pregnancy disease develops.

Regardless of whether the disease occurs in fat animals or in thin and poorly nourished animals, the pathology is the same. Only the predisposing conditions differ. In well-nourished animals an attack may be precipitated by cessation of feeding because of storms, a radical change in diet that lowers appetite, irregular feeding, or the upsets of a long drive or railroad journey. Outbreaks have developed when owners, thinking their animals were too fat, reduced the rations. Lack of exercise is also a contributing factor in fat ewes.

Most cases, however, develop in sheep that are in poor condition and on inadequate diets, such as straw, cornfodder, wild hay, or poor pasture, and too little grain. The increasing demands of the growing fetuses finally become too great for the limited supply of carbohydrates, and pregnancy disease results.

R. F. Bourne, formerly of Colorado Agricultural and Mechanical College, in his discussion of the physiology of pregnancy disease, pointed out that the body's supply of carbohydrate is represented by the relatively small amounts of sugar in the blood and lymph. In addition, there is a considerable reserve of glycogen stored in the various tissues, 80 percent of which is in the liver and skeletal muscle. When the intake of carbohydrate is insufficient to meet the increasing demands, the liver gives up glycogen to make up the deficit. The glycogen in the liver cells is then replaced by fat, which may increase from a normal 3 percent to as much as 30 percent by weight in that organ. The reserve glycogen stored in the muscle is not immediately available for use but is released in the form of lactic acid under the influence of exercise and is utilized to replenish the depleted supply of glycogen in the liver. That helps explain the well-established value of moderate exercise in the prevention of pregnancy disease, particularly in fat ewes.

As the reserves of glycogen are depleted, the body turns increasingly to the fats as a source of body energy. Fats, however, burn well only in the presence of an adequate amount of blood sugar, and since this is low, the resultant imperfect metabolism evolves quantities of unburned intermediate products, known as ketone bodies. The ketone bodies accumulate first in the blood and later in the urine, and are always present in pregnancy disease. The resultant ketosis further depresses the appetite, and the already damaged liver cannot efficiently utilize the fatty acids for energy in place of glycogen. The condition thus becomes progressively worse, the animal becomes comatose, and a fatal toxemia develops.

THE FIRST SYMPTOMS are loss of appetite, dullness, and an inclination to lag behind and remain outside the flock. The ewe becomes unsteady and urinates frequently. There is grinding of the teeth and labored breathing.

Vision is impaired, and blindness may result. There is a tendency to walk in circles or push against some solid object. Finally, the ability to stand is lost; in a few hours or at most in 1 or 2 days, the animal becomes prostrate.

The ewe remains recumbent in a comatose condition, sometimes on her side but more frequently lying on the breast, with the head turned to one side. Occasionally the fetuses are delivered, in which case recovery is prompt. Otherwise the disease is fatal in 1 to 7 days. The temperature remains normal throughout the course of the disease. The urine is usually acid and becomes strongly positive for ketone bodies.

Almost invariably more than one fetus is found at autopsy. The most striking pathologic change is in the liver, which is light yellow, friable, and perhaps mottled. The cut surface is found to be greasy as a result of the fatty infiltration. In extreme cases, because of the high fat content, it will be found that pieces of liver will float in water. The kidneys and sometimes the heart show microscopic evidence of fatty infiltration, but usually no gross changes are evident.

THE MANAGEMENT of pregnancy disease resolves itself into two phases prevention and treatment.

Pregnant ewes should be fed an abundance of a balanced ration, which must be increased during the last 2 months of gestation. It may consist of good pasture or a liberal amount of legume hay, such as alfalfa or clover. The amount of grain fed should not be less than one-half pound, and may be gradually increased to 1 pound during the last month of pregnancy. It is desirable that the ewe herself should be gaining some weight in addition to the. weight of the fetus.

In the face of an outbreak it is advisable to supplement the grain mixture by adding directly to it small amounts (up to one-fourth pound) of blackstrap molasses or corn sugar (dextrose).

Radical changes in diet should be avoided. Intake should not be cut sharply Care should be taken that the sheep do not go unfed during periods of storm or while being shipped. A moderate amount of exercise is important. An adequate water supply should be provided. A constant supply of salt is desirable.

The theory of treatment is simple: It is necessary to raise and maintain the sugar level of the blood. In practice, however, treatment on an economically feasible basis is difficult.

Loss of appetite is a constant symptom, and force feeding, is necessary until the animal again begins to eat. That may be done by injections of dextrose (in a 10 percent solution) intravenously, intraperitoneally, or subcutaneously. Dextrose or molasses in water may be given by mouth, but, since a comatose sheep may be unable to swallow, it should be administered by a stomach tube. Injections must be given daily or, if treatment is by stomach tube, 2 or 3 times a day.

It is evident that the treatment of affected sheep involves considerable time, labor, and expense, and the results generally have not been encouraging. Most of the ewes that are down and comatose eventually die, but a reasonable proportion of those showing symptoms but still on their feet may be expected to recover. Probably the chief benefit of adding sugar to the ration derives from tiding over ewes that are starting to show symptoms.

Other treatments that have been used on an experimental basis include injections of adrenocorticotropic hormone (ACTH) and cortisone. The value of concentrated vitamins, injectable amino acids, and rumen inoculation is also being investigated. Those treatments, alone or in combination, show promise, but they are costly.

W. A. ANDERSON is a veterinarian at the Animal Disease Research Laboratory, Denver, Colo. He received his degrees from Colorado Agricultural and Mechanical College and Purdue University and has been associated with the Department of Agriculture since 1936.

C. L. DAVIS received his degree in veterinary medicine from Colorado Agricultural and Mechanical College in 1921. In 1922 he joined the Bureau of Animal Industry of the Department of Agriculture.