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"Metabolic and Nutritional Diseases"

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Metabolic and Nutritional Diseases

By: "Goat Handbook, United States, 1992"
Original Document: Web Site

  • About the Author
  • 1) PREGNANCY TOXEMIA
    Also known as pregnancy disease, ketosis or twin lamb disease. Pregnancy toxemia is a metabolic disease of goats and sheep in late pregnancy. Factors important in the development of the disease are: (1) Presence of two or more fetuses; (2) Undernourishment during late pregnancy when the fetuses have the most rapid growth; (3) Addition of stress such as severe weather, sudden changes in feed, other disease or transportation upon the previous factors. The disease usually appears in the last 30 days of pregnancy and is more common after the first pregnancy. The does show signs of ketonemia, ketonuria, acidosis and central nervous system involvement. The mortality rate is high in affected animals. Most information available is the result of studies in sheep.

    2) Cause
    As pregnancy progresses, an increasing demand is on the available blood glucose supply of the doe or ewe because of fetal development. The principal source of energy to the fetus is glucose and utilization by the fetus occurs at the detriment of the mother. Glucose requirements during late pregnancy are increased 70-800ver the nonpregnant state since 800f fetal growth occurs during the last 40 days of pregnancy. Blood sugar levels decrease as pregnancy progresses (hypoglycemia) from a normal 35-45 mg per 100 ml blood to 20-25 mg per 100 ml blood in late pregnancy. Pregnancy toxemia may develop when levels decrease to about 18 mg per 100 ml blood. The severity of hypoglycemia will be directly affected by undernourishment of the mother or by increased requirements of the fetus(es).

    3)
    As the glucose supply diminishes from increasing fetal demands and decreased glucose production due to undernourishment, energy requirements are furnished by other metabolic pathways, i.e. from free fatty acids and amino acids. Breakdown of the free fatty acids results in increased production of ketones, acetoacetate and B-hydroxybutyrate. As hypoglycemia becomes more severe, the ketone level in the blood increases (ketonemia) and ketosis occurs.

    4)
    As ketosis increases, the bicarbonate level in the blood decreases and acidosis may result. When the bicarbonate level declines sufficiently, the animal will become comatose. During the later stages of pregnancy toxemia, water consumption decreases, urine output is decreased and kidney function is impaired. The blood sugar level may increase severely (hyperglycemia) during the late stages of the disease as a result of the response of the adrenal glands to stress.

    5)
    Circumstances which cause severe hypoglycemia will usually result in pregnancy toxemia. Under-nourishment of the doe may not meet the demands for glucose production. The level of nutrition should be increasing as pregnancy progresses so that the doe will be able to provide fetal requirements. The doe should be gaining weight during pregnancy. As previously mentioned, multiple fetuses greatly increase the glucose requirements. A gradual onset of undernourishment, as would be seen if the feed intake was not increased during pregnancy, may be tolerated by the doe and toxemia may not develop. However, if the animal is starved for several days, pregnancy toxemia may develop readily. Sudden changes in weather, infections or transport may result in periods of inappetence and may trigger pregnancy toxemia. Excessively fat animals may develop periods of poor appetite under stressful situations.

    6) Clinical Signs
    Clinical signs are those observed with involvement of the central nervous system. Initially, the animal tends to separate from others. There is mild depression. Evidence of blindness develops, the animal runs into objects, shows little or no reaction when approached, and wanders aimlessly. Dullness and depression become progressively severe. There is reluctance to move. Eventually they go down in sternal or lateral recumbency and show little or no response to their environment. The does become comatose and eventually die.

    7)
    Occasionally, animals may show a short period or intermittent periods of hypersensitivity. There may be quivering, twitching of the ears, muzzle or eyelids or spasms of certain muscles. Incoordination may be evident. Recumbent animals may have convulsive paddling movements.

    8)
    Chewing, teeth grinding or vigorous licking movements may be seen. Mild scouring may be present. A snuffling respiration due to excessive nasal secretion may be common. Drooling of saliva is also seen.

    9)
    Temperature and pulse are within normal limits. Respiration is usually normal until the later stages when it may become labored. The appetite is poor or absent. Ketones may be detected in the urine. 10)
    In some herds, 200r more may be affected. Mortality may reach 80 Some may recover spontaneously following parturition or abortion.

    11) Post Mortem Findings
    The liver is enlarged and has a pale yellow to orange coloration. The adrenal glands may be enlarged. The uterus contains two or more fetuses.

    12) Treatment
    Oral administration of glycerol or propylene glycol or intravenous administration of glucose may be effective in the early stages of the disease. Insulin may be used with these treatments for better utilization of glucose. During the late stages of the disease, glucose administration may be ineffective or detrimental because the blood glucose levels may be very high.

    13)
    During the later stages of the disease, acidosis and dehydration may be important factors. Intravenous administration of large volumes of electrolyte solutions with sodium bicarbonate may be important. Corticosteroids may not be effective in the later stages unless given at dosages utilized to combat endotoxic shock.

    14)
    Cesarean section or other methods of terminating pregnancy may be effective in some cases.

    15) Prevention
    An adequate nutritional level throughout the pregnancy will prevent pregnancy toxemia. Protein and energy levels during the last 30-40 days of pregnancy should meet the doe's maintenance requirements as well as the growth requirements of the fetuses. Allowing the animal to become excessively fat should be avoided.

    16) Management during late pregnancy should be directed at avoiding appetite problems in the animals. Avoid sudden feed changes, diminish stresses of severe weather, delay or avoid transportation and prevent concurrent disease problems.

    17) Parturient Hypocalcemia
    Also known as milk fever. Parturient hypocalcemia is a metabolic disease in does following kidding characterized by poor milk production, poor appetite, lethargy and low blood calcium levels. A hyperirritability characterized by tetany may occasionally occur.

    18) Cause
    Much research has been done on hypocalcemia in dairy cows but knowledge is still incomplete.

    19)
    Following kidding, most does may have a lowered calcium level in the blood (hypocalcemia). This is partially due to the drain on available calcium by the production of colostrum. (Colostrum contains twice as much calcium as milk). Calcium is supplied from two sources: 1) dietary; 2) mobilization of calcium from the bone. Normally, calcium requirements following kidding are provided primarily from the diet since mobilization of calcium from the bone does not provide significant amounts until about 10 days after parturition. A loss of gastrointestinal function for any reason, before or at parturition, may cause a severe drop in the blood calcium level. Signs of hypocalcemia may develop. Since older animals have more digestive upsets at parturition, they have more problems with hypocalcemia.

    20)
    A high level of calcium in the ration during gestation places almost complete reliance on the dietary source of calcium. If the prepartum diet is low in calcium, calcium mobilization from the bone is instituted to meet the calcium needs. If a gastrointestinal dysfunction occurs at parturition, the effects are not severe since part of the calcium requirements is supplied by mobilization from the bone.

    21) Clinical Signs
    Usually high producing older does are affected shortly after kidding. The does show lethargy, poor appetite and poor milk production. Occasionally, hypocalcemia tetany may be observed. The doe is hyperirritable and may show muscle twitching of the lips, eyelids and ears. Trembling or twitching of other muscles of the body may also occur. Convulsions may develop.

    22)
    Blood calcium levels may be 5-7 mg per 100 ml blood. The response to calcium therapy may be diagnostic.

    23) Prevention
    The problem often involves many does in the milking herd. Usually, there is excessive calcium in the gestation diet from a mineral source and/or high quality legume hay. Correction of the calcium imbalance is necessary. A low calcium level during late pregnancy will help to control the problem.

    24) No information available.

    25) Polioencephalomalcia
    Polioencephalomalacia, also known as cerebrocortical necrosis. Polioencephalomalacia (PEM)is a disease of ruminant animals characterized by derangement of the central nervous system due to necrosis of the cerebral cortex of the brain.

    26) Cause
    The cause and development of the disease have not been entirely elucidated. Thiamine is produced in the rumen. In PEM, thiaminase, an enzyme that destroys thiamine, is thought to be produced by certain bacteria within the rumen and thiamine deficiency develops. A thiamine - analogue is also produced within the rumen which may replace thiamine in important metabolic reactions in the brain. Necrosis of the brain occurs.

    27) Clinical Signs
    Young animals on high grain diets are affected more often. Older animals and pastured animals may be occasionally involved.

    28)
    The onset is often sudden with blindness and disorientation. The head may be elevated. Excitement may be seen but is usually replaced with dullness. The animal may go down on its side with its head thrown back. The legs may be rigidly extended. Convulsions may occur. If untreated, death usually occurs within a few days.

    29)
    The appetite is lost and the animal does not drink. Temperature and respiratory rate are usually normal but the heart rate may be depressed.

    30) Treatment
    Administration of large doses of thiamine intravenously and/or intramuscularly early in the disease will usually produce a dramatic improvement within a few hours. In the later stages of the disease, the brain necrosis may be too severe for the animal to recover.

    31) Prevention
    Until further elucidation of the cause and development of the disease, little can be done to economically prevent the disease. If a case of PEM is diagnosed in a group of animals, it is advisable to inject the remaining animals with thiamine to prevent further cases.

    32) Calculosis
    Calculosis, also known as urinary calculi, urolithiasis, kidney/bladder stones or waterbelly. Calculosis is a metabolic disease of male ruminants characterized by formation of concretions within the urinary tract with obstruction to the outflow of urine. This often results in rupture of the bladder or the urethra

    33) Cause
    The disease occurs in animals on a high concentrate diet with a mineral imbalance resulting in excessive phosphorus intake. A high phosphorus level develops in the blood and in the urine. Magnesium and ammonium phosphate precipitate to form a concretion or calculus. The size may vary from sand-like particles to as much as 5-10 mm.

    34)
    In the female ruminants, the calculi are passed easily through the short expandable urethra. In the male ruminant, the urethra is long and does not expand easily. The calculus must pass around three curves in the urethra. In sheep and goats, the urethral process is a short (2-3 cm) extension of the urethra beyond the tip of the penis. The diameter of the urethral process is slightly smaller than the remaining urethra. Calculi have a tendency to lodge at the lower curve of the penis or at the urethral process.

    35)
    Once calculi have lodged, the wall of the urethra is damaged. Urine flow is obstructed and pressure may build up in the bladder until the bladder ruptures. If severe damage occurs to the wall of the urethra, it may rupture and urine may flow into surrounding tissues.

    36)
    Urinary calculi problems are seen most frequently during the winter or periods of very warm weather when water consumption may be reduced.

    37) Clinical Signs
    Signs do not develop until there is partial or complete obstruction of the urethra. Uneasiness, frequent attempts to urinate and straining are seen early. Crystal deposits may collect on the preputial hairs. The animals may refuse food, isolate from the group and kick at the abdomen. If the bladder ruptures, the abdomen may enlarge. If the urethra ruptures, the lower abdominal wall may become thickened from urine infiltration. If the bladder or urethra rupture, the animals may show temporary improvement. However, as time progresses, the animal becomes depressed and death eventually results.

    38) Treatment
    Once clinical signs develop, damage to the urethra may be severe and while the animal's life may be saved, its reproductive capabilities may be lost. Since the calculi may frequently lodge in the urethral process, this may be easily removed and may eliminate the obstruction. Removal of the urethral process has no effect on the reproductive abilities of the buck.

    39) Prevention
    The calcium-phosphorus ratio should be 1.5-2:1. Often in breeding males, it is advisable to decrease the grain and increase the roughage. Adequate clean water should be available. Prevent freezing of the drinking water in the winter.

    40)
    If calculosis is a herd problem, feed ammonium chloride 0.5-10r gradually increase the salt in the diet to 5-10.

    Rated 4.5 by 38 responses.

    About the author/references: Extension Goat Handbook - This material was contributed from collections at the National Agricultural Library. However, users should direct all inquires about the contents to authors or originating agencies. D. R. Nelson; U. of Illinois, Urbana. S. B. Guss; Pennsylvania State U., University Park

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