- Iodine Deficiency (Goiter)
- Iron Deficiency Anemia
- Rickets and Osteoporosis
- Vitamin E/Selenium Deficiency
Hyperplastic thyroid glands (goiter) occasionally occur in swine. Goiter usually occurs as a result of one of the following: iodine deficiency in the pregnant sow; a genetic defect in the sow for the biosynthesis of thyroid hormones; ingestion by the gestating sow of goitrogenic substances (certain plants, drugs, or chemicals); or iodine toxicity from dams being fed an excess of iodine.
In swine, goiter usually occurs in iodine deficient regions where iodized salt has not been included in the dam’s feed. Deficiency of iodine leads to the birth of weak or dead pigs that are largely devoid of hair. Many of the pigs have a mucinous edema, especially over enlarged foreparts of the body. The skin in these areas is thick and doughy. The tongue is often edematous and may protrude from the oral cavity. Enlarged thyroid glands (goiter) in piglets may not be visible externally but often can be palpated or observed at necropsy. In mature swine, iodine deficiency is not usually a significant disease although gestation may be prolonged by as much as seven days. Iodine deficiency is easily avoided by using iodized salt in the ration of gestating sows.
Piglets are born with very little iron reserve. Colostrum and milk from the sow provide relatively little iron, perhaps only 15-50% of the daily requirement. Rapid growth and expansion of blood volume in suckling piglets ensures that a deficiency of iron and anemia will develop unless another source of iron is made available. This is especially the case in pigs raised in confinement without access to soil or feces containing iron. A small amount of copper is essential for utilization of iron. Copper deficiency can also lead to anemia that has many of the same clinical signs and lesions.
Signs and lesions of iron deficiency vary in piglets of different ages. Piglets not supplemented with iron will rapidly lose body condition and thrift after only about one week. At necropsy, these pigs will have pallor, a thin-walled heart, and edema of the lungs, muscles and connective tissues. In piglets that have received an insufficient supply of iron to successfully reach weaning at three to four weeks of age, rapid breathing and sudden deaths can occur. At necropsy there is marked enlargement of the heart and spleen, hydropericardium, ascites, edema in various tissues and fatty changes in the liver. Iron deficient piglets four to ten weeks of age will show similar signs and lesions. They are quite susceptible to bacterial infection and have little resistance to environmental chilling.
Diagnosis can often be made on the basis of a history that documents a lack of supplementation with iron; clinical signs and postmortem lesions will reinforce the diagnosis. Additionally, several laboratory procedures can be used to confirm the anemia. Among these is a study of stained blood smears that reveals a microcytic, hypochromic anemia. Hematology and serum chemistry will reveal reduced serum iron and transferrin saturation and a low hematocrit.
Prevention is possible by administration of supplemental iron (100-200mg). This can be done with water-soluble iron given per os or by parenteral injection of iron dextran. Parenteral administration is most commonly practiced and has the advantage of precise dosage. Iron dextran should only be injected into the neck muscles in order to prevent any possibility of staining valuable areas of the carcass. For the same reason, iron dextran should not be administered parenterally beyond seven days of age. Both forms of administration, when improperly used, can lead to iron toxicity and deaths.
Pigs deficient in vitamin E/selenium are highly susceptible to iron toxicity. Pigs raised outdoors with access to soil usually do not have an absolute requirement for iron supplementation but many producers still find it a beneficial practice even in these situations.
Parakeratosis is a zinc-responsive dermatosis usually observed in 2- to 4-month-old swine. Pigs not allowed access to soil or not supplemented with zinc are more likely to have parakeratosis. The disease is caused by a relative deficiency of zinc. The deficiency is usually caused by feeding an unbalanced diet that has one or more of the following features: excessive calcium; excessive phytic acid (sometimes present in soybean protein); or a low concentration of essential fatty acids. These features all adversely affect availability of dietary zinc. In addition, enteric pathogens or changes in intestinal flora can adversely influence zinc absorption. Parakeratosis most often is caused by consumption of excessive calcium.
Affected pigs show few signs of illness other than skin lesions and reduced growth rate. Initial lesions appear as reddened macules and papules on the ventrolateral abdomen and medial surface of the thighs; these lesions often go unobserved. The lesions are slowly covered by thick, roughened scales and crusts. More obvious lesions soon become apparent on the lower legs and on the dorsum. Lesions sometimes can be seen around the eyes, ears, snout and tail and eventually may become generalized. Affected areas of the skin are hyperkeratotic and there may be fissuring of the epidermis with secondary infection of the fissures. A unique feature occasionally seen is a focal or diffuse hyperkeratosis on the tongue. Parakeratosis is a microscopic feature of affected epidermis and gives this dermatosis its name.
Parakeratosis must be differentiated from sarcoptic mange and greasy pig disease (exudative dermatitis). Parakeratosis is nonpruritic whereas sarcoptic mange is pruritic. Greasy pig disease tends to occur in younger, smaller pigs. Pigs with parakeratosis will recover if excessive calcium is removed from the ration and it is properly supplemented with zinc. Most good commercial or carefully compounded rations now are supplemented with adequate levels of zinc salts. Although once common, parakeratosis seldom occurs today unless a feed mixing error occurs.
Rickets is a disease of growing bones. Consequently, it usually is seen in young, weaned, growing pigs in which there is a deficiency, an imbalance, or a failure of utilization of calcium, phosphorous or vitamin D. Rickets usually is caused by a dietary deficiency of vitamin D or phosphorus. The basic abnormality is a failure of mineralization of osteoid and cartilaginous matrix, especially in growth plates. This is most obvious as a thickening and irregularity of growth plates in long bones. In confined animals not exposed to sunlight or supplemented, vitamin D may be inadequate. In pastured swine fed little or no grain or protein supplement, phosphorus may be inadequate.
Signs of rickets include poor growth, short stature, enlargement of the ends of long bones, lameness and deformation of the weight-bearing long bones. Necropsy lesions include an unusual number of recent or healing fractures, ribs that bend markedly before they fracture, and widened, thickened and irregular growth plates. Abnormal growth plates are best seen on longitudinally-sawed long bones.
Osteoporosis is a lesion of mature bones. It follows removal of much of the mineral content of the bones. It results from an imbalance between bone formation and resorption in favor of resorption. In the process there may be a softening of the bone (osteomalacia). Osteoporosis occurs often in prolific sows that mobilize minerals for high milk production. Gilts in their first lactation also are susceptible since their skeletal development may have been incomplete and there was no mineral reserve prior to pregnancy. Osteoporosis often results in fractures in the latter part of a nursing period, immediately after weaning, or during mating. Lack of exercise in confinement likely contributes to osteoporosis but inappropriate ration formulation or mixing is the most important etiological factor.
Signs of osteoporosis include lameness, recumbency, fractures and paraplegia. At necropsy, fractures often can be demonstrated in the femur, humerus or lumbar vertebrae. There may be distortions or deformities of the pelvis.
Properly balanced rations, including adequate calcium, phosphorus (in the proper ratio) and vitamin D are essential for prevention of rickets and osteoporosis. Adequate exercise also is important for normal skeletal development and maintenance. Treatment tends to be unrewarding for both rickets and osteoporosis.
Feeds high in the concentration of polyunsaturated fatty acids, copper, vitamin A or mycotoxins can either destroy vitamin E or make it less bioavailable. Grains from soils deficient in selenium, or selenium antagonists in mixed feeds, can result in feeds low in selenium. Both vitamin E and selenium work as antioxidants.
There are three closely related, overlapping syndromes associated with vitamin E and/or selenium deficiency. The most common is mulberry heart disease (MHD). The true causal mechanism is not known but the condition can usually be prevented with additional vitamin E supplementation. MHD usually occurs when vitamin E is low but is also seen in the face of seemingly adequate levels of vitamin E in tissue or serum. MHD is manifested by sudden death in pigs a few weeks to four months of age that were believed to be in excellent health. The condition was named after the mottled appearance of the heart muscle in affected pigs. Typically, there are alternating areas of necrosis and hemorrhage throughout the myocardium. The pericardial sac is distended with fluid and fibrin strands. Straw-colored fluid is often present in the pleural cavity and lungs are edematous. Microscopically there are degenerative changes in arteriole walls at many sites. Supplementation with vitamin E, either parenterally or orally, will prevent deaths from this disease.
Hepatosis dietetica (HD) is a much more rarely encountered presentation of vitamin E and/or selenium deficiency since legal levels of selenium supplementation in livestock feed were raised to 0.3 ppm. Clinically, HD presents as sudden deaths with few or no preceding signs. This syndrome was named on the basis of hepatic lesions and the belief that they are related to the pig’s diet. There are irregular focal to large areas of hepatic necrosis and hemorrhage; some lobules are distended and reddened. The gall bladder often is edematous. Myocardial necrosis and pulmonary edema may be present. Supplementation with selenium will ameliorate HD.
White muscle disease (WMD) is a presentation of vitamin E and/or selenium deficiency that is much more common in lambs, calves and chickens rather than swine. Skeletal muscle pallor or streaks of white, gritty mineralization are observed, particularly in the longissimus dorsi muscle. Microscopically, characteristic necrosis and/or mineralization of individual muscle fibers are observed.
Since these deficiencies are similar, it is not surprising that lesions of the syndromes sometimes overlap. Diagnosis can often be made on the basis of gross lesions, microscopic lesions in heart, liver, or muscles, and analysis for vitamin E/selenium levels in the liver or serum.
For prevention or treatment of a deficiency, pigs can be injected with vitamin E and/or selenium and tissue levels will be increased rapidly. Also, prevention is possible through supplementation of feed or drinking water. Sows injected in late gestation give birth to pigs with increased levels of both compounds. The syndromes described above may not always be responsive to supplemental vitamin E and selenium. MHD is more responsive to vitamin E; HD more so to selenium.
Pigs on pasture usually get enough vitamin E and selenium unless the soil is deficient in selenium. In outbreaks, feed content and quality as well as feed storage conditions should be examined carefully to determine why the feed is deficient. Improper feed storage, high copper levels, high fat levels, and poor quality feed constituents can result in destruction of vitamin E in a feed otherwise formulated adequately.
Pigs deficient in vitamin E and/or selenium may be more susceptible to other diseases. Also, deficient small piglets are quite susceptible to iron toxicity. If treated with iron dextran for anemia prevention, many deaths may occur. Myocardial lesions will closely resemble those of mulberry heart disease (MHD).