Diagnosis of nutritional deficiencies by observation is difficult. Quite often, the clinical signs are the result of a complex of mismanagement and infectious diseases, including parasitism, as well as malnutrition. For most nutritional deficiencies, the signs are not specific, eg, poor appetite, reduced growth, and unthriftiness. Deficiency of a single nutrient may bring about inanition, and the subsequent starvation may cause multiple deficiencies. Then, too, a nutritional deficiency may exist without the appearance of definite signs. In the field, the deficiency may be only slight or borderline, which makes diagnosis difficult.
Diagnosis of a deficiency by observing the response to nutritional therapy is not always clear, particularly for longterm deficiencies, the lesions of which may be irreversible. A nutritional deficiency should be diagnosed positively only after observance of several of the expected clinical signs and a careful review of the dietary, disease, and management history of the animals.
Protein deficiency, which may result from suboptimal feed intake or a deficiency of one or more of the essential amino acids, causes reduced gains, poor feed conversion, and fatter carcasses in growing and finishing pigs. In lactating sows, milk production is reduced, excess weight loss occurs, and sows may fail to exhibit postweaning estrus or have delayed return to estrus. For optimal use of protein, all essential amino acids must be liberated during digestion at rates commensurate with needs. Therefore, protein supplements should not be handfed at infrequent intervals but should be mixed with the grain or be available at all times with grain on a free-choice basis.
No evidence has been presented to support the theory of “protein poisoning” in pigs. Diets containing as much as 35–50% protein were found to be laxative and less efficiently used, but no toxic effects were noted.
Certain long-chain polyunsaturated fatty acids are essential for swine. Linoleic acid is essential in the diet and is used to produce longer-chain fatty acids that are probably also essential. A linoleic acid deficiency induces hair loss, scaly dermatitis, skin necrosis on the neck and shoulders, and an unthrifty appearance in growing pigs. Conventional swine diets generally contain adequate fat from the natural ingredients to furnish ample amounts of essential fatty acids.
Deficiencies of calcium or phosphorus result in rickets (see Rickets) in growing pigs and osteomalacia (see Osteomalacia) in mature pigs. Signs include deformity and bending of long bones and lameness in young pigs, and fractures and posterior paralysis (a result of fractures in the lumbar region) in older pigs. Sows that produce high levels of milk and nurse large litters are particularly susceptible to posterior paralysis toward the end of lactation or after weaning if dietary calcium or phosphorus is deficient. These signs can also result from a deficiency of vitamin D, but phosphorus deficiency is the most common cause.
Pigs fed diets low in salt (NaCl) grow poorly and inefficiently, due largely to a marked reduction in feed intake. Though not specific for salt deficiency, poor hair and skin condition may also develop. There have been reports of salt-deficient pigs attempting to consume urine of other pigs.
Sows fed diets deficient in iodine produce hairless pigs that are weak or stillborn. With a borderline deficiency, the newborn pigs may be weak only at birth, but their thyroids are enlarged and have histologic abnormalities. (Also see Non-Neoplastic Enlargement of the Thyroid Gland.) Some feedstuffs (including soybeans and soybean meal) contain goitrogens that may cause marginal goiter if iodine is not included in the diet. Iodized salt at recommended levels prevents this deficiency.
Deficiencies of iron and copper reduce the rate of Hgb formation and produce typical nutritional anemia. Signs of nutritional anemia in suckling pigs include low Hgb and RBC count, pale mucous membranes, enlarged heart, skin edema about the neck and shoulders, listlessness, and spastic breathing (thumps). Iron deficiency is more common than copper deficiency and is most common in nursing pigs that do not receive an iron injection or oral iron early in life.
A deficiency of zinc results in parakeratosis (see Parakeratosis) in growing pigs, particularly when fed diets high in phytic acid (or phytate, the primary form of phosphorus in cereal grains and oilseed meals) and more than the recommended amount of calcium. The exact mode of action of zinc in the prevention of parakeratosis is not known.
Deficiencies of selenium and/or vitamin E can cause sudden death of young, rapidly growing pigs (see Nutritional Myopathy of Pigs). In addition, selenium/vitamin E deficiency in nursing pigs makes them more susceptible to iron toxicosis from iron injections (see Iron Toxicity in Newborn Pigs.)
Most commercial diets are fortified with vitamins, and vitamin premixes are readily available for farm-mixed feeds, so deficiencies are less common than they were years ago. Deficiency of vitamin A results in disturbances of the eyes and the epithelial tissues of the respiratory, reproductive, nervous, urinary, and digestive systems. Reproduction is impaired in sows, and they may farrow blind, eyeless, weak, or malformed pigs. Herniation of the spinal cord in fetal pigs is reported as a unique sign of vitamin A deficiency in pregnant sows. Growing pigs deficient in vitamin A show incoordination and develop night blindness and respiratory disorders. Vitamin A deficiency is rare due to the ability of the liver to store this vitamin.
Signs of vitamin D deficiency include rickets, stiffness, weak and bent bones, and posterior paralysis. These signs are indistinguishable from those of a calcium or phosphorus deficiency (see Mineral Deficiency).
Vitamin E deficiency can result in poor reproduction and impaired immune system. Many of the signs of vitamin E deficiency are similar to those of selenium deficiency (see Mineral Deficiency).
Pigs deficient in vitamin K have prolonged blood clotting time and may die from hemorrhages. Certain components in moldy feed can interfere with vitamin K synthesis. Also excessive levels of dietary calcium interfere with vitamin K activity, causing these signs.
In pigs deficient in riboflavin, reproduction is impaired; postpubertal gilts fail to cycle but show no other clinical signs. Deficient sows are anorectic and farrow dead pigs 4–16 days prematurely. The stillborn pigs have very little hair, often are partially resorbed, and may have enlarged forelegs. Growing pigs fed diets low in riboflavin gain weight slowly and have a poor appetite, a rough coat, an exudate on the skin, and possibly cataracts.
Pigs deficient in niacin have inflammatory lesions of the digestive tract and exhibit diarrhea, weight loss, rough skin and coat, and dermatitis on the ears. Intestinal conditions can be due to niacin deficiency or bacterial infection. Deficient pigs respond readily to niacin therapy and, although not a cure for infectious enteritis, adequate dietary niacin probably allows the pig to maintain its resistance to bacterial invasion.
Growing pigs and pregnant sows develop a typical “goose-stepping” gait, ataxia, and a noninfectious bloody diarrhea when maintained on diets deficient in pantothenic acid. When the deficiency becomes severe, anorexia develops.
Pigs with a choline deficiency exhibit incoordination and an abnormal shoulder conformation. At necropsy, they may have fatty livers and usually show kidney damage. Sows deficient in choline have reduced litter size and may give birth to spraddle-legged pigs.
Biotin deficiency includes excessive hair loss, skin ulcerations and dermatitis, exudates around the eyes, inflammation of the mucous membranes of the mouth, transverse cracking of the hooves, and cracking or bleeding of the footpads.
Neonatal pigs fed synthetic diets low in vitamin B12 show hyperirritability, voice failure, and pain and incoordination in the hindquarters. Histologic examination of the bone marrow reveals an impaired hematopoietic system. Fatty livers are also noted at necropsy.
Last full review/revision July 2011 by Gary L. Cromwell, PhD