McMillen et al. (1948) raised pigs on pasture beginning with an average body weight of 23 pounds and supplied them with a corn-soybean meal ration plus casein, complex minerals, liberal amounts of A and D supplements, thiamin, riboflavin, niacin and pyridoxine. The pigs began "goose-stepping" in seven weeks. However, the control pigs which received 25 mg of pantothenic acid per lb of feed remained normal. McMillen et al. (1948) observed a similar prevention of goose-stepping by pantothenic acid supplementation in dry-lot raised pigs. Such gait incoordination was observed in gilts provided with only 2 mg of supplemental pantothenic acid per lb of ration (Davey and Stevenson, 1963).
Pigs suffering from pantothenic acid deficiency have scaly skin and thin hair and a brownish secretion around the eyes. The dermatosis associated with deficiency appears principally on the shoulders and behind the ears; the skin appears dirty and scaly. Skin becomes reddened, and the bristles on the rump and along the spine loosen and fall. The dermatosis extends to the mucosa, where it becomes manifest as necrotic enteritis, ulceration and hemorrhages in the large intestine (Ullrey et al., 1955). As a consequence, the feces contain blood. Goodwin (1962) observed various degrees of gastritis and, occasionally, peritonitis and intestinal fissures.
Ullrey et al. (1955) observed pathologic changes in some of the other organs of sows and baby pigs maintained on pantothenic acid-deficient diets. These changes included fatty liver degeneration, enlarged adrenals and enlarged heart, with some related flaccidity of the myocardium and intramuscular hemorrhages. Histopathologic studies showed degenerative changes and necroses of the tissue cells. Stothers et al. (1955) observed a decrease in thickness of the glomerular layer of the adrenals in addition to many of the other symptoms of pantothenic acid deficiency reported by other researchers. Follis and Wintrobe (1945) compared the influence of pyridoxine or pantothenic acid deficiencies on nervous tissues of young pigs. These authors reported that while the most prominent and initial feature in pyridoxine deficiency was degeneration of the peripheral process of the sensory neurons, chromatolysis was the first evidence of damage to the afferent neuron in animals subjected to pantothenic acid deficiency.
Pantothenic acid is particularly important in sow fertility, with insufficient quantities of the vitamin resulting in complete reproductive failure (Ullrey et al., 1955). Estrus occurred but the sows failed to retain the embryos following breeding. Female hogs fed low-pantothenic acid diets developed fatty livers, enlarged adrenal glands, intramuscular hemorrhage, heart dilation, diminution of ovaries and improper uterus development (Ullrey et al., 1955). Davey and Stevenson (1963) reported in one of their trials that litter weights at weaning were reduced with lower pantothenic acid levels and appeared to be due to a reduction in litter size. The incidence of stillbirths was inversely related to dietary pantothenic acid levels. The data from their experiments suggested that reproductive performance and growth could be improved if pantothenic acid was increased from 2.0 mg to 5.4 mg per lb of feed. Davey and Stevenson (1963) concluded that a minimum of 5.4 mg of pantothenic acid per lb is required in swine diets for maximum reproduction. Ensminger et al. (1951) reported that although gilts on a low-pantothenic acid diet became pregnant, they did not farrow or show any signs of pregnancy. Necropsy of gilts revealed macerating feti in the uterine horns in all cases. Minimal pantothenic acid sufficient to result in normal farrowing may still result in an abnormal locomotion in suckling pigs from sows that had received diets low in the vitamin (Teague et al., 1971). Sucking movements in the deficient piglets are impaired as is the use of the tongue (Christensen, 1983).
