The chemical structure of biotin includes a sulfur atom in its ring (like thiamin) and a transverse bond across the ring (Illus. 11-1). It is a monocarboxylic acid with the sulfur as a thioether linkage. Biotin, with its unusual structure, contains three asymmetric carbon atoms; therefore, eight different isomers are possible. Of these isomers, only one, d-biotin, contains vitamin activity. The stereoisomer l-biotin is inactive.
Biotin crystallizes from water as long white needles. Its melting point is 232° to 233°C. Free biotin is soluble in dilute alkaline solutions and hot water and practically insoluble in fats and organic solvents. Biotin is quite stable under ordinary conditions. It is destroyed by nitric acid, other strong acids, strong bases and formaldehyde and also inactivated by oxidative rancidity reactions (Scott et al., 1982). Also, it is gradually destroyed by ultraviolet (UV) radiation. Structurally related analogs of biotin can vary from no activity to partial replacement value to antibiotin activity. Mild oxidation converts biotin to the sulfoxide, and strong oxidation converts it to sulfone. Strong agents result in sulfur replacement by oxygen, resulting in oxybiotin and desthiobiotin. Oxybiotin has some biotin activity for chicks (one-third) but less for rats (one-tenth). A prominent nutrient-drug interaction is that biotin-dependent enzymes are reduced with the epilepsy drug carbamazepine (Rathman et al., 2002). Biotin exists in natural materials in both bound and free forms, with much of the bound biotin apparently not available to animal species. For poultry, and presumably for pigs, often less than half of the microbiologically determined biotin in a feedstuff is biologically available (Scott, 1981; Frigg 1984, 1987). Naturally occurring biotin is found partly in the free state (fruit, milk, vegetables) and partly in a form bound to protein in animal tissues, plant seeds and yeast. Naturally occurring biotin is often bound to the amino acid lysine. The few animal studies of biotin metabolism revealed that biotin is absorbed as the intact molecule in the first third to half of the small intestine (Bonjour, 1984). There is also absorption of biotin from the hind gut of the pig, with disappearance of 50% and 61% of infused biotin between the cecum and feces that was accompanied by a more than a four-fold increase of plasma biotin concentration and a more than six-fold increase of urinary biotin excretion (Barth et al., 1986). Kopinski and Leibholz (1985) reported that post-ileal absorption was 10% to 15% of that from the small intestine after oral ingestion. Of a labeled biotin dose infused into the cecum of mini-pigs, 80% appeared in portal blood (Drochner and Volker, 1984) with the largest proportion appearing in feces. Kopinski et al. (1989a, b) reported similar findings in that absorption of free biotin in the post-ileal digestive tract was about 8% as efficient as that from a similar labeled dose of orally administered biotin. Information on biotin transport, tissue deposition and storage in animals and humans is very limited. McCormick and Olson (1984) reported that biotin is transported as a free water-soluble component of plasma, taken up by cells via active transport, and attached to its apoenzymes. Whitehead and Bannister (1980) reported that plasma biotin concentration gives a good indication of biotin intake in young pigs. All cells contain some biotin, with largest quantities in liver and kidney. Intracellular distribution of biotin corresponds to known localization of biotin-dependent enzymes (carboxylases). Cooper et al. (1997) investigated the distribution of biotin in tissues of pigs and chickens using an indirect peroxidase-antiperoxidase immunohistochemical technique. In both species, immunoreactive biotin was detected in many tissues, including liver, kidney, pancreas, testis, brain, choroid plexus, adipose tissue, adrenal gland, cardiac skeletal muscle, skin lymphoid tissues, and epithelium of the respiratory and digestive systems. Investigations into biotin metabolism in animals are difficult to interpret, as biotin-producing microorganisms exist in the intestinal tract distal to the cecum. Often the amount of biotin excreted in urine and feces together exceeds total dietary intake, whereas urinary biotin excretion is usually less than intake. Efficient conservation of biotin, together with the recycling of biocytin released from the catabolism of biotin-containing enzymes, may be as important as intestinal bacterial synthesis of the vitamin in meeting biotin requirements (Bender, 1992). Carbon-14-labeled biotin showed the major portion of intraperitoneally injected radioactivity to be excreted in the urine and none in the feces or expired as CO2 (Lee et al., 1973). In rats and pigs, biliary excretion of biotin and metabolites is negligible (Zempleni et al., 1997).
Biotin is an essential coenzyme in carbohydrate, fat and protein metabolism. It is involved in conversion of carbohydrate to protein and vice versa, as well as conversion of protein and carbohydrate to fat. Biotin also plays an important role in maintaining normal blood glucose levels from metabolism of protein and fat when the dietary intake of carbohydrate is low. As a component of several carboxylating enzymes, it has the capacity to transport carboxyl units and to fix carbon dioxide (as bicarbonate) in tissue (Camporeale and Zempleni, 2006). In carbohydrate metabolism, biotin functions in both carbon dioxide fixation and decarboxylation, with the energy-producing tricarboxylic acid (TCA) cycle dependent upon the presence of this vitamin. Data from Hamilton et al. (1983) suggest an effect of biotin on hepatic pyruvate carboxylase activity in young pigs. Specific biotin-dependent reactions in carbohydrate metabolism are as follows (Mock, 2007):
In protein metabolism, biotin enzymes are important in protein synthesis, amino acid deamination, purine synthesis and nucleic acid metabolism. Biotin is required for transcarboxylation in degradation of various amino acids. Acetyl-coenzyme A (CoA)-carboxylase catalyzes addition of carbon dioxide to acetyl CoA to form malonyl CoA. This is the first reaction in the synthesis of fatty acids. Biotin is required for normal longchain unsaturated fatty acid synthesis and is important for essential fatty acid metabolism. Deficiency in rats and chicks inhibited arachidonic acid (20:4) synthesis from linoleic acid (18:2) while increasing linolenic acid (18:3) and its metabolite (22:6) (Kramer et al., 1984; Watkins and Kratzer, 1987a). Biotin deficiency resulted in reduced arachidonic acid (20:4) in chicks and therefore reduced plasma prostaglandin E2 (PGE2) as a result of less of the prostaglandin precursor (20:4) (Watkins and Kratzer, 1987b; Watkins, 1989).
More recently, evidence has emerged that biotin also plays unique roles in cell signaling, epigenetic control of gene expression, and chromatin structure (Rodríguez-Meléndez and Zempleni; 2003). Biotin regulates the genetic expression of holocarboxylase synthetase and mitochondrial carboxylases in rats (Rodríguez-Meléndez et al., 2001). Manthey et al. (2002) reports that biotin affects expression of biotin transporters, biotinylation of carboxylases and metabolism of interleukin-2 in Jurat cells.
Biotin deficiency has adverse effects on cellular and humoral immune function (Camporeale and Zempleni, 2006). Synthesis of antibodies is reduced in biotin-deficient rats. Biotin deficiency in mice decreases both the number of spleen cells and the percentage of B lymphocytes in the spleen.
The dietary biotin requirement (NRC, 1998) for breeding swine is estimated to be 0.2 mg per kg (0.09 mg per lb) and for growing pigs, 0.05 to 0.08 mg per kg (0.02 to 0.04 mg per lb) of diet. Requirements for biotin are difficult to establish due to biotin variability in feed content and bioavailability. Likewise, it is difficult to obtain a quantitative requirement for biotin, as the vitamin is synthesized by many microorganisms and certain fungi. These microorganisms are found in the lower part of the intestinal tract, a region in which absorption of nutrients is generally reduced. There is evidence in the pig, however, that intestinal microflora make a significant contribution to the body pool of available biotin (Barth et al., 1986). Kopinski et al. (1989a) reported that this microbially synthesized biotin is of little benefit to the pig. What is not known for the various species is the extent of microbial synthesis or the biotin availability to the host. It has also been reported that microorganisms contribute to animal and human requirements, as the use of some sulfa drugs, such as sulfathalidine, can induce deficiency under some circumstances. Rate and extent of biotin synthesis may depend on the level of other dietary components. It has been shown that in rats and poultry, polyunsaturated fatty acids (PUFAs), ascorbic acid and other B- vitamins may influence the demand for biotin. Addition of PUFAs to fat-free, biotin-deficient diets increased severity of dermal lesions (Roland and Edwards, 1971). Biotin is rapidly destroyed as feeds become rancid. Pure biotin was inactivated to an extent of 96% in 12 hours when linoleic acid of a high peroxide number was added to the diet (Pavcek and Shull, 1942). In the presence of alpha-tocopherol, this destruction amounted to only 40% after 48 hours. Recently, Bonomi et al. (1996) conducted an experiment with biotin, which was microencapsulated by a fatty acids film and then fed to swine. These authors recommended the addition of between 200 and 400 ppb for growing swine to improve weight gain, feed utilization, yield of ham, meat digestibility, and meat tenderness. Newport (1981) concluded that until they reached at least 28 days of age, 10 µg of biotin per kg (4.5 µg per lb) dry matter was likely to be adequate for pigs weaned at two days of age and provided a milk substitute until 28 days of age. Peo et al. (1970) investigated the effect of protein source and antibiotic on response to biotin supplementation in baby pig diets and found no significant effects due to biotin supplementation at a level of 440 or 880 µg per kg (200 or 400 µg per lb). Washam et al. (1975) found no benefit of including 165 µg biotin per kg (75 µg per lb) in a pelleted corn-based 18% protein starter swine ration. Average daily gain and feed:gain were not improved by the addition of biotin. Adams et al.(1967) reported a 7.5% increase in weight gain and a 5% improvement in feed efficiency when 6.8 kg (15 lbs) specific pathogen-free (SPF) pigs were fed a corn-milo-soybean diet supplemented with biotin at 110 µg per kg (50 µg per lb) of diet. Partridge and McDonald (1990) studied the effects of supplemental biotin at the rate of 500 µg per kg (227 µg per lb) of diet when fed to pigs weighing 15 to 88 kg (33 to 40 lb). They reported that feed:gain ratio was improved during the grower phase. There was also a tendency for improvements in feed:gain ratio in the starter and finisher phases and in carcass grading. Although it is recognized that biotin is essential for growing pigs, nutritionists have generally assumed that intestinal bacterial synthesis and basal diet ingredients adequately meet this need (Kornegay, 1986, Kopinski et al., 1989c, d).
A review of the literature examining the benefits of supplemental biotin to the growing pig is summarized in Table 11-1. Of the data available, several investigators have reported significant improvements in rate of gain and (or) feed conversion. However, in a majority of the studies there is only a trend for improvement in feed conversion. The addition of biotin at a level of 55 to 880 µg per kg (25 to 400 µg per lb) of diet appeared to improve feed conversion numerically regardless of the type of diet used, indicating that most practical diets are marginal in available biotin and not adequate to allow for optimal performance. Variation in responses to biotin supplementation for growing performance in pigs may depend on certain factors, such as age and dietary components, including high levels of copper supplementation and the PUFA content of the diet (Menten et al., 1987; Scherf, 1988; Kornegay et al., 1989; McDowell, 2000). Results of Hamilton and Veum (1986) suggested that biotin supplementation of corn-soybean meal diets did not improve the performance of growing pigs because the basal diet provided adequate biotin levels (0.17 to 0.22 ppm). Partridge and McDonald (1990) suggested that the financial savings would greatly exceed the cost of providing biotin at a concentration of 100 µg/kg because of the likely improvement in feed:gain ratio.
Kornegay et al. (1990) summarized field trial and university research on the effects of biotin supplementation on sow and gilt reproductive performance from 1977 to 1989. Reported supplemental biotin levels ranged from 100 to 550 µg per kg (45.5 to 250 µg per lb) of diet, with basal diets containing a wide variety of feedstuffs of varying composition and with total biotin levels ranging from 90 to 170 µg per kg (40.9 to 77.3 µg per lb) of diet. Many of these studies have shown beneficial effects of biotin supplementation on sow reproductive performance, including litter size, conception rate and interval from weaning to first estrus. The reduction in the interval from weaning to first estrus seems to be more responsive to supplemental biotin when delayed return to estrus was observed in control animals.
Although improvements in sow reproductive performance have been reported in several single-parity studies, research involving four and five parities indicated that improvements in litter size were most obvious in parities subsequent to the first. Luce et al. (1995) indicated that biotin supplementation was not efficacious when included in wheat-soybean meal diets for bred gilts. The calculated biotin value of the basal diet was 1.32 mg per kg (0.6 mg per lb), which was lower than the recommended 2 mg per kg (0.9 mg per lb) for bred gilts and sows (NRC, 1998). When 400 mg of biotin per ton of feed was supplied along with the basal diet, no differences in various indices of reproductive performance were observed due to supplementation. Penny et al. (1981) reported that the effect of biotin supplementation on sow reproduction depended on parity. For a 12 month-period, gilts and sows were assigned to the control group or the biotin supplementation group, which received 1,160 µg of biotin per day during pregnancy and 2,320 µg of biotin per day during lactation. Biotin had no effect in first-parity gilts. In the second and fourth parities, there were significant improvements due to biotin supplementation for the number of live pigs born. For some unapparent explanation, although significance was approached in the third parity, the effect was only a tendency. There was no effect from the fifth parity onward. Penny et al.(1981) concluded that biotin supplementation can increase the number of live pigs born in second and subsequent litters. Biotin may increase uterine space and placental development during mid-pregnancy (Scherf and Scott, 1989). Simmins (1985) reported the same number of corpora lutea, heavier ovaries and an increase in the length of the uterine horn of biotin-supplemented gilts compared with unsupplemented controls. Uterine horn length is a significant factor in determining the final volume of the uterus. Biotin additionally may act through prostaglandins, which are involved in the stretching phase of uterine enlargement via its role in carboxylation reactions involving PUFA synthesis (Scherf and Scott, 1989). Foot and toe lesions, which often develop into severe problems in breeding herds maintained in confinement, may be associated with lameness and consequent culling (Penny et al., 1963; Smith and Robertson, 1971; Fritschen, 1979). It has been well established that experimentally induced biotin deficiency in young pigs (Cunha et al., 1946; Glattli et al., 1975; Kopinski et al., 1989c, d) and sows (Misir and Blair, 1986a) causes cracks in the sole and hoof that are responsive to biotin supplementation.Numerous investigators (Brooks et al., 1977; Comben, 1978; Halama, 1979; Pedersen and Udesen, 1980; Penny et al., 1980; Brooks and Simmins, 1981; Brulisauer and Triebel, 1983; Bryant and Kornegay, 1984; Bryant et al., 1985a, c; Simmins and Brooks, 1988; Kornegay et al., 1990) have suggested that foot lesions in developing gilts and reproducing sows housed in confinement can be reduced, although not prevented, by adding biotin to diets containing commonly used feedstuffs; others (Grandhi and Strain, 1980; Hamilton and Veum, 1984; Lewis et al., 1991; Watkins et al., 1991) have reported no change in the incidence of foot lesions with biotin supplementation. Biotin supplementation was more beneficial in preventing foot lesions than in curing established foot lesions (Penny et al., 1980). Bryant et al. (1985c) indicated that the reduction in the number and frequency of foot lesions resulting from supplemental biotin increased as the prevalence of foot lesions increased in the swine herd. Brooks (1982) speculated that the variation of response to biotin supplementation may be due in part to the fact that clinical signs associated with biotin deficiency may resemble conditions having an alternative etiology and that response depends on the opportunities for resolution of the lesions (i.e., pigs housed on poorly designed floors have little opportunity for recovery, as continuous traumatic injury exceeds the capacity of the hoof for growth and repair).Simmins and Brooks (1980, 1985) investigated the effect of dietary biotin on physical characteristics of pig hoof tissue using a puncture and compression strength test and examined specific regions of the hoof horn and claw. It has been reported that biotin increases the compressive strength and hardness of the hoof wall and decreases the hardness of heel bulb tissue (Brooks and Simmins, 1981; Webb et al., 1984), although the mode of action of biotin in the maintenance of hoof integrity is unclear.
Biotin is present in many foods and feedstuffs. However, corn, wheat, other cereals, meat and fish are relatively poor sources. Less than half of the biotin in various feedstuffs, as determined by microbiologic assay, is biologically available (Frigg, 1976; 1984; 1987). Kopinski et al. (1989e) used ileocecal cannulas to evaluate the biotin availability in feedstuffs for pigs and used terminal ileum collection for the same purpose in chickens. From these results, Kopinski et al. (1989c) conclude that for either the chicken or the pig, commonly used Australian feedstuffs do not provide good sources of available biotin. Thus, it is important to know the chemical form of biotin (e.g., bound or unbound) as well as its overall content in feed. Kopinski et al. (1989b) suggested that urinary excretion may provide a useful measure of biotin availability in the pig. Table 11-3 illustrates the wide variations of biotin content within the same feedstuffs and the extreme range of biotin bioavailability. For alfalfa meal, corn, cottonseed meal and soybean meal, bioavailability of biotin is estimated at 100%. However, biotin availability is variable for other feedstuffs, for example, 20% to 50% in barley, 62% in corn gluten meal, 30% in fish meal, 20% to 60% in sorghum, 32% in oats and 0% to 62% in wheat (McDowell, 2004).
Oilseed meals, alfalfa meals and dried yeasts are good sources of biologically available biotin. Meat and fish meals contain biotin of relatively poor biologic availability. Sauer et al. (1988) determined an apparent biotin digestibility of soybean meal to be 55.4%, while that of meat and bone meal to be only 2.7% and canola meal, 3.9%. Grains are poor sources, with biotin in corn and oats more available than in wheat, hull less barley or regular barley. Frigg (1976) reported that the biotin in wheat and barley may be totally unavailable. Sorghum was rated an availability of 10% to 20% compared with 75% to 100% for corn (Buenrostro and Kratzer, 1984). Anderson et al. (1978) determined the biotin content of corn, barley, sorghum and wheat. Using a chick bioassay, Anderson et al. (1978) compared their results with those of authors who have performed microbiologic assay. They determined that corn has an availability close to 100%, but available biotin contents are low in wheat, barley and sorghum.
The biotin content of cereal grains appears to be considerably influenced by variety, season and yield (in particular the endosperm: pericarp ratio) (Brooks, 1982). Harvest conditions, post-harvest treatment and storage conditions all appear to play a part in determining biotin content and may also affect the availability. Biotin in feedstuffs may be destroyed by heat curing, solvent extraction and improper storage, while pelleting has little effect on biotin content of feed (McGinnis, 1988). Losses of biotin during storage can occur. Biotin is readily destroyed by rancid fat (Pavcek and Shull, 1942). Preparing fresh feeds, storing them for only short periods and keeping them dry and in a well-ventilated storage area will minimize rancidity problems. Hamilton and Veum (1984) have suggested that overdrying, poor storage conditions and presence of mold, may reduce the availability of biotin in corn. Also, the diet should be low in pro-oxidants and (or) properly protected by an effective antioxidant to avoid destruction of biotin, vitamin E, selenium and other nutrients.
There is considerable variation in biotin content within individual sources, For example, 59 samples of corn analyzed for biotin varied between 56 and 115 µg per kg (26 and 52 µg per lb), and 62 samples of meat meal ranged from 17 to 323 µg per kg (8 to 146 µg per lb) (Frigg, 1987). In comparison to cereal grains, oilseed meals are better sources of total biotin. Soybean meal, for instance, contains a mean biotin content of 270 µg per kg (122 µg per lb) with a range of 200 to 387 µg per kg (91 to 176 µg per lb) (Frigg and Volker, 1994).
Biotin is commercially available as a 100% crystalline product, as various dilutions and premixes and as low potency spray-dried preparations. The vitamin form is d-biotin, which occurs in nature and is the commercially available form. A 2% spray-dried biotin product is also available for use in either feed or drinking water.
Biotin is important for normal function of the thyroid and adrenal glands, the reproductive tract and the nervous system. Its effect on the cutaneous system is most dramatic, since severe dermatitis is the major obvious clinical sign of biotin deficiency in livestock. Biotin deficiency was produced in 1946 in swine by feeding a purified diet containing sulfathalidine or raw egg white (Lindley and Cunha, 1946; Cunha et al., 1946). For many years it was concluded that biotin supplementation was not needed, since it is synthesized by intestinal microorganisms and is widely distributed in feed. Nevertheless, clinical signs of deficiency were observed by feed company personnel and scientists under field conditions. However, it was the 1970s before a greater awareness of biotin field deficiencies became apparent (Cunha, 1984). Biotin deficiency results in reduced growth rate and impaired feed conversion and produces a wide variety of clinical signs. Clinical signs associated with biotin deficiency include alopecia; a dermatitis characterized by dryness, roughness and a brownish exudate; ulceration of the skin; inflammation of the oral mucosa; hindleg spasticity; and transverse cracking of the soles and tops of hooves (Cunha, 1977). Many of the symptoms of biotin deficiency were observed in suckling pigs by Lehrer et al. (1952). Illus. 11-2 and Illus. 11-3 show clinical signs of biotin deficiency in swine.
Growth depression may become evident in biotin-deficient swine before clinical signs are seen. The first clinical signs are generally excessive hair loss and dermatitis, with complete hair loss in severe cases. Dermatitis first appears as scaly skin, often starting on the ears, neck, shoulder and tail and eventually spreading over the entire body. In later stages, crust and cracks appear on the face and extremities. After five to seven weeks on a biotin-deficient diet, swine may show hoof defects. Foot lesions may be the most characteristic sign of biotin deficiency. In a biotin deficiency, the hoof horn becomes soft and rubbery and poorly resistant to abrasions. The slow growth and repair process in the hoof tissue and the considerable weight on the feet add to the problem. Depending on the type of flooring on which the animal is kept, this may have little effect or may lead to the development of cracks and necrotic lesions, resulting in extreme lameness (Glattli et al., 1975; Pluym et al., 2011). Secondary infections may gain entry through hoof cracks and infect the joints, which may lead to premature removal from the herd. Feeding and breeding are also adversely affected. With hoof defects in particular, the sow becomes unable to support the weight of the boar. Also, because the hog’s ability to eat may be impaired, these problems obviously lead to economic losses. Supplementation of the diet of breeding sows with biotin from an early stage of development made a significant contribution to the maintenance of hoof horn integrity (Simmins and Brooks, 1988). Tagwerker (1983) noted that foot lesions were responsible for 4% to 8% of all sows culled in Europe. Also, he noted a Denmark study that reported 8.5% of biotin-supplemented sows having hoof lesions, compared with 25% for controls. After biotin supplementation in Holland, culling rate due to lameness was decreased from 25% to 14% (de Jong and Sytsema, 1983). Cunha (1984) noted that in most of the 40 countries he had visited during the past 30 years, biotin deficiency signs were observed in swine operations. Deficiency signs observed under field conditions occurred in only 10% to 20% of sows or fewer. Baby pigs nursing these sows usually showed no biotin deficiency signs but responded to biotin supplementation. Unfortunately, many swine producers are of the opinion that it is natural for a swine herd to have a few animals with hair loss, dermatitis and cracked feet and therefore are not overly concerned when a small percentage of sows exhibit these clinical signs (Cunha, 1984). Biotin supplementation of sow diets has significantly improved reproductive performance, including the number of pigs farrowed and weaned, litter weaning weight and number of days from weaning to estrus (Brooks et al., 1977; Simmins and Brooks, 1983; Misir and Blair, 1984; Kornegay, 1986). In a field study, sows had severe lameness and impaired reproduction (Fonge, 1977). After these sows received supplemental biotin, normal foot health and normal reproductive performance were restored. Researchers found that sows housed in total confinement showed a positive response in conception rate and interval from weaning to first estrus and a trend to larger litters when supplemented with biotin (Bryant et al., 1985b). In an earlier study (Brooks et al., 1977), sows fed supplemental biotin had more pigs born alive (9.8 versus 8.1), more pigs weaned (7.8 versus 6.8), increased litter weight at weaning (71.0 versus 64.5 kg) and reduced time interval from weaning to first estrus after weaning (6.2 versus 15.3 days), compared with unsupplemented controls.
The economics of biotin supplementation in swine diets is often given much attention with regard to vitamin supplementation formulations (i.e., vitamin premixes). The most likely reason for this is that biotin is thought to be the most expensive vitamin in swine diets. However, based on the requirements and recommended industry levels for biotin supplementation, biotin in swine diets costs less than other vitamins, such as choline and vitamin E. To this point, the nutritionist must consider the extreme variation of biotin content and bioavailability in feedstuffs used for swine diets. It makes these feed components dietary unreliable as a consistent source of biotin. Therefore, under practical commercial production conditions, criteria such as growth rate, feed conversion, reproductive efficiency and other parameters associated with biotin-responsive conditions should be considered when formulating swine diets. Although swine and poultry showed clinical signs of deficiency under experimental conditions in the 1940s, for many years it was believed that supplemental biotin was not needed in swine and poultry diets because of the wide distribution of biotin in feedstuffs and the potential synthesis by intestinal microflora. In the late 1960s and early 1970s, interest in swine and poultry was rekindled when more field cases of deficiency occurred than in the past. Also, since then, well-controlled research has more clearly defined the occurrence of biotin deficiency and the values of supplementation in the practical swine ration. Interferences with the biosynthesis of biotin by intestinal bacteria can individually or collectively lead to a biotin deficiency. These interferences can be in the form of therapeutic administration of antibacterial agents and modern housing systems limiting animals’ access to feces. There are several factors that affect the intestinal microbial populations of pigs that may change nutrient absorption and excretion (e.g., biotin). Wilt and Carlson (2009) studied the effect of supplemental zinc oxide at high levels (3,000 mg per kg or 1,364 mg per lb) and an antimicrobial agent (carbadox) on need for biotin in nursery pigs. Results indicated that feeding nursery pigs 440 µg per kg (200 µg per lb) of biotin improved daily gains independent of zinc and carbadox supplementation. Additionally, biotin deficiencies are now more prevalent because of restricted use of biotin-rich feedstuffs and limited bioavailability of biotin in some grains (e.g., wheat, barley, sorghum) and in some animal protein sources (e.g., meat meal, poultry by-product meal). Biotin antagonists (e.g., molds and feed rancidity) and improved plant genetic characteristics for greater crop production have also contributed to limiting biotin utilization by swine. Cunha (1984) has summarized the possible reasons for more frequent occurrence of biotin deficiencies in swine (Table 11-4).
Table 11-4: Possible Explanations Why Biotin Deficiencies Became More Prevalent in Swine Operations in Recent Years
Adapted from Cunha (1984) - Courtesy of Hoffman-La Roche, Inc.
For swine already diagnosed with biotin deficiencies, supplemental programs may need higher than required levels of biotin to cure pigs. Some reports conclude that foot lesions in adult sows healed in a matter of weeks (Tagwerker, 1974) when sows were supplemented with high levels of biotin, while Brooks et al. (1977) found biotin supplementation to result in a 28% reduction in lesions after six months. Pigs housed on badly designed floors have little opportunity for recovery, as traumatic injury exceeds capacity of the hoof for growth and repair. Brooks (1982) summarized data from Great Britain, Denmark, and Switzerland and concluded that where foot lesions already existed, dietary supplements of 2,000 to 3,000 µg of biotin per kg (909 to 1,364 µg per lb) of diet were beneficial. Losses of biotin during storage can be considerable. Biotin is readily destroyed by feed rancidity (Pavcek and Shull, 1942). Preparing fresh feeds, storing them for only short periods and keeping them dry and in a well-ventilated storage area will minimize rancidity problems. Also, the diet should be low in feedstuffs high in pro-oxidants and/or properly protected by an effective antioxidant to avoid destruction of biotin, vitamin E, selenium and other nutrients. Biotin is relatively stable in multivitamin premixes and in natural sources in feeds and is fairly stable during processing. Using presently available feedstuffs and under modern swine production conditions, a marginal biotin deficiency is possible. Supplemental d-biotin should be added to swine rations at levels that provide an appropriate margin of safety to offset the factors influencing the biotin needs of swine.
Studies with swine indicate that this species can safely tolerate dietary levels four to 10 times their nutritional requirement of biotin (NRC, 1998). In view of the poor retention of biotin, it is probable that swine can tolerate much higher levels.
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