Biotin in swine production: A review

Livestock Production Science, 14 (1986) 65--89

65

Elsevier Science Publishers B.V., A m s t e r d a m -- Printed in The Netherlands

BIOTIN

IN SWINE PRODUCTION:

A REVIEW

E.T. K O R N E G A Y

Department o f Animal Science, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061 (U.S.A.) (Accepted 30 J u l y 1985)

ABSTRACT Kornegay, E.T., 1986. Biotin in swine p r o d u c t i o n : a review. Livest. Prod. Sci., 14: 65--89. Biotin, an essential water-soluble vitamin, is a c o f a c t o r of a n u m b e r of e n z y m e systems responsible for c a r b o x y l a t i o n and transcarboxylation reactions. These reactions play a major role in the m e t a b o l i s m of carbohydrates and nucleic acids, in the synthesis of fatty acids, proteins and purines, and in the d e a m i n a t i o n of amino acids. In the past, it was believed that supplemental biotin was not required in swine diets because of its wide distribution in feedstuffs generally used in the f o r m u l a t i o n of swine diets, and its k n o w n synthesis by the pig's intestinal microflora. Interest in biotin nutrition for swine, however, was rekindled w h e n several field reports in the mid-1970s described disease c o n d i t i o n s similar to those reported for e x p e r i m e n t a l l y induced biotin deficiencies ( p o o r growth in y o u n g pigs, low plasma biotin levels, alopecia and pustule f o r m a t i o n in the skin and lesions of the h o o f and sole of the toes). These conditions were reported to be responsive to biotin s u p p l e m e n t a t i o n in m a n y cases, but control treatments, were usually not included so that definitive conclusions could not be made. Results from p r o p e r l y controlled research are now available, especially from long-term sow studies (three to four parities), which suggest that supplemental biotin may improve one or m o r e of the following: p o o r litter size, c o n c e p t i o n rate or weaning to estrus interval, toe lesions and p o o r haircoat condition. Milk biotin c o n c e n t r a t i o n and plasma biotin c o n c e n t r a t i o n of sows and piglets were reported to be elevated w h e n supplemental biotin was fed. The a m o u n t of biotin in feedstuffs varies from 20 to 2600 parts per billion (p.p.b.), but availability values have n o t been d e t e r m i n e d for pigs, although chick bioavailability values suggest that biotin in c o m m o n l y used grain and protein sources is p o o r l y available. N u m e r o u s environmental and nutritional factors m a y influence the occurrence of a biotin deficiency in swine or alter the level of biotin required in the diet to meet the animal's needs. Using presently available feedstuffs and under m o d e r n swine p r o d u c t i o n conditions, a marginal biotin deficiency is possible. There are, however, m a n y unanswered questions and a need for m o r e research to b e t t e r understand the role of biotin in swine nutrition. Swine producers experiencing p o o r reproductive p e r f o r m a n c e in their sow herds, associated with excessive loss of hair and severe foot lesions, should evaluate the biotin c o n t e n t o f their sow diet and consider supplemental biotin.

INTRODUCTION B i o t i n is w e l l e s t a b l i s h e d as a n e s s e n t i a l w a t e r - s o l u b l e , s u l f u r - c o n t a i n i n g v i t a m i n t h a t is w i d e l y d i s t r i b u t e d i n n a t u r e ( H a r d i n g e a n d C r o o k s , 1 9 6 1 ; 0301-6226/86/$03.50

© 1986 Elsevier Science Publishers B.V.

66 Scheiner and de Ritter, 1975). However, it is present in relatively small concentrations and bioavailability appears to be limited (Wagstaff et al., 1961; Anderson and Warnick, 1970; Scheiner and de Ritter, 1975; Frigg and Brubacher, 1976}. Because of the wide range of metabolic functions (metabolism of carbohydrates and nucleic acids, synthesis of f a t t y acids, proteins and purines and deamination of amino acids), a deficiency of biotin has profound effects on the animal and a wide range of clinical symptoms have been described in different species (Balnave, 1977; Scott, 1981; Whitehead, 1981). The role of biotin in the health and nutrition of humans and animals was discussed at an International Conference on Biotin sponsored by the New York Academy of Science in 1984. Several decades have passed since Cunha et al. (1946) first produced a biotin deficiency in young pigs by feeding a semi-purified diet containing raw egg whites (egg whites contain avidin, which binds biotin); however, the role and need for supplemental biotin for swine-fed practical diets is still n o t completely clear. For m a n y years after biotin was identified as an essential vitamin for the pig, it was believed that supplemental biotin was not needed in pig diets because of its wide distribution in generally used feedstuffs and its known synthesis by the animal's intestinal microflora (Simmins and Brooks, 1983). Interest in biotin nutrition for swine was rekindled during 1968 to 1978 when several reports (Cunha et al., 1968; Cunha, 1971; Tagwerker, 1974; Comben, 1978}, primarily of field cases, suggested that disease conditions observed in swine in modern production systems fed on c o m m o n l y used feedstuffs resembled a biotin deficiency. These disease conditions were reported to be responsive to biotin supplementation in most cases. Scientists were skeptical because adequate control treatments were not included. As a result, a few scientists in several countries undertook controlled sow studies to determine the need for supplemental biotin in sow diets, and at the same time field studies were continued. Major changes occurred during this same period in the production, processing and storage of feedstuffs used in swine diets and in the breeding, feeding and housing of swine. These changes and other factors may have influenced the level of biotin required in swine diets. They include: (a) an increase in total confinement housing, particularly of the breeding herd, which reduces the opportunity for coprophagy; (b) an increase in the number of farrowings per sow per year and a reduction in the daily feed intake during gestation, which increases the need for vitamin fortification; (c) strong selection pressure for swine with a faster growth rate, more efficient feed conversion, lower fat and higher muscle content; (d) wide variation in the biotin content within and among feedstuffs and decreased use of biotin-rich feedstuffs; (e) deactivation or loss of biotin in feeds due to processing and storage, contact with rancid fats or oils, or to the presence of biotin antimetabolites or antagonists;

67

(f) limited bioavailability of biotin in many feedstuffs (based on chick growth assay); (g) reduction of biotin biosynthesis in the gastrointestinal tract by various diet components, especially antibiotics; (h) disease or disorders that impair absorption of biotin. One or more of these factors may increase the need of pigs for supplemental biotin. Various aspects of biotin nutrition in swine were discussed by Kornegay and Bryant (1981), Brooks (1982) and Penny and Johnston (1983). Since then, several significant studies including long-term sow studies have been reported. The objective of this paper is to provide a current, comprehensive review of the status of biotin in swine nutrition. FUNCTION

Biotin is a cofactor in a number of carboxylation and transcarboxylation enzyme systems that play an essential role in carbohydrate metabolism, fatty acid synthesis, amino acid deamination, purine synthesis and nucleic acid metabolism (Lynen, 1967; Olson and Suttie, 1977). These enzyme systems have the capacity to transport carboxyl units and to fix carbon dioxide (as bicarbonate) in tissue. Four of these biotin-dependent enzymes are significant in mammalian metabolism (Anonymous, 1979). These include pyruvate carboxylase, which converts pyruvate to oxaloacetate (gluconeogensis and lipogenesis), propionyl-CoA carboxylase, which converts propionyl-CoA to methylmalonyl-CoA (for catabolism of amino acids and odd numbered fatty acids), B-methylcrotonyl-CoA carboxylase, which converts B-methylcrotonyl-CoA to 3-methylglutaconyl-CoA (catabolism of leucine) and acetyl-CoA carboxylase, which forms malonyl Co-A (also l~pogenesis). Most biotin-dependent carboxylases have three protein components: (a) biotin carboxylase, (b) a carboxyl transferase and (c) a biotin-containing carboxyl carrier protein (McCormick, 1975). Autoradiographic studies in chicks using 3H-biotin revealed that labelled biotin is incorporated into a variety of tissues in a pattern that is in agreement with its known biochemical function (Frigg and Torhorst, 1982). High labelling was found in differentiated cells, e.g. in hepatocytes, proximal tubular cells of kidney, villous epithelia of small intestine and fat cells; whereas rapidly proliferating tissue compartments were only weakly labelled, e.g. undifferentiated kidney cortex, bone marrow, lymphatic tissue. The rate of incorporation of biotin into the tissue was much faster in biotin deficient chicks. ABSORPTION AND EXCRETION

In rats and pigs, orally, parenterally and intramuscularly administered biotin is rapidly absorbed and there is a rapid rise in blood biotin levels, but with a return to the initial levels within 12--48 h depending on the

68 dosage (Baker et al., 1969; Gl~ittli e t al. (cited by Tagwerker, 1977); V61ker et al., 1977; Bryant et al., 1982). Relatively high levels of administered biotin caused only small or no increase in the biotin concentration of pyruvate carboxylase activity in the liver (V61ker et al., cited by Tagwerker, 1977; Bryant et al., 1985c). Lee et al. (1972) and McCormick (1975) reported that excess biotin is partly oxidized in the liver of rats and that most of it is excreted via the urine within a matter of hours. V61ker et al. (cited by Tagwerker, 1977), showed that about 22% of the biotin administered to pigs was excreted via the kidney, whereas the biotin content of the faeces did not appear to be influenced by dietary biotin (Table I). TABLE I Biotin: excretion in the pig~

A B C D

Biotin supplements in feed (meg kg -1)

Average daily intake (mcg)

0 300 900 2700

220 960 2700 7900

Average excretion (percent ofintake) Faeces

Urine

150 28 12 7

4 23 22 22

~V~lker et al. (cited by Tagwerker, 1977). Microbial synthesis of biotin takes place in the lower parts of the intestinal tract where absorption of nutrients is believed to be rather limited (Tagwerker, 1977; Kopinski et al., 1983). Drochner and V61ker (1984) injected labelled biotin into the cecum of pigs and found that only a minute fraction was absorbed and excreted in the urine; the major part of the biotin was found in the faeces. The intestinal tract may also harbor biotin-consuming organisms, which compete with the host for biotin (V61ker et al., cited by Tagwerker, 1977). This hypothesis is supported by the research in which broiler chicks fed marginally deficient biotin diets became biotin deficient when inoculated with Lactobacillus acidophilus (Buenrostro and Kratzer, 1983). Misir and Blair (1984a), using a chick bioassay, suggested that dietary fiber might interfere with the absorption of biotin from the gut. VARIABILITY AND BIOAVAILABILITY OF BIOTIN IN FEEDSTUFFS Feedstuffs consumed provide the major source of biotin for the pig. The a m o u n t of biotin in the diet available to the pig depends upon the quantity in the feedstuff and its biological availability. These may vary considerably from one feedstuff to another (Table II). The a m o u n t of

69 TABLE II Microbiologically analyzed and available biotin content in various feed ingredients ~ Ingredient

Analyzed biotin Inclusion in content (ug]kg) the diet (%)

No. of groups:

Mean (percent availability ± S.D°)

Barley Oats Rye Rice polishings Sorghum Wheat Wheat bran Wheat germ Wheat middlings Peanut meal Sunflower meal Alfalfa meal Grass meal Molasses beet Skim milk powder Whey powder Tapioca meal

130 262 89 375 214 90 343 245 190 1630 1001 567 432 757 204 302 59

8 8 8 8 8 12 8 8 8 8 8 8 12 8 8 8 8

21.6 40.8 --3.0 23.4 24.5 4.0 18.3 54.9 6.4 52.8 38.8 55.5 66.6 74.8 64.8 117.0 6.4

40 40 40 10 40 40 15 10 20 7 10 12 15 8 10 10 20

± 4.1 ± 2.8 ± 9.3 _+ 3.9 ± 1.7 ± 7.0 ± 5.9 ± 8.2 ± 8.7 ± 5.0 ± 2.9 -+ 8.7 ± 9.4 + 12.0 ± 15.5 ± 18.8 ± 18.2

'Frigg (1984). :Each group consisted of eight chicks; half the groups males, half females. b i o t i n p r e s e n t in c o m m o n l y used feed ingredients varies f r o m 20 t o 2 6 0 0 p.p.b. (Frigg, 1 9 7 6 ; 1 9 8 4 ) . Yeast and vegetable p r o t e i n s such as p e a n u t s are p a r t i c u l a r l y rich in biotin. H o w e v e r grains, w h i c h c o n t a i n low levels o f biotin, are the p r i m a r y ingredients in m o s t c o m m e r c i a l sow and pig diets. Biotin availability values have n o t been d e t e r m i n e d using pigs, t h u s we can o n l y e x t r a p o l a t e f r o m c h i c k e n and t u r k e y data. Based o n m i c r o b i o l o g i c a l d e t e r m i n a t i o n s , t h e b i o t i n c o n t e n t o f several f e e d s t u f f s was r e p o r t e d t o be o n l y partially available t o c h i c k e n s and t u r k e y s (Frigg, 1 9 7 6 , 1 9 8 4 ; Frigg and B r u b a c h e r , 1 9 7 6 ; A n d e r s o n a n d Warnick, 1 9 7 0 ; A n d e r s o n et al., 1 9 7 8 ; Misir and Blair, 1 9 8 4 a , b). T h e biotin c o n t e n t o f c o r n was r e p o r t e d to be low (45 p.p.b.), b u t it a p p e a r e d to be t o t a l l y available (Frigg, 1976). Biotin in milo, barley a n d oats was r e p o r t e d t o be o n l y 20 t o 30% available. N o g r o w t h was o b t a i n e d with w h e a t , indicating very p o o r bioavailability. Baker {1978) r e p o r t e d the bioavailability o f biotin t o be 122, 61, 6 9 and 45% f o r c o r n , s o r g h u m , barley and w h e a t , respectively. T h e r e f o r e , w h e n certain grains are fed, especially w h e a t , t h e biotin available to t h e animal m a y be limited. DEFICIENCY SYMPTOMS R e s e a r c h using several m a m m a l i a n species has s h o w n t h a t b i o t i n is req u i r e d f o r d e v e l o p m e n t a n d m a i n t e n a n c e o f the skin, hair, f o o t pads and

70 hooves and reproductive and nervous systems (Balnave, 1977; Scott, 1981; Whitehead, 1981). Biotin deficiency signs produced in young pigs fed a synthetic diet containing raw egg white (Cunha et al., 1946), have been confirmed by others (Lehrer et ai., 1952; Biihlmann, 1973; Pohlenz, 1974; Gl~ittli et al., 1975; Geyer et al., 1981, 1983; Hamilton et al., 1982). These symptoms include decreased growth rate, alopecia, dry scaly skin with brownish exudate, transverse grooves on the tongue, spasticity of the hind legs, erosion of the soft toe heel and extensive cracking of the toe heel and horn, and low plasma levels, with the sequence of development similar to the order of presentation (Gl~ttli, 1976). Geyer et al. (1981) reported that weanling pigs fed a biotin-deficient diet (5% egg white) showed the most marked changes after 8 to 10 weeks on the deficient diet. Alopecia, pustule formation in the skin and formation of weak, brittle and crusty horn material in circumscribed areas of the dorsal and lateral aspects of the toes were the most marked findings. Sows that were believed to be biotin deficient have exhibited alopecia, dry scaly skin, erosion of the soft heel and extensive cracking of the toe heel and horn {Brooks et al., 1977; Brooks and Simmins, 1981; de Jong and Sytsema, 1983; Misir and Blair, 1983). Additionally, poor reproductive performance has been reported for biotin deficient sows (Brooks et al., 1977; Simmins and Brooks, 1983; Tribble et al., 1983; Misir and Blair, 1984d; Bryant et al., 1985c). GROWTH RATE Biotin deficiency produced by feeding diets containing certain sulfa drugs to inhibit bacterial synthesis of biotin in the gut (Lindley and Cunha, 1946; Cunha et al., 1948), or by feeding diets containing avidin, which binds biotin (Cunha et al., 1946; Gl~ittli et al., 1975; Hamilton et al., 1982) caused reduced growth rate in young pigs. Lehrer et al. (1952) obtained clinical biotin deficiency symptoms in baby pigs fed a synthetic milk diet free of biotin, but reported no depression in growth rate. Improvements in growth rate due to biotin supplementation have been reported in alleged field cases of biotin deficiency (Cunha, 1971; Gl~ittli, 1975, 1976). Adams et al. (1967) fed early-weaned pathogen-free pigs on a basal corn--milo-soybean diet calculated to contain 286 #g biotin kg -1 diet. The addition of 110 ~g biotin kg -1 diet increased growth rate and feed efficiency by 15 and 17%, respectively. Combs (unpublished data, 1967) and Peo et al. (1970) reported only slight improvements in rate of growth and feed efficiency of young pigs fed supplemental biotin (55--880 p.p.b.). On the other hand, Hanke and Meade (1972), Washam et al. (1975), Kopinski et al. (1982) and Brooks et al. {1984, and unpublished data, 1984} reported no growth response to biotin supplementation of diets containing several natural feedstuffs. Tagwerker (1974) reported results of field trials in a number of countries

71

where the performance of growing pigs was improved by supplemental biotin. However, Zivkovic et al. (1970), Meade (1971), Easter et al. {1978), and Bryant et al. (1985b) reported no improvement in feedlot performance of growing/finishing pigs fed diets containing several commonly used feedstuffs. Gl~ittli (1976) reported that in an experimentally induced biotin deficiency, growth depression usually became apparent before clinical symptoms were noted. This may not be the case in swine fed commonly used feedstuffs, as decreases in foot lesions have been reported for growing pigs fed supplemental biotin with no effect on growth rate (Bryant et al., 1985b). FOOT HEALTH

Foot and toe lesions are known to be closely associated with lameness (Penny et al., 1963; Smith and Robertson, 1971; Fritschen, 1979) and have increased in swine housed in confinement. Poor floor surfaces are a primary cause and differences in claw size are known to increase the development of foot lesions (Penny et al., 1963; Fritschen, 1979; Jensen, 1979; Bryant et al., 1985a; Lepine et al., 1985). With the exception of biotin supplementation, other attempts to reduce the incidence and severity of foot lesions by altering the nutrition of swine have generally been unsuccessful (Kornegay, 1984). It is well established that an experimentally induced biotin deficiency in young pigs (Cunha et al., 1946; Gl~ittli et al., 1975; Gl~ittli, 1976; Geyer et al., 1983) and sows (Misir and Blair, 1983, 1984d) causes cracks in the sole and hoof that are responsive to biotin supplementation. Numerous reports in controlled and field studies 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 (Brooks et al., 1977; Comben, 1978; Halama, 1979; Triebel and Lobsiger, 1979; Pedersen and Udesen, 1980; Penny et al., 1980; Brooks and Simmins, 1981; Money and Laughton, 1981; Kopinski et al., 1982; Briihsauer and Triebel, 1983; de Jong and Sytsema, 1983; Bryant and Kornegay, 1984; Bryant et al., 1985d). Other researchers (Bane et al., 1980; Grandhi and Strain, 1980; Hamilton and Veum, 1984), however, have reported no change in incidence of foot lesions when biotin was supplemented to diets containing commonly used feedstuffs (sse Fig. 1 for a description of a classification system used by several researchers). Bryant and Kornegay (1984) reported that females fed a biotin-supplemented (220 p.p.b, during growth and 440 p.p.b, during gestation and lactation) corn- or wheat-based soybean meal diet (90--110 p.p.b, biotin) had fewer heel cracks, white-line horn cracks, heel--horn junction cracks and side-wall cracks than females fed the unsupplemented basal; the biotin response increased with age with the major effect occurring between 521 and 1090 days of age. Although the mode of action of biotin in the maintenance of hoof integ-

72

crac~

Longitudinal side wall

/

Vertical side-wall horn crack

Fig. 1. Toe lesion classificationsystem, adapted from Brooks et al. (1977).

rity is n o t clearly understood, it has been established that biotin increases the compressive strength and hardness of the h o o f wall, and decreases the hardness of the heel bulb tissue {Brooks and Simmins, 1981; Webb et al., 1984). A softening o f the h o o f wall was reported in earlier studies for biotin-deficient swine {Brooks et al., 1977; Comben, 1978), b u t the failure of Simmins and Brooks {1983) to find a significant increase in h o o f wall strength {compressive test) may have been a result of them choosing the leading edge of the h o o f to test. Webb et al. {1984) reported that the lateral wall of the h o o f {mid-abaxial side wall) was responsive to biotin supplementation, b u t that the leading edge of the h o o f was not. The leading edge of the h o o f was stronger and harder than the mid-abaxial wall. Webb et al. {1984) also found that biotin supplementation decreased the hardness of the heel bulb. A soft heel bulb presumably functions as a cushion, spreading the load evenly and minimizing stresses, and also absorbing strain energy. Both the keratin of the hard h o o f and the soft heel bulb need to be elastic and strong so as to have resilience as suggested by Shigley {1963} and Greenough et al. (1981). Penny et al. {1980) suggested that biotin supplementation was more

73 beneficial in preventing foot lesions than in curing established f o o t lesions. This hypothesis is supported by the research of Brooks and Simmins (1981) and Triebel and Lobsiger (1979), and indirectly by the findings of Bryant and Kornegay (1984). Bryant et al. (1985d) indicated that the reduction in the number and frequency of foot lesions resulting from biotin supplementation was generally greater as the presence of foot lesions increased in the herd. Geyer (1979) reported that it takes longer for the repair of horn lesions in sows than in growing gilts because of the slower growth rate of the horn of sows compared with growing pigs (5--6 vs 10 mm every 28 days), and because of the absolute size of the horn being much larger in the sow. Sp6rri (1976) showed that it t o o k a b o u t 2 months to see major reductions in the incidence and severity of f o o t lesions in pregnant sows fed a therapeutic level of biotin. In a Yugoslavian study (Bujas et al., cited b y Tagwerker, 1977) sows with severe lameness because of extensive f o o t lesions on the soft sole and dry eczematous skin were treated twice weekly with 5 mg injections of biotin, or a combination of injections and biotin feeding (550 p.p.b, in the diet). Four weeks of the combined treatment resulted in an almost complete cure, while injections used alone appeared to be a little less effective. Brooks (1982) points out that the variation in response to biotin supplementation m a y be explained by two factors. First, the clinical symptoms associated with biotin deficiency are not dissimilar from conditions having an alternative aetiology. Consequently, an improvement will not be achieved if the initial diagnosis of biotin deficiency was incorrect. Secondly, the response depends upon the opportunities provided for resolution of the lesions. Pigs housed on poorly designed floors have little o p p o r t u n i t y for recovery, as continuous traumatic injury exceeds the capacity of the h o o f for regrowth and repair. Thus, nutritional effects m a y be masked by the effect of p o o r floors. On the other hand, Geyer et al. (1984) have demonstrated that biotin has a marked influence on the development of a normal, resistant epidermis in the toe as well as in the skin and suggest that a toe horn of good quality has a better chance to resist the severe mechanical influences from b o d y weight movement and stable floors. Brooks (1982), based on only indirect evidence, suggested that the rate and magnitude of the recovery from foot lesions is directly related to the level and duration of biotin supplementation. He suggested that the lower level of supplementation can protect clinically healthy gilts thereby preventing the development of f o o t lesions, b u t higher levels are necessary to treat sows with foot lesions. Bryant and Kornegay (1984) reported that supplemental biotin did not affect the size (width and length) of front and hind medial and lateral toes of growing gilts and reproducing sows. Biotin supplementation has not been reported to improve overall structural soundness scores (Hamilton and Veum, 1984; Bryant et al., 1985d).

74 H A I R C O A T CONDITION

The role of biotin in maintaining a good haircoat condition and reducing dermatitis in experimentally induced biotin deficiencies is well documented for growing pigs (Cunha et al., 1946; Bfihlmann, 1973; Gl~ittli et al., 1975; Geyer et al., 1981, 1983) and sows (Misir and Blair, 1983; 1984b). Gl~ittli (1976) reported an improvement in skin lesions and amelioration of the haircoat when piglets affected with various eczematous skin lesions, exudative epidermitis and fissures on the coronet were supplemented with 5 mg biotin per head per day in the feed. They further showed that biotin deficient piglets were more susceptable to a dermal infection b y Staphylococcus hyicus (Gl~ittli, 1976; Von Stuker and Gl~ittli, 1976). In field trials, Cunha et al. (1968), Halama (1979) and Bautista (1984) reported a reduction in skin dermatitis and hair loss for sows after biotin supplementation. Bryant et al. (1985d) recorded a greater number of hairs per square centimeter and improved haircoat condition when sows were fed corn--soybean or wheat--soybean meal based diets supplemented with biotin; however, improvements were not observed until females were over 240 days of age. A histological examination of skin samples taken from the point of the shoulder and from the lower part of the ham of sows after three or four parities failed to show any differences between biotin supplemented and non-supplemented sows. An alteration in the fatty acid composition in adipose tissue occurs in a biotin deficiency (Biihlmann, 1973; Brooks, 1983; Misir and Blair, 1983; 1984d); there is a decrease in saturated fatty acids and an increase in unsaturated fatty acids. In field trials, Comben (1978) reported that many sows exhibited dry scaly skin and hair loss. However, there was no consistent response to biotin supplementation. Also, Penny et al. (1980) and Hamilton and Veum (1984) failed to demonstrate a difference in skin and haircoat condition between biotin-supplemented and non-supplemented sows. REPRODUCTION

The role of biotin in the reproductive process was established in rats (Kennedy and Palmer, 1946) and chickens (Cravens et al., 1942) in the 1940s. Terroine (1960) reported that a biotin deficiency severely retarded all facets of reproduction in rats and chicks. A dose--response relationship between biotin deficiency and congenital malformations was recently reported in mice and hamsters (Watanabe, 1983; Watanabe and Endo, 1983, 1984). However, the mean weight of live fetuses was only slightly reduced in biotin-deficient groups and their dams did n o t exhibit overt signs o f biotin deficiency such as alopecia, dermatitis or nervous irritability. Although Cunha et al. (1968) was the first author to suggest an improvement in sow reproductive performance from biotin supplementation, Michel and Mastachi {1981) and Misir and Blair (1983; 1984c,d) were first to

75 Ph.A .0,-~

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report experimentally induced biotin deficiency in reproducing sows. In addition to reduced reproductive performance (reduced litter size and increased weaning to first estrus interval), they reported deterioration in the skin and foot condition, alteration in the fatty acid composition of backfat and a drop in serum concentration of biotin. These conditions were responsive to biotin supplementation. Reports from field trials and controlled university studies in several countries during the last eight years have shown a beneficial effect of supplemental biotin on litter size, conception rate or interval from weaning to first estrus in sows (Brooks et al., 1977; Easter et al., 1979; Halama, 1979; Pedersen and Udesen, 1980; Michel and Mastachi, 1981; Penny et [] 20--J

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PARITY Fig. 2. Weaning to estrus or rebreeding interval of sows fed control and biotin-supplem e n t e d diets.

77

al., 1981; Serrano and de la Calera, 1981; Emms et al., 1983; Simmins and Brooks, 1983; Tribble et al., 1983; van der Heyde, 1983; Bautista, 1984; Bryant et al., 1985c), although differences were not statistically significant (P<0.05) in all reports (Table III). Other reports (Grandhi and Strain, 1980; Newman and EUiott, 1980; Hamilton and Veum, 1984) failed to show major improvement from supplemental biotin. The supplemental biotin levels reported ranged from 100 to 2000 p.p.b, diet and included basal diets containing feedstuffs of varying composition with total biotin levels ranging from 90 to 170 p.p.b. Age at puberty seems to be unaffected by biotin supplementation (Simmins and Brooks, 1983; Bryant et al., 1985c). Bryant et al. (1985c) and Halama (1979) reported an improvement in conception rate for sows fed supplemental biotin, but Grandhi and Strain (1980) failed to obtain a response. Several reports (Brooks, 1978; Halama, 1979; Pedersen and Udesen, 1980; Simmins and Brooks, 1983; Bautista, 1984; Bryant et al., 1985c) reported a reduction in the weaning to estrus interval for biotinsupplemented sows, while others (Grandhi and Strain, 1980; Penny et al., 1981; Emms et al., 1983; Tribble et al., 1983; Hamilton and Veum, 1984) observed no improvement due to biotin supplementation (Fig. 2). A significantly larger number of total or live pigs farrowed was reported for biotin-supplemented sows (Brooks et al., 1977; Halama, 1979; Penny et al., 1981; Emms et al., 1983; Simmins and Brooks, 1983; Tribble et al., 1983; Bryant et al., 1985c), and non-significant improvements were shown by others (Easter et al., 1979; Pedersen and Udesen, 1980; van der Heyde, 1983; Bautista, 1984). Improvements in total or live pigs farrowed were not observed for sows or gilts fed supplemental biotin (Grandhi and Strain, 121

I

I

supplemented

r]

unsupplemented

In

mi~

,- ,o.

il Ni

10,3

'

10

9.8

9

. ~i

~.~

;1111111 1

2

3 PARITY

4

Overall

Fig. 3. Live pigs per litter -- means (unweighted) of Bryant et al. (1985c), Simmins and Brooks (1983) and Tribble et al. (1983) for sows fed c o n t r o l and b i o t i n - s u p p l e m e n t e d diets.

78

1980; Hamilton and Veum, 1984). However, Hamilton and Veum {1984) reported that sows fed supplemental biotin for five parities weaned more pigs per litter overall than control sows. Several (three or four) parity studies (Halama, 1979; Penny et al., 1981; Simmins and Brooks, 1983; Tribble et al., 1983; Bryant et al., 1985c), reported biotin responses only after the first parity (Fig. 3). Improvements observed in live pigs farrowed were believed to be due to biotin supplementation. These seemed to persist as larger litters were weaned from supplemented sows (Halama, 1979; Pedersen and Udesen, 1980; Simmins and Brooks, 1983; Tribble et al., 1983; Bryant et al., 1985c). ASSESSMENT OF BLOOD AND TISSUE BIOTIN LEVELS

At present there is no readily applicable test to determine the biotin status of an animal, although some effort has been expended in developing such methods for several species during the past few years. Whitehead (1981) suggested that the most specific criteria for identifying and quantifying a biotin deficiency are biochemical. However, these methods are often very expensive and the animal has to be killed. Plasma biotin concentration may be useful as a test to evaluate the biotin status of a herd. Biotin levels in blood have been reported to be related to biotin intake for chickens (Frigg et al., 1973), humans (Berger, 1950) and pigs (Tagwerker, 1974; Gl~ttli et al., 1975; Brooks et al., 1977; Bryant et al., 1982, 1985b,c; Bri]lisauer and Triebel, 1983; Misir and Blair, 1983a, 1984c; Simmins and Brooks, 1983). Variability between individuals has been reported (Tagwerker, 1974; Brooks, 1982; Bryant et al., 1982, 1985c). Thus several animals should be sampled when using plasma biotin levels to assess the biotin status of a herd. Tagwerker (1974) reported that clinical s y m p t o m s of biotin deficiency were not observed in pigs having a plasma biotin concentration over 50 ng d l - ' . Bryant et al. {1985b,c) reported plasma biotin concentrations of 60--70 ng dl -~ for growing/finishing gilts and reproducing sows fed diets without supplemental biotin, while gilts or sows consuming the diet with supplemental biotin had plasma biotin concentrations of 100 to 150 ng dl -~ (Table IV). Brooks and Simmins (1980) observed plasma biotin levels of 192--196 ng dl -~ for sows fed supplemental biotin versus 103--111 ng dl -~ for sows without supplemental biotin. It has been shown that plasma biotin concentrations increased rapidly after feeding (Tagwerker, 1974; Brooks, 1982). Bryant et al. (1982) reported no diurnal variation in plasma biotin concentrations when growing-finishing gilts were fed twice daily; however, there was a rapid increase (proportional to the amount injected) when gilts were given a single injection of biotin with a less rapid decline over time (Fig. 4). This suggests that the plasma biotin levels of animals fed at least twice a day reach an equilibrium and do not vary greatly. The porcine placenta appears capable of accumulating large quantities

79 TABLE IV Least-squares means for various bichemical criteria as influenced by biotin supplementation 1 Item

Supplemental biotin (~g kg -~ ) 0

440

S.E. 2

Sow

Plasma biotin (ng d1-1 )3 Initial Gestation, d 109 s Weaning' Milk biotin (ug 1-1)3 Liver biotin (ug g-~ DM) 3 Liver pyruvate carboxylaseactivity 6

60 51 69 24 0.96

(55) 4 (97) (88) (23) (39)

10.2

(30)

141 132 150 68 1.34

(55) (107) (93) (30) (36)

4.3 2.9 3.1 2.8 0.06

10.5

(28)

2.31

Pig Plasma b i o t i n ( n g dl-1) 3 Day 0 Day 14 Liver b i o t i n ( ~ g g -~ DM)

425 (11) 62 (11) 0.79(17)

1299 (17) 313 (18) 0.73(24)

111 22

1Bryant et al. (1985c). 2Standard error of the treatment mean. 3Biotin effect (P<0.001). 4No. of observations/mean in parentheses. 5Mean for four parities. ~Expressed as nmo114 CO 2 converted per min per mg protein.

of biotin and of transporting them to the fetus, as evidenced by the very high plasma biotin levels in the fetus at birth (425 ng d1-1 for non-supplemented sows and 1299 ng d1-1 for biotin-supplemented sows; Table IV). At 14 days plasma biotin levels had decreased to 62 ng d1-1 in pigs nursing the non-supplemented sows and to 313 ng d1-1 for pigs nursing the supplemented sows. Liver biotin content, however, was not affected by biotin supplementation of sow diets. Sows consuming biotin-supplemented diets had a threefold increase in milk biotin concentration (Bryant et al., 1985c; Table IV}. Liver biotin concentration was higher for third or fourth parity sows fed supplemental biotin than for control sows {1.34 vs 0.96 p.p.m. DM), b u t liver pyruvate carboxylase activity was n o t different. Kopinski et al. (1982} observed elevated liver and kidney biotin c o n t e n t for 5-day-old pigs fed a cornflour-casein diet supplemented with 100 p.p.b, of biotin for 89 days. Breeding age gilts, fitted with ileal and cecal fistulas, were fed either a corn soybean meal diet (11.9% crude protein and 110 p.p.b, biotin} or a basal semipurified diet (11.9% crude protein and 10 p.p.b, biotin} with or without added biotin (270 or 700 p.p.b.) and/or 100 g per day of spray

80

100-

90ng per

80-

dl

70-

60-

50-

40.

3O

.

0

.

.

2

.

4

.

.

6

;

8

10

.

.

.

2 14 hours

Legend:

TRT

.

16 post

;

;

:

.

18

,

20

22

,

4 26

.

,

28

30

,

,

2 34

,

36

injection

~_ s h a m

a

~

~

low

; ; ; ; high

Fig. 4. Plasma biotin concentrations for gilts receiving three levels of biotin injection (Bryant et al., 1982).

dried egg albumen with cecal infusions of 2.56 g day -1 of oxytetracycline for 49 days (Hamilton et al., 1985a). The addition of biotin did not affect nitrogen or energy utilization at the end of the small or large intestine (Hamilton et al., 1985a), total aerobic or anaerobic bacterial fecal counts (Hamilton et al., 1985b), or plasma urea N and glucose levels (Hamilton et al., 1985c). Liver pyruvate carboxylase activity and histological examination of tongue, kidney and skin tissues did not reveal any symptoms of a biotin deficiency (Hamilton et al., 1985c). An experimentally induced biotin deficiency in weanling pigs did not influence the plasma levels of glucose and fatty acids and blood levels of lactic acid and pyruvic acid, but did decrease liver DNA and pyruvate carboxylase activity (Hamilton et al., 1982).

81 MISCELLANEOUS In a review of "The clinical symptoms of biotin deficiency in animals", Balnave (1977) pointed out that antibody production was impaired and resistance to certain diseases was reduced in biotin deficiency of rats and chicks. Wound healing was retarded in biotin-deficient rats and they were more susceptible to cold exposure. More recently, Kung et al. (1979) reported that the c y t o t o x i c T-cell response was altered in biotin-deficient rats. The role of biotin in antibody production, wound healing and disease resistance, however, has n o t been demonstrated in swine. Biotin has been implicated in the treatment and prevention of greasy pig disease (Gillespie, 1982; Fox, 1984); however, its role is n o t known and its effectiveness has not been well documented. Brooks et al. (1984, and unpublished data, 1984) have studied the interactive effects of growth stimulating copper levels and supplemental biotin in growing pigs. Preliminary data suggest that supplemental biotin enhances the growth response to copper. They indicate, however, that additional research is needed. REQUIREMENT We can only make an educated projection as to the most desirable level of biotin to use. Brooks (1978), based on the extrapolation of chicken data (Whitehead et al., 1974) to the sow using metabolic b o d y weight as the bases, estimated the total dietary biotin requirement of the sow to be 250--300 p.p.b, bioavallable biotin. Cereal grain-based diets usually supply from 90 to 170 p.p.b, total biotin of which, based on chick availability data, about 30--50% would be available. Using the estimated requirement suggested by Brooks (1978), and assuming that the availability of biotin synthesized in the large intestine is minimal, 100--200 p.p.b, of supplemental biotin could be required to meet the daily requirement of the pig. As discussed in the Introduction, several factors m a y influence the a m o u n t of biotin that is needed in the diet to meet the daily requirement of the pig. A suggested allowance of 300 p.p.b, for growing and breeding pigs is given in the Ministry of Agriculture, Fisheries and F o o d Booklet No. 2089. The Agricultural Research Council (ARC, 1981) does not give a requirement, but suggests that dietary biotin m a y be necessary for very young pigs and sows. The National Research Council (NRC, 1979) suggest a level of 100 p.p.b, for all classes, b u t indicate that requirements have not been established. FUTURE RESEARCH NEEDS Findings from well controlled short-term and long-term studies, field

82

studies and reports are accumulating that show that under some conditions supplemental biotin will improve litter size, conception rate, weaning to estrus interval, f o o t lesions and haircoat conditions of swine; however, many questions concerning the availability, requirement and role of biotin remain unanswered: 1. The availability of the biotin in various feedstuffs for swine is unknown. Present availability values were derived using chicks; they may or may not be applicable to swine. 2. The role of bacterial synthesis and the extent of absorption and utilization is unknown; indirect evidence suggests that it may vary for different sizes of swine. 3. The influence of various dietary factors (fat and fatty acids, copper, ascorbic acid, bacterial fermentation, amino acid and fiber) is poorly understood or unknown. 4. The biotin requirement and the need for supplemental biotin for the various classes of swine under differing environmental and nutritional conditions is virtually unknown. 5. The mechanism of involvement of biotin in f o o t health, skin and haircoat condition and reproduction is not clearly understood. 6. The role of biotin in disease resistance is not known for swine. 7. Easy to use and reliable methods of assessing the biotin status of various classes of swine are not available.

REFERENCES Adams, C.R., Richardson, C.E. and Cunha, T.J., 1967. Supplemental biotin and vitamin B for swine. J. Anita. Sci., 1 6 : 9 0 3 (Abstr.). Anderson, J.O. and Warnick, R.E., 1970. Studies of the need for supplemental biotin in chick rations. Poult. Sci., 49: 569--578. Anderson, P.A., Baker, D.H. and Mistry, S.P., 1978. Bioassay determination of the biotin content of corn, barley, sorghum and wheat. J. Anita. Sei., 47: 654--659. Anonymous, 1979. Multiple biotin-dependent carboxylase deficiencies associated with defects in immunity. Nutr. Rev., 37 : 289--301. ARC, 1981. The nutrient requirements of pigs. Agricultural Research Council, Commonwealth Agricultural Bureaux, Slough, England. Baker, D.H., 1978. Nutrient bioavailability in feedstuffs: methodology for determining amino acid and B-vitamin availability in cereal grains and soybean meal. Georgia Nutr. Conf., 15--17 February, pp. 1--2. Baker, H.O., Frank, O., Thompson, A.D. and Feingold, S., 1969. Vitamin distribution in red blood cells, plasma, and other body fluids. Am. J. Clin. Nutr., 22: 1469--1475. Balnave, D., 1977. Clinical symptoms of biotin deficiency in animals. Am. J. Clin. Nutr., 30: 1408--1413. Bane, D.P., Hilley, H.D. and Meade, R.J., 1980. Influence of d-biotin and housing on hoof lesion in swine. J. Anita. Sci., 51 (Suppl. 1): 138. Bautista, G.C., 1984. Efecto de la suplementacion de biotina ,, reproductive de la cerda. Thesis, Universidad autonomu D,

83 Berger, H., 1950. Urinary excretion o f biotin in children without pathological skin conditions with special reference to the relations of seborrhoeic dermatitis and eczema. Int. Z. Vitaminforsch., 22: 190--199. Brooks, P.H., 1978. The effect of dietary biotin on the incidence of foot lesions and on the reproductive performance of the sow. Proc. Vitamin Day Symp. Roche Products, Paris, 28 pp. Brooks, P.H., 1982. Biotin in pig nutrition. Pig News Inf., 3 : 29--32. Brooks, P.H., 1983. Vitamin responsive conditions in breeding pigs. Recent Adv. Anim. Nutr., pp. 81--102. Brooks, P.H. and Simmins, P.H., 1980. Recent findings on the effect of biotin supplementation on reproductive performance and the maintenance of hoof integrity in the female pig. In: Recent Research on the Response of Pooltry and Pigs to Supplementary Biotin. Roche Information Service No. 1775. Brooks, P.H. and Simmins, P.H., 1981. The effect of supplementing breeding pig diets with biotin on the maintenance of hoof integrity. In: D. Giesecke, G. Dirksen and M. Stangassinger (Editors) Proc. 4th Int. Conf. Production Diseases in Farm Animals, Munich, West Germany, pp. 1--4. Brooks, P.H., Morgan, D.T. and Hastings, K.E., 1984. The effect of dietary biotin on the response of promotes. Proc. 8th Int. Pig Vet. Congr., 27--31 Aug., Ghent, Belgium, p. 316. Brooks, P.H., Smith, D.A. and Irwin, V.C.R., 1977. Biotin supplementation of diets; the incidence of foot lesions and the reproductive performance of sows. Vet. Rec., 101 : 46--50. BrUlisauer, F. and Triebel, D.F., 1983. Einfluss einer erhShten Biotindosierung. St. Galler Bauer 70, No. 6, pp. 11--12. Bryant, K.L. and Kornegay, E.T., 1984. Influence of supplemental biotin on growth and development of toes and toe lesions and on hair quality in female swine. Proc. 8th Int. Pig Vet. Congr., 27--31 Aug., Ghent, Belgium, p. 314. Bryant, K.L., Kornegay, E.T., Knight, J.W., Notter, D.R. and Bartlett, H.S., 1982. Influence of biotin injection on plasma biotin concentrations in swine. VPI and SU Livest. Res. Rep., No. 2, pp. 53--58. Bryant, K.L., Kornegay, E.T. and Notter, D.R., 1985a. Supplemental biotin for swine. IV. Influence of toe size, toe location and biotin level on toe lesions and the influence of biotin level on hair scores in confinement housed gilts and sows. J. Anita. Sci., 61 : in press. Bryant, K.L., Kornegay, E.T., Knight, J.W., Webb, Jr., K.E. and Notter, D.R., 1985b. Supplemental biotin for swine. I. Influence on feedlot performance, plasma biotin and toe lesions in developing gilts. J. Anita. Sci., 60: 136--144. Bryant, K.L., Kornegay, E.T., Knight, J.W., Webb, Jr., K.E. and Notter, D.R., 1985c. Supplemental biotin for swine. II. Influence of supplementation to corn- and wheatbased diets on reproductive performance and various biochemical criteria of sows during four parities. J. Anita. Sci., 60: 145--153. Bryant, K.L., Kornegay, E.T., Knight, J.W., Veit, H.P. and Notter, D.R., 1985d. Supplemental biotin for swine. III. Influence of supplementation to corn- and wheatbased diets on the incidence and severity of toe lesions, hair and skin characteristics and structural soundness of sows housed in confinement during four parities. J. Anim. Sci., 60: 154--162. Buenrostro, J.L. and Kratzer, F.H., 1983. Effect of lactobacillus innoculation and antibiotic feeding of chickens on availability of dietary biotin. Poult. Sci., 52: 2022-2029. Bilhlmann, R., 1973. Changes in fat metabolism with biotin deficiency in swine. Ph.D. Dissertation, University of Basle. Comben, N., 1978. Biotin for breeding sows. Field experiences 1976--1978. Proc. Roche Syrup. October, London, pp. 1--22.

84 Cravens, W.W., Sebesta, E.E., Halpin, J.G. and Hart, E.B., 1942. Effect of biotin on reproduction in the domestic fowl. Proc. Soc. Exp. Biol. Med., 50 : 101--104. Cunha, T.J., 1971. Present status on vitamin K and biotin for the pig. Feedstuffs, 43 (9): 20. Cunha, T.J., Adams, C.R. and Richardson, C.E., 1968. Observations on the biotin needs of the pig. Feedstuffs, 40(43): 22--26. Cunha, T.J., Lindley, D.C. and Ensminger, M.E., 1946. Biotin deficiency syndrome in pigs fed desiccated egg white. J. Anita. Sci., 5 : 219--225. Cunha, T.J., Colby, R.W., Bustad, L.K. and Bone, J.F., 1948. The need for and interrelationship of folic acid, anti-pernicious anemia liver extract, and biotin in the pig. J. Nutr., 36: 215--225. De Jong, M.F. and Sytsema, J.R., 1983. Field experience with d-biotin supplementation to giltand sow feed. Vet. Q., 5: 58-67. Drochner, W. and VSlker, L., 1984. Unpublished data quoted in W. Drochner, Spurenelement- und Vitaminversorgung des Ferkels. Proc. Int. TAD-Symp., Cuxhaven/Wingst (in press). Easter, R.A., Corley, J.R., Esch, N.W. and Wende, D.L., 1979. Vitamin B6, biotin, folacin and thiamin supplementation of corn--soybean meal diets. J. Anita. Sci., 49(Suppl. 1): 239. Easter, R.A., Michel, E.J., Anderson, P.A. and Corley, J.R., 1978. Effect of vitamin B6 and biotin additions to corn--soybean meal diets for growing--finishing swine. J. Anita. Sci.,47:300 (Abstr.). Emms, Y., Mercy, A.R. and Steele, P., 1983. The effects of biotin supplementation on reproductive performance of sows. XXII World Vet. Congr., Aug. Perth, Australia, p. 17. Fox, R.J., 1984. Countering biotin deficiency. Pig Am., September: 24. Frigg, M., 1976. Bio-availabilityof biotin in cereals.Poult. Sci., 55: 2310--2318. Frigg, M., 1984. Available biotin content of various feed ingredients. Poult. Sci., 63: 750--753. Frigg, M. and Brubacher, G., 1976. Biotin deficiency in chicks fed a wheat-based diet. Int. J. Vit. Nutr. Res., 46: 314--321. Frigg, M. and Torhorst, J., 1982. Autoradiographic localisation of 3H-biotin in chick tissues. Int. J. Vit. Nutr. Res., 52: 417--422. Frigg, M., Weiser, H. and Bollinger, A., 1973. Biotin deficiency in chicks. Clinical and chemical alterations. Proc. 5th Int. Congr. World Vet. Poult. Assoc., Munich, Vol. 2, p. 1286. Fritschen, R.D., 1979. Housing and its effect on feet and leg problems. Proc. Pig Vet. Soc., 5: 95--98. Geyer, H., 1979. Morphologie und Wachstum der Schweineklaue. Grundlagen f~irStallboden-gestaltung und Klauenpathologie. Habilitationsschrift Zilrich. Kurzfassung: Schweiz. Arch. Tierheilk.,121: 275--293. Geyer, H., Pohlenz, J. and Volker, L., 1981. Morphologische und histochemische Untersuchungen von Haut, Schleimh~uten und Klauen bei Schweinen mit experimentellem Biotinmangel. Zentralbl. Veterinaermed. A., 28: 574--592. Geyer, H., Schulze, J. and Tagwerker, F., 1983. Macro- and micropathological claw lesions in biotin-deficient pigs. 5th World Conf. Anita. Prod., 14--19 August, Tokyo, p. 138. Geyer, H., Schulze, J. and Tagwerker, F., 1984. Claw alterations in the young pig induced by experimental biotin deficiency. Int. Pig Vet. Congr., Aug. 27--31, Ghent, Belgium, p. 315. GiUespie, T.G., 1982. Biotin supplementation in greasy pig disease. Mod. Vet. Pract., 63: 724--726. Gl~ttli, H.R., 1975. Zur Klinik des experimentell erzeugten Biotinmangels beim Schwein und Mitteilung erster Ergebnisse aus Feldversuchen. Schweiz. Arch. Tierheilkd., 117: 135--144.

85 Gl~ttli, H.R., 1976. Experimental biotin deficiencies and biotin responsive condition in pigs. Proc. 4th Int. Pig Vet. Congress, Ames, Iowa, p. A10. G1;~ttli, H.R., Pohlenz, J., Streiff, K. and Ehrensperger, F., 1975. Clinical deficiency in pigs. Zentralbl. Veterinaermed. A., 22: 102--116. Grandhi, R.R. and Strain, J.H., 1980. Effect of biotin supplementation on reproductive performance and foot lesions in swine. Can. J. Anim. Sci., 60 : 961--969. Greenough, P.R., MacCullum, F.J. and Weaver, A.D., 1981. Lameness in Cattle. 2nd edn. Wright, Bristol, p. 97. Halama, A.K., 1979. Biotin deficiency in breeding pigs. Wien. Tierarztl. Monatsschr., 66(12): 370--374. Hamilton, C.R. and Veum, T.L., 1984. Response of sows and litters to added dietary biotin in environment-regulated facilities. J. Anita. Sci., 59: 151--157. Hamilton, C.R., Veum, T.L., Jewell, D.E. and Siwecki, J.A., 1982. The biotin status of weanling pigs fed semipurified diets as evaluated by plasma and hepatic parameters. Int. J. Vit. Nutr. Res., 53: 44--50. Hamilton, C.R., Dove, C.R., Zinn, G.M. and Veum, T.L., 1985a. Effect of dietary biotin on non-gravid gilts. I. Nitrogen and energy balance. University of Missouri Swine Res. Rep., pp. 64--73. Hamilton, C.R., Dove, C.R., Iannotti, E. and Veum, T.L., 1985b. Effect of dietary biotin on non-gravid gilts. II. Total aerobic and anaerobic fecal counts. University of Missouri Swine Res. Rep., pp. 74--78. Hamilton, C.R., Dove, C.R., Zinn, G.M. and Veum, T.L., 1985c. Effect of dietary biotin on non-gravid gilts. III. Metabolic parameters and histopathology. University of Missouri Swine Res. Rep., pp. 79--83. Hanke, H.E. and Meade, R.J., 1972. Biotin and pyridoxin additions to diets for pigs weaned at an early age. University of Minnesota Swine Res. Rep., pp. 18--19. Hardinge, M.G. and Crooks, H., 1961. Lesser known vitamins in foods. J. Am. Diet. Assoc., 38: 240--245. Jensen, A.H., 1979. The effect of environmental factors, floor design and materials on performance and on foot and limb disorders in growing and adult pigs. Proc. Pig Vet. Soc., 5: 85--93. Kennedy, C. and Palmer, L.S., 1946. Biotin deficiency in relation to reproduction and lactation. Arch. Biochem., 7: 9--13. Kopinski, J.S., Bryden, W.L. and Leibholz, J., 1982. Biotin deficiency in the young pig. Proc. Nutr. Soc. Aust., 7 : 1 5 1 (Abstr.). Kopinski, J.S., Bryden, W.L. and Leibholz, J., 1983. Biotin synthesis and absorption in the pig. Proc. Nutr. Soc. Aust., 8 : 2 0 5 (Abstr.). Kornegay, E.T., 1984. Influence of nutrition on toe and hoof development, bone mineralization and structural soundness in swine. Florida Nutr. Conf., 11--13 January, pp. 129--149. Kornegay, E.T. and Bryant, K.L., 1981. The role of supplemental biotin in swine nutrition. Feedstuffs, 53(10): 32--34. Kung, J.T., MacKenzie, C.G. and Talmage, D.W., 1979. The requirement for biotin and fatty acids in cytotoxic T-ceU response. Cell Immunol., 48: 100--110. Lee, H.-M., Wright, L.D. and McCormick, D.B., 1972. Metabolism of carboxyl-labeled ~4C-biotin in the rat. J. Nutr., 102 : 1453--1464. Lehrer, W.P., Jr., Wiese, A.C. and Moore, P.R., 1952. Biotin deficiency in suckling pigs. J. Nutr., 47 : 203--212. Lepine, A.J., Kornegay, E.T., Notter, D.R., Veit, H.P. and Knight, J.W., 1985. Foot and leg measurements, toe lesions, soundness scores and feedlot performance of crossbred boars as influenced by nutrition and age. Can. J. Anim. Sci., 65: 459--472. Lindley, D.C. and Cunha, T.J., 1946. Nutritional significance of inositol and biotin for the pig. J. Nutr., 32: 47--59. Lynen, F., 1967. The role of biotin-dependent carboxylations in biosynthetic reactions. Biochem. J., 102: 381--400.

86 McCormick, D.B., 1975. Biotin. Nutr. Rev., 33: 97--102. Meade, R.J., 1971. Biotin and pyridoxine supplementation of diets for growing pigs. University of Minnesota Swine Res. Rep., p. 45. Michel, E. and Mastachi, I., 1981. La biotine en la nutricion de la cerda gestante. AgroSentesis, 12 (2) : Sintesis Porcina, 12(1) : 3sp--10sp. Misir, R. and Blair, R., 1983. Effects of biotin deficiency on changes in hair coat, skin and foot condition and backfat composition of sows. J. Anita. Sci., 57(Suppl. 1): 257. Misir, R. and Blair, R., 1984a. Bioavailable biotin from cereal grains for broiler chicks as affected by added dietary fiber. Poult. Sci., 63(Suppl. 1): 152. Misir, R. and Blair, R., 1984b. Bioavailable biotin from cereal grains for turkey poults. Can. J. Anita. Sci., 6 4 : 1 0 8 9 (Abstr.). Misir, R. and Blair, R., 1984c. Effect of biotin deficiency on the reproductive performance of sows over two parities. Can. J. Anim. Sci., 6 4 : 1 9 6 (Abstr.). Misir, R. and Blair, R., 1984d. Effect of biotin supplementation on the performance of biotin deficient sows. J. Anim. Sci., 59(Suppl. 1): 254. Money, D.F.L. and Laughton, G.L., 1981. Biotin-responsive lameness in New Zealand pigs. N.Z. Vet. J., 28: 33--34. Newman, C.W. and Elliott, D.O., 1980. Supplemental pyridoxine, biotin and choline in gestation diets of first parity sows. J. Anirn. Sci., 50(Suppl. 1): 215. NRC, 1979. Requirements of Domestic Animals, No. 2. Nutrient Requirements of Swine. 8th edn. National Academy of Science--National Research Council, Washington, DC, 52 pp. Olson, R.E. and Suttie, J.W., 1977. Vitamin K and v-carboxyglutamate biosynthesis. Vit. Horm., 35: 59--108. Pedersen, O.G. and Udesen, F., 1980. Testing biotin in sows. Communication No. 18, Danish Committee on Pig Breeding and Production, Joint Office of Cooperative Slaughterhouses, Copenhagen. Penny, R.H.C. and Johnston, A.M., 1983. Biotin supplementation of sow diets. Vet. Ann., 23: 137--142. Penny, R.H.C., Osborne, A.D. and Wright, A.I., 1963. The causes and incidence of lameness in store and adult pigs. Vet. Rec., 75: 1225--1240. Penny, R.H.C., Cameron, R.D.A., Johnson, S., Kenyon, P.J., Smith, H.A., Bell, A.W.P., Cole, J.P.L. and Taylor, J., 1980. Foot rot of pigs: the influence of biotin supplementation on foot lesions in sows. Vet. Rec., 107 : 350--351. Penny, R.H.C., Cameron, R.D.A., Johnson, S., Kenyon, P.J., Smith, H.A., Bell, A.W.P., Cole, J.P.L. and Taylor, J., 1981. Influence of biotin supplementation on sow reproductive efficiency. Vet. Rec., 109: 80--81. Peo, E.R., Jr., Wehrbein, G.F., Moser, B., Cunningham, P.J. and Vipperman, Jr., P.E., 1970. Biotin supplementation of baby pig diets. J. Anita. Sci., 3 1 : 2 0 9 (Abstr.). Pohlenz, F., 1974. Klinische und morphologische Befunde beim experimentellen Biotinmangel des Schweines. Fortschr. Veterin~rmed. Heft, 20:10. Kongressbericht, pp. 249--252. Scheiner, J. and de Ritter, E., 1975. Biotin content of feedstuffs. J. Agric. Food Chem., 23: 1157--1162. Scott, M.L., 1981. Importance of biotin for chickens and turkeys. Feedstuffs, 53(8): 59--67. Serrano, Robres A. and de la Calera, Garcia F., 1981. Influence of a continuous biotin supplementation in the feed on the reproductive performance of breeder sows. Proc. 32nd Ann. Meeting Europ. Assoc. Anita. Prod., Zagreb, pp. 1--8. Shigley, J.E., 1963. Mechanical Engineering Design. McGraw-Hill, New York, p. 110. Simmins, P.H. and Brooks, P.H., 1983. Supplementary biotin for sows: effect on reproductive characteristics. Vet. Rec., 112 : 425--429.

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RESUME

Kornegay, E.T., 1986. La biotine en production porcine : une revue. Livest. Prod. Sci., 1 4 : 6 5 - - 8 9 (en anglais). La biotine, vitamine hydrosoluble indispensable, est le cofacteur de nombreux syst~mes enzymatiques responsables de r~actions de caxboxylation et de transcarboxylation. Ces r~actions jouent un rSle essentiel dans le m~tabolisme des glucides et des acides nucl~iques, dans la synth~se des acides gras, des prot~ines et des purines, et dans la d~samination des acides amines. O n croyait autrefois qu'il n'6tait pas n~cessaire de suppl~menter en biotine les aliments destines au porc car elle est largement r~pandue dans les mati~res premieres couramment utilis~es dans les r~gimes, et parce qu'eUe est

88 synth~tis~e par la flore intestinale du porc. Mals l'int~r~t pour cette vitamine en nutrition porcine a ressurgi ~ la suite de plusieurs rapports d'~levages du milieu des ann~es 1970 d~crivant des maladies d o n t les symptSmes ~taient similaires ~ ceux observes ~ la suite de carences exp~rimentales en biotine (mauvaise croissance des jeunes porcs, falble taux plasmatique de biotine, alop~cie et formation de pustules sur la peau, l~sions de l'onglon et de la sole des doigts). On a constat~ ~ plusieurs reprises que ces manifestations r~pondaient ~ la supplementation en biotine, mais il n'y avait g~n~ralement pas d'animaux t~moins si bien qu'il n'~tait pas possible de conclure de fa~on d~finitive. Des r~sultats d'exp~riences bien contrSl~es, en particulier d'~tudes ~ long terme sur truies (trois quatre port~es successives), sont ~ present disponibles. Iis sugg~rent que la biotine peut am~liorer un ou plusieurs des crithres suivants : faible taille de portcSe, taux de conception, intervalle sevrage-oestrus, l~sions des doigts et mauvais ~tat des soies. Les teneurs en biotine du lait et du plasma des truies et des porcelets sont plus ~lev~s apr~s supplementation du r~gime en biotine. Les aliments contiennent 20 ~ 2 600 ppb de biotine, reals sa disponibilit~ pour le porc n'a pas ~t~ d~terminde. Cependant, les valeurs obtenues chez le poulet sugg~rent que la biotine des c~r~ales et des sources azot~es usueUes est faiblement disponible. De nombreux facteurs de l'environnement et de ralimentation peuvent influencer la manifestation d'une carence en biotine chez le porc, ou modifier le taux de biotine du r~gime n~cessaire aux besoins de ranimal. En utilisant les aliments actuellement disponibles dans les conditions modernes de production porcine, une carence marginale en biotine est possible. De nombreuses questions restent n~anmoins sans r~ponse, et d'autres ~tudes sont n~cessaires pour une meilleure comprehension du rSle de la biotine darts la nutrition du porc. Les producteurs de porcs constatant de mauvaises performances de reproduction associ~es ~ des pertes excessives de soies et des l~sions graves des pattes peuvent ~valuer la teneur en biotine du r~gime des truies et envisager une suppl~nentation en biotine.

KURZFASSUNG Kornegay, E.T., 1986. Die Bedeutung yon Biotin in der Schweineproduktion: Ein iJberblick, Livest. Prod. Sci., 14 : 65--89 (auf englisch). Biotin, ein lebensnotwendiges und wasserl~sliches Vitamin, ist als Reaktionspartner in einer Anzahl von E n z y m e n verantwortlich fiir die Bildung der Karboxylgruppe und deren Ubertragung bei chemischen Reaktionen. Diese Reaktionen spielen eine wesentliche Rolle im Stoffwechsel der Kohlenhydrate und Nukleins~iuren, bei der Synthese yon Fetts~iuren Eiweissen und Purinen sowie bei der Abspaltung yon Aminos~iuregruppen. In der Vergangenheit nah.m m a n an, dass eine Biotinerg~/nzung in der Schweinefiitterung nicht erforderlich sei, weil Biotin in den ~blicherweise bei der Rezeptur der Rationen verwendeteten Futtermitteln ausreichend vorkommt und es ausserdem bekannt war, dass Biotin yon der Darmflora des Schweines synthestisiert werden kann. Das Interesse an der Biotinern~hrung der Schweine wurde jedoch wieder geweckt, als Mitte der 70er Jahre verschiedene Meldungen aus der Praxis iiber Krankheitserscheinungen berichteten, die denjenigen glichen, die bei experimentellem Biotinmangel erzeugt werden konnten (schlechtes Wachstum bei jungen Schweinen, niedriger Biotingspiegel im Blut, Haarlosigkeit und Pustelbildung der Haut sowie Verletzungen an Huf und Sohle). Zwar wurde fiir diese Zust~inde in vielen F~/llen die Biotinversorgung verantworlich gemacht, jedoch konnten keine klaren Schlussfolgerungen gezogen werden, da Kontrollbehandlungen gewShnlich nicht vorhanden waren. N u n liegen jedoch Ergebnisse exakter Forschungsarbeiten vor -- insbesondere aus Langzeitstudien mit Sauen (3 -- 4 Gravidit~iten) -- die darauf hindeuten, dass eine Biotinzufiitterung zu einer Verbesserung eines oder mehrerer der folgenden Merkmale fiihren kann: Geringe WurfgrSsse, Konzeptionsrate bzw. Intervall

89 zwischen dem Absetzen und der n~ichsten Brunst, Fussverletzungen und geringe Behaarung. Ausserdem soll der Biotingehalt in Milch und Blut bei Sauen und Ferkeln ansteigen, sobald Biotin zusiitzlich gefiittertwird. Der Gehalt an Biotin schwankt in den Futtermitteln zwischen 20 und 2600 ppb, jedoch liegen noch keine Werte fiber die Verfiigbarkeit bei Schweinen vor, obwohl die H S h e der biologischen Verwertbarkeit bei Hiihnern darauf hinweist, dass das Biotin beim Einsatz herkSmmlicher Getreide- und Eiweissquellen nur gering verfiigbar ist. Zahlreiche Umwelt- und Ern~ihrungsfaktoren kSnnen das Auftreten eines Biotinmangels beim Schwein beeinflussen bzw. den ffir den Bedarf des Tieres erforderlichen Biotingehalt im Futter ver~indern. Ein marginaler Biotinmangel ist beim Einsatz yon zur Zeit gebr~iuchlichen Futtermitteln und unter den Bedingungen einer modernen Schweineproduktion durchaus mSglich. Natiirlich gibt es eine Reihe unbeantworteter Fragen, aus denen sich die Notwendigkeit ergibt, mehr Forschung hinsichtlich eines besseren Verst~ndnisses iiber die Rolle des Biotins in der Schweineern~ihrung zu betreiben. Wenn Schweineproduzenten eine geringe Fortpflanzungsleistung verbunden mit iiberm~sigem Haarausfall sowie h~iufigen Fussverletzungen in ihrem Sauenbestand beobachten, sollten sie den Biotingehalt ihres Sauenfutters berechnen und eine Biotinzufiitterung erw~igen.