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Poultry: Biotin

Deficiency

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 and poultry.

Biotin requirement in the turkey is higher than that of the chick, so more field problems with biotin deficiency have arisen in turkeys. Biotin deficiency in chicks and poults results in a wide range of clinical signs (Illus. 1, 2, 3 and 4) with considerable variation in time of appearance of individual signs (NRC, 1994). Principal effects in both species are reduced growth rate and feed efficiency, disturbed and broken feathering, dermatitis and leg and beak deformities. First signs of a deficiency are usually growth depression and loose feathering; signs of dermatitis appear next; and finally, disorders of the leg (perosis) and beak become apparent. However, Li et al. (1994) noted that the first signs of biotin deficiency of broiler chicks were lesions on the foot pads in the second week, while growth reduction did not occur until the third week.

Illustration 1
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With dermal lesions, bottoms of feet become rough and callused and contain deep fissures that show some hemorrhaging. Foot problems are usually exacerbated by bacterial invasion of lesions. Also, toes may become necrotic and slough off. Tops of feet and legs usually show only a dry scaliness. Lesions appear in the corner of the mouth and slowly spread to the whole area around the beak. Eyelids eventually swell and stick together.

Dermal lesions have a characteristic order of appearance, although speed of onset depends on severity of deficiency. For chicks fed severely biotin-deficient diets, dryness and flakiness of the feet first become noticeable at about 14 days of age, and slight encrustations and superficial fissures develop on the undersurfaces of the feet at about 18 days (Whitehead, 1978). These increase in severity until by about 25 days, the fissures are hemorrhagic. Between three and four weeks, dermatitis may also appear on the eyelids, and as this develops, the bird becomes unable to keep the lids apart, and they eventually stick together.

Dermal lesions are similar to those of pantothenic acid deficiency. However, with biotin deficiency, lesions occur first on feet and later around the beak and eyes, whereas in pantothenic acid deficiency, signs occur first in corners of mouth and eyes and only in prolonged cases appear on the feet. Because of the difficulty of making a differential diagnosis between the two vitamins, it is often necessary to examine the diet composition and decide which is more likely to be deficient. In commercial poultry production both vitamins should be supplemented in a corn-soybean meal ration.

Biotin deficiency is a cause of hock disorders in both poults and chicks. The major deficiency sign affecting market turkeys is severe leg weakness. Lesions caused by biotin deficiency are brought about by chondrodystrophy, a condition in which bone mineralization is normal but linear growth of long bones is impaired. Chondrodystrophy caused by biotin deficiency can result in shortening of metatarsal bones and perosis. Perosis occurs when irregular bone development results in enlargement and deformity of the hock joint (Illus. 5). Crippling in turkeys can occur as early as three to four weeks of age. Often it seems to disappear at six to seven weeks. Then it reappears with great severity between 13 to 16 weeks (Scott, 1981). At this stage the birds are unable to walk and thus can be trampled or cannibalized by other turkeys. Perosis can occur at any stage. In general, young chickens are less susceptible to leg disorders than poults, although biotin deficiency does cause problems of the same type in chicks as in poults (Whitehead, 1978). Once the deformities of perosis occur, biotin administration is not effective.

Illustration 5

Bain and Newbrey (1988) report that "twisted leg" is the most common limb disorder in broiler chickens and that biotin deficiency adversely affected tibiotarsal bone growth. Tibiotarsal bones are frequently longitudinally distorted in biotin-deficient poultry. Presumably, reduced biotin prevents ready formation of prostaglandins from essential fatty acids, and bone growth fails to respond to stresses during development (Watkins et al., 1989).

Low dietary fat and the necessity for fatty acid synthesis lead to an abnormal array of fatty acids that predisposes poultry to a fatty liver and kidney syndrome (FLKS) (Whitehead, 1988). This condition, which has caused heavy economic losses in commercial broiler flocks, was found to be due to suboptimal dietary biotin coupled with certain nutritional and environmental stress factors. Situations increasing the metabolic rate of biotin-dependent enzymes, such as low fat or protein levels, aggravate the condition. Although the signs of FLKS are not those of classic biotin deficiency, they can be virtually eliminated by supplementation of chick starter or breeder diets with biotin.

For turkeys, dry and brittle feathers usually accompany the other signs of clinical biotin deficiency. Bronze poults can exhibit white barring of the feathers, usually affecting just tom turkeys. Likewise, deficient chicks have rough and broken feathering, with head and breast feathers often having a spiky, matted appearance.

Poor egg production and hatchability result from clinical biotin deficiency (Robel, 1991; NRC, 1994). For breeder chickens, biotin deficiency reduces hatchability but is less likely to affect egg production. Clinical signs and conditions associated with biotin deficiency in chick embryos and (or) newly hatched chicks include bone deformities (perosis); impaired muscular coordination (ataxia); skeletal deformities (e.g., crooked legs); extensive foot webbing; abnormal cartilage development (chondrodystrophy); embryonic mortality; twisted, malformed beak ("parrot beak"); and reduced size. Ferguson et al. (1961) reported that biotin deficiency in turkeys resulted in a marked decrease in hatchability and a high rate of embryonic mortality during the first week of incubation. At the end of the second week, hatchability decreased from 83% to 14%. At the end of the third week hatchability was zero. Embryonic mortality because of inadequate biotin occurs largely during the last three days of incubation. Feeding the biotin-deficient diet resulted in an abrupt decrease in egg production after 13 weeks.

 

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