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Poultry: Vitamin K
Deficiency

The major clinical sign of vitamin K deficiency in all species is impairment of blood coagulation. Other clinical signs include low prothrombin levels, increased clotting time and hemorrhaging. In its most severe form, a lack of vitamin K will cause subcutaneous and internal hemorrhages, which can be fatal. Vitamin K deficiency can result from dietary deficiency, lack of microbial synthesis within the gut, inadequate intestinal absorption or inability of the liver to use the available vitamin K. Clinical signs of vitamin K deficiency are similar in all poultry species, with most research completed with newly hatched chicks and growing broilers.

A deficiency of vitamin K causes a reduction in the prothrombin content of the blood and, in the chick, may reduce the quantity in the plasma to less than 2% of normal. Since the prothrombin content of the blood of normal, newly hatched chicks is only about 40% that of adult birds, very young chicks are readily affected by a deficiency of vitamin K. A carryover from the parent hen to the chick has been demonstrated (Almquist, 1971). Laying hens fed on a diet containing vitamin K1 or vitamin K3 at 10 to 100 mg per kg (4.5 to 45 mg per lb) produced vitamin K-rich eggs (Suzuki and Okamoto, 1997). Therefore, breeder hen diets should be supplemented with vitamin K to ensure good chick health. Laying hens fed a diet deficient in vitamin K produce eggs low in the vitamin, and when the eggs are incubated, the chicks produced have low reserves and a prolonged clotting time. Adverse effects on blood clotting are not apparent until after hatching, when hemorrhaging and mortality may occur should trauma be encountered. As a consequence, the chicks may bleed to death from an injury as slight as that caused by debeaking or wing banding (Illus. 1).
Illustration 1

In very young chicks deficient in vitamin K, blood coagulation time begins to increase after five to 10 days of age, with clinical signs occurring most frequently in chicks two to three weeks after they begin consuming a vitamin K-deficient diet. Hemorrhages often occur in any part of the body, either spontaneously or as a result of an injury or bruise. Postmortem examination usually reveals accumulations of blood in various parts of the body; sometimes there are petechial hemorrhages in the liver and almost invariably there is erosion of the gizzard lining.

Even though inadequate dietary vitamin K alters bone osteocalcin, signs associated with the skeletal system are not as apparent as blood clotting problems. Although blood clotting was impaired and there was a reduction in bone gamma-carboxyglutamic acid concentrations, vitamin K deficiency did not functionally impair skeletal metabolism of laying hens or their progeny (Lavelle et al., 1994).

Vitamin K-dependent gamma-carboxylated proteins have been identified as ligands for a unique family of receptor tyrosine kinases with transforming ability. The involvement of vitamin K metabolism and function in two well-characterized birth defects, warfarin embryopathy and vitamin K epoxide reductase deficiency, suggests that developmental signals from vitamin K-dependent pathways may be required for normal embryogenesis (Saxena et al., 1997). 

Borderline deficiencies of vitamin K often cause small hemorrhagic blemishes on the breast, legs and wings, and in the abdominal cavity and on the surface of the intestine (Illus. 2). Chicks show an anemia that in part may be caused by loss of blood, but also by the development of a hypoplastic bone marrow (Illus. 3). Even a borderline deficiency of vitamin K is of economic importance in broiler production because the hemorrhagic areas that occur in the legs or throughout the body may result in a high percentage of condemnations during inspection at the processing plant (Scott et al., 1982). A condition manifested by numerous small hemorrhages scattered throughout all tissues has been reported frequently in the commercial broiler industry (Almquist, 1978).
Illustration 2
Illustration 3

A number of considerations influence the likelihood of a vitamin K deficiency in poultry, including dietary sources of the vitamin, level of vitamin K in the maternal diet, intestinal synthesis, coprophagy, presence of sulfa drugs and other non-nutrients in the diet, and disease conditions. Chicks suffering from coccidiosis, a disease that causes severe damage along the intestinal tract, may bleed excessively or fatally. When sulfaquinoxaline or certain other drugs are present in the feed or in the drinking water or when coccidiosis is being treated, supplementary vitamin K is needed at levels up to 10 times that needed in the absence of these drugs (Scott et al., 1982). Antimicrobial agents suppress intestinal bacteria that synthesize vitamin K and in their presence the bird may be entirely dependent on dietary vitamin K (NRC, 1994). Arsenilic acid increases the need for dietary vitamin K in both breeder and chick diets.

In poultry, little intestinal synthesis occurs because of the short digestive tract. The young chicken's large intestine or colon, a major area of bacterial activity, comprises less than 6% of the total length of the intestinal tract, while the figure for the adult of the same species is 7% (Griminger, 1984). In other domestic animals, the relative length varies from 13% for the dog to 28% for the rabbit. Also, poultry cannot utilize the vitamin K synthesized by intestinal flora because the synthesis is taking place too close to the distal end of the intestinal tract to permit significant absorption.

Rapid rate of food passage through the digestive tract may also influence vitamin K synthesis in poultry. Passage time in pigs, for a specific portion of the diet, may occur about 15 hours after feeding, but most of a given meal will be retained in the tract appreciably longer. A comparable time period for chickens would be approximately three hours (Griminger, 1984).
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