In considering vitamin K deficiency, Kindberg and Suttie (1989) noted that vitamin K deficiency is strongly dependent upon the assay used. The authors indicated that direct measurements of prothrombin concentration or alterations in liver vitamin K-dependent carboxylase activity are more sensitive and more readily quantitated criteria of sufficiency than one-stage prothrombin times.
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.
Schendel and Johnson (1962) were able to produce a vitamin K deficiency in the baby pig by using a sulfa drug and an antibiotic and by carefully minimizing coprophagy by cleaning the feces from wire bottom cages where pigs were housed. Likewise, hemorrhagic disease occurred in piglets weaned at five to six weeks of age within two weeks after transfer onto flat decks (Hoppe, 1987). This vitamin K-responsive outbreak had occurred because of (1) the diet being virtually free of vitamin K; (2) dietary inclusion of sulfonamide, a known vitamin K antagonist; and (3) flat deckhousing, which precludes intake of microbial vitamin K from feces or litter.
Clinical and subclinical signs of vitamin K deficiency include both increased prothrombin and blood-clotting time, internal hemorrhage, and anemia due to blood loss (Seerley et al., 1976; Cunha, 1977; Newsholme et al., 1985). Newborn pigs may be pale with loss of blood from the umbilical cord. Until recently, vitamin K deficiency under natural conditions was not expected, as it was thought that the pig synthesized most if not all of the vitamin that was required. However, in the late 1960s and early 1970s there were prevalent reports of a bleeding disease of young pigs on commercial diets that was successfully overcome by vitamin K supplementation. Observations from Australia and New Zealand were of hemorrhaging in the navel of newborn pigs (Cunha, 1977).
Pigs placed on a high-sugar diet suffered heart lesions and hemorrhagic syndrome, which could be prevented by provision of vitamin K (Brooks et al., 1973). A number of field trials in the United States have reported a hemorrhagic syndrome for growing pigs. In one study, hemorrhagic syndrome occurred nine days after pigs were fed a standard diet, while those receiving either 2.5% dehydrated alfalfa meal or supplemental vitamin K remained in good health (Fritschen et al., 1970). Gross visible signs for hemorrhagic syndrome include large subcutaneous hemorrhages, blood in urine and abnormal breathing. Additional clinical signs from field observations are that some pigs will develop enlarged blood-filled joints and become lame, whereas others may have swellings along the body wall that are filled with unclotted blood. Hematomas (or blood swellings) in the ears also occur (Cunha, 1977). Hemorrhagic conditions in the growing pig have in some cases been associated with ingestion of molds, such as aspergillus or moldy materials, and have usually responded to vitamin K therapy.
The exact causes of more recent needs for vitamin K supplementation are not definitely known. Cunha (1977) and Scott et al. (1982) have summarized likely reasons for vitamin K deficiency under field conditions:
- As confinement feeding has increased, less pasture and alfalfa, both of which are good sources of vitamin K, are used for production of higher energy, more efficient diets. Likewise there has been a trend toward the use of solvent-extracted soybean meal and other oil seed meals and higher quality (less putrefied) fish meals, which are lower in vitamin K than the original expeller meals, and somewhat putrid fish meals.
- Hemorrhaging gastric ulcers, which occur frequently, may increase vitamin K needs.
- Mycotoxins produced by certain molds that may be present in the feed.
- Antimetabolite (antivitamin K) may be in the feed and thus increase vitamin K needs.
- Use of slatted floors lessens the opportunity for coprophagy: feces are an excellent source of vitamin K.
- Use of sulfa drugs, antibiotics and other medications that may reduce intestinal synthesis of the vitamin.
- Breeding of strains of pigs that possibly require more vitamin K. Increased litter size and rate of gain may also be increasing the need for vitamin K.
