Header for print stylesheet
You are here:    

Companion Animals: Vitamin B12

Deficiency

The general signs of a vitamin B12 deficiency in most animal species are a loss of appetite, variable feed intake and a dramatic growth suppression. In addition, sometimes there is rough skin and hair coat, vomiting and diarrhea, voice failure, and a slight anemia (Catron et al., 1952). Clinical cases in dogs and cats proven to be due solely to vitamin B12 deficiency have been limited. The megaloblastic anemia and the neurological symptoms observed in vitamin B12 deficiency in pernicious anemia in humans have not been observed in most other animals, including dogs and cats.

A positive diagnosis of vitamin B12 deficiency is usually made by the finding of subnormal serum and tissue B12 concentrations. Low serum levels are associated with low body content of the vitamin. In addition to serum vitamin B12, elevations of methylmalonic acid and total homocysteine are very sensitive and specific in diagnosing vitamin B12 deficiency and can be used to help differentiate vitamin B12 deficiency from folic acid deficiency (Stabler et al., 1996). Serum concentrations of vitamin B12 have been determined in dogs (Caprelli et al., 1994; Davenport et al., 1994) and cats (Dunn et al., 1984) to evaluate status of the vitamin. Vitamin B12 deficiency has been confirmed by elevated urinary methylmalonic acid in dogs (Williams et al., 1969; Chanarin et al., 1973) and cats (Vaden et al., 1992). A clinical test for vitamin B12 deficiency in dogs is to load the animal with a precursor of methylmalonic acid (e.g., valine) and measure urinary excretion of methylmalonic acid (Williams et al., 1969; Chanarin et al., 1973).

A. Deficiency in Dogs

Normally, dogs have not shown any signs of vitamin B12 deficiency, yet they definitely have a requirement for this vitamin because clinical signs appear in dogs in certain disease conditions and when animals are fed low dietary concentrations of the vitamin (Ralston Purina, 1987). Lavrova (1969) found that dogs with internal biliary fistulas had vitamin B12 malabsorption and macrocytic anemia, as well as bone marrow abnormalities. The anemia was generally macrocytic hypochromic, macrocytic normochromic, normocytic hypochromic, or normocytic normochromic in type. The bone marrow erythropoietic centers appeared hypoplastic. Arnrich et al. (1952) observed that cocker spaniel puppies fed a 20% purified casein diet for 20 weeks grew better when 50 µg vitamin B12 per kg (22.7 µg per lb) diet was added to the diet, even though there were no signs of anemia. Campbell and Phillips (1953) reported impaired reproduction and also found that puppies grew better when their diets provided 22 µg per kg (10 µg per lb) vitamin B12.

An inherited intestinal vitamin B12 malabsorption disorder has been reported in dogs as a result of a defective brush-border expression of intrinsic factor-vitamin B12 receptor (Fyfe et al., 1989; 1991b). Vitamin B12-deficient dogs developed chronic inappetence, lethargy, a chronic nonregenerative anemia and failure to thrive at 12 weeks of age. Vitamin B12-deficiency has been identified in 50% of German shepherds with degenerative myelopathy; however, the clinical signs were not responsive to vitamin B12 treatment (Toenniessen and Morin, 1995).

B. Deficiency in Cats

Vitamin B12-deficient kittens exhibited poor growth, lethargy, emaciation and a high level of methylmalonic acid excretion (Keesling and Morris, 1975; Vaden et al., 1992). Morris (1977) reported that kittens given a vitamin B12-deficient diet at first grew normally for three to four months, after which growth ceased. Subsequently, body weight was lost at an accelerating rate until supplementation was initiated with parenteral vitamin B12, which restored weight gain.

 

references

view references

footer for print stylesheet