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Significance and application of B-vitamins to dogs and cats: A survey
Abstract
A deficiency of B-vitamins develops in dogs and cats as a result of digestive disturbances and infections. It inhibits the appetite and reduces the vitality and the activity of the immune system. The stores of B-vitamins in the form of their co-enzymes are low and after ten days of anorexia the administration of a preparation is advisable. The signs of B-vitamins deficiency are described and recommendations for an optimal supply together with methods of administration are described.
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Biotin deficiency was produced in growing kittens by feeding a diet containing dried, raw egg white. After receiving either an 18.5% egg white diet for 25 weeks, or a 32% egg white diet for 12 weeks, they exhibited dermal lesions characterized by alopecia, scaly dermatitis and achromotrichia, which increased in severity with the deficiency. Females developed accumulations of dried salivary, nasal and lacrymal secretions in the facial region although a male did not. There was a loss of body weight in all cats as the deficiency progressed. Hepatic propionyl CoA carboxylase activities were measured on biopsy samples of liver during biotin deficiency and after biotin supplementation. In the deficient state, activities were 4% and 24% of that following biotin supplementation. Propionyl carboxylase activity in the liver of the cat was comparable to that reported in the rat and chick in the deficient and normal states. Subcutaneous injection of 0.25 mg biotin every other day while continuing to receive the egg white diet caused remission of clinical signs, a body weight gain and increased food intake.
A six-month-old beagle was presented with a three-month history of failure to gain weight, lethargy, intermittent vomiting and seizures. Hypoglycaemia, portosystemic shunt, lead intoxication, gastrointestinal diseases and hereditary metabolic disorders were considered. Laboratory test results of low serum cobalamin (Cbl) concentrations, anaemia, leucopenia and methylmalonic aciduria while the dog was receiving a balanced commercial canine diet were suggestive of a congenital selective Cbl malabsorption. Treatment with repeated injections of parenteral cyanocobalamin (CN-Cbl) at 50 microg/kg every two weeks corrected the Cbl-deficient state and reversed all the clinical abnormalities. Selective Cbl malabsorption has previously been described in giant schnauzers and border collies and represents a unique readily treatable hereditary metabolic disorder.
Pantothenic acid, a B-vitamin, is essential for all mammalian species that have been studied: humans, calves, pigs, dogs, rodents, and cats, as well as for poultry and fish. The different species develop various deficiency signs such as growth retardation; anorexia; changes in hair, feather, or skin; locomotor abnormalities; gastrointestinal problems; compromised immunofunctions; impaired adrenal functions; altered lipid and carbohydrate metabolism; and adverse breeding outcome. Because there are no reliable and sensitive criteria for assessing pantothenate status, the dietary requirements of different species are most frequently set at the level that results in maximum growth. The pantothenate requirement varies widely among different species and strains, and depends on the age, growth rate, and breeding stages of the animals. This review summarizes the deficiency signs and the requirements for pantothenate of different species, and discusses various factors that affect pantothenate requirements of the animals.
Cats were fed purified diets containing varying levels of calcium pantothenate. In pantothenic acid-deficient cats the most prominent changes were growth failure and histologic changes in the small intestines and the liver. The results of gross and histologic examinations, measurements of acetylation of urinary p-aminobenzoic and the ratio of urinary pantothenic acid to creatinine indicate that in this study, cats required approximately 5 mg of calcium pantothenate/kg of diet.
Vitamin B6 deficiency, characterized by failure of growth, emaciation, convulsions, anemia and oxalate nephrocalcinosis, has been produced in cats.The presence of large quantities of oxalate in the kidneys and urine of cats deficient in vitamin B6, in amounts sufficient to cause marked renal damage, is attributable to excessive endogenous formation of oxalate.The implications of these findings in relation to human disease states associated with oxalate are discussed.
Thiaminase I and II activity of Baltic herring, vendace, smelt and dace was measured. All four fish species were found to contain thiaminase activity. The amounts of thiaminase activity in mug of thiamine split per 100 g of fish tissue per hour at 37 degrees C were: in Baltic herring 115 +/- 60, in dace 11500 +/- 2050, in smelt 25 +/- 25 and in vendace 30+/- 15.
Twenty-eight cats belonging to a cat rescue society developed clinical signs consistent with thiamin deficiency after being fed a proprietary canned food containing inadequate amounts of the vitamin. Five of the cats died but the others recovered after appropriate therapy. The diagnosis was based on clinical signs, histopathological findings, food analysis and response to treatment.
Inherited selective intestinal malabsorption of cobalamin (Cbl) was observed in a family of giant schnauzer dogs. Family studies and breeding experiments demonstrated simple autosomal recessive inheritance of this disease. Affected puppies exhibited chronic inappetence and failure to thrive beginning between 6 and 12 wk of age. Neutropenia with hypersegmentation, anemia with anisocytosis and poikilocytosis, and megaloblastic changes of the bone marrow were present. Serum Cbl concentrations were low, and methylmalonic aciduria and homocysteinemia were present. Parenteral, but not oral, cyanocobalamin administration rapidly eliminated all signs of Cbl deficiency except for low serum Cbl concentrations. Cbl malabsorption in affected dogs was documented by oral administration of [57Co]cyanocobalamin with or without simultaneous oral administration of intrinsic factor or normal dog gastric juice. Quantitation and function studies of intrinsic factor and transcobalamin-II from affected dogs revealed no abnormality. Other gastrointestinal functions and ileal morphology were normal, indicating a selective defect of Cbl absorption at the level of the ileal enterocyte. Immunoelectron microscopy of ileal biopsies showed that the receptor for intrinsic factor-Cbl complex was absent from the apical brush border microvillus pits of affected dogs. This canine disorder resembles inherited selective intestinal Cbl malabsorption (Imerslund-Gräsbeck syndrome) in humans, and is a spontaneously occurring animal model of early onset Cbl deficiency.
Serum immunoglobulin concentrations and densities of IgA-producing immunocytes in intestinal mucosa were compared in a group of clinically healthy dogs of various breeds, a group of clinically healthy German shepherd dogs, and a group of German shepherds with bacterial overgrowth in the proximal small intestine. Serum concentrations of IgA, but not IgM or IgG, were significantly lower in the clinically healthy German shepherd dogs than in other purebreed and mixbreed dogs, indicating that production of IgA by gut-associated lymphoid tissue might be relatively low in this breed. However, densities of IgA-producing cells were not significantly different comparing these two groups, suggesting that any impairment of mucosal IgA production is more likely to be related to defective synthesis or secretion of IgA than to reduced numbers of IgA-producing immunocytes. Comparable findings in German shepherd dogs with small intestinal bacterial overgrowth provided further indirect evidence that local immunity might be defective in this breed, since these luminal bacteria would be expected to stimulate mucosal IgA production. However, it is not clear whether such a defect is directly responsible for the overgrowth, or whether there is an indirect relationship between defective local immunity and bacterial overgrowth in German shepherd dogs.
In a collaborative study with small-animal veterinary surgeons, dogs with fur and skin conditions were treated with biotin (approximately 5 mg biotin/10 kg body weight/day) for 3 to 5 weeks. In total 119 cases could be treated which were reported to show symptoms such as dull coat, brittle hair, loss of hair, scaly skin, pruritus or dermatitis. Cases requiring other treatments with e.g. glucocorticoids, were excluded from the study. In 60% of the cases all symptoms were reported to be cured after the biotin treatment and in a further 31% an improvement was noted; in only 9% no effect was recorded. All breeds responded but to a variable extent: e.g. in Poodles the response was lower (no response in 6 out of 11 cases) than in Alsatians where all improved and 14 out of 29 were completely cured. The results confirm the favourable effect of biotin for treatment of fur and skin conditions in dogs.
Blood concentrations of thiamin, biotin, nicotinates, pantothenates, folates, riboflavin, vitamins A, B6, B12, C, E, beta-carotene and choline were analyzed in healthy animals (23 horses, 25 dogs, and 29 cats). B-Complex vitamins and choline also were analyzed in the liver of the dogs and cats. Vitamin concentrations in the blood and livers of dogs were similar; however, blood vitamin A and beta-carotene concentrations were lower in the cat than in the dog. Horses had a higher B12 blood concentration than did the dogs and cats. These data can be useful for detecting overt and hidden vitamin deficits in these species due to various conditions.
Two 4 x 4 Latin square experiments were conducted with English Pointer puppies to determine the growth promoting capacity of D-tryptophan (trp) relative to L-trp and to estimate the trp requirement of the growing dog. Based upon a multiple linear regression slope-ratio technique, D-trp had an efficacy value of 35.5 +/- 6.4% relative to L-trp. The urine of dogs fed D-trp contained 14.6% of the ingested trp; no measurable trp was recovered in the urine of dogs fed L-trp. The trp requirement for maximal weight gain was at least .16% for 6-to 10-wk-old dogs, between .12 and .16% for 10- to 12-wk-old dogs and less than or equal to .12% for 12- to 14-wk-old dogs. The overall requirement for the 6- to 14-wk age period was .15%. Total N, as well as urea-N, in urine decreased and N retention increased with increasing levels of dietary L-trp; NH3-N, creatinine-N and fecal-N were unaffected by treatment.
Cubilin is an endocytic receptor of the apical brush border membrane that is essential for intrinsic factor-mediated cobalamin absorption in small intestine. However, cubilin is more highly expressed in kidney and yolk sac, and recent molecular characterization of the receptor has focused on these tissues. The aim of this investigation was to examine tissue-specific cubilin expression and posttranslational modifications with an emphasis on the gastrointestinal tract. Intrinsic factor-cobalamin binding activity, cubilin immunoreactivity, and cubilin mRNA levels were determined in multiple segments of canine gastrointestinal mucosa and other tissues. These aspects of cubilin expression varied in parallel, suggesting that the major determinant of regional cubilin expression in the gastrointestinal tract is modulation of cubilin mRNA. Cell fractionation indicated that ileal cubilin is not strongly membrane associated. An approximately 185-kDa brush border specific and two >400-kDa precursor forms of cubilin were identified. Asparagine-linked oligosaccharide modifications characterized by differential glycosidase digestion of affinity-purified cubilin from ileal mucosa and renal cortex differed, but ileal and renal intracellular cubilin comigrated on SDS-PAGE at approximately 400 kDa after oligosaccharide removal, thus reconciling previous conflicting size estimates of the cubilin polypeptide.
Riboflavin deficiency has been produced in cats fed isonitrogenous purified diets varying in carbohydrate and fat content and containing different quantities of riboflavin. In a number of instances cataracts developed in cats receiving amounts of riboflavin slightly below their minimal requirement. Fatty livers and testicular hypoplasia were present as well as skin changes which were less dramatic than in other species. Anemia and central nervous system changes were not observed. High-carbohydrate, low-fat diets appear to exert a sparing influence on the cats' riboflavin requirement. Urinary and fecal riboflavin determinations indicate that this effect is largely due to increased intestinal synthesis and utilization of riboflavin.