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1. Professor’s, Department of Veterinary Pathology, College of Veterinary Science, GADVASU, Ludhiana, Punjab-141004. 2. Assistant Professor, Dept. of Vety. Pathology, College of Veterinary Science, GADVASU, Ludhiana, Punjab-141004. 3. Corresponding Author: Dr. Sambhaji G. Chavhan, Assistant Professor, Department of Veterinary Pathology, Veterinary College, KVAFSU, Bidar, Karnataka-585401. Email: email@example.com, Website: www.vetclinpath.in
Vitamins are organic compounds needed in small amounts for the normal growth and activity of the body. Most of the vitamins cannot be synthesized by the body but are naturally found in foods obtained from the plants and animals. Vitamins are either water-soluble or fatsoluble and water-soluble vitamins are excreted rapidly than fat soluble vitamins. Vitamin D is not a single compound but different compounds are reported to have a vitamin D activity (Smith, 1982). Among them vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol) are important. Vitamin D3 was found to be approximately ten times more toxic than vitamin D2 (Chen and Bosmann, 1964; Hunt et al., 1972). The vitamin D3 toxicity reported to cause generalized calcification mainly of soft tissues (Long, 1984). Nowadays use of vitamin D3 (cholecalciferol) in commercial pet, livestock and infant feed supplements, multivitamin preparations and as a rodenticide increased risk of toxicity. Various plant species reported to have a high concentration of vitamin D analogue have been reported as a source of vitamin D3 toxicity in livestock. The most common source of vitamin D3 toxicity in dogs and cats is accidental ingestion of rodenticide baits containing cholecalciferol (Rumbeiha, 2006). So, in present article we summarized various aspects of vitamin D3 toxicity in detail. Sources of Toxicity: Vitamin D3 nowadays also used as rodenticide. The rodenticide preparations are available in different formulations like granules, flakes, tablets, baits containing 0.075% cholecalciferol. The most common source of vitamin D3 toxicity in dogs and cats is accidental ingestion of rodenticide baits containing cholecalciferol (Rumbeiha, 2006).
Vitamin D3 is widely used as feed supplement in commercial livestock, pet and infant feeds. The presence of excessive amount of vitamin D3 in commercial feed supplements reported causing toxicity especially in pets, swine and human infants (Stevenson et al., 1976; Long, 1984; Morita et al., 1995; Roberson et al., 2000).
Thus. soft tissues tend to become calcified while a bone tends to be rarified. Acute oral LD50 in dogs of technical material in oil has been reported to be 85 mg/kg. This has lead to an underestimate of the actual hazard of the rodenticide products for this species. heart and lungs cause structural damage that leads to decreased functional capacity of these tissues and organs. 40 IU vitamin D = 1 mcg.5 . Younger animals appear at higher risk to the development of toxicosis. 2 . Morrow. Relay toxicosis: not reported in experimental studies. osteoporosis and renal failure (Beasly. Vitamin D2 and D3 accelerate these mechanisms many a times leading to marked hypercalcemia as result of which calcium salts are deposited in soft tissues such as kidneys. 2009). heart and lungs. The cause of death reported in vitamin D3 toxicity includes cardiac and renal failure (Beasly. 1999). kidneys. Sandhu and Brar. 1999. stimulating bone resorption and decreasing renal excretion of calcium. Administration of 10 . toxicoses have occurred in dogs from the ingestion of cholecalciferol at 0. The mineralization of vital organs viz. Cestrum diurnum and Solanum nigricans are reported to have a high concentration of vitamin D3 analogue. In high doses. 2001. The loss of function contributes to the development of ongoing end stage clinical signs as well as long term signs in animals that survive. Mechanism of Action: Physiologically vitamin D and its metabolites maintain normal calcium levels in blood by increasing intestinal absorption of calcium. The grazing of livestock on pastures containing these plant species have been reported to cause a disorder called enzootic calcinosis or Manchester wasting disease (Beasly. Accidental ingestion of human medications containing vitamin D analogues used for treatment of number of diseases like hypophosphatemic disorders. osteomalacia. blood vessels.3 mg/kg body weight.025 mcg of cholecalciferol. hypoparathyroidism. Toxicity: Based upon clinical reports. Thus. 1999). The plant species like golden oat grass (Trisetum flavescens). 1 IU of vitamin D3 = 0.20 mg/kg to dogs of cholecalciferol-based rodenticide resulted in death in 4 dogs.
3 .. aorta etc. kidneys. once daily.) can be observed (Chavhan et al. Corticosteroids (cortisone and prednisone): Dogs & cats: 1-2 mg/kg. Histopathologically. Treatment: No specific antidote available for cholecalciferol toxicity. nervous signs like aimless running. Affected animals cannot walk properly/ shows tumbling movements and even cannot open mouth. exhibited snoring sound during respiration. Treatment of Vitamin D3 toxicosis is aimed primarily at lowering the elevated serum calcium levels. dehydration and weakness. The stomach and intestines may reveal bloody ingesta in the lumen with marked hemorrhages on mucosa. rigidity of limbs and difficulty in movement. 2011). lungs. diagnosis can be done from gross postmortem and histopathological findings (calcification/mineralization of various visceral organs). the pasture should be checked for presence of calcinogenic plants. Anorexia. orally or intramuscular.Clinical Signs: Diarrhoea. Diagnosis: History of ingestion of rodenticide or in case of grazing livestock. The pin point white chalky deposits of calcium can be observed on capsules of both kidneys. The following drugs can be used to lower the calcium level. 2011). heart.. severe progressive emaciation. The gross postmortem findings include white chalky deposits of calcium on epicardial surface of heart and serosal surface of intestine. dullness. Ruffled body coat. 2-3 times daily. Difficulty in respiration. Clinical signs. the mineralization of various visceral organs (viz. elevated level of calcium. Clinicopathological findings: Increased plasma levels of calcium (hypercalcemia). subnormal body temperature and progressive wasting. phosphorus and Blood Urea Nitrogen (BUN). rolling and epileptic seizures can be seen (Chavhan et al. phosphorus and BUN. shivering and epistaxis. In dead animals. Before death. Salmon calcitonin: Dogs & cats: 4-6 IU/kg.
7. Missouri.pp:629-642. USA. USA. Kothule VR and Kammon AM. Pesticides: Organic Rodenticides (Vitamin D Compounds).3-2 mg/kg. Fluid therapy along with diuretics (frusemide) helps to reduce hypercalcemia. International Veterinary Information Service (www. 2nd Edn.org). Brar RS. Emesis or gastric lavage. 3. Vet. pp:380-382. Kalyani Publishers. Sandhu HS and Brar RS. 17: 54-57. 12: 905-911. Pamidronate: Dogs: 1. Sodhi S. 6. 1976. 2001. Acute toxicosis in swine associated with excessive dietary intake of vitamin D. 102: 975-986. Shimada A. 2009. In: Textbook of Veterinary Toxicology. Morita T. Med. Toxicology International 18(1): 35-43. 2nd Edn. 5. Vet. Can. pp: 244-246. Hunt RD. Gadhave PD.ivis. 1995. Rumbeiha W K. Vet. administration of activated charcoal and osmotic cathartic helps to remove unabsorbed toxicant. 87: 148-154. Cornell University Press. REFERENCES 1. Clinicopathological Studies on Vitamin D3 Toxicity and Therapeutic Evaluation of Aloe vera in Rats. 12. Awakura T. It may be repeated at 96 hours. New York. 1984. Prognosis: Prognosis of vitamin D based rodenticide toxicosis is guarded. 1972. Banga HS. Nagai T and Haruna A. Nutr. if the clinical signs are severe or advanced. slow IV in 0. Beasley V R. Smith SE. Ludhiana. Roberson RJ. Sci. 1982. Saunders Elsevier. 8. Small Animal Toxicology. 2. Specific toxicants: cholecalciferol. J. Morrow C. J. Ithaca. Comstock Publishing Associate. Nutr. 57: 831-837. A comparison of the toxicity of ergocalciferol and cholecalciferol in Rhesus monkeys (Macaca mulatta). (ed). Garcia FG and Walsh RJ. USA. Hypervitaminosis D in rabbits. India. In: Swenson MJ. Vitamins. 1999. ********************************************************* 4 . Jour. Swecker WS and Hullender LL. 4. J. Hypercalcemia and 9. In: Peterson M E and Talcott P A (ed). 2000. Stevenson RG. JAVMA 216: 1115-1118. Sandhu HS. Comparision of the hypercalcemic action of vitamins D2 and D3 in chicks and the effect on tetracycline fixation by bone. Vitamin D toxicosis in cats: Natural outbreak and experimental study. Umemura T. Med. JAVMA 184: 164-170. 10. 2006. Duke’s Physiology of Domestic Animals. Chavhan SG. Cholecalciferol poisoning. Chen PS and Bosman HB.9% sodium chloride solution over a period of 2-4 hours. Long GG. 11. 1965. Palmer NC and Finley GG. hypervitaminosis D in two lambs. Veterinary Toxicology. 2011.
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