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:, Website:

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).

The loss of function contributes to the development of ongoing end stage clinical signs as well as long term signs in animals that survive. 2001. blood vessels. Mechanism of Action: Physiologically vitamin D and its metabolites maintain normal calcium levels in blood by increasing intestinal absorption of calcium. 1999. Thus.    Relay toxicosis: not reported in experimental studies. osteomalacia. Toxicity:  Based upon clinical reports. 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.  In high doses. Sandhu and Brar. Administration of 10 .   Younger animals appear at higher risk to the development of toxicosis. 40 IU vitamin D = 1 mcg. osteoporosis and renal failure (Beasly.  Accidental ingestion of human medications containing vitamin D analogues used for treatment of number of diseases like hypophosphatemic disorders.  The mineralization of vital organs viz. The plant species like golden oat grass (Trisetum flavescens).3 mg/kg body weight. 1999). heart and lungs. Morrow. Cestrum diurnum and Solanum nigricans are reported to have a high concentration of vitamin D3 analogue. Acute oral LD50 in dogs of technical material in oil has been reported to be 85 mg/kg. heart and lungs cause structural damage that leads to decreased functional capacity of these tissues and organs.5 .025 mcg of cholecalciferol. 1999). stimulating bone resorption and decreasing renal excretion of calcium. Thus. toxicoses have occurred in dogs from the ingestion of cholecalciferol at 0. The cause of death reported in vitamin D3 toxicity includes cardiac 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. 1 IU of vitamin D3 = 0. soft tissues tend to become calcified while a bone tends to be rarified. 2009).20 mg/kg to dogs of cholecalciferol-based rodenticide resulted in death in 4 dogs. kidneys. This has lead to an underestimate of the actual hazard of the rodenticide products for this species. 2 . hypoparathyroidism.

orally or intramuscular. Difficulty in respiration.Clinical Signs:       Diarrhoea. Before death.) can be observed (Chavhan et al.. rigidity of limbs and difficulty in movement. Clinical signs. phosphorus and Blood Urea Nitrogen (BUN). Histopathologically. subnormal body temperature and progressive wasting. The following drugs can be used to lower the calcium level. Diagnosis:    History of ingestion of rodenticide or in case of grazing livestock. 2011). shivering and epistaxis. Ruffled body coat. elevated level of calcium. Affected animals cannot walk properly/ shows tumbling movements and even cannot open mouth. lungs. heart. Clinicopathological findings:  Increased plasma levels of calcium (hypercalcemia). nervous signs like aimless running. The gross postmortem findings include white chalky deposits of calcium on epicardial surface of heart and serosal surface of intestine. Treatment of Vitamin D3 toxicosis is aimed primarily at lowering the elevated serum calcium levels. The pin point white chalky deposits of calcium can be observed on capsules of both kidneys. 3 . exhibited snoring sound during respiration. 2011). The stomach and intestines may reveal bloody ingesta in the lumen with marked hemorrhages on mucosa. Treatment:  No specific antidote available for cholecalciferol toxicity. phosphorus and BUN.   Corticosteroids (cortisone and prednisone): Dogs & cats: 1-2 mg/kg. In dead animals. 2-3 times daily. rolling and epileptic seizures can be seen (Chavhan et al. the pasture should be checked for presence of calcinogenic plants. severe progressive emaciation. dehydration and weakness. kidneys. Salmon calcitonin: Dogs & cats: 4-6 IU/kg. aorta etc. dullness. the mineralization of various visceral organs (viz. Anorexia.. diagnosis can be done from gross postmortem and histopathological findings (calcification/mineralization of various visceral organs). once daily.

Sandhu HS.3-2 mg/kg. 2nd Edn. Sci. Pesticides: Organic Rodenticides (Vitamin D Compounds). Rumbeiha W K. Shimada A.ivis. 2. Banga HS. In: Textbook of Veterinary Toxicology. Vet. Kalyani Publishers. 10. 1972. Vitamin D toxicosis in cats: Natural outbreak and experimental study. Missouri. 2001. 3. 12: 905-911. Clinicopathological Studies on Vitamin D3 Toxicity and Therapeutic Evaluation of Aloe vera in Rats. Prognosis: Prognosis of vitamin D based rodenticide toxicosis is guarded.9% sodium chloride solution over a period of 2-4 hours. A comparison of the toxicity of ergocalciferol and cholecalciferol in Rhesus monkeys (Macaca mulatta). Med. Veterinary Toxicology. 1976. It may be repeated at 96 hours. Nutr. Umemura T. 2006. Chavhan SG. Vet. Acute toxicosis in swine associated with excessive dietary intake of vitamin D. 4. ********************************************************* 4 . Duke’s Physiology of Domestic Animals. Palmer NC and Finley GG. 2009. 87: 148-154. J. Hypervitaminosis D in rabbits. JAVMA 216: 1115-1118. 1995. J. 6. Awakura T. Cholecalciferol poisoning. J.  Pamidronate: Dogs: 1. Cornell University Press. Stevenson RG. USA. Beasley V R. 2nd Edn. Gadhave PD. Smith SE. In: Peterson M E and Talcott P A (ed). USA.pp:629-642. 1999. 2000. International Veterinary Information Service (www. (ed). Vet. Morrow C. 17: 54-57. if the clinical signs are severe or advanced. Vitamins. pp: 244-246. Comparision of the hypercalcemic action of vitamins D2 and D3 in chicks and the effect on tetracycline fixation by bone. 57: 831-837. Roberson RJ. 2011. Toxicology International 18(1): 35-43. Saunders Elsevier. Brar 8. 1982. 5. Sandhu HS and Brar RS. Hypercalcemia and 9. New York. Small Animal Toxicology. Emesis or gastric lavage. administration of activated charcoal and osmotic cathartic helps to remove unabsorbed toxicant. Comstock Publishing Associate. Specific toxicants: cholecalciferol. Long GG. Nutr. Med. USA. Kothule VR and Kammon AM. Garcia FG and Walsh RJ. Swecker WS and Hullender LL. JAVMA 184: 164-170. 1965. In: Swenson MJ. pp:380-382. Hunt RD. Nagai T and Haruna A. 7. REFERENCES 1. 12. Morita T. 102: 975-986. hypervitaminosis D in two lambs. 1984. Fluid therapy along with diuretics (frusemide) helps to reduce hypercalcemia. Jour. 11. slow IV in 0. Ithaca. Sodhi S. India. Chen PS and Bosman HB. Can. Ludhiana.

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