Symptoms of Vitamin D Deficiency in Raccoon Dogs and Methods of Prevention and Treatment
The absorption of VD not only promotes the absorption of calcium and phosphorus in the intestines, but also acts on bone tissue. Although raccoon dogs are physiologically predisposed against VD absorption, conventional farming practices mostly use fish as feed, so VD deficiency is generally uncommon; however, in early-weaned raccoon dog pups, the disease readily occurs when the calcium-to-phosphorus ratio in the artificially fed diet is imbalanced, when inorganic salts, vitamins and protein are deficient, or when the pups suffer from gastroenteritis and are kept in dark, unsanitary cages without ultraviolet exposure. The clinical manifestations of VD deficiency are mainly digestive dysfunction, lameness, arched back, enlargement and deformity of the vertebrae, facial bones and limb joints, and may lead to death. Based on the treatment of 8 clinically admitted cases of VD deficiency in raccoon dogs, the author summarizes the findings as follows:
1 Pathogenesis
VD is a sterol substance with many types, the main ones being VD2 (ergocalciferol) and VD3 (cholecalciferol). VD2 is the product of ultraviolet irradiation of ergosterol from yeast or ergot; VD3 is the product of ultraviolet irradiation of 7-dehydrocholesterol in animal skin and fat. Only after VD is absorbed by the body and hydroxylated into its active form can it exert its physiological functions. Under normal living environments and feeding conditions, animals do not develop VD deficiency. Therefore, lack of ultraviolet exposure, calcium deficiency in food, and an improper calcium-to-phosphorus ratio are the main factors leading to VD deficiency in raccoon dogs.
2 Clinical Symptoms
In the early stage, affected raccoon dogs generally show decreased appetite, slightly poor spirits, indigestion, rough fur, weakness of the hind limbs, and reluctance to move. After about 4 weeks, the affected animals can no longer bear weight normally on their front and hind limbs and crawl, with deformation of the vertebrae and long bones of the limbs, arched back, and enlarged joints, accompanied by severe digestive disturbance, presenting as constipation or alternating constipation and diarrhea, though constipation is more common. In severe cases at the late stage, the animals die of exhaustion.
3 Treatment Measures
Clinically, a diagnosis can basically be confirmed based on medical history and clinical symptoms, combined with X-ray findings where conditions permit.
3.1 Intramuscular injection of VD 20,000 IU per dose, once a week, for 3 to 5 consecutive times. Oral calcitriol may also be given, along with calcium supplementation.
3.2 For affected raccoon dogs with severe disease or poor response to treatment, intramuscular injection of the anabolic hormone nandrolone phenylpropionate, 2 to 4 mL per dose, once every 2 weeks. At the same time, appropriately increase the protein content in the feed so that it can better exert its anabolic effect.
3.3 Intramuscular injection of vitamin D calcium colloid, 2 mL per dose, once a day, for 5 to 7 consecutive times. At the same time, appropriately add bone meal to the daily diet. After 1 month of treatment, the condition improved markedly, but a few more severely affected animals still showed varying degrees of lameness.
4 Summary
4.1 The effectiveness of treatment for this disease is related to the duration and severity of the illness. The shorter the course of the disease, the milder the condition, and the more timely the treatment, the better the therapeutic effect; conversely, the poorer the effect.
4.2 VD not only promotes the absorption of calcium and phosphorus in the intestines, but also acts on bone tissue. VD deficiency in growing young raccoon dogs can induce rickets; therefore, when treating VD deficiency in raccoon dogs, calcium supplementation for the affected animals should also be considered.
4.3 Scientific feeding and prevention of picky eating are important measures for preventing this disease.