How are nutritional and metabolic diseases in foxes diagnosed, prevented and treated?
Nutritional and metabolic diseases refer to conditions where the nutrients contained in the feed, especially vitamins and minerals, are supplied in amounts that cannot meet the growth and development needs of the fox's body. Sometimes nutritional and metabolic diseases occur not because the nutrient content of the feed is insufficient, but because the animal's digestive function is impaired. When formulating feed, attention should also be paid to the interrelationships between vitamins and between minerals (complementary or antagonistic). The nutritional and metabolic diseases that fur-bearing animals are prone to mainly include the following five types.
(1) Vitamin A deficiency
Vitamin A deficiency is a disease characterized by keratinization of epithelial cells, and foxes are susceptible to it.
[Causes]
When the vitamin A in the feed does not reach the fox's requirement, or when the vitamin A in the diet is destroyed due to prolonged storage, oxidation, spoilage and deterioration, or improper formulation, or when digestive tract diseases affect the absorption of vitamin A, these are the main causes of this disease.
[Symptoms]
This disease mainly manifests as keratinization of the skin and mucous membranes. When silver foxes suffer from this disease, demyelination of nerve fiber myelin sheath phospholipids occurs, follicular degeneration occurs in female foxes, and degeneration of the seminiferous tubule epithelium occurs in male foxes, thereby affecting the reproductive function of foxes.
The clinical manifestations in young foxes and adult foxes are basically the same. Generally, when vitamin A is insufficient, clinical symptoms appear after 2 to 3 months. The early symptoms are neurological disorders, convulsions, head tilting backward, and the sick fox losing balance and falling down. The sick fox's stress response is enhanced, and it becomes highly excited by minor stimuli, running in circles along the cage and walking unsteadily. The intestinal function of young foxes is damaged to varying degrees, with diarrhea symptoms appearing, and the feces mixed with large amounts of mucus and blood; sometimes pneumonia symptoms appear, with stunted growth and slow tooth replacement.
[Pathological anatomical changes]
Dead carcasses are generally relatively emaciated and anemic. Young foxes often have tracheitis and bronchitis. Gastritis and enteritis changes are also often found in young foxes, with ulcers found in the stomach and stones found in the kidneys and bladder.
[Diagnosis]
The diagnosis can be confirmed by measuring the vitamin A content in the blood of sick foxes and the liver of dead animals, or by adding vitamin A to the diet for therapeutic diagnosis.
[Prevention and treatment]
To prevent the occurrence of this disease, the first step is to ensure the supply of vitamin A in the diet, and pay attention to the supply of vegetables, fish and liver in the feed. To treat this disease, vitamin A can be added to the feed. The therapeutic dose is 5 to 10 times the requirement, with 3000 to 5000 IU per day per silver fox and arctic fox.
(2) Vitamin E deficiency
Vitamin E is the general term for several types of biological phenols with vitamin E activity. Its main function is to act as a biological antioxidant. When foxes are deficient in vitamin E, reproductive function disorders occur.
[Symptoms]
When female foxes are deficient in vitamin E, they show prolonged estrus, infertility and increased rates of empty pregnancy, and the young foxes born are listless, weak, unable to suckle, with increased mortality; male foxes show reduced or absent libido and impaired spermatogenesis. Foxes in good nutritional condition have yellow-stained and degenerated fat, and often die suddenly in autumn.
[Prevention and treatment]
To prevent this disease, sufficient vitamin E should be provided according to the different physiological periods of the fox, and when the feed is not fresh, vitamin E should be supplemented in increased amounts.
When treating this disease, vitamin E should first be supplemented at 5 to 10 mg per kg of body weight, and the following prescription drugs may optionally be added:
(1) Vitamin B12, 50 to 100 mg per kg of body weight.
(2) Penicillin, 100,000 to 200,000 IU per kg of body weight; sulfadiazine 0.05 to 0.1 g per kg of body weight.
(3) Lactasin 0.2 g per kg of body weight, mixed into the feed; oxytetracycline 50,000 IU per kg of body weight, intramuscular injection.
(3) Vitamin C deficiency
When foxes are deficient in vitamin C, it often causes "red paw disease" in young foxes.
[Symptoms]
When pregnant female foxes are deficient in vitamin C during gestation, it mostly causes newborn foxes to suffer from red paw disease. When young foxes within 1 week of age suffer from red paw disease, its characteristic symptoms are: edema of the limbs, highly flushed skin, thickened joints, swollen and thickened toe pads, and edema of the tail. After a period of time, ulcers and fissures appear between the toes. If the pregnant female fox is severely deficient in vitamin C during gestation, the young foxes develop edema of the paw pads during the embryonic period or after birth, which is mild at first and then gradually becomes severe. On the second day after birth, the paw pads are accompanied by mild congestion, at which time the tail tip becomes thickened and the skin is flushed. Sick young foxes often emit screams, crawl around restlessly, tilt their heads backward, and become exhausted.
[Prevention and treatment]
To prevent this disease, it is necessary to ensure that the feed contains a complete variety and sufficient quantity of vitamins. When feeding unfresh vegetables, vitamin C refined products must be supplemented, at more than 20 mg per day per animal. Vitamin C decomposes easily at high temperatures, so it must be mixed evenly with cool water. After the female fox gives birth, timely examination should be carried out; if foxes with red paw disease are found, timely treatment should be given. Administer 3% to 5% vitamin C solution, 1 mL per day per animal, twice daily. It can be administered orally with a dropper until the swelling subsides.
(4) B vitamin deficiency
The occurrence of B vitamin deficiency in fur-bearing animals is caused not only by insufficient content in the feed, but also mainly by fat oxidation in the feed, insufficient amounts, and the destruction and loss of B vitamins during feed storage.
1. Vitamin B1 deficiency
[Causes]
In addition to the above points, the causes of vitamin B1 deficiency include long-term feeding of freshwater fish or certain marine fish containing thiaminase that destroys vitamin B1, or diets using yeast as the source of B vitamins in the feed (although yeast is rich in B vitamins, it does not contain much vitamin B1), which easily causes the occurrence of this disease.
[Symptoms]
When vitamin B1 in the feed is insufficient, this disease is caused after 20 to 40 days. Affected animals show reduced or absent appetite, leaving large amounts of food uneaten, physical weakness, emaciation, unsteady gait, convulsions and spasms, and if not treated in time, death occurs after 1 to 2 days. When severely deficient in vitamin B1, lesions occur at nerve endings, disorders occur in tissues and organs, the sick fox's body temperature drops, cardiac function weakens, anorexia and refusal to eat occur, and digestive function is disturbed. When female foxes are deficient in vitamin B1, gestation may be prolonged, the rate of empty pregnancy increases, and weak young are born.
[Prevention and treatment]
To prevent the occurrence of this disease, the vitamin B1 content in the feed must be ensured, and foxes must not be fed fish containing thiaminase for long periods. Freshwater fish must be cooked before feeding.
If this disease is discovered early, vitamin B1 can be used for treatment, and yeast should be added to the feed to increase feed rich in vitamin B1. Silver foxes and arctic foxes should be fed 8 to 10 mg of vitamin B1 per day per animal for 10 to 15 consecutive days. When neurological symptoms appear and the animal refuses to eat, vitamin B1 injection can be used, and silver foxes or arctic foxes can be injected with 0.5 to 1 mL.
2. Vitamin B2 deficiency
[Symptoms]
When vitamin B2 is deficient, it causes dermatitis in animals, depigmentation of the coat, and slow growth. It also often causes damage to nervous function, unsteady gait, incomplete paralysis or paralysis of the hind limbs, spasms and coma. Cardiac function weakens. The entire body coat falls out, the fur becomes depigmented, female foxes have delayed estrus, and infertility may also occur; newborn young foxes are underdeveloped, with cleft palate and shortened bones. Arctic foxes show hairless young or grayish-white down during the nursing period. At 5 weeks of age, young foxes are completely without coat and have thick fatty skin, weakened motor function, and cloudy, milky-white lenses.
[Prevention and treatment]
Affected silver foxes and arctic foxes can be fed 3 to 3.5 mg of riboflavin per day per animal, while improving feeding management and increasing yeast supplementation. If the feed has a high fat content, the riboflavin supply should be increased. For female foxes during gestation and nursing, an additional 2.5 mg of riboflavin per day per animal should be provided.
3. Vitamin B6 deficiency This disease mostly occurs during the fox breeding period. When vitamin B6 is insufficient, male foxes develop azoospermia, female foxes experience empty pregnancy or fetal death, and young foxes show stunted growth and development. Therefore, once vitamin B6 is lacking in the feed, it will cause great losses to fox farming production.
[Symptoms]
Affected foxes show reduced appetite, keratinization of epithelial cells, and in those with acanthosis, paralysis of the hind limbs and microcytic anemia occur; the empty pregnancy rate of pregnant female foxes increases; the mortality rate of newborn young foxes increases; male foxes lose sexual function or sexual reflexes, with azoospermia; male fox testes are noticeably reduced in size, with degeneration inside the testes; young foxes show stunted growth and development; female foxes show delayed estrus and gestation.
[Prevention and treatment]
To prevent the occurrence of this disease, the amount of vitamin B6 in the diet is required to be no less than 0.9 mg per 100 g of dry matter, or 0.25 mg per 418 kg of feed. If affected foxes are found, vitamin B6 preparations should be used promptly for treatment. During the estrus period, use 1.2 g, once daily; during the coat growth period, use 0.9 mg; during the growth period, use 0.6 mg, which can be mixed into the feed. If it is an injection, the dosage can be calculated proportionally for intramuscular injection.
4. Vitamin B12 deficiency Vitamin B12 deficiency or insufficiency can cause anemia in foxes. When vitamin B12 is lacking in the feed, deficiency symptoms appear after 36 weeks in adult foxes and after 15 weeks in young foxes.
[Symptoms]
Sick foxes show anemia due to impaired blood formation, pale visible mucous membranes, complete loss of appetite, emaciation and weakness. If it occurs during gestation, the mortality rate of young foxes is high. When silver foxes suffer from this disease, they show systemic anemia, pale mucous membranes, poor development of young foxes, atrophy and shrinking of parenchymal organs, and thinning of the edges of the liver and spleen.
[Prevention and treatment]
To prevent this disease, vitamin B12 in the feed should be supplied according to the standard, that is, the vitamin B12 content per 418 kg of feed should be 1.5 to 2.5 mg.
When using vitamin B12 to treat this disease, the dosage is 10 to 15 g per kg of body weight by intramuscular injection. Inject once every 1 to 2 days until cured.