In order to maximize the genetic potential of livestock and poultry growth and reproduction, more than 36 kinds of nutrients are absolutely essential, and to maintain the proper nutrient content and nutrient balance in the feed. Veterinarians often encounter this situation by determining whether the nature of a disease is nutritional or whether nutrition has become a specific clinical problem. When an essential nutrient is severely deficient, characteristic symptoms are often exhibited. Before or at the same time as the appearance of characteristic symptoms, it is often accompanied by non-characteristic symptoms such as decreased feed intake, slow growth, coarse coat, reduced production performance (breeding, egg production, lactation), and reduced resistance to disease. When a certain nutrient is partially lacking, only these non-specific symptoms may be observed. This situation makes the lack of part of the nutrient difficult to identify, because many factors including infectious diseases and toxins can cause these non-specific symptoms. Important nutrients in livestock nutrition include: protein and amino acids, carbohydrates, fats, vitamins, trace elements, and water. Now the classification of livestock and poultry nutritional deficiency is reported as follows: 1. Causes of porcine nutritional deficiency: Reduced feed intake: Reduced bioavailability of nutrients in dietary raw materials; Changes in nutrient content in dietary raw materials; Errors in diet formulation and configuration; Changes in pig nutritional requirements, etc. . 1, protein, amino acid deficiency: reduced food intake, slow growth. Reduced feed efficiency, depression, impaired fertility in sows and boars, increased back fat at necropsy; decreased serum protein and serum albumin levels in primary piglets, anemia, systemic edema, increased liver lipid levels; increased plasma urine levels, Reduced anti-bacterial infectivity 2. Iron deficiency: Reduced food intake, slow growth, and low feed efficiency. Hair is rough, skin pale, shrinking, breathing difficulties. Erythrocyte hypochromic anemia, heart and spleen enlargement, fatty hepatomegaly, ascites, erythroblast condensation in the bone marrow. Serum iron and iron transfer protein percent saturation decreased, hemoglobin levels decreased (≤ 7g/100ml), blood thin, water samples, disease resistance decreased 3, selenium deficiency: consistent with vitamin E deficiency, sperm production and exercise Reduced sex, serum and skeletal muscle selenium levels decreased, glutathione peroxidase activity decreased. 4. In the absence of zinc: anorexia, slow growth, low feed efficiency, parakeratosis, prolonged delivery during childbirth, increased stillbirth rate, reduced weight of newborn piglets and decreased individual Zn levels in serum, tissues, and milk, serum albumin and Reduced alkaline phosphatase levels, decreased thymus weight, slower testicular development, lack of fat storage, lipid atrophy, thymic cell failure, keratinization of the tongue, esophagus, and gastric orifice, decreased immune response 5, vitamin E deficiency: lactation stopped , Decreased litter size, longer delivery time, frail piglets, sudden death (rapid growth pigs): hepatic necrosis (nutrition of liver disease), degeneration of myocardium (Mulberry heart), degenerative thrombotic vascular injury, secondary angle of the stomach Histology, stomach ulcers. Anemia, yellowing of adipose tissue, degeneration of bones, elevated levels of serum glutamate-acetate transaminase and glutamate pyruvate transaminase, decreased immune response 6, deficiency of vitamin B group: vitamin B1 deficiency: anorexia, growth Slow, vomiting, sudden death of cardiac hypertrophy, slow heartbeat, increased plasma pyruvate levels, decreased body temperature, degeneration of cardiac muscle, and heart relaxation. In the absence of vitamin B6: anorexia, slow growth. Convulsions, periocular discharge, dyskinesia, coma, death of erythrocyte hypochromic anemia, elevated serum iron levels, hepatic fatty infiltration, elevated levels of 7-globulin-like blood protein, hemoglobin, red blood cell, and lymphocyte counts cut back. In the absence of vitamin Bl2: anorexia - slow growth, reduced number of litters, small primary birth weight, allergies, rough skin and hair, hind legs dysregulation of normal red blood cell anemia, increased neutrophil count, lymphocyte count decreased by 7, In the absence of vitamin c (ascorbic acid): systemic freckle bleeding. Vitamin C (ascorbic acid) is a water-soluble antioxidant that is involved in the oxidation of aromatic amino acids, the synthesis of norepinephrine and carnitine, and the reduction of cellular hemagglutinin to be transferred to cells. Ascorbic acid is also required for hydroxylation of valine and lysine, and hydroxylated valine and lysine are components of collagen. The principle of glue is essential for the growth of cartilage and bones. Vitamin C promotes the formation of bone matrix and tooth dentin. two. Poultry deficiency deficiencies: Reduced feed intake; Reduced bioavailability of nutrients in dietary raw materials: Changes in nutrient content in dietary raw materials: Errors in diet formulation and configuration; Changes in poultry nutritional needs, etc. . 1. Protein/amino acid deficiency: Unlike the characteristic symptoms caused by vitamin or mineral deficiency, the symptoms of essential amino acid deficiency are non-specific: growth retardation, decreased feed intake, reduced egg production and egg weight, and adult poultry Weight loss and so on. The critical deficiency of amino acids often leads to an increase in feed intake, or the feed intake remains unchanged and body weight gain and muscle tissue increase simultaneously decrease, resulting in a significant increase in body fat. A severe lack of amino acids can also cause changes in body composition. The lack of certain amino acids has Other additional effects. Since methionine has a noteworthy role in methyl metabolism, its deficiency can exacerbate choline or vitamin BI2 deficiency. In bronze turkeys, the lack of lysine causes a decrease in the deposition of pigments, but its biochemical mechanism is still unknown. At the same time, the lack of lysine can cause growth retardation in poultry. The lack of arginine tends to cause the feathers of the wings to roll upwards, causing the chicks to appear distinctly feathery. It has been reported that there are several other amino acids that also have clusters of feather growth and structure. When the dietary protein level exceeds the animal's requirement, the excess protein is degraded by the body and the released nitrogen is converted to uric acid. A large excess of protein can cause hyperuricemia and joint gout, especially in genetically sensitive birds. 2, when the iron is lacking: Causes the hemoglobin to be too little the red blood cell anemia, causes the plasma non-heme iron content to reduce, and hinder colored breed feather pigmentation. The lack of iron in laying hens results in anemia in the developing embryos of the laying eggs at hatching. And reduce the hatching rate. The chicks that lived during hatching were weak and unwilling to exercise, but they could recover after adding iron. The hen's hemoglobin level will be reduced during the first part of laying, but this obviously has nothing to do with the amount of iron or copper in the diet because the hens will rapidly increase their hemoglobin levels when they begin to hold their nests. Therefore, the common occurrence of low hemoglobin in spawning is more likely to be caused by changes in hormonal activity than in the absence of iron or copper. According to reports, chicks are deficient in iron. The number of hydrochloric acid synthesized from tryptophan decreases. 3, lack of selenium: larvae exudative quality and young turkey muscle stomach and heart muscle disease, duckling selenium plasma glutathione peroxidase and body weight gain decreased, mortality increased. Ducks that died of selenium deficiency exhibited necrosis of myogastric and intestinal smooth muscles, myocardium, and skeletal muscles, as well as symptoms of hydrocephalus and ascites. Vitamin E and selenium have a coordinated effect on the prevention of these diseases. The severely selenium-deficient chicks showed poor growth and poor feather development, poor fat indigestion, pancreatic atrophy and fibrosis, and decreased selenium glucosylperoxidase activity in the pancreas. According to relevant reports, continuous sampling studies were performed on pancreatic lesions. The lesions began in six ages and showed the formation of vacuoles and transparent bodies of the exocrine pancreas. As the deficiency develops, the cytoplasm degenerates until the acinus is replaced by a ring of cells in which the fibrous tissue is embedded in the center of the cavity. Feeding 100IU/kg of vitamin E and promoting its absorption with bile salts can maintain a high level of plasma tocopherol, which can greatly reduce the incidence of exudative diathesis. The chicken's pancreas does not show exudative qualities until severely degenerated. 4. Zinc deficiency: Symptoms of zinc deficiency include slow growth, poor feather growth, increased ankles, short and thick long bones, skin scales and dermatitis mainly in the feet, and clumsy arthritic gait. Zinc-deficient chicks show an increase in hematocrit due to redistribution of water in the body, not due to changes in drinking water. Ducks showed poor growth and epidermal lesions on the feet, especially between the digits. Pathological changes in epidermitis are evident in the interdigital toes, tongue mucosa, and other parts of the gastrointestinal tract. Hyperkeratosis and echinoderms are tongue and toe problems. According to reports, chickens raised on diets deficient in zinc cannot produce antibodies against T cell-dependent antigens, even if lymphocytes can produce immunoglobulins. 5, vitamin E deficiency: chickens can occur brain encephalomalacia, exudative quality and muscular dystrophy; Turkey can occur ankle swelling and muscle stomach muscle atrophy; duck muscle atrophy. Vitamin E may also be necessary for the normal development of duck embryos. Alcohol type vitamin E is a very effective antioxidant. It is an important protective agent for essential fatty acids and other unsaturated fatty acids, vitamin A, vitamin D, glucosinolates, and lutein in feeds. Tests showed that when the dietary selenium content reached 0.04 ~ O. 1mg/kg. It can prevent and treat the exudative quality caused by vitamin E deficiency in chicks, O. 1. - ~ 0, 2mg/kg of selenium can effectively prevent the occurrence of muscle stomach and heart muscle disease in young turkeys. Vitamin E plays a multifaceted role in poultry nutrition. It is not only required for the normal breeding of poultry, but also as the most effective anti-oxidation thorn in nature, it can prevent brain softening, synergy with selenium can prevent exudative quality and turkey myopathy, synergistic with selenium and cystine. Rejection can prevent the occurrence of nutritional muscle atrophy. Deficiency and histopathological changes Adult chickens and turkeys consume only a very low level of vitamin E over a longer period of time, and do not show an external lack of symptoms. However, hatching rates of eggs produced by vitamin E-deficient chickens and turkeys are significantly reduced. Eggs produced by vitamin E-deficient hens die on the fourth or later embryonic day. Mortality depends on the severity of vitamin E deficiency. Embryos in turkeys can cause cataracts in both eyes, leading to blindness. Male birds do not take vitamin E for a long time and their sexual desire is not strong. Semen quality is not the same, testicles become smaller and degenerate. 6, vitamin B deficiency when the lack of vitamin B1: Chicks are very sensitive to thiamine deficiency, feeding diets lacking thiamine about 10 days after the emergence of multiple neurological symptoms. Suddenly, the diseased chicken showed a "stargazing" posture. The head was extremely bent and bowed like an angled bow. Because the leg paralysis was unable to stand and walk, the diseased chicken took the ankle and the tail to touch the ground. Sitting on the ground or lying on the side of the floor, serious failure died. About 3 weeks after the adult chicken thiamine deficiency, there are clinical symptoms. In the beginning of the illness, the appetite decreased, the growth was slow, the feathers were dull, the legs were weak and the gait was unstable. The cockscomb often has a blue-purple color. Afterwards, the neurological symptoms gradually became apparent. It began with flexor muscle paralysis of the toes, followed by upward development. The extensors of the legs, wings, and neck were clearly paralyzed. Some chickens have anemia and diarrhea. The body temperature dropped to 35.5 °C. The respiratory rate is progressively reduced. Failed to die. Diseased ducks often have paroxysmal onset of neurological symptoms, head to side, or head up. As the disease progresses, the number of episodes increases and gradually becomes severe. The body is convulsed or thundered and reversed by rain. In the absence of vitamin B2: After the chicks are fed a diet lacking riboflavin, diarrhea occurs at 1 to 2 weeks of age, and the appetite is still good, but the growth is slow, and weight loss is weak. The characteristic symptom is that the toes are twisted inward and cannot walk, and the ankle joints are grounded. The wings are maintained to maintain the balance of the body and the legs are paralyzed. Leg muscles are atrophic and loose. The skin is dry and rough. The diseased chicks starved to eat without food. In the late period of brooding chicken disease, the legs lie open and lie down. The egg production of the hen is reduced and the protein is thin. The hatching rate of eggs decreased. The riboflavin content in the hen's diet is low, and the riboflavin content of the eggs it produces and the hatched chicks is also low. Riboflavin is essential for normal embryonic development and hatching. When the riboflavin in the hatching eggs is used up, the chick embryo will die. Dead embryo showed nodular villi, curved neck, short body, deformed joints, edema, anemia, and degeneration of kidney and other pathological changes. Sometimes hatchlings can also be hatched, but most of them have congenital symptoms of numbness, small size and puffiness. In the absence of vitamin B6, chicks have decreased appetite, poor growth, anemia, and characteristic neurological symptoms. The chicken's nerves vibrate on both feet and die with a strong licking. When some chickens were convulsed, they ran without purpose, wings flew, turned to one side or completely overturned on the ground. Their heads and legs swiftly swayed. This kind of intense activity and struggle led to the death of the sick chickens. Some of the other chickens had no severe neurological symptoms and severe brucellosis. The histological features of bony bruxism are that the vesicular region of the cartilage of the sacroiliac joints is disorderly arranged and the blood vessels unevenly project into the bone plate. Causes the bone to bend. The loss of appetite in adult chickens, egg production and hatching rate decreased significantly, due to the body's amino acid metabolism, protein deposition rate decreased, slow growth; glyphosate and succinyl-CoA condensed porphyrin group hindered the role of iron Absorption occurs when absorption and utilization decrease. The diseased chickens then lost weight and gradually died of failure. Broilers had subcutaneous edema, enlarged internal organs, and degeneration of the spinal cord and peripheral nerves. Some show liver degeneration. In the absence of vitamin Bl2: Diseased chicks have slow growth, reduced appetite, and anemia. In the absence of vitamin B12 in growing chicks and adult chickens, no characteristic symptoms were reported. If the lack of choline as a methyl source, methionine in the feed at the same time may be short bone rough. Increase vitamin B2 at this time can prevent bone shortness disease, due to the vitamin Bl2 on the synthesis of methyl can play a role. It has been demonstrated that young hens suffering from vitamin BI2 deficiency have a low response to ethylene estradiol treatment at low choline and low egg nitrogen levels and are significantly lower than those fed vitamin BI2. According to relevant reports, the vitamin B1 deficiency is increased in non-protein nitrogen in the blood, and if it is fed with vitamin B2 liver essence, it can be reduced to normal. When vitamin B12 deficiency occurs in adult hens, the vitamin B12 in the eggs is insufficient, and then the embryonic mortality rate peaks when the eggs are hatched to the l6th to 18th days. The characteristic lesions are slow growth of chicken embryos, reduced embryo size, diffuse edema of the skin - muscle atrophy, enlarged heart and morphological abnormalities, goiter, hepatic steatosis, yolk sac, heart and lungs, etc. Bleeding. Some of them also exhibit pathological changes such as bone shortness.
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