Meat chicken leg disease and diet nutrition

Drumstick disease is a complex multifactorial disease. In current production practice, regardless of whether it is self-contained powder or feed pellets, it has a certain incidence of leg problems, and is increasingly complex and serious, resulting in increased mortality. It has a great impact on the economic benefits of farmers.

1 dietary energy, protein and amino acid levels

In order to make broiler have faster growth rate and higher feed utilization rate, oil is usually used to make high-energy diets, but high-energy and high-protein diets, in addition to leading to ascites, and death, can easily lead to higher The incidence of leg problems. In order to meet the growth needs of poultry and avoid the occurrence of leg problems, the protein concentration in the diet should decrease as the age increases, and the energy must be increased accordingly. That is, during the growth period, the ratio of dietary energy to protein should continue to increase. Rizk (1980)'s experimental study showed that when the lysine content in the diet ranged from 0.5% to 1.0%, the incidence of broiler spondylolisthesis and curling claws increased from 22% to 33%. Cauliner (1992) reported that 50% of 10-day-old chicks supplemented with 0.5% lysine had foot problems in 18% protein feeds, and about 0.7% of chicks were supplemented with 0.75% lysine. % leg disorder. In production practice, it has also been found that when a feed with a high protein content (especially animal protein) is fed to chickens, a large amount of urate is deposited in the joints to form joint gout, which is due to dyslipidemia. .

2 constant elements

The appropriate levels of calcium, phosphorus, and available phosphorus in the diet and the ratio between them have a certain degree of influence on leg disease in broilers. Broilers have the most calcium and phosphorus requirements, and are prone to calcium and phosphorus deficiency. When calcium and phosphorus are lacking or there is sufficient supply of calcium and phosphorus, but the ratio between the two is not proper or VD is lacking, broilers still cannot absorb calcium well. Phosphorus causes chickens to suffer from osteomalacia, osteoporosis and soft, numbness in the feet, difficulties in standing, and often sideways symptoms. Hulan (1986) showed that the ratio of calcium to available phosphorus in broiler brooding and finishing diets was 1.75-3.03, and the incidence of leg abnormalities was the lowest. Leach (1972) pointed out that dietary calcium, phosphorus (or calcium, phosphorus ratio) and fluoride levels play a decisive role in the induction or prevention of ostrich osteochondritis (TD). Lee et al. (1984) and Roland et al. (1990) obtained the same conclusion. The current recommended values ​​for calcium and phosphorus are 0.8-0.9 g/kg and 0.3-0.4 g/kg, respectively, consistent with normal bone development. High-phosphorus, high-chlorine diets can make broiler leg disease appear, especially high-chloride diets are more likely to cause osteomalacia than high-phosphorus diets. The uptake of high-phosphorus or high-chlorine diets destroys the body's acid-base balance and affects calcium metabolism. Such as the combination of plasma calcium and free calcium, the regulation between parathyroid hormone (pTH) and Ca2+, and more importantly, the conversion of 25-(OH)2D3 from kidney to the activity of α-hydroxylase of 1.25-(OH)2D3. Interference. Excessive chlorine causes acidosis, which can reduce the serum 1,25-(OH)2D3 content, affecting the normal development and calcification of cartilage. Adding spikes or potassium ions to the diet can limit the onset of high chloride diets, which may regulate the body's acid-base balance. High magnesium diets can reduce the incidence of TD caused by high chloride or high phosphorus diets. Studies have shown that ingestion of high-magnitude diets increases the calcium and phosphorus levels in young chickens (Roland et al. 1990). Magnesium as an anti-leg disease factor in diets is achieved by promoting the deposition of calcium and phosphorus in the bone tissue of the chicks and increasing calcification, and it may have jaw-effects with chlorine in the diet.

In the absence of potassium, it can cause gait instability and impediment to growth. If there is a lack of chlorine, the kidneys are damaged. The chicks also exhibit special neurological reactions, falling before the body, and legs stretching.

3 Electrolyte balance

A high balance of dietary electrolytes helps prevent leg problems. When dietary electrolyte balance (dEB) was between -200 and 400 mmol/kg, the highest TD incidence (>20%) was in the dEB=-200 mmol/kg group, and the lowest TD incidence (<3 %) In the dEB group of 400, there was a tendency for TD to decline as dEB increased (Austic and Paience, 1988).

Mineral balance in diets affects bone calcification. Excessive levels of chloride in the form of amino acid hydrochloride and calcium chloride in diets can reduce ash content in chicken bone (Edwards, 1984). Skeletal calcification can also occur in chickens with K deficiency, which may be caused by intracellular acidosis due to the abnormal acid-base balance caused by low potassium levels. Hulan et al. (1987) showed that the supply of Na and K in diets affected the incidence of TD in broilers and was related to the levels of dietary Ca and Cl. The increase of Ca, Na, or K in diets decreased the incidence of TD. When the level of steel in diets was low, the effects of TD were reduced only when the K and Cl contents in the diet were high. A high level of available phosphorus (0.65%) in the diet when the Cl content in the diet is high (0.36%) results in a significant increase in the incidence of TD in the broiler (Lilburm et al., 1989). The results of Halley et al. (1987) showed that the blood pH of broilers tends to decrease as the content of anions in the diet increases; excessive levels of H(superscript -) and HCO3- are lower in the blood; the excess of blood alkali and the incidence of TD are significant. Negative correlation.

4 trace mineral elements

Trace elements associated with leg problems include manganese, copper, zinc, nickel and selenium. Manganese is required for the synthesis of oligosaccharides and proteoglycans in the process of glycosyltransferases. Mucopolysaccharides and collagen are the units of bone organic matter. When manganese is deficient, the synthesis of mucopolysaccharides is hindered, and the content of mucopolysaccharides in bones is reduced and calcified. Matrix formation is hindered, affecting the strength of the skeleton, and the classic symptom is slippery cavitation. High calcium and high phosphorus can lead to the formation of calcium phosphate precipitates in the intestine, precipitation of manganese adsorption and discharge together with the digestive tract to exacerbate the lack of manganese. It is generally believed that the minimum requirement of manganese for growing poultry under normal dietary conditions is 40 mg/kg. In order to safely adapt to variations in calcium and phosphorus intake, 50 mg/kg of manganese need to be supplemented in the diet. When the broiler's skeleton is abnormal, the abdomen's skin appears as a piece of phosphorus, and it is easy to fall into pieces. This is the performance of zinc deficiency. The minimum amount of zinc needed for chick growth is 35-40 mg/kg for soy feed and 25-30 mg/kg for animal feed. Currently supplemented with meat and bone meal in feed has received a good preventive effect, because it is rich in zinc, meat powder containing 50mg/kg, bone powder containing 150-200 mg/kg. The role of copper is mainly due to the copper-containing metalloproteinase hydroxylase oxidase which is necessary for the covalent cross-linking of collagen molecules to form fibrils. When feeding copper-deficient diets, symptoms of lameness occur at 2-4 weeks of age and the bones become brittle. Easy to fold, the cartilage at the skeletal site thickens, showing symptoms of movement disorders, paralysis of numbness. The minimum requirement for copper in broilers does not exceed 3-5 mg/kg diet. Due to the high content of copper in vegetable feeds, in most cases it is not necessary to add copper to broiler feeds; there are also few reports of copper deficiency in production. Aluminum in the diet can affect bone calcification by interacting with phosphorus. For every unit of dietary aluminum added, 0.76g of phosphorus needs to be added to prevent the decrease of plasma phosphorus and maintain the mineral deposition of bone tissue. . Nieson (1970) was the first to confirm that nickel is an essential nutrient for growth in chicks, and chicks fed a diet lower than 44 mg/kg had a short and thick leg, a tiny hocks, and 3-5 mg/kg of nickel in the diet. Prevent the occurrence of TD. However, the mechanism is not yet clear. In practice, deficiency of selenium and VE often occur at the same time. Selenium deficiency can affect the absorption of VE. Causes chickens to soften their brains, lick their legs, paralyze, and ataxia. Zhu Yisun (1998) reported that a chicken farm breeds three types of yellow chickens, and when it is 280 days old, it is changed from feeding full-grain pellet feed to self-contained powder. After 35 days of feeding powder, selenium deficiency occurs in breeder chickens. Clinically, diarrhea, lameness, lying in the ground, extreme exhaustion, and individual madness and other symptoms.

5 vitamins

Biotin (VH) is a sulfur-containing compound in the B vitamins. It was confirmed as early as in the 1940s that short bone thickening is a characteristic symptom of biotin deficiency, similar to the symptoms of manganese deficiency. Vitamin B1 (thiamine) is related to carbohydrate metabolism. When it is lacking, it triggers glucose metabolism disorder. It is the lack of energy supply to the nervous tissue, which affects the nerve function, thus causing multiple neuritis or peripheral nerve paralysis. The diseased chicken put the body to sit. On the legs of the curls, the head is backwards, and the front and back are extremely curved and assume a "stargazing" posture or penguin posture. The symptoms of vitamin B2 (riboflavin) deficiency are inward curling of the paws of the diseased chickens, paralysis of the two limbs, landing on running joints, difficulty walking, slow growth, muscle atrophy and relaxation of the legs, dry and rough skin. At the time of necropsy, the sciatic nerve and arm nerves were clearly swollen and soft, and the swelling of the sciatic nerve was 4-5 times higher than normal. Vitamin E deficiency, the disease of the abdomen, wings inside, subcutaneous tissue edema of the inner thigh or effusion, due to brain softening, often manifested ataxia, head down or backward contracture, leg spasmodic convulsions, walking inconvenience, Finally can not stand. The symptoms caused by vitamin D deficiency are also called osteoporosis and rickets, which are caused by calcium and phosphorus metabolism disorders in the body. The symptoms are exactly the same as calcium and phosphorus deficiency. Lack of nicotinic acid (VPP) can cause the swelling of young chickens' hocks and the bending of leg bones. The first symptom of choline (VB4) deficiency is enlargement of the hump, with a needle-point hemorrhage on the surface, a thickening of the posterior pulp bone, displacement of the articular cartilage, and detachment from the condyle. Pantothenic acid and folic acid deficiency all show bone shortness and coarseness. The former also has paternal horns, toes and decapitated cavities, and the latter has anemia.

6 The special role of feed ingredients

6.1 Tannins are fed on sorghum-enriched sorghum chickens, which cause leg bending and joint swelling.

6.2 Antitrypsin factor and guineous enzyme Edwards (1985) found that different sources of beancake powder have different effects on chicken legs. The analysis showed that the bean cake powder containing high antitrypsin factor and urease activity caused a high incidence of TD, and the pancreas of the chicken was also swollen.

6.3 Isothiocyanate (ITC), OxThrough Alkylthione (OZT) High levels of rapeseed cake (> 1000 mg/kg) in brood diets increase the incidence of leg deformation in broiler chickens and add manganese. Cannot improve the situation. New low-toxic rapeseed cake has a weak pathogenic effect.

7 The role of nutrients

7.1 Interactions between minerals The levels of calcium and phosphorus in diets are too high. They form flocculant precipitates in the alkaline environment of the intestine, and manganese, zinc and other trace elements are excreted in the faeces. Excessive levels of calcium and phytic acid in diets will hinder the use of trace elements such as copper and zinc, which will increase the incidence of leg problems.

7.2 Vitamin E and Fatty Acids Zinc is required for â–³6-desaturase, prostaglandin synthetase, etc. in essential fatty acid metabolic pathways. Bettger (1980) found that increased levels of unsaturated fatty acids in the diet increased the incidence of chickens and zinc deficiencies such as dermatitis and TD. Zinc deficiency is reduced if the level of saturated fat and VE is increased.

7.3 Biotin, folic acid and pantothenic acid Robble. (1970) reported that biotin alone had little effect on the treatment of joint anomalies in the event of an outbreak of syndromes similar to biotin deficiency; although folate and pantothenic acid were not effective when biotin was not present, it was clearly associated with the use of biotin. Reduced morbidity.

7.4 There is a strong interaction between the appropriate concentration of 1,25-(OH)2D3 or 25-(OH)D3 in the diet and the calcium and phosphorus nutrition levels of the vitamin D metabolite. Generally, the calcium level in the diet is increased. Low, the greater the dose of metabolites required to prevent TD from occurring. The efficacy of 1,25-(OH)2D3 and 25-OH)D3 is very strong. The concentration of the former in the diet is generally only 2-10 μg/kg, while the latter is about 75-250 μg/kg. The excessive dose of metabolites leads to hypercalcemia and inhibits growth, and the difference between the effective dose and the toxic dose of 1,25-(OH)2D3 is very small. Therefore, it is necessary to carefully determine the feed according to the calcium and phosphorus levels in the diet. dose.

In summary, the analysis of the production of broiler leg disease and the nutritional status of feed is an indispensable aspect. It is necessary to comprehensively and objectively find out the cause of the disease and it is necessary for diagnosis and further treatment.

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