Etiological analysis of gout in chickens

Gout is due to the disturbance of uric acid metabolism in chickens, the increase of the concentration of uric acid in the blood, and the excretion of a large amount of uric acid through the kidneys; kidney damage and renal function decline caused by various reasons further hinder the excretion of uric acid and form a metabolic disease of uricosis, which mostly occurs in broilers and cages. The main causes of chicken gout are as follows:

1. Lack of VA

VA has the function of protecting mucous membrane. When lacking, it can cause keratosis and squamous metaplasia of renal tubules, collecting ducts and ureters. Due to keratosis and metaplasia of the epithelium, mucus secretion decreases, and urate excretion is blocked to form an embolic substance-urate stone, which blocks the lumen and leads to gout. When the unreasonable combination of trace elements and vitamins and the storage time of feed essence are too long, it will cause a great deal of damage to vitamin A. due to the lack of vitamin A, the renal epithelium is damaged, the glomerular filtration rate decreases obviously, and the excretion of uric acid and phosphorus is blocked. When yeast protein is used instead of fishmeal, because the main component of yeast protein is nuclear protein, and the end product of its metabolism in poultry liver is uric acid, the concentration of uric acid in blood is too high, and uric acid is deposited on the surface of internal organs and kidneys, resulting in massive destruction of nephron and renal failure, so vitamin A must be supplemented in this diet.

2. Feed too much protein feed

Bean cake, animal offal, fish meal and meat and bone meal are high in protein. Because there is no arginine enzyme in the liver of birds, ammonia can not be synthesized into urea, and the kidney can not carry ammonia because there is no glutamine synthetase, so the protein metabolites of birds are excreted in the form of uric acid through purine nucleotide synthesis and decomposition pathway. Kidney is the most important and critical organ of uric acid metabolism in birds, and it is also the only excretion channel of uric acid in birds. When the kidney function of poultry is normal, uric acid can be excreted quickly through the kidneys, so that the blood to maintain a certain level of uric acid (1.5---3.0mg), will not cause disease. However, when renal dysfunction or excessive uric acid products increase the concentration of uric acid in the blood, which combines with Na+ and Ca2+ in the blood to form uric acid widely deposited in the body, coupled with ureteral block, uricemia will inevitably occur. As a result, the liver and kidney are enlarged and brittle, and the renal tubules and ureters are dilated due to the obstruction of urate crystals, and white calcareous dung is excreted. Due to the friction stimulation of urate deposits in the joint cavity, erosion and exudation occur on the articular surface, resulting in joint swelling, dyskinesia or paralysis. Some chicken farmers pursue too high the growth rate and laying rate, adding too much protein feed (such as bean cake, animal offal, fish meal, etc.) to the feed, the uric acid produced by nucleic acid decomposition exceeds the excretion capacity of the body, a large amount of urate will be deposited in the internal organs or joints, resulting in gout.

3. Feed high calcium feed

Some feed manufacturers only pursue profit but not quality, and excessively add stone powder and shell powder to the feed products, resulting in high calcium and low phosphorus, resulting in a serious imbalance of calcium and phosphorus. In addition, some chicken farmers feed their chicks with egg-laying feed, while others consciously feed them with broiler feed, or add too much shell powder and stone powder to the feed, resulting in secondary hypercalcemia, which leads to an increase in parathyroid hormone secretion, which increases the concentration of calcium in renal tubular epithelial cells. under certain conditions, calcium salt is deposited in the kidney and gradually calcified. When the calcified renal tubular epithelial cells fall off into the renal tubular lumen, they become the basis for the formation of renal calculi. At the same time, due to the continuous destruction of nephron, the number of organically active nephron decreases gradually, which is not enough to compensate for all renal function, resulting in compensatory renal enlargement and chronic renal insufficiency. When the Ca2+ in the feed is too high, a large amount of calcium salt will be precipitated from the blood and deposited in the viscera or joints, resulting in calcium gout.

4. Unreasonable use of some antibiotics

Many drugs have harmful effects on the kidney, such as sulfonamides and aminoglycoside antibiotics, Ganmaotong and so on are excreted through the kidney and have potential toxic effects on the kidney. If the drug is used for too long and too much, it will cause kidney damage. In particular, sulfonamides have high solubility in alkaline conditions and easy crystallization and precipitation in acidic conditions. If sulfonamides are used in large doses for a long time without cooperating with NaHCO3 and other alkaline drugs, sulfonamides will be crystallized and deposited in the kidney and ureter, affecting the function of the kidney and ureter, causing excretion disorders, and causing urate deposition in the body to form gout. Especially when some chicken farmers get sick, all antibiotics are used in turn, and the dose is too high, especially the high dose of sulfonamides for a long time, it is easy to cause chicken gout. As for the long-term use of oxytetracycline and chloramphenicol, as long as the normal amount of oxytetracycline will not cause damage to the kidney; although tetracycline has a certain nephrotoxic effect, it has no adverse effect on the kidney with normal function.

5. Insufficient drinking water

Lack of drinking water is a cause of gout in poultry. In hot summer or long-distance transportation, if drinking water is insufficient, it will cause dehydration of the body, promote urine concentration, and the metabolites of the body can not be excreted out of the body in time, resulting in urate deposition in the ureter and renal ureter blocked by urate crystallization. induce gout.

6. Feed inferior feed

Feed shoddy fish meal. When feed prices soar, leading to a substantial decline in the efficiency of chicken farming, some chicken farmers have difficulties in cash flow and use cheap fish meal, which is low in protein, high in salt and often mixed with urea; some even get moldy. High contents of salt, urea, mold and their toxins are the factors that can not be ignored in renal injury.

Feeding inferior bone meal is another important factor in the occurrence of gout. There are many manufacturers processing bone powder in various places, and the source of bone is insufficient, so it is difficult to guarantee the quality of bone powder. Some bone meal is crushed without degreasing, degumming and drying. The fat, colloid and water in it make the bone powder rancidity and mildew easily. Some even mixed with a large amount of shell powder in the bone powder, resulting in high calcium and low phosphorus, causing gout after feeding chickens.

7. Disease factors

The main diseases related to chicken gout are renal infectious bronchitis (IB), infectious bursal disease (IBD), salmonellosis and so on. Infectious bronchitis is a highly contagious disease in chickens, which usually mainly affects the respiratory tract, but some strains such as Holte, Gray, Italian and AustralianT have strong nephritis, resulting in nephritis and renal dysfunction. Young chickens are most sensitive to renal damage caused by infectious bronchitis, and the first infection may occur long before renal function decline and death. When the reserve hens are sexually mature, in order to lay eggs, they are fed a diet with a higher calcium content. If the kidneys have been damaged during the breeding or breeding period, the damaged kidneys cannot excrete high levels of calcium as normal, leading to gout. In addition, avian glomerulonephritis virus (ANV) is an enterovirus that proliferates in kidney cells and can cause inflammation of the kidney, leading to renal failure and secondary gout.