What causes gout in chickens? A comprehensive analysis of the causes
Gout is a metabolic disease caused by a disturbance in uric acid metabolism in the chicken's body, in which the uric acid concentration in the blood rises, large amounts of uric acid are excreted through the kidneys; kidney damage and reduced kidney function caused by various factors further obstruct uric acid excretion, resulting in uric acid poisoning. It occurs mostly in broiler chickens and caged @#@230@#@. The main causes of gout in chickens are as follows:
1. VA deficiency
VA has the function of protecting mucous membranes; when deficient, it can cause keratinization and squamous epithelial metaplasia of the renal tubules, collecting ducts and ureters. Due to keratinization and metaplasia of the epithelium, mucus secretion decreases, urate excretion is obstructed and embolic material forms - urate stones - blocking the lumen and thereby causing gout. When trace elements and vitamins are combined unreasonably and the concentrate feed is stored for too long, large amounts of vitamin A are destroyed; deficiency of vitamin A leads to renal epithelial damage, a marked decrease in glomerular filtration rate, and obstructed excretion of uric acid and phosphorus. When yeast protein is used to replace fishmeal, since the main component of yeast protein is nucleoprotein, its end product after metabolism in the poultry liver is mainly uric acid, causing the uric acid concentration in the blood to be too high; uric acid is deposited on the surface of internal organs and in the kidneys, ultimately destroying large numbers of nephrons and causing renal failure. Therefore, vitamin A must be supplemented adequately in such diets.
2. Feeding too much protein-rich feed
Soybean cake, animal offal, fishmeal and meat-and-bone meal are relatively high in protein. Because the poultry liver does not contain arginase and cannot synthesize urea from ammonia, and the kidney cannot carry ammonia because it lacks glutamine synthetase, the protein metabolic products of poultry are excreted in the form of uric acid through the pathways of purine nucleotide synthesis and decomposition. The kidney is the most important and most critical organ for uric acid metabolism in the poultry body, and is also the only excretory channel for uric acid in poultry. When poultry kidney function is normal, uric acid can be excreted quickly through the kidneys, maintaining a certain uric acid level in the blood (1.5---3.0mg), and will not cause disease. But when kidney function is impaired or uric acid products are excessive, the uric acid concentration in the blood rises and combines with Na+ and Ca2+ in the blood to form urates that are widely deposited in the body; together with obstruction of the ureters, uricemia will inevitably occur. This causes enlargement and brittleness of the liver and kidneys, dilation of the renal tubules and ureters due to blockage by urate crystals, and excretion of white lime-like loose droppings. In the joint cavity, friction and irritation from urate deposits cause erosion and exudation of the articular surface, leading to joint swelling, movement disorders or paralysis. Some chicken farmers pursue growth speed and egg production rate too aggressively and add excessive protein feed (such as soybean cake, animal offal, fishmeal, etc.) to the feed; the uric acid produced by nucleic acid decomposition exceeds the body's excretion capacity, and large amounts of urates are deposited in the internal organs or joints, causing gout.
3. Feeding high-calcium feed
Some feed manufacturers pursue only profit and not quality, adding too much stone powder and shell powder to finished feed, resulting in high calcium and low phosphorus and thus a severely imbalanced calcium-to-phosphorus ratio. In addition, some chicken farmers use layer feed to feed chicks, and some chicken farmers, in order to speed up the growth of egg-type chicks, deliberately feed broiler feed, or add too much shell powder, stone powder, etc. to the feed, which secondarily causes hypercalcemia. Hypercalcemia leads to increased parathyroid hormone secretion, raising the calcium ion concentration in renal tubular epithelial cells; under certain conditions, calcium salts are deposited in the kidneys and gradually calcify. When calcified renal tubular epithelial cells desquamate into the renal tubular lumen, they become the basis for kidney stone formation; the cells continuously desquamate and gradually aggregate to form kidney stones. At the same time, because nephrons are continuously destroyed, the number of functional nephrons gradually decreases, becoming insufficient to compensate for all kidney function, thereby causing compensatory kidney enlargement and chronic renal insufficiency. When Ca2+ in the feed is too high, large amounts of calcium salts precipitate from the blood and are deposited in the internal organs or joints, forming calcium-salt gout.
4. Unreasonable use of certain antibacterial drugs
Many drugs have damaging effects on the kidneys, such as sulfonamides, aminoglycoside antibiotics, and Ganmaotong, which are excreted through the kidneys in the body and have potential toxic effects on the kidneys. If the drug is used for too long or in too large a dose, it will cause kidney damage. This is especially true of sulfonamides, which have high solubility under alkaline conditions but readily crystallize and precipitate under acidic conditions. If sulfonamides are used in large doses for a long time without being combined with alkaline drugs such as NaHCO3, the sulfonamides will crystallize and precipitate and be deposited in the kidneys and ureters, affecting the function of the kidneys and ureters, causing excretion disorders, and causing urates to be deposited in the body to form gout. In particular, some chicken farmers use all antibiotics in turn when the flock becomes ill, and with excessive doses, especially the large-dose, long-term use of sulfonamides, it is very easy to cause gout in chickens. As for long-term use of oxytetracycline and chloramphenicol, as long as the normal dose is used, they will not cause damage to the kidneys; although tetracycline has a certain nephrotoxic effect, it has no adverse effect on kidneys with normal function.
5. Insufficient drinking water
Insufficient drinking water is a predisposing factor for gout in poultry. In hot summer or during long-distance transport, if drinking water is insufficient, it will cause dehydration of the body, promote urine concentration, and prevent the body's metabolic products from being excreted in time, causing urates to be deposited in the ureters; the renal ureters are blocked by urate crystals, inducing gout.
6. Feeding inferior-quality feed
Feeding inferior-quality fishmeal. When feed prices soar and the profitability of chicken raising drops sharply, some chicken farmers, facing difficulties in cash flow, use cheap fishmeal. This fishmeal is low in protein and high in salt, and is often mixed with urea; some fishmeal is even moldy. High levels of salt, urea, mold and its toxins are factors that cannot be ignored in causing kidney damage.
Feeding inferior-quality bone meal is another important factor in the occurrence of gout. There are many bone meal processing plants in various places, but the supply of bones is insufficient, so quality is difficult to guarantee; some bone meal is crushed without degreasing, degumming or drying. The fat, gelatin and moisture it contains make the bone meal very prone to rancidity and mold. Some even mix large amounts of shell powder into the bone meal, causing high calcium and low phosphorus, which causes gout after being fed to chickens.
7. Disease factors
The diseases related to chicken gout mainly include nephropathogenic infectious bronchitis (IB), infectious bursal disease (IBD), salmonellosis, etc. Infectious bronchitis is a highly contagious disease of chickens, usually mainly affecting the respiratory tract, but certain strains such as Holte, Gray, Italian and AustralianT are strongly nephrotropic, causing nephritis and weakened kidney function. Young chickens are most sensitive to the kidney damage caused by infectious bronchitis, and initial infection may occur long before kidney function declines and death occurs. When replacement pullets reach sexual maturity, they need to be fed a diet with a relatively high calcium content for egg production; if the kidneys were damaged during the brooding or growing period, such damaged kidneys cannot excrete high levels of calcium as normal kidneys do, thus causing gout. In addition, avian nephritis virus (ANV) is an enterovirus that proliferates in kidney cells and can cause inflammation of the kidneys, leading to renal failure and secondary gout.