GOUT IN POULTRY

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GOUT IN POULTRY

Aditya Sharma1, Sheikh Uzma Farooq2, Akashdeep Jalandhari3, Muskan4

1Department of Veterinary Pathology, Khalsa College of Veterinary and Animal Sciences, Amritsar

2Department of Veterinary Pharmacology and Toxicology, Khalsa College of Veterinary and Animal Sciences, Amritsar

3,43rd Prof Student, Khalsa College of Veterinary and Animal Sciences, Amritsar

INTRODUCTION:-

Poultry birds excrete nitrogenous waste from their body as uric acid with mucous in their urine. The proper excretion of uric acid occurs only if the kidneys are properly functioning. In mammals, uric acid is converted to less harmful substance by the activity of the enzyme uricase. But in poultry, uricase is absent. Therefore, uric acid is the final excretory product. Any renal dysfunction decrease the clearance of uric acid from the blood of birds which leads to hyperuricemia and eventually the urates in the blood start depositing on or within the kidneys or other tissues of body – which is known as gout. Therefore, gout is a metabolic disease characterized by deposition of urates on the surfaces of various internal organs or various joints. Uric acid is not toxic but precipitated urate crystals cause mechanical damage to the tissues where they deposit. Both in broilers and layer chicks, gout can be seen from 4th day onward and can be a serious problem between 2nd and 3rd week. Birds usually die from kidney failure. In gout, blood levels of uric acid can be as high as 44 mg/100 ml as compared to 5-7 mg/ 100 ml in a normal bird.

TYPES OF GOUT :-

The two major types of gout in poultry are differentiated by site of uric acid deposition – visceral and articular gout. In both forms, deposits consist of needle shaped crystals called tophi.

  • Visceral gout is considered to be the acute form of disease causing huge mortality characterized by the urate deposits on serosal surfaces, most often in the liver, kidney, pericardium, heart and air sacs. Visceral gout is more common in broilers as young as 2-3 days old. In layers, pullets above 14 weeks are more likely to be affected.
  • Articular gout is considered to be the chronic form of the disease and is less common. Lesions observed are urate deposition around joints, ligaments and tendon sheaths. There is a predilection for peripheral articulation. Clinical signs observed are shifting leg lameness with joints becoming warm, swollen and tender. It is a condition in chicken that has been recognized for more than 30 years.
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PATHOGENESIS OF GOUT:-

  • Uric acid is the end product of purine and protein metabolism in poultry. Uric acid is formed by the liver and excreted by the kidneys.
  • Birds are uricotelic, lack the enzyme uricase and this along with the process of water conservation allows them to excrete urine in the form of semi-solid uric acid in the feces.
  • Disruption in the metabolic process of excretion of uric acid leads to gout.
  • So, gout can arise either due to production of uric acid over the capacity of kidneys to excrete it, or due to compromised kidney function failing to excrete the produced uric acid.

SYMPTOMS OF GOUT :-

General and non-specific symptoms like depression, reduced feed intake, ruffled feathers, emaciation, lameness, moist vent, enteritis etc. are observed, that are inconclusive of gout.

Specific diagnosis is made on post-mortem, wherein lesions reveal urate deposition in various locations. There is irregular and excessive enlargement of kidney lobules.

POST MORTEM LESIONS:-

  1. Presence of white chalky deposits on the suface of heart, liver, kidneys and lungs. These deposits are seen as white chalky coating.
  2. The chalky deposits first begin on the heart and then spread.
  3. The kidneys are swollen, congested and typically greyish white in colour.
  4. One or both ureters may be distended with white material.
  5. In the articular gout, when joints are opened, the tissue surrounding the joints is white due to urate deposition.

CAUSES OF GOUT:-

The causes of avian gout are varied, ranging from management and/ or nutrition-related, to pathogens and/or the presence of mycotoxins in feed.

  1. In terms of nutrition, special attention must be paid to the calcium/phosphorus balance, sodium and vitamin D3. In general, any condition favoring an increase of uric acid in blood favors precipitation in tissue and, as a consequence, development of gout.
  2. Excess dietary calcium with low available phosphorus results in the precipitation of sodium-urate crystals and calcium pyrophosphate (pseudogout).
  3. In younger birds, gout due to sodium intoxication may be observed at sodium levels exceeding 0.4% in water and 0.8% in feed
  4. Another nutrition-related cause is the protein level in feed which in excess of 30% causes uric acid production leading to excretory loads in kidneys.
  5. Sulphates decrease calcium resorption causing excess calcium secretion through the urine. This favors gout, as well as any other factor contributing to urine alkalinity.
  6. Renal disease, failure or obstructed ureters .
  7. Urolithiasis, or the formation of stones in the urinary system.
  8. Hereditary defects that affect uric acid metabolism.
  9. Viral infections, such as infectious bronchitis virus, avian nephritis virus, and Type A influenza virus.
  10. Exposure to mycotoxins, such as oosporein. Nephrotoxin exposure, such as to aminoglycoside, potassium dichromate, or mercuric chloride.
  11. Exposure to pesticides, herbicides, or other toxins.
  12. Deficiency of vitamin A or B12.
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REMEDIES:-

Treatment depends on according causes which has been discussed above in causes of gout development in poultry.

  1. Should be supplied plenty of water, adequate drinkers, and water pipe for egg layer chicken.
  2. Feed containing higher protein than the recommended level as per the age and breed should be avoided. Provide a low protein diet for 3-5 days based on need depending on the severity of gout in acute cases.
  3. Use of urine acidifiers which decrease urate deposition on kidney and other visceral organs.
  4. Ensure adequate levels of A, D3, K and B complex vitamins, and minerals.
  5. Excessive use of sodium bicarbonate eg more than 2kg/ton should be avoided.
  6. Supplying broken maize which is considered as a low purine diet and lesser uric production, thereby urate deposition also decreased in visceral organ in poultry, at least for 3 days.
  7. Providing 0.6% methionine hydroxyl analog free acid with 3% calcium in the diet decreases the production of uric acid in the liver.
  8.  Allopurinol which is available at 2.5-5% should be given 10-40mg in drinking water twice daily and never stop dosage until mortality zero.

PREVENTION:-

For the prevention of gout in poultry in laying chicken it is necessary to have:

1) Nutritionally and Scientifically balanced feed containing proper guideline:-

  • Proper Calcium-phosphorus ratio.
  • Vitamin A, D3, and other essential vitamins and minerals are provided.
  • Required level of sodium, chloride and other ions should be maintained.
  • Conventional sources of protein should be also considered.

2) Determining the feed for mycotoxin content and if found positive change the feed or use suitable toxin binders to fix it.

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3) Judicious use of drugs such as antibiotics especially sulpha drugs and anticoccidials to avoid kidney damage.

4) Fresh potable water accessible to birds all the time to promotes excrete uric acid quickly.

5) Copper sulfate should not be used for medication in all cases, if used should be used under the directions of a registered veterinarian or a poultry practitioner.

CONCLUSION:-

Gout in India is still one of the major causes for huge mortality and morbidity in poultry, causing great monetary losses to the producers. Breeder management along with adequate farm and hatchery management are crucial in preventing incidences of gout. Gout due to water deprivation, particularly in the winter season in India’s northern states, should be taken care of by providing optimal brooding temperatures. The producer should be proactive enough to include optimal additives/supplements in water that would aid in cutting down the usual mortality pattern. Any practice that encourages flushing out uric acid crystals should be adopted.

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