Gout is the deposition of uric acid or urates in tissues. In birds uric acid is the end product of nitrogen metabolism. Uric acid is not toxic but precipitated crystals can cause mechanical damage to tissues. Gout is rare in passerine birds. Psittacine birds are more frequently affected. There are two major forms of gout differentiated by the sites of uric acid deposition. These are synovial and visceral gout. In both forms, deposits consist of needle shaped crystals called tophi.

Synovial and visceral gout may occur separately or in conjunction. Synovial gout is considered to be the chronic form of the disease and is the more common. Lesions observed are urate deposition around joints, ligaments, and tendon sheaths. There is a predilection for peripheral articulations. Deposits may have a creamy, pasty or gritty consistency. They may be extremely painful and disfigure the leg. The hock, joints of the feet, and tendon sheaths of the forewing are usually affected. Clinical signs observed are shifting leg lameness, seeking out larger perches, and staying close to floor of cage. Joints may be warm, swollen and tender. Pain usually increases until the bird refuses to move, although some with marked lesions remain unaffected.

Visceral gout is considered to be the acute form of the disease and it is more insidious and difficult to detect. Lesions are pale urate deposits on serosal surfaces, most often in liver, kidney, pericardium, heart and air sacs. Clinical signs are not diagnostic. Anorexia, depression, emaciation, lethargy, and change in temperment may be observed. Birds may die suddenly or waste away gradually.

Diagnosis of both forms is made on the basis of: 1) gross lesions, 2) microscopic examination showing needle-shaped or amorphous crystals (tophi), and 3) the murexide test. (The murexide test is performed by placing a sample of material from the lesions plus one drop nitric acid on a glass slide. This is evaporated slowly over a bunsen burner, allowed to cool, and then one drop of ammonia is added. A red-purple color is positive for urates.)

The exact cause of gout is not known. Uric acid is produced mainly in the liver and is excreted by the kidneys. High blood levels of uric acid fabor its precipitation in tissues. Several predisposing factors may be involved in urate deposition. These include: 1) water deprivation, 2) high protein diets or overeating which can increase uric acid levels in the blood and lead to precipitation in tissues or 3) impaired renal function.

The prognosis for affected birds is very poor. It is not possible to cure birds with gout. Urates already deposited in tissues can not be resorbed. However, pain can be alleviated and further precipitation of urates prevented.

Therapy consists of a combination of dietary, environmental, and local and systematic treatments. 1) environmental; smooth, flat perches placed at low levels, easily accessible food and water, and freedom to exercise, 2) dietary; low protein seed mixes plus vitamin A, vegetables and fruits, 3) local therapy; surgical removal and cauterization may be done in some instances. This is indicated in large deposits causing great pain, swelling and inflammation, but heal very poorly, and 4) systematic drug therapy: a) analgesiscs: Aspirin, and Atophan b) Zyloprim: Allupurinol.

Daily treatment is essential in affected birds for the rest of their lives and some clients may not be willing or able to do this. In some cases, pain and lesions are so severe that euthanasia must be recommended.

Gout (visceral and articular)

Uric acid is the end product of protein and purine metabolism (uricotelic) in birds, where as in mammals’ urea is the end product (ureotelic)

Birds lack the enzyme carbamyl phosphate synthetase to dispose of ammonia and the enzyme uricase to decarboxylate uric acid to allantoin

Gout is a metabolic condition where abnormal accumulation of white chalky or white semifluid-like urates in soft tissues of various organs in the body

Gout occurs as two distinct syndromes, visceral and articular gout

These two syndromes differ in age of onset, frequency, sex predilection, gross and microscopic lesions, pathogenesis and causes

Great deal of confusion exists between the two syndromes because urate deposition takes place in joints in visceral gout also

Term "visceral gout" should be replaced with the term "visceral urate deposits"

See table 4 to help clarify differences between the two syndromes

Table 4: Differences between Visceral Gout and Articular Gout in Birds

	Visceral gout (Visceral urate deposition)	Articular gout
1. Onset:	It is usually an acute condition but can be chronic.	It is usually a chronic disease.
2. Frequency:	It is very common.	It is rare or sporadic.
3. Age:	1 day and above.	4-5 months and above. However, immature genetically susceptible chickens may be induced by high protein levels in the diet.
4. Sex:	Both males and females are susceptible.	Mostly males.
5. Gross lesions
Kidney:	Kidneys are almost always involved and they look grossly abnormal with deposition of white, chalky precipitates.	Kidneys are normal grossly. Kidneys may become abnormal with white urate deposits if the bird gets dehydrated.
Soft tissues:	Visceral organs like liver, myocardium, spleen or serosal surfaces like pleura, pericardium, air sacs, mesentery, etc. are commonly involved.	Soft tissues other than synovium are rarely involved, however, comb, wattles, and trachea have been observed to be involved.
Joints:	Soft tissues around the joints may or may not be involved. Surfaces of muscles, synovial sheaths of tendons and joints are involved in severe cases.	Soft tissues around the joints are always involved, especially feet. Other joints of the legs, wing, spine, and mandible are also commonly involved.
6. Microscopic lesions:	Generally no inflammatory reaction in synovium or visceral surfaces. Kidney has inflammatory reaction around tophus.	Granulomatous inflammation in synovium and other tissues.
7. Pathogenesis:	It is generally due to failure of urate excretion (renal failure).	It is probably due to a metabolic defect in the secretion of urates by the kidney tubules.
8. Causes:	1. Dehydration. 2. Nephrotoxicity: calcium, mycotoxins, (ochratoxins, oosporein, aflatoxins, etc.), certain antibiotics, heavy metals (lead), ethylene glycol, ethoxyquin etc. 3. Infectious agents: nephrotropic IBV and avian nephritis virus (chickens), polyomavirus, PMV-1 (pigeons), Salmonella sp., Yersinia sp., Chlamydia psittaci, Eimeria truncata, microsporidia, cryptosporidia, Aspergillus sp., etc. 4. Vitamin A deficiency 5. Urolithiasis 6. Neoplasia (lymphoma, primary renal tumors) 8. Immune mediated glomerulonephritis 9. Anomalies 10. Others?	a. Genetics. b. High protein in the diet. c. Others?

Ref: Shivaprasad, H. L. An overview of anatomy, physiology and pathology of urinary system in birds, AAV Proceedings, pp. 201-205, 1998