Avian Gout
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.