Infectious causes of Gout

Toxic causes

Control of Gout

Difference between Visceral Gout and Articular Gout in Birds

Introduction: 

Today's bird is genetically engineered for higher productivity. Selection is based on production parameters. In the process, the health of the vital organs is ignored. this has resulted in increased incidence of metabolic disorders. The kidney is one such vital organ of the bird with diverse metabolic and excretory functions, viz:

Maintaining the chemical composition of body fluids

Removal of metabolic waste and toxic products

Regulation of blood pressure and blood volume

Conservation of fluids and electrolytes.

The kidney is affected by a number of specific diseases and disorders. One of the important disorders associated with kidney damage is GOUT. Gout is a condition in which kidney function has decreased to the point where uric acid accumulates in the blood and body fluids. Avian Gout is a metabolic condition where abnormal accumulation of white, chalky uric acid or urates occurs in soft tissues of various organs in the body. There are two major forms of gout differentiated by the sites of uric acid deposition - visceral and articular gout. In both forms, deposits consist of needle-shaped crystals called tophi.

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 prediliction for peripheral articulations. Clinical signs observed are shifting leg lameness with joints becoming warm, swollen and tender. It is a condition in chickens that has been recognized for more than 30 years. Visceral gout is considered to be the acute form of the disease causing huge mortality and characterized by urate deposits on serosal surfaces, most often in the liver, kidney, pericardium, heart and air sacs. Visceral gout is more common in broilers as yound as 2-3 days old. In layers, pullets above 14 weeks are more likely to be affected.

In birds, uric acid is the end product of nitrogen metabolism. Uric acid is a nitrogenous waste from protein breakdown. In mammals, it is converted to less harmful substances with the help of the enzyme uricase. But in birds, this enzyme is absent. Hence, uric acid is the final excretory product. Uric acid is produced mainly in the liver and is excreted by the kidneys. High blood levels of uric acid favor its precipitation in tissues. Uric acid is not toxic but precipitated crystals can cause mechanical damange to tissues. Whenever there is kidney damage, excretion of uric acid gets affected and uric acid starts accumulating in the blood and later in tissues. 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.

The causes of gout are many as kidney damange occures due to multietiological factors. The causes of gout can be broadly categorized as:

• Nutritional and metabolic factors
• Infectious causes
• Toxicity and other reasons

NUTRITIONAL CAUSES OF GOUT

Excess dietary calcium with low available phosphorus results in precipitation of calcium-sodium-urate crystals. High levels of vitamin D_{3 can also increase calcium absorption from the gut which can favor formation and deposition of urate crystals.}

• Excessive use of sodium bicarbonate : Sodium bicarbonate is used to combat heat stress and thus improve egg shell quality in layers. This results in alkalinity of urine favoring kidney stone formation
• Prolonged Vitamin A deficiency causes sloughing of tubular epithelium and subsequent blockade resulting in accumulation of urates in the kidney. However, incidence of gout due to Vitamin A deficiency is least under field conditions.
• Excess Sodium : Gout due to sodium intoxication is seen in younger birds when the sodium level exceeds 0.4% in water and 0.8% in feed. This generally happens when fishmeal is used in the diet ( even with normal salt content), since fishmeal is rich in salt content. Total content of sodium chloride in feed should not exceed 0.3%.
• Excess of Protein : More than 30% of protein in the diet causes excessive uric acid production which in turn, creates an excretory load on the kidney. At the same time, the presence of sulphates decreases calcium resorption causing excessive calcium secretion through urine. This condition favors gout.
• Water deprivation : This leads to concentration of uric acid and other minerals in the blood and later in the kidney. Water deprivation especially in summer is dangerous. This can happen during transportation of birds or due to blockage of nipples, inadequate number of waterers, extra height of water line, overcrowding, water withholding for long durations during vaccination, etc. Hard water with higher metallic salt content is also a load on the kidney.

INFECTIOUS CAUSES OF GOUT

The major infectious causes include Avian Nephritis virus, infectious bronchitis and baby chick nephropathy. Infectious Bronchitis (IB) of nephrotropic strain causes gout in chicken. The virus causes severe kidney damage. Sub-clinical infection combined with other factors like high protein, high calcium etc. results in gout. This is common especially in younger chicks as they pick up infections in the early stages.

TOXIC CAUSES

Various chemicals and toxins are involved in kidney damage:

• Mycotoxin : Mycotoxins are the most common cause of kidney damage and among mycotoxins, ochratoxins and oosporin are important. The combination of ochratoxins with aflatoxins is found to be more dangerous. Because of kidney damage uric acid excretion is reduced resulting in accumulation of uric acid in the body.
• Antibiotics like gentamycin, sulfonamides and nitrofurosones are known to cause renal damage especially in young chicks. The drugs, which get excreted through the kidney, have their own imbalancing effect on pH and renal metabolism.
• Disinfectants like Phenol and Cresol, if used erroneously, can cause residual toxicity.
• Copper sulphate used in water results in water refusal, dehydration and gout.

Gout is characterised by depression, dehydration and sometimes, greenish diarrhoea. Affected chicks appear dull with ruffled feathers and moist vent. Mortaligy among young chicks is high. There is irregular and excessive enlargement of kidney lobules and cutting open the kidney reveals urate crystals. Chalky white deposition of urate crystals is seen all over the visceral organs like the heart, liver and kidney, under the skin etc.

CONTROL OF GOUT

• Provide plenty of water
• Avoid a diet higher in protein than the recommended level as per the age and breed.
• Review IB vaccination programme. In areas, where IB is endemic it is advisable to vaccinate with nephrotropic strain at around 4 days. Day one beak dip vaccination has proved to be beneficial in broilers.
• Use of urine acidifiers. Ammonium sulphate 5.0 g / kg and ammonium chloride 10 g / kg increases the acidity of the urine and helps in uric acid excretion.
• Meet the dietary calcium and phosphorus level carefully. It is better to provide calcium in the form of grit rather than powder as grit dissolves slowly and helps to maintain blood calcium level.
• Analyse the feed for mycotoxin content and if found positive change the feed or use suitable toxin binders.
• Regular checking of watering system for height, blockage, adequate flow of water etc.
• Judicious use of drugs which cause kidney damange.
• Ensure adequate levels of AB₂D₃K and B complex vitamins.
• Excessive use of soidum bicarbonate i.e., more than 2 kg / ton should be avoided.
• Use of electrolytes through water may assist in controlling mortality.
• In acute cases, potassium chloride 1 g / litre can be used.
• Provide broken maize at least for 3 days and jaggery 5 g / litre for 3 - 5 days in acute cases of mortality.
• If the transportation of chicks from hatchery to farm is too long ensure proper temperature and humidity to avoid dehydration.

In conclusion, kidney damage can occur due to a variety of reasons and results in accumulation of uric acid crystals in the body. Hence, prevention and control of gout requires a multifaceted approach in terms of management, disease control and nutrition. Although gout has been recognised for some time as a cause of pullet and broiler chick mortality, it continues to be a diagnostic challenge. Chickens affected by renal damage can continue to be productive until less than one-third of their normal kidney mass remains functional. Compensatory enlargement of remaining normal kidney tissue is responsible for maintaining adequate renal function, at least for a while. Gout, when recognized as a problem in the field, is likely to be a multi-factorial problem and identifying a specific cause is often difficult. Another reason for diagnostic difficulty is that kidney damage occurring during the growing period often has no apparent signs until the birds later come into egg production and are fed high-calcium diets. Field cases and research have demonstrated the importance of interaction between two or more contributing factors, especially nutrition, management and infectious causes.

Thorough investigation to determine the cause of kidney damage and gout helps in streamlining therapeutic and control measures.

Table Ref : H.L. Shivaprasad, University of California, Davis