Avian Urolithiasis (Visceral Gout): An Economically Important Metabolic Syndrome in Broiler Chickens

Introduction:

“Avian urolithiasis’’ or Gout is a metabolic disorder occurs in poultry and other domestic birds related with kidney dysfunctions. It is characterized by high level of uric acid in the blood (hyperuricemia) and leads to deposition of urates on the surface of visceral organs or various joints particularly hock joint (articular gout). In avian, uric acid is end product of protein or nitrogen metabolism due to absence of uricase enzymes. In gout, blood levels of uric acid are higher than the normal when it exceeds 10mg/dl lead to gout. It can be as high as 44mg/100ml compared to 5-7mg/100ml in a normal bird. The syndrome occurs usually in two separate form visceral gout and articular gout. Visceral gout is a condition in which white chalky uric acid or urate crystals (tophi) (monosodium urates) deposits are seen in soft tissues of various organs in body. Due to its striking lesions, visceral gout has also been describe as acute toxic nephritis, renal gout, kidney stones, nutritional gout and nephrosis. It is responsible for high morbidity and mortality in fast growing and high producing broilers. Visceral gout has emerged as a syndrome of major concern causing heavy economic losses in broiler industry, particularly of broiler chicks and poses a challenge to control because of its multi factorial etiology .The syndrome occurs worldwide which is most common cause of mortality in growing broiler chickens. In worst situation mortality had been seen up to 90% in past. However, 8-15 % mortality is most common in broilers.

Prevalence: 

The visceral gout in fowls was first time described in India by Iyer (1941). Visceral gout is a condition of chickens that has been recognized for more than 30 years. This condition can occur as an individual problem at any age but outbreaks are seen in young chicks in the first or second week of life (baby chick nephropathy) and could be of multi factorial origin. Year wise incidence of the disease ranged between 4.01 to 9.37% with an overall average relative incidence of 7.15% (Chaudhary, 2016). Sayed (2001) reported the incidence of visceral gout was increased during winter months which were attributed to environmental cold stress, making the birds more susceptible to visceral gout followed by summer and monsoon. The highest incidence 93.07% was recorded in colder season in broilers by Shrivastava (2001). He reported higher susceptibility of this condition in broiler between 0-3 weeks of age. Greater the severity of gout resulted in poor feed conversion ratio (FCR) and lower body weight gain. Visceral gout assumes prime economic importance in poultry industry due to increased incidence causing production loss, mortality and lack of availability of specific treatment.

Etiology:

Visceral gout is a metabolic disease and multi etiological factors alone or in combination are known to influence occurrence of this syndrome.

This comprises of

Nutritional and metabolic causes

1. Excess dietary calcium and vitamin D3 with low phosphorous supplementation in the diet of immature pullets.

2. Rearing diets that contain limestone and sodium bicarbonate in particle form which may results in excess calcium intake and imbalance of Ca: P ratio.

3. Marginally low available phosphorus in rearing diets has been associated with higher gout incidence.

4. Sodium bicarbonate can contribute to gout by making the urine more alkaline, which, with high levels of calcium, is an ideal medium for the formation of kidney stones.

5. Vitamin A deficiency over a long period of time can cause damage to the lining of the ureters, which leads to urethral ducts get occluded by the desquamated metaplastic squamous epithelium preventing the excretion of uric acid and facilitating its accumulation in the blood (Ali et al., 2012).

7. Excess of dietary protein (30–40 %)

8. High amount of salt (more than 0.3 %)

9. Poor quality of protein (High amount of nonessential amino acids)

Managemental causes

1. Water deprivation either because of mechanical malfunction or less water in the diet (dehydration).

2. Consumption of hard water with a high amount of minerals (i.e., calcium and copper sulfate).

3. Brooding management (type of brooder, temperature).

Infectious causes:

 Viral agents known to be involved in gout are infectious bronchitis, avian nephritis virus, reo virus and astro virus. Nephropathogenic or nephrotropic strains of infectious bronchitis have a special predilection for the kidneys in youngpoultry causing enlargement of kidney and distended with urates.

Toxins: 

Products used on a routine basis that have potential for human error and resulting toxicity are antibiotics, anti-coccidials, minerals, vitamins, manufactured chemicals and pesticides. Fungal toxins (Mycotoxins, ocharatoxins, aflatoxins, oosporein etc.) in poultry feed are nephrotoxic. Other causes includes heavy metal poisoning and the inappropriate use of antibiotics (such as gentamycin, nitrofurosones and sulfonamides etc.), anti-coccidials, chemicals, pesticides, disinfectants (i.e., cresol and phenol) etc.

Development of disease / Pathogenesis

The kidney is a vital organ of the bird with diverse metabolic and excretory function viz. maintaining the chemical composition of body fluids, removal of metabolic waste products, regulation of blood pressure and blood volume and conservation of fluids and electrolytes. Avians are uricotelic due to that they are more prone to gout. As that uric acid is the main excretory end product of protein or nitrogen metabolism in the absence of uricase enzymes in birds. Gout is mainly due to damaged kidneys (nephropathy), it leads to accumulation of uric acid in blood (Hyperurecaemia). There isprecipitation of monosodium urate monohydrate (MSU) crystals in joints called articular gout and on visceral surfaces called visceral gout (Lumeij, 2008). Visceral gout is an acute form of deposition of urate crystals. These crystals stimulate phagocytosis by neutrophils and initiate the inflammatory cascade (Arun and Azeez, 2004).An elevated serum urate level, together with local factors, can result in the deposition of urate crystals into the joints is more advanced stage and found rarely. Its crystallization depends on the concentrations of both urate and cation levels. Chronic cumulative urate crystal formation in tissue fluids leads to MSUM crystal deposition (tophus) in the synovium and cell surface layer of cartilage. These “crystal shedding” facilitates crystal interaction with synovial cell lining and residential inflammatory cells, leading to an acute gouty flare.

Signs and pathological lesions

• Chalk-like urate deposits on pericardial sac and liver capsule

• Increased thirst (polydipsia)

• Dehydration and sometimes greenish diarrhea

• Joints may be enlarged, stiff and painful, shifting weight from one foot to the other and have a shuffling gait

• The bird may be unable to perch, spending most of his time on the floor of the cage.

• If the wings are affected, the bird may be unable to fly

• Birds often have reddened, swollen feet that progress to blisters and sores. Joint become painful and joint immobilization due to depot of urate crystals

• Gouty plaques are found (shiny, raised, whitish deposits) under skin

• Decreased appetite

• Lethargy

• General debility and weight loss

• Feather plucking, dull plumage and self-trauma

• Abnormal droppings with chalky urates in their stool.

• Change in temperament

The gross lesions include woolen pale kidneys with urate deposits and dilated ureters filled with chalky white material. The kidneys are congested and greyish white with a soft in consistency. The other noticeable findings observed are presences of chalky white masses surrounding the heart, kidneys, liver intestines, peritoneum, spleen, lungs, air sacs, muscles and inner lining of proventriculus. Generally no inflammatory reaction in synovium or visceral surfaces has been observed.

Microscopically, the kidneys shows severe lesions characterized by moderate to severe tubular dilation, necrosis and large deposits of radiating fine needle shaped crystals in the tubular lumen and in the interstitium and also in myocardium. These deposits are surrounded by a zone of granulomatous inflammation. The crystals appeared black against a yellow background on DeGalantha staining confirming theme to be of urates and the cases of gout. Kidney lesions were mainly of nature of visceral gout characterized by granular degeneration, vacuolation and desquamation of tubular epithelium, foci of necrosis and massive infiltration of heterophils in the interstitium in acute stage of the syndrome.

Managemental approaches to prevent gout/

Prevention and control

As described visceral gout is of multifactorial origin when incidence occurs identifying the cause is often difficult. Different managemental strategies can alleviate the problems in poultry flocks.

Housing management

Minimize the stress from the hatchery level to the chicks up to all life stages. With minimizing dehydration. Maintain proper ventilation, brooding temperature and humidity (60-70%) during early chick stage. Provide adequate number of drinker to the flock with appropriate height.

Nutritional management

Preventive measures concern with nutrition includes

1. Ensure adequate hydration. Water deprivation should be avoided in rearing of boiler and laying flocks.

2. Use of Jaggery 2 to 5 grams per liter of water or recommended electrolyte doses in water.

3. Feed pullets should not contain more than 1 per cent calcium in powdered form up to 16 weeks of age. High calcium intake in immature pullets can cause serious kidney damage.

4. Available phosphorus levels should be 0.45-0.50 per cent in rearing diets. Insufficient phosphorus predisposes the kidneys to calcium damage.

5. Pre-lay ration should not be used before 16 weeks of age, or when the flock shows signs of sexual maturity (blooming of the combs). A calcium content of 2.50-2.75 per cent should be sufficient.

6. If sodium bicarbonate is used to improve egg shell quality, use the minimum recommended level and only when needed. A flock with gout should not be medicated with sodium bicarbonate or fed a ration that is highly alkaline (high levels of sodium or potassium).

7. Review all calcium and phosphorus levels in the feeding program. Pullet and layer feeds should be routinely analyzed for calcium and phosphorus level.

8. Feed samples are assayed for the presence of the mycotoxins like citrinin, ochratoxin and oosporein routinely.

9. Avoid a diet with higher protein content than the recommended level as per the age group of poultry. Depending upon severity manipulate the diet with low protein for few days.

10. Adequate level of phosphorus should be supplied as per the recommended level in concern with calcium to balance Ca: P ratio.

11. Birds with incidence of gout may be supplement or rear on natural vegetables, some of the fruit and plant based compounds such as flavonoid due to richness of vitamin A, antioxidant and anti-inflammatory actions.

12. Supply adequate amount of vitamin A as per recommendation and additional supplementation is needed when gout is prevalent in flock (Omega-3 fatty acids).

13. Use toxin binders and liver tonics to keep minimum levels of fungal toxins in feed. Use recommended levels of aluminum-free Sodium bicarbonate (baking soda) in feed during high temperatures.

Other measures:

Field cases and research reported the interaction between infectious bronchitis (IB) and nutritional as well as managemental factors for triggering visceral gout in poultry. Considering this point as per recommendations and following standard of vaccination schedule for IB vaccines should be administered in poultry birds. Kept in mind for various serotypes of bronchitis vaccines in endemic areas and specifically against nephropathogenic strains will improve immunity of birds against this infection. Some of antiviral drugs should also be helpful for immunity elevation. In broiler breeder and broiler farms infectious bronchitis virus vaccination programme should be review.

Treatments

• Based on history and incidence occurrence in flock the supportive treatment should be given to the birds which cannot be corrected completely kidney damage but may help full to alleviate from this condition and turns to normal functioning of kidney.

• This condition of kidney damage is linked with loss of water and electrolytes so check proper hydration and give fluid therapy and electrolyte supplementation intravenously or in drinking water.

• Techniques involved for reducing gout by using urine acidifier preparations, such as ammonium chloride, DL-methionine, ammonium sulfate, potassium chloride and methionine hydroxy analogue (MHA) which acidifies the urine and increases the solubilization of calcium and urates crystals in urine.

• Use some of the diuretics preparations like Lasix, Zyloric have also been used.

• Use some the pain relieving medication generally of non-steroidal anti-inflammatory (NSAIDs) compounds like meloxicam, aspirin and Celebrex etc.

• Use some of the herbal compounds like coconut water is of a good diuretic action.

Conclusion: The incidence of visceral gout in chicks is indicative of kidney damage occurred at an earlier stage in the poultry. As per the research findings, strongly inkling this syndrome withnutritional causes of Ca:P imbalance and the viral infection of IB as principal cause of visceral gout in broilers leads to mortality. Other factors also likely to be an underlying cause include dehydration, electrolyte imbalance and mycotoxins possibly need to recognize. The prognosis of affected flocks with visceral gout is generally poor that cannot be cured but proper nutritional and housing management and proper endemic strain specific vaccination can alleviate the problems which reduces mortality in broiler chicken flocks.

Dr. A. B. Parmar, Dr. V. R. Patel, Dr. J. M. Patel and Dr. Y. D. Padheriya

College of Veterinary Science & Animal husbandry, Navsari Agricultural University,

Navsari -396 450. Gujarat, India.