Review Article

Review - Gout In Chicken

Kanakuntla Sandhyarani*, Dhoppalapudi Madhuri, Yadala Ravikumar

Department of Veterinary Pathology, College of Veterinary Science, P.V.N.R.T.V.U, Korutla, India

Received | September 13, 2021; Accepted | January 18, 2022; Published | February 15, 2022

*Correspondence | Kanakuntla Sandhyarani, Department of Veterinary Pathology, College of Veterinary Science, P.V.N.R.T.V.U, Korutla, India; Email: sandyroyal777@gmail.com

Citation | Sandhyarani K, Madhuri D , Ravikumar Y (2022). Review - gout in chicken. Adv. Anim. Vet. Sci. 10(3): 702-711.

DOI | http://dx.doi.org/10.17582/journal.aavs/2022/10.3.702.711

ISSN (Online) | 2307-8316

 

INTRODUCTION

Gout is a common metabolic disorder that results in abnormal accumulation of urates in domestic birds (Ali and Sultana, 2012). In case of gout, the blood levels of uric acid can be as high as 44 mg/100ml as compared to 5-7mg/100ml in a normal bird. Kidney is one of the vital organs with many functions in birds that affected by some diseases and disorder and the most important of them is gout syndrome. The primary function of the kidney is to maintain the chemical composition of body fluids (blood). It serves a variety of other functions in the body like removal of metabolic waste and toxic products; conserving fluids and vital electrolytes; regulation of blood volume and production of hormones that regulate blood pressure and production of red blood cells. When renal function stops, uric acid, normally excreted by the kidney in the urine, is then deposited any place that blood is circulated (Alice mitchell, 2015). Hyperuricemia is a central risk factor for gout and increases the risk for other chronic diseases, including cardiometabolic disease, kidney disease, and hypertension (Hong et al., 2020). Hyperuricemia is the outcome of a combination of an endogenous purine metabolism disorder and an exogenous environmental disruption (Dalbeth, 2016). The high levels of uric acid subsequently precipitates as monosodium/calcium urate crystals in a variety of locations, particularly in the kidneys and on the serous membranes of the liver, heart, air sacs and joints. These crystals, being insoluble in tissue fluids and having sharp ends, cause physical damage to the tissues leading to a cascading inflammatory reaction  However, other mammals, such as rats, mice, and rabbits, contain uricase and can metabolize urate to allantoin, which is soluble in water and easy to excrete (Lee et al., 2013). Chickens affected by renal damage can continue to be productive until less than one third of their normal kidney mass remains functional. Gout is not a single disease entity, but rather the result of kidney damage from a number of potential causes, which can be infectious, nutritional, toxic or possibly a combination of factors. The disturbed balance of the minerals like calcium and phosphorous in diet can result in various pathological conditions including renal failure and development of gout in chicken. High dietary calcium concentration (>2%) causes nephrosis and visceral gout in broilers. Mineral imbalance, particularly of calcium and phosphorus, is one of such problems responsible for economic losses to farm holders, who often formulate the poultry rations themselves. Some infectious agents like IBV, CAstV and ANV along with lack of proper managemental practices causes renal failure leads to gout. Although gout has been recognised for some time as a cause of excessive pullet and layer mortality, it continues to be a diagnostic challenge. Birds can be in full production and exhibit few external symptoms until shortly before death (Alice mitchell, 2015).

Incidence Of Gout

Season

The highest prevalence of this disease was recorded during colder months followed by summer and lowest in rainy season (Srivastava et al., 2002; Jana et al., 2008; Yadav et al., 2020; Lakkawar et al., 2018; Panigrahi, 2017). There is also excess formation and decreased dissolution of uric acid at colder temperature leads to cold stress and results in high mortality. Higher prevalence of gout in rainy season than summer season could be ascribed to poor hygienic conditions prevailing during rainy season (Sayed, 2001).

Age

Age wise susceptibility and mortality due to visceral gout is highest among young chicks in comparison to adult birds (Mallinson et al., 1984; Wideman, 1988; Wideman et al., 1994; Jana et al., 2008; Singh et al., 2013; Panigrahi, 2017, Yadav et al., 2020). When pullets sexually mature, they are placed on higher-calcium diets to meet the demands of egg production. If the kidneys were previously damaged, they may no longer function normally with the higher level of calcium excretion, and the result is likely to be gout (Alice mitchell, 2015).

Causes

Gout is one of the conditions affecting poultry and was initially thought to be a nutritional problem. However, with the advent of science and development of diagnostic assays, viruses have been detected from gout cases (Panigrahi, 2017). Gout is a multifcatorial metabolic disease result of kidney damage from any of a number of potential causes (Alice mitchell, 2015). Raised levels of uric acid in the blood (hyperuricaemia), which may be due either to over production of uric acid or impaired destruction of uric acid because of deficient enzymes systems or to its decreased excretion, either due to impaired filtration or altered excretion in the tubules as may occur in drug therapy like aspirin, mercuric salts etc. (Ali and Sultana, 2012).

Nutritional Causes

One of the important factors for the incidence of visceral gout was dietary calcium percentage in the broiler starter ration. Different standard specifications have been given by Bureau of Indian Standards (BIS, 1992) as maximum inclusion of calcium is 1.2 per cent, whereas Leeson and Summers (2008) had mentioned 1 per cent inclusion of calcium as most appropriate. Inclusion of high calcium(>2%) in broilers diet lead to some disorders in the physiologic process of kidneys consequently resulting in urates depositions on serous surfaces of viscera especially kidneys which are the signs of gout syndrome that causes huge mortality among flocks (Pater et al., 2007; Feizi et al., 2011). An increase in dietary protein can cause an increase in kidney size and glomerular filtrate rate (GFR), with subsequent glomerular injury, accumulation of mesangial deposits, and eventually results in glomerulosclerosis (Khan and Alden, 2001; Pater et al., 2007; Singh et al., 2013; Hong et al., 2020). Based on recommendations of BIS 2007, the optimum crude protein levels are 22 and 20 per cent for broiler starter and broiler finisher ration respectively. Healthy kidneys are not affected by high dietary protein levels. Nevertheless, in case of pre-existing kidney damage, feed containing more than 30 per cent of crude protein can be dangerous that leads to excessive uric acid production which further worsens the kidney function. Adulteration of protein supplements with urea increases the nitrogenous component, further enhancing the uric acid production. This coupled with kidney damage can lead to gout. (Alice and mitchell, 2015).

Minerals

Calcium: Phosphorus ratio - Excess dietary calcium with low available phosphorus results in precipitation of calcium-sodium-urate crystals. Excess dietary calcium fed to immature pullets over a period of time will result in kidney damage that may lead to gout. Phosphorus has been shown to partially protect the kidney against calcium induced damage and also it acts as a urinary acidifier and helps to prevent stones from forming in the kidney. But marginally low available phosphorus in rearing diets has been associated with higher gout incidence (Alice mitchell, 2015). The kidney performed its normal physiological functions only when calcium and phosphorus are maintained in a specific ratio of 2:1 that necessitates maintenance of different physiological mechanisms including secretions, excretions and resorption etc. An imbalance of these minerals in diet can result in renal failure and development of gout in chicken (Ali and sultana, 2012). Outbreak of gout attributed to disproportionate Ca: P ratio (3.5: 1) and 16.39% crude protein in the feed has been reported (Mir et al., 2005; Guo et al., 2005). Higher levels of dietary proteins cause excess uric acid production and nephropathy while higher dietary levels of calcium and low levels of phosphorus lead to increased retention and decreased excretion of uric acid (Mir et al., 2005).

Sodium: Sodium intoxication puts extra stress on kidneys. Hard water with higher salt content is also a load on kidneys. Sodium bicarbonate is sometimes used to improve egg shell quality or combat the effects of heat stress. (Poultry gout, growel agrovet private limited, 2016). 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. (Alice mitchell, 2015; Ali et al., 2018; Ejaz et al., 2005).

Sulphates: Decreased calcium resorption causing excessive calcium secretion through urine favours gout.

Dehydration

Dehydration due to water deprivation is also a common cause for visceral deposition of urates (Onderka, 1987). Managemental causes like Improper brooding temperature in which too high or too low brooding temperature, heats up or chills the water respectively – thereby reducing the water intake and hence increasing chances of development of gout. Inadequate number of waterer/nipples, Improper height of waterers, Water withdrawal during vaccination, too low water pH – leads to water rejection by poultry or irritates the epithelium. Chicks held for a long in hatchery or transported for a long distance without water leads to renal failure and results in gout (Alice mitchell, 2015).

Vitamins

High levels of vitamin D3 increases calcium absorption from the gut which can favour further formation and deposition of urate crystals. Prolonged vitamin A deficiency causes sloughing of tubular epithelium and subsequent blockade resulting in accumulation of urates in the kidney (Alice mitchell, 2015).

Infectious causes

Among the infectious causes, the viral pathogens like Avian Nephritis Virus (ANV), Nephropathic Infectious Bronchitis Virus (IBV) and Chicken Astrovirus (CAstV)( Bulbule NR et al., 2013) are listed, but the IBV may lead to permanent kidney damage with high mortality (Singh et al., 2010). The most prevalent strain of IBV was Masachusette strain; its outbreaks caused visceral gout and nephrosis in commercial young broiler chicken and widely spread throughout the country in a short period, therefore caused huge economic losses (Gaba et al., 2010; Ali and sultana, 2012; Panigrahi, 2017). The disease, when vertically transmitted, affects the kidney of progeny leading to gout in young chickens (Alice mitchell, 2015).

Miscellaneous causes

There are several mycotoxins that are nephrotoxic and/or hepatotoxic in laying hens, including citrinin, ochratoxin A, oosporein, and deoxynivalenol (DON) cause damage to kidney and liver thereby uric acid excretion is reduced resulting in accumulation of uric acid in the body.(Guo et al., 2005; Sid and Fettah, 2011; Bulbule et al., 2013; Alice mitchell, 2015). Metabolic cause like Ascites – Hypoxic conditions increases the production of uric acid. Ascites in initial stages can lead to symptoms of gout (Alice mitchell, 2015). Antibiotics like gentamycin, sulphonamides and nitrofurosones are known to cause renal damage especially in young chicks. The drugs which get excreted through the kidneys have their own imbalancing effect on pH and renal metabolism. Disinfectants like phenol and cresol if used erroneously cause residual toxicity. Chemicals like copper sulphate used in water results in water refusal, dehydration and gout (Yadav et al., 2020). Anticoccidials, manufactured chemicals, and pesticides can also induce gout in poultry.

TYPES OF GOUT

There are two major forms of gout which are differentiated by the sites of uric acid deposition- visceral and articular gout. In both forms, deposits consist of needle shaped crystals called tophi.

Visceral gout

A condition in which white uric acid or urate crystals deposits are seen in soft tissues of various organs in body. 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. Whenever there is kidney damage, excretion of uric acid gets affected and uric acid starts accumulating in the blood and later in tissues (Banday et al., 2009).

Articular gout

It is a chronic form of the disease and is less common which occurs when uric acid and urates are deposited in the ligaments and tendons, but more commonly in the legs or synovial fluid and synovial membranes of toes and wing joints, and incite a chronic granulomatous reaction to urate crystals (tophi). Deposits of MSU can also be detected around the joints (periarticular gout). The joints become swollen, red, tender swell, and warm to touch. This condition is rarely seen and usually a chronic condition. Kidneys are generally normal and may become abnormal with white urate deposit if bird gets dehydrated. A bird with articular gout prefers to sit on a flat surface instead of perching because of the pains. If forced to walk, the bird becomes noisy due to discomfort. It may also be depressed and dehydrated, with greenish diarrhoea. In addition, the bird will look dull, its feathers ruffled and the vent moist. It is unusual for gout to affect more than one or two joints at a time. When gout crystals form in the feet, they usually also form in the wing. The most commonly affect wing joint is the birds wrist (carpus) (Ali and sultana, 2012).

Pathophysiology of gout

Gout occurs due to decrease in kidney function to the point where uric acid (a nitrogenous waste) accumulates in the blood and body fluids.The pathogenesis of visceral gout is not completely understood but generally is considered to be the acute form of disease causing huge mortality characterized by the urate deposits on serosal surfaces, most often in the heart, kidney, liver, and air sacs as reported by Mc Gavin and Zachary (2007), Saif (2008), Sandhyarani et al. (2019). The damaged kidneys appear atrophied or missing portions of kidney lobes with whitish gritty material in kidneys and enlarged ureters. Compensatory enlargement of remaining part of normal kidney can be observed in an attempt to maintain adequate renal function (Siller et al., 1981; Goryo et al., 1984; Jones et al., 1998; Banday et al., 2009). Birds are uricotelic, that is, in them , the waste product of protein metabolism is mainly in the form of uric acid. This is because they lack the enzyme uricase, which converts uric acid into allantoin. Moreover uric acid is water insoluble. Therefore any injury or damage to bird’s kidney, from whatever cause, interferes with eliminaton of uric acid, which then accumulates in the blood (hyperuricaemia) and leads to visceral gout. On the other hand, mammals are ureotelic where the waste product of protein metabolism is in the form of urea which is water soluble, and therefore mammals are not prone to gout like birds. Some times precipitated monosodium urate crystals in turn, triggers a chain of events that end in joint injury. Once crystals are deposited into a joint, they can be released into the joint space and initiate an inflammatory cascade causing acute gouty arthritis.The released urate crystals are chemotactic and also activate complement which results in generation of C3a and C5a which induce accumulation of neutrophils and macrophages in the joints and synovial membranes. Phagocytosis of crystals causes release of toxic free radicals and leukotrienes, particularly B4. Death of the neutrophils releases destructive lysosomal enzymes. Macrophages also participate in joint injury. After ingestion of urate crystals, macrophages secrete a variety of pro-inflammatory mediators, such as inteleukin-1, IL-6, IL-8 and tumour necrosis factor (TNF). These not only intensify the inflammatory response, but also activate synovial cells and cartilage cells to release proteases that causes the tissue injury and develops acute arthritis (JL VEGAD). These acute flares resolve, but the crystals remain in the joint. The way to ultimately correct the underlying metabolic problem of hyperuricemia and the crystal deposition is to lower the serum urate level and dissolve the crystal deposits. This will stop both the acute attacks and the progressive joint damage (Ali and sultana, 2012).

 

 

Clinical Symptoms

The ante-mortem clinical manifestation of affected chicks are dullness, dehydration, ruffled feathers, seggregatory behavior, restlessness, moist vent with whitish pasty droppings, difficulty in movement and standing on legs, painful joints and may continually shift weight from one foot to the other and have a shuffling gait. The bird may be unable to perch, spending most of the 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 pain and joint immobility that urate deposits cause. At postmortem, all the carcasses were emaciated and dehydrated with moderate enlargement of hock and phalangeal joints. Other signs include decreased appetite, lethargy, general debility and weight loss, feather plucking, dull plumage and Self-trauma, abnormal droppings, chalky urates in their stool and change in temperament (Ali and sultana, 2012, Patel et al., 2014, Akter and Sarkar, 2015).

Clinical Pathology

The birds affected with gout have a significant increase in serum uric acid (>5-7mg/100ml) and serum creatinine

 

levels (>0.7-22mg/dl). This elevation in the level of serum uric acid might be due to failure of excretory function of kidney and to the increased degradation of nucleic acid released as a result of degenerative changes in various organs (Chandra et al., 1985). The observations like hyperuricaemia due to repeated use of NSAIDs at therapeutic level for prolonged period may induce marked renal dysfunction (Shafi et al., 2012). Similarly, Chandra et al. (1984) and Guo et al. (2005) had reported in their study that increased levels of uric acid in the birds provided with high calcium and high protein diets. Creatinine originates from the non enzymatic conversion of creatinine in muscle and filtered by glomerulus and excreted in the urine, so it can be used as a rough index of glomerular filtration (Benjamin, 1978). These parameters are markers of renal injury, possibly due to MSU crystal products in the kidney. The mean values of TEC, Hb, TLC and PCV in the affected birds were significantly (P>0.01) high (Jana et al., 2008; Singh et al., 2013; Yadav et al., 2020). The observation of increased levels of PCV, TEC, Hb values were possibly due to dehydration as a result of diarrhoea. The leucocytosis in the affected birds was mainly contributed by the absolute increase of lymphocytes was suggestive of the onset of cellular immunological response of the body of affected birds to any infection (Yadav et al., 2020) and may have stimulatory effect on bone marrow leading to leukocytosis (Thanagari et al., 2012; Singh et al., 2013; Shafi et al., 2015; Salam, 2017). The liver function markers AST and ALT were significantly increased in the birds effected with gout induced by high protein diet (Hong F et al., 2020) and diclofenac (Sandhyarani et al., 2019) which is an indication of hepatic injury. Antioxidant profile reveals decreased glutathione stimulating hormone (GSH) and increased thiobarbituric acid reactive substances (TBARS) in kidney and liver tissue (Singh et al., 2013; Akter and sarker, 2015; Sandhyarani et al., 2019). Glutathione (GSH) is an important intracellular peptide with multiple functions ranging from antioxidant defense to modulation of cell proliferation (Lu, 1999). Glutathione plays a very important role in the detoxification and elimination of xenobiotics. Glutathione participates in many cellular reactions and effectively scavenges free radicals and other reactive oxygen species (ROS). Glutathione deficiency contributes to oxidative stress and therefore cause aging and the pathogenesis of many diseases. Most of the cellular GSH (85–90%) was present in the cytosol, with the remainder in all organelles (including the mitochondria, nuclear matrix, and peroxisomes (Wu et al., 2004). An exposure to xenobiotics induces mitochondrial injury involves generation of reactive oxygen species (ROS), causing oxidative stress to hepatocytes and results in depletion of GSH levels in poultry birds (Sokol et al., 2001). TBARS assay has been found to be one of the better predictor of oxidative damage (Morrow, 2000). Lipid peroxidation can be used as the hepatic oxidative stress parameters for measuring the damage that occurs in membranes of tissue due to result of free radical generation. The increase in superoxide dismutase levels and malondialdehyde (MDA) activity in renal tissue may indicate peroxidative damage and cause cell damage in kidney tissue (Gokcimen et al., 2001). Significant (P≤0.05) increase in serum aminotransferase, alkaline phosphatases, serum total proteins and serum albumin were also found in natural cases of gout positive birds (Feizi et al., 2011; Singh et al., 2013; Behtari and Feizi, 2015; Sandhyarani et al., 2019). Increase in total proteins in gout cases may be due the ammonia and carbonmonoxide if accumulated in sheds may affect the normal ventilation and ultimately reduced water intake lead to non availability of adequate water to flush out the urinary system leading to its clogging (Phatak, 2001). Lipid metabolic markers, such as total cholesterol (TC), triglycerides (TG),total bilirubin (TB), and direct bilirubin (DB) were decreased in the birds fed with high protein diet which induces an abnormal claw morphology in chicken, MSU crystal production in synovial fluid and other tissues induces renal injury in chickens and results in gout. (Hong et al., 2020).

Postmortem Lesions

Grossly, dry platery patches of white chalky urate deposits were observed on the serosal surfaces of pericardium, air sacs, peritoneum, liver, kidneys and ureters. Congestion of viscera might be due to emaciation and dehydration of birds leading to haemoconcentration (Satalkar, 2007). Nephropathy, observed consistently, was characterized by unilateral to bilateral enlargement which bulged out of the bony depression and moderate to severe congestion of kidneys. Kidneys appeared frosted due to accumulation of urate crystals, minute pin point haemorrhages along with chalky white deposits of urate crystals on the serosal surface. Ureters of either side were found to be distended with retained semi fluid to semisolid chalky white urates, giving cord-like appearance to ureters. The ureters were markedly enlarged due to blockages by uroliths and the entire obstructed kidney showed varying degree of degeneration (Lakkawar et al., 2018). Microscopically, marked congestion, hameorrhages involving glomeruli, cortical and medullary tubules, collecting ducts and medullary tracts and focal to diffuse degenerative changes in tubular epithelium like vacuolar degeneration, desquamated and necrosed tubular epithelial cells. Kidney parenchyma exhibited aggregates of uric acid crystals characterized by needle shaped urate crystals as pink radiating amorphous material surrounded by a narrow zone of inflammatory cells (Muhammed et al., 2012; Bulbule et al., 2013; Akter and sarker, 2015). Chandra and Balwant (1980) described the extent of damages to kidney was directly correlated to the degree of urate deposition. Hyaline casts were present in few tubular lumens. Glomerular changes included atrophy, distortion and segmentation (Mir et al., 2005).

Liver is enlarged, friable with white chalky urate deposition on the surface of the capsule. Liver section reveals severe sinusoidal congestion, haemorrhages in parenchyma, fatty change and foci of necrotic hepatocytes (Feizi et al., 2011; Sultana et al., 2012; Patel et al., 2014; Nitin and Ghosh, 2014; Amaravathi et al., 2015; Akter and sarker, 2015; Behtari and Feizi, 2015; Ramzan et al., 2015). Liver parenchyma shows amorphous radiating uric acid crystals mixed with necrotic debris surrounded by a narrow zone of inflammatory cells (Mudasir et al., 2017; Sandhyarani et al., 2019). Also the subcapsular hepatocytes were flattened with elongated nucleus and intense cytoplasmic basophilia along with proliferation of fibrous connective tissue in glisson’s capsule (Mir et al., 2005).

In heart, the entire pericardium is covered with urate deposits of varying degrees on its serosal surface i.e uric acid pericarditis (Yewale, 2010). Pericardium is firmly adhered to heart. Myocardium of the heart showed urate deposition along with destruction of myocardial cells and infiltration of inflammatory cells. Lesions of heart included myocardial congestion because of severe engorgement of blood vessels and focal to diffuse haemorrhages between muscle fibers (Ramzan et al., 2012; Patel et al., 2014; Mudasir et al., 2017).

Lungs showed deposition of urates in the parenchyma, air capillaries and parabronchi. The air capillaries near tophi are collapsed and the remaining which are away from urate deposition showed emphysema. Oedematous fluid was present in air capillaries and atria (Mir et al., 2005).

Spleen showed splenitis and subcapsular haemorrhages. Urate deposits were observed in the subcapsular region as well as in the parenchyma (Mir et al., 2005).

Dry platery patches of white chalky urate deposits on the breast muscles, neck and on serosal surfaces of pericardium, peritoneum, mesentery, proventriculus, gizzard, testes,ovaries, over the abdomen and chest wall are also observed. Microscopically Proventriculus revealed oedema, haemorrhage and heterophilic infiltration in the serosa. Bursa of Fabricius presented mild depletion of lymphocytes in the follicles (Mir et al., 2005). These uric acid crystals were observed in black color by De Galantha’s stain (Mohan et al., 2012; Patel et al., 2014; Patil et al., 2015; Sandhyarani et al., 2019).
In the articular form white chalky nodules known as tophi found in tissues. It may occur in subcutaneous tissue other than joint which may cause ulcer but without severe pain (Ali and sultana, 2012). On opening the joints, white semifluid deposits of urates are present within the joints.

The deposits are also observed in almost all other joints including shoulder, elbow, carpus and phalanges in wings and hip, knee and toe joints in the limbs. Rarely some deposits were also observed in the cervical articulations. Arthritis with segmental necrosis of periarticular muscles and

intermuscular oedema are also observed (Mir et al., 2005).

PREVENTION AND CONTROl

• • A feed analysis is necessary, ensures the bird receives an appropriate intake of minerals, proteins and vitamins.
• • For the prevention of gout in poultry, it is necessary to have scientifically balanced feed in respect of:

-Calcium-phosphorus ration depending on the type of ration.

-Vitamin A, D3 and other essential vitamins.

-Required level of sodium, chloride and other ions.

-Excessive use of sodium bicarbonate i.e. more than 2kg/ton should be avoided.

-Conventional sources of protein should be used.

• • Analyse the feed for mycotoxin content and if found positive, change the feed or use suitable toxin binders.
• • Judicious use of drugs such as antibiotics, sulpha drugs and anticoccidials to avoid kidney damage.
• • Fresh potable water accessible to birds all the time.
• • Copper sulphate should not be used for medication, if used should be used under the directions of a veterinarian or a poultry practitioner.

 

TREATMENT

• • Provide plenty of water and adequate drinkers.
• • Avoid a diet higher in protein than the recommended level as per the age and breed. Provide low protein diet for 3-5 days based on need depending on severity of gout.
• • Review IB vaccination programme. In the 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: Any one of the following urine acidifiers may be given in water or feed.
• • Ensure adequate levels of A, D3, K and B complex vitamins.
• • Vinegar: 1-2 ml per litre water up to 24 hours.
• • Potassium chloride: 1gram per litre water up to 24 hours.
• • Ammonium chloride: Two and half kg/ton feed for 7 days.
• • Ammonium sulphate: Two and half kg/ton feed for 7 days.
• • Use of electrolytes through water may assist in controlling mortality.
• • Provide broken maize at least for 3 days and jaggery 5g/litre for 3-5 days in case of mortality.
• • Allopurinol which available at 2.5-5% should be given 10-40mg in drinking water twice daily and never stop dosage until mortality percentage become zero.
• • Provide 0.6% methionine hydroxyl analogue free acid with 3% calcium in the diet (Banday, 2009).

 

Conclusion

Gout is causing great monetary losses to the producers and considered as one of the major causes for huge mortality in poultry.

Most of the research work is done on gout and observe a strong link for bronchitis and calcium/phosphorus imbalance are the major causes of gout in chicken leads to high mortality. The other factors such as vitamins, chemicals, mycotoxins, water deprivation and electrolyte imbalanc are need to be recognized as possible contributing factors for gout. Likewise, in pullets and layers, the diet that increases urine alkalinity in combination with high calcium can contribute to gout. Chicken mortality due to gout can be reduced by increasing the acidity of the urine to dissolve existing kidney stones or to prevent additional kidney stones from forming. A regular feed analysis is necessary, ensures the bird receives an appropriate intake of minerals, proteins and vitamins. Breeder management along with hatchery and adequate farm management are crucial in preventing incidences of gout.

Conflict of interest

The authors have declared no conflicts of interest.

novelty statement

The current manuscript denotes how all nutritional, infectious and managemental factors contribute to cause gout in chicken individually. The gout causes, symptoms, patho-physiology, clinical pathology, gross and microscopic lesions are furnished thoroughly in the manuscript. Hence one can analyse the results of the feed, blood and serum sample of suspected birds to reduce the morbidity and mortality of birds in the flock.

Authors contribution

All authors contributed equally.

REFERENCES

Ahmed MS, Anjaneyulu Y, Lakshman M, Rama Rao SV (2003). Urolithiasis in broiler breeders- A pathological study. Indian J. Vet. Pathol. 27(1):63- 64.

Akter R, Sarker MAW (2015). Effect of diclofenac sodium in broilers. Bangladesh J. Vet. Med. 13(1):19-24. https://doi.org/10.3329/bjvm.v13i1.23710

Ali, Sultana (2012), GOUT OF POULTRY. https://www.researchgate.net/publication/279201331_GOUT_OF_POULTRY

Ali R, Kamil SA, Amin U, Mir MS, Shah A, Kashani B, Dar TA, Shah SA, Qureshi S 4. (2018). Clinicopathology of sodium bicarbonate induced gout in broiler chicken model. Indian journal of veterinary pathology. 42(1): 58-63. https://doi.org/10.5958/0973-970X.2018.00010.X

Alice Mitchell (2015), Gout management in poultry. Poultry welfare: Poultry health. (The poultry site).

Amaravathi M, Satheesh K, Reddy CB, Dhyana VR (2015). A report on visceral gout in broilers. International J. Livest. Res. 5(8):81-4. https://doi.org/10.5455/ijlr.20150829120837

Banday MT, Bhakt M, Hamid SA (2009). Avian Gout: Causes Treatment and Prevention. Srinagar, Kashmir, India. 5:26.

Behtari M, Feizi A (2015). Investigation of production performance and measurement of some serum biochemical parameters in broiler breeder farm with gout syndrome. Int. J. Biol. Pharma. Allied Sci. 4 (2): 728-738.

Benjamin, MM (1978). Outline of Veterinary Clinical Pathology. 3rd Edition. Iowa State University Press. Part 2, 177-178.

Bulbule NR, Mandakhalikar KD, Kapgate SS, Deshmukh VV, Schat KA, Chawak MM (2013). Role of chicken astrovirus as a causative agent of gout in commercial broilers in India. Avian Pathology. 42(5):464-473. https://doi.org/10.1080/03079457.2013.828194

Bureau of Indian Standards BIS, (2007).

Carro MD, Falkenstein E, Radke WJ, Klandorf H (2010). Effects of allopurinol on uric acid concentrations, xanthine oxidoreductase activity and oxidative stress in broiler chickens. Comp. Biochem. Physiol. C Toxicol. Pharmacol. 151:12–17. https://doi.org/10.1016/j.cbpc.2009.07.010

Chandra M, Balwant S (1980). Uric acid nephritis in domestic fowl in Punjab. Indian J. Poult. Sci. 15 (2): 83-89.

Chandra M, Singh B, Soni GL, Ahuja SP (1984). Renal and biochemical changes produced in broilers by high-protein, high-calcium, urea-containing, and vitamin-A-deficient diets. Avian Dis. Jan 1:1-1. https://doi.org/10.2307/1590124

Chandra M, Singh B, Gupta PP, Ahuja SP, Singh N (1985). Clinicopathological, haematological and biochemical studies in some outbreaks of nephritis in poultry. Avian Dis. 29: 590- 600. https://doi.org/10.2307/1590650

Dalbeth N, Merriman T R, Stamp LK (2016). Gout. Lancet. 388:2039–2052. https://doi.org/10.1093/med/9780198748311.001.0001

Echols MS (2006). Evaluating and treating the kidneys. Clin. Avian Med. 2:451-491.

Ejaz S, Kim BS, Lim CW (2005). Gout induced by intoxication of sodium bicarbonate in Korean native broilers. Drug Chem. Toxicol. 28(2):245-261. https://doi.org/10.1081/DCT-52559

Feizi A, Dadian F, Nazeri M (2011). Evaluation the effect of dietary calcium percentage on incidence of gout syndrome in broiler chicks. Australian J. Basic Appl. Sci. 5 (11): 1750-1755.

Feizi A, Nazeri M (2011). Evaluation the effect of dietary calcium percentage on incidence of gout syndrome in broiler chicks. Res. J. Biolog. Sci.6(8): 349-52.

Gaba A, Hanish D, Pal JK, Prajapati KS (2010). Isolation, identification and molecular characterization of IBV variant from out break of visceral gout in commercial broilers. Vet. World. 3 (8): 375-377.

Gokcimen A, Aydin G, Karaöz E, Malas MA, Öncü (2001). Effect of diclofenac sodium administration during pregnancy in the postnatal period. Fetal Diagnos. Therap. 16(6):417-22. https://doi.org/10.1159/000053951

Goryo M, Umemura T, Itakura C (1984). Concurrence of nephrosis‐nephritis due to infectious bronchitis virus and infectious bursal disease in broiler chickens. Avian Pathol. 13(2):191-200. https://doi.org/10.1080/03079458408418523

Gowthaman V, Singh SD, Dhama K, Barathidasan R, Srinivasan P, Saravanan S, Gopalakrishnamurthy TR, Deb R, Mathapati B, Ramakrishnan MA (2015). Detection and partial genetic characterisation of a novel variant of Avian nephritis virus in Indian poultry flocks showing diverse clinical signs. Acta Vet. Hungarica. 63(4):499-507. https://doi.org/10.1556/004.2015.046

Guo X, Huang K, Tang J (2005). Clinico-pathology of gout in growing layers induced by high calcium and high protein diets. Brit. Poult. Sci. 46(5):641-646. https://doi.org/10.1080/00071660500302661

Hong F, Zheng A, Xu P, Wang J, Xue T, Dai S, Pan S, Guo Y, Xie X, Li L, Qiao X (2020). High-protein diet induces hyperuricemia in a new animal model for studying human gout. Int. J. Molecul. Sci. 21(6):2147. https://doi.org/10.3390/ijms21062147

Jana S, Niyogi D, Mandal S, Ganguly S and Mukhopadhaya SK (2008). Haematological and Serum biochemical alteration in gout of broiler birds. Indian J. Anim. Hlth. 47 (2): 113-115.

Jones TC, Hunt RD, King NW (1998). The urinary system. In: Veterinary Pathology, Williams and Wilkins Maryland, USA, 1111-1148. https://doi.org/10.1007/978-3-642-80335-2

Khan NM, Alden CL (2001). Kidney. In: Handbook of Toxicologic Pathology (Haschek, WM et al. eds.), Academic Press, San diego, CA, 2: 255-335.

Lakkawar AW, Kumar R, Venugopal S, Uma S, Sathiyaseelan M, Nair MG, Sivakumar M (2018). Pathology and management of gout in Giriraja breeder chicks. J. Entomol. Zool. Studies. 6(1):550-4.

Lee IR, Yang L, Sebetso G, Allen R, Doan TH, Blundell R, Lui EY, Morrow CA, Fraser JA (2013). Characterization of the complete uric acid degradation pathway in the fungal pathogen Cryptococcus neoformans. PLoS ONE. 8:e64292 https://doi.org/10.1371/journal.pone.0064292.

Leeson S (2007). Vitamin requirements: is there basis for re-evaluating dietary specifications?. World’s Poult. Sci. J. 63 (2): 255-266. https://doi.org/10.1017/S0043933907001444

Lu SC (1999). Regulation of hepatic glutathione synthesis: current concepts and controversies. FASEB J. 13 (10): 1169-1183. https://doi.org/10.1096/fasebj.13.10.1169

Mallinson ET, Rothenbacher H, Wideman RF, Snyder DB, Russek E, Zuckerman AI, Davidson JP (1984). Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. Avian Dis. 1:25-43. https://doi.org/10.2307/1590126

Mc Gavin MD, Zachary JF (2007). Pathologic Basis of Veterinary. 6th ed, Mosby, Inc. Elsevier Inc, Missuori.1488.

Mir MS, Darzi MM, Khan AA, Ganaie NA, Gupta S, Nashiruddullah N, S. A. Kamil (2005). Investigation of an outbreak of Gout in Kashmir Favorella Poultry. Indian J. Vet. Pathol. 29(1): 35-37.

Morrow JD (2000). The isoprostanes: their quantification as an index of oxidant stress status in vivo. Drug Metabol. Rev. 32 (3-4): 377-385. https://doi.org/10.1081/DMR-100102340

Mohan K, Jayakumar K, Narayanaswamy HD, Manafi M, Pavithra BH (2012). An initial safety assessment of hepatotoxic and nephrotoxic potential of intramuscular ketoprofen at single repetitive dose level in broiler chickens. Poult. Sci. 91(6):1308-14. https://doi.org/10.3382/ps.2011-01929

Mudasir M, Dogra S, Badroo GA, Nashirrudullah N, Batoo AS, Javaid M, Bhat MA (2017). Pathomorphological Study of Visceral Gout in Desi Fowl. Int. J. Curr. Microbiol. App. Sci. 6(10):5039-5042. https://doi.org/10.20546/ijcmas.2017.610.478

Muhammad R, Muhammad A, Khawaja TM (2012). Toxicity of flunixin meglumine in broiler chickens. J. Pharmaceut. Sci. Re. 4(2): 748-1754.

National Research Council (NRC), (1994).

Nitin S, Ghosh RC (2014). Pathology of gout induced by high protein diets in growing broilers. Asian J. Anim. Sci. 9 (2): 149-153. https://doi.org/10.15740/HAS/TAJAS/9.2/149-153

Onderka DK, Hanson JA, Leggett FL, Armstrong LD (1987). Renal pathology in chicks following water deprivation. Avian Dis. 31:735-739. https://doi.org/10.2307/1591024

Panigrahi S (2017). Epidemiological studies on chicken astroviruses in gout affected broiler chicken flocks. Doctoral Dissertation. LUVAS.

Patel NJ, Joshi BP, Prajapati KS, Patil VM (2014). Pathomorphological changes of aceclofenac toxicity in layer chicks. Vet. World. 7(2): 90-94. https://doi.org/10.14202/vetworld.2014.90-94

Pater KA, Ghodasara DJ, Dave CJ, Jani PB, Joshi BP, Prajapati KS (2007). Experimental studies on etiopathology of visceral gout in broiler chicks. Indian J. Vet. Pathol. 31(1): 24-28.

Patil VM, Patel NJ, Jivani BM, Dave CJ, Joshi BP (2015). Toxicopathological studies of aceclofenac in broiler chicks. Indian J. Vet. Pathol. 39 (2): 149-153. https://doi.org/10.5958/0973-970X.2015.00034.6

Phatak RK (2001). Management of gout in tropical countries. South Asian Regional Poultry Conference and Exhibition. 24-26.

Ramzan M, Ashraf M, Mahmood KT (2012). Toxicity of flunixin meglumine in broiler chickens. J. Pharmaceut. Sci. Res. 4 (2): 1748- 1754.

Ramzan M, Ashraf M, Hashmi HA, Iqbal Z, Anjum AA (2015). Evaluation of diclofenac sodium toxicity at different concentrations in relation to time using broiler chicken model. J. Toxicolog. Sci. 25 (2): 357-65.

Rivera-Paredez B, Macías-Kauffer L, Fernandez-Lopez JC, Villalobos-Comparán M, Martinez-Aguilar MM, de la Cruz-Montoya A, Ramírez-Salazar EG, Villamil-Ramírez H, Quiterio M, Ramírez-Palacios P, Romero-Hidalgo S (2019). Influence of genetic and non-genetic risk factors for serum uric acid levels and hyperuricemia in Mexicans. Nutrients. 11(6):1336. https://doi.org/10.3390/nu11061336

Saif YM (2008). Diseases of Poultry. 12th ed, Blackwell Publishing Ltd, Iowa, pp.1409.

Salam SGRA (2017). Immunomodulatory and hematological effects induced by diclofenac, ibuprofen or paracetamol toxicity in Swiss albino mice. European J. Biolog. Res. 7 (4): 348-359.

Sandhyarani K, Madhuri D, Jeevanalatha M, Dhanalakshmi K (2019). Histopathological changes in liver and heart of diclofenac induced visceral gout in broilers and its amelioration with ayurvet product. Pharma. Innovat. 8(4): 250-255.

Sandhyarani K, Madhuri D, Jeevanalatha M, Dhanalakshmi K (2019a). Kidneys: Histopathological Changes in Diclofenac Induced Visceral Gout in Broilers and its Amelioration with Natural Herbals. Pharma. Innovat. 9(8): 103-110.

Satalkar AA (2007). Efficacy of Boerhavia diffusa on Experimentally Induced Gout in Broilers. M.V.Sc. Thesis. Maharastra Animal and Fishery Science University, Nagpur.

Sayed A (2001). Gout in poultry. Kemin Direct. 2(3): 10–12.

Shafi M, Hussain K, Garg UK, Baba OK (2015). Haemato-biochemical and Immunological Study on NSAIDs Induced Acute Toxicity in Broiler Chicken. J. Anim. Res. 5 (2): 297-302. https://doi.org/10.5958/2277-940X.2015.00051.0

Sid H, Fettah A (2011). Kidney damage is emerging in laying hens. Poult. World. www.worldpoultry.net/Breeders/General/2011/4/Kidneydamage-is-emerging-in-laying-hens-WP008719W/

Siller WG (1981). Renal pathology of the fowl- A review. Avian Pathology. 10(3):187-262. https://doi.org/10.1080/03079458108418474

Singh F, Shakya S, Rawat N (2010). Isolation and identification of nephropathogenic avian bronchitis virus. Indian Vet. J. 87 (10): 957-959.

Singh N, Ghosh R C, Singh A (2013). Prevalence and haemato–biochemical studies on naturally occurring Gout in Chhattisgarh. Adv. Anim. Vet. Sci. 1 (3): 9 – 11.

Sokol RJ, Straka MS, Dahl R, Devereaux MW, Yerushalmi B, Gumpricht E, Elkins N, Everson G (2001). Role of oxidant stress in the permeability transition induced in rat hepatic mitochondria by hydrophobic bile acids. Pediat. Res. 49(4):519-31. https://doi.org/10.1203/00006450-200104000-00014

Srivastava N, Joshi BP, Jani PB and Prajapati KS (2002). Epidemiological studies on visceral gout in broiler chicks. National symposium on Recent Advance in Diagnosis of: Livestock, Poultry and Wildlife with special Emphasis on Hill Area Diseases and XIX Annual Conference of Indian Association of Veterinary Pathologists. Palampur, Hamnchal Pradesh, India.

Sultana S, Ali MZ, Rahman MT (2012). Effect of different dietary calcium and phosphorus ratio on urinary system and incidence of gout in broiler chicks. J. Innovat. Develop. Strat. 6(2): 19-23.

Thanagari BS, Fefar DT, Prajapati KS, Jivani BM, Thakor KB, Patel JH, Ghodasara DJ, Joshi BP, Undhad VV (2012). Haemato-biochemical alterations induced by diclofenac sodium toxicity in Swiss albino mice. Vet.World. 5 (7): 417-419. https://doi.org/10.5455/vetworld.2012.417-419

Vegad JL (2008). Poultry Diseases a Guide for Farmers and Poultry Professionals. 2nd Edition. International Book Distributing Co. India, Chap. 3: 94-96.

Wideman RF (1988). Avian kidney anatomy and physiology. Crit. Rev. Poult. Biol. 1:133176.

Wideman RF Jr, Cowen BS (1987). Effect of dietary acidification on kidney damage induced in immature chicken by excess calcium and infectious bronchitis virus. Poult. Sci. 66:626-633. https://doi.org/10.3382/ps.0660626

Wideman RF, Ford BC, May JD, Lott BD (1994). Acute heat acclimation and kidney function in broilers. Poult. Sci. 73:75-88. https://doi.org/10.3382/ps.0730075

Wu G, Fang YZ, Yang S, Lupton JR, Turner ND (2004). Glutathione metabolism and its implications for health. J. Nutrit. 134(3):489-92. https://doi.org/10.1093/jn/134.3.489

Yadav BS, Niyogi D, Gupta RK, Singh SV, Saif M, Jaiswal SK (2020). Incidence and clinico-pathological study of gout in broiler birds of Faizabad and Sultanpur districts of Eastern Uttar Pradesh. Explor. Anim. Med. Res. 10:88-91.

Yewale VD (2010). Studies on Infectious Bronchitis virus as a cause of visceral gout in broiler chicks. Thesis submitted to Anand Agricultural University, Anand, Gujarat.