Avian Visceral Gout: A Clinicopathological Study in Broiler Chickens

¹University of Verona, Italy

²Department of Livestock & Dairy Development Quetta, Pakistan

³Sindh Agriculture University Tandojam, Pakistan

*Corresponding author: Adnan Yousaf, Sindh Agriculture University Tandojam, Pakistan, Phone: +923005662008, E-mail: [email protected]

Received Date: August 11, 2025

Published Date: October 17, 2025

Citation: Yousaf A, et al. (2025). Avian Visceral Gout: A Clinicopathological Study in Broiler Chickens. Mathews J Vet Sci. 9(7):87.

Copyrights: Yousaf A, et al. © (2025).

ABSTRACT

In April 2025, an outbreak of visceral gout occurred in a flock of intensively reared commercial broiler chickens. Affected birds presented with characteristic clinical signs including hyporexia, adipsia, lethargy, ruffled plumage, progressive emaciation, and abnormal fecal output. Postmortem examination revealed pathognomonic white, chalky urate deposits on the serosal surfaces of multiple organs, with particularly severe involvement of the pericardium and liver. Histopathological assessment of renal tissue confirmed extensive tubular necrosis and luminal obstruction with birefringent urate crystals, consistent with advanced urate nephropathy. The therapeutic strategy implemented involved a multi-pronged nutritional approach aimed at reducing nitrogenous waste and supporting renal function. This included immediate dietary protein restriction to decrease endogenous uric acid production, oral supplementation with jaggery (a natural source of readily available carbohydrates) to promote energy intake and reduce protein catabolism, and administration of B-complex vitamins to support metabolic recovery. Additionally, electrolyte therapy was provided to correct fluid imbalances and promote urate excretion. This combined intervention successfully halted disease progression and facilitated flock recovery.

Keywords: Visceral Gout, Broiler Chicks, Urate Crystals, Tubular Degeneration.

INTRODUCTION

Renal pathologies represent a significant health challenge in avian medicine, with epidemiological studies suggesting they account for approximately 29.6% of all disease presentations in poultry [1]. The economic and welfare impacts of these conditions are substantial, as exemplified by severe outbreaks of visceral gout in commercial broiler operations in Gulf countries between 2011 and 2012, where mortality rates reached 40% in affected flocks [2]. Avian gout is a metabolic disorder stemming from renal dysfunction, which can be precipitated by a complex interplay of infectious agents (e.g., infectious bronchitis virus), nutritional imbalances (e.g., excessive dietary protein or calcium, vitamin A deficiency, dehydration), and toxic insults (e.g., mycotoxins, nephrotoxic antibiotics) [3]. The pathophysiology of gout is uniquely linked to avian nitrogen metabolism. Birds are uricotelic, meaning uric acid is the primary end product of protein and purine catabolism. A critical physiological distinction from mammals is the absence of the hepatic enzyme uricase, which in other species converts uric acid into the highly soluble compound allantoin. To circumvent the insolubility of uric acid at physiological pH, birds have evolved a sophisticated renal transport system where it binds to specific carrier proteins in the proximal tubules to remain in solution for excretion [4]. Compromise of renal function or a systemic overproduction of uric acid overwhelms this mechanism, leading to hyperuricemia. The subsequent precipitation of monosodium urate crystals in tissues, while biochemically inert, induces severe mechanical damage, inflammation, and organ dysfunction through physical distortion and pressure necrosis.

Gout presents in two distinct clinical forms:

1. Visceral Gout: The more acute and common form in poultry, characterized by pathognomonic white, chalky urate deposits on the serosal surfaces of the heart (uremic pericarditis), liver, kidneys, and air sacs.
2. Articular Gout: A chronic form involving painful deposition of urates in synovial joints and tendon sheaths, leading to lameness and swollen, deformed joints.

Both forms have been extensively documented across various avian species, including pheasants, Japanese quail, ducks, and commercial chickens [5,6]. The following report details a confirmed case of visceral gout in a flock of Rajasri layer chickens, describing the antemortem presentation, key pathological findings, and the implemented therapeutic and management strategies that were successful in mitigating losses.

CASE PRESENTATION

In April 2025, an outbreak of visceral gout was documented in a commercially reared broiler flock. Affected birds displayed characteristic clinical signs including pronounced hyporexia, adipsia, generalized lethargy, ruffled plumage, progressive emaciation, and passage of abnormal droppings. Postmortem examinations were conducted and revealed extensive visceral gout, marked by chalky white urate deposits on the serosal surfaces of the pericardium, liver, intestinal loops, air sacs, kidneys, and ureters. The most prominent gross lesions included uremic pericarditis and hepatitis, indicative of severe systemic urate deposition.

Histopathological assessment of renal tissue confirmed severe nephropathy, featuring extensive tubular degeneration and necrosis, luminal distension with proteinaceous casts, and conspicuous accumulation of birefringent urate crystals findings consistent with advanced urate nephrosis.

Disease management was initiated through a multifaceted therapeutic strategy focused on reducing renal metabolic load and supporting recovery. This involved immediate dietary modification to a low-protein formulation to limit endogenous uric acid production, provision of oral jaggery (an unrefined sugar product) dissolved in drinking water to supply readily metabolizable energy and reduce catabolism, and supplementation with B-complex vitamins alongside electrolyte therapy to correct dehydration, support metabolic cofactor status, and promote diuresis. This integrated nutritional and supportive intervention proved effective in curbing mortality and facilitating clinical recovery within the flock.

This case underscores the critical importance of prompt diagnosis and comprehensive dietary management in controlling metabolic disorders such as gout in intensively reared poultry.

MATERIALS AND METHODS

Mortality was observed within a commercial broiler flock during the second week of age. Affected birds exhibiting nonspecific clinical signs were submitted for diagnostic postmortem examination. A diagnosis of visceral gout was established based on the presence of pathognomonic gross lesions, including chalky white urate deposits on the pericardium, liver, and other serosal surfaces, and subsequently confirmed by histopathological analysis.

For microscopic evaluation, samples of renal tissue were systematically collected and trimmed into standardized 1×1 cm³ sections to ensure uniform fixation. These specimens were immersion-fixed in 10% neutral buffered formalin (NBF) for a minimum of 48 hours to adequately preserve cellular architecture and prevent artifactual changes. Following fixation, the tissues underwent routine histological processing through a series of graded alcohols and xylenes for dehydration and clearing, were infiltrated with and embedded in paraffin wax, and sectioned at a thickness of 5 μm using a rotary microtome. The resulting sections were mounted on glass slides, stained with hematoxylin and eosin (H&E), and coverslipped for detailed light microscopic examination [7].

This standardized tissue processing protocol enabled the clear identification of characteristic histologic lesions associated with urate nephropathy, including tubular necrosis, luminal dilation, and the presence of intratubular urate crystals surrounded by granulomatous inflammation and giant cells, thereby providing a definitive diagnosis.

RESULTS

In April 2025, a sudden spike in mortality was documented within a commercial broiler flock. Birds presenting clinical signs were notably lethargic, exhibited markedly reduced consumption of both feed and water, showed ruffled plumage and progressive weight loss, and passed abnormal droppings.

A thorough postmortem examination was conducted on multiple affected birds. Consistently observed gross findings included poor body condition indicative of emaciation and signs of dehydration, such as darkened, shrunken musculature and taut skin. The most significant lesions were associated with widespread visceral gout. Key pathological observations were:

• Liver: The organ was mildly enlarged, showed diffuse congestion, and was stippled with granular, chalky white urate deposits on both its capsular and cut surfaces (Figure 1).
• Multiple Serosal Surfaces: Extensive, patchy to coalescing deposits of urates were evident on the serosa of the intestines, the pleural and abdominal air sacs, and the epicardial surface of the heart (Figure 2).
• Heart: A defining lesion was severe fibrinous pericarditis, characterized by a layer of fibrin intermixed with urate crystals covering the pericardium and epicardium (Figure 2).

These collective findings provided a clear and definitive gross pathological diagnosis of advanced visceral gout.

Figure 1. Liver showing chalky white deposits, congestion and mild enlargement.

Figure 2. Deposition of chalky white materials on pericardial sac.

Histopathology

Microscopic examination of renal tissue sections revealed severe and widespread nephropathy consistent with advanced urate nephrosis. The parenchyma exhibited multifocal hemorrhages, indicative of vascular damage. There was extensive degeneration of the tubular epithelium, characterized by cellular swelling, loss of brush borders, and pyknotic nuclei. This progressed to overt tubular necrosis, with sloughing of epithelial cells into the lumen and formation of granular and cellular casts.

The most prominent histopathological feature was the presence of extensive, multifocal aggregates of pale eosinophilic, needle-shaped urate crystals deposited within the tubules and the surrounding interstitium. These crystalline deposits were consistently surrounded by a robust inflammatory response, specifically a granulomatous reaction featuring numerous multinucleated giant cells, macrophages, and lymphocytes, which formed distinct granulomas aimed at walling off the insoluble crystalline material.

The combination of acute tubular injury and the severe granulomatous interstitial nephritis provided histopathological confirmation of renal failure as the underlying cause of the visceral gout observed grossly.

DISCUSSION

Gout is a metabolic disorder characterized by persistent hyperuricemia, leading to the precipitation and deposition of monosodium urate crystals in various tissues. In the present case, the diagnosis was confirmed by the presence of pathognomonic chalky white urate deposits on visceral serosae, supported by histopathological findings including renal tubular necrosis, intratubular urate crystallization, and associated granulomatous inflammation. These pathological features align with previously documented cases of avian visceral gout [8,9].

In the context of Gulf countries n broiler production systems, the emergence of gout is often multifactorial, arising from interactions between nutritional, environmental, infectious, and management-related stressors:

1. Nutritional Imbalances

Diets containing excess calcium (>1.2% in starter rations) or a distorted calcium-to-phosphorus ratio promote nephrocalcinosis and impair renal function. High crude protein formulations (>23%) elevate endogenous production of uric acid, the main nitrogenous waste product in birds, overwhelming renal excretory capacity. Deficiencies in fat-soluble vitamins, particularly vitamin A (essential for epithelial integrity) and vitamin D₃ (involved in calcium homeostasis), further predispose birds to renal damage and dysfunction.

2. Hydration and Environmental Stress

Chronic dehydration, often resulting from inadequate water access or high environmental temperatures common in arid regions, leads to the production of highly concentrated urine. This increases the risk of urate crystallization within the renal tubules and ureters. Additionally, poor water quality, frequently reported in certain areas of the Kingdom of Gulf countries (KSA) due to high mineral content (elevated sulfates, nitrates, and sodium), places additional osmotic stress on the kidneys and exacerbates renal compromise.

3. Infectious and Toxicological Trigger

Nephropathogenic strains of Infectious Bronchitis Virus (IBV) exhibit a specific tropism for renal tissues, causing tubular epithelial necrosis and acute renal failure. Mycotoxins, particularly ochratoxin A and aflatoxins, are potent nephrotoxins that disrupt protein synthesis, promote oxidative stress, and directly damage renal tubular cells, synergizing with other risk factors to precipitate gout outbreaks.

4. Management-Related Factors

The overuse of additives such as sodium bicarbonate can alter urine pH and electrolyte balance, facilitating urate precipitation. Furthermore, physiological stress associated with live vaccination protocols (e.g., against Infectious Bursal Disease) may transiently suppress immune function and elevate metabolic stress, compounding preexisting renal vulnerability.

This multifactorial etiology underscores the importance of integrated flock management strategies targeting nutrition, water quality, biosecurity, and environmental conditions to mitigate the risk of gout in broiler production systems

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