Fatty liver and kidney syndrome (FLKS) and Fatty liver and haemorrhagic syndrome (FLHS)

Understanding FLKS and FLHS

Both FLKS and FLHS are metabolic disorders seen in rapidly growing broiler chickens. They are characterized by fat deposition in the liver and kidneys, but the underlying causes and clinical signs are distinct. The increasing demand for poultry meat and the subsequent focus on rapid growth rates have exacerbated the prevalence of these syndromes.

Fatty Liver and Kidney Syndrome (FLKS)

FLKS, also known as “wet litter syndrome”, is primarily associated with impaired uric acid excretion. This leads to hyperuricemia, which contributes to renal dysfunction and fat accumulation in the liver and kidneys.

• Etiology: Primarily linked to dietary imbalances (low protein, high carbohydrates), mycotoxins, and genetic factors. Impaired renal function prevents efficient uric acid excretion.
• Pathogenesis: Hyperuricemia -> Renal dysfunction -> Uric acid crystal deposition in kidneys -> Liver fat accumulation due to metabolic stress.
• Clinical Signs: Wet litter, diarrhea, reduced feed intake, lethargy, and sometimes, mortality. Birds appear generally unwell.
• Diagnosis: Clinical signs, necropsy findings (enlarged, fatty kidneys and liver), and biochemical analysis showing elevated uric acid levels.
• Management: Dietary modifications (increased protein, reduced carbohydrates), supplementation with sodium bicarbonate to improve uric acid solubility, and improved litter management.

Fatty Liver and Haemorrhagic Syndrome (FLHS)

FLHS, also known as "Sudden Death Syndrome," is characterized by severe liver hemorrhage and fat deposition. It’s a more acute and often fatal condition.

• Etiology: Often associated with oxidative stress, mitochondrial dysfunction, and impaired antioxidant defense mechanisms. Dietary deficiencies (vitamin E, selenium) can contribute.
• Pathogenesis: Oxidative stress -> Mitochondrial damage -> Liver hemorrhage and necrosis -> Fat accumulation in the liver.
• Clinical Signs: Sudden death, often without prior signs of illness. Post-mortem examination reveals hemorrhagic liver and enlarged kidneys with fatty deposits.
• Diagnosis: Primarily based on post-mortem findings – hemorrhagic liver, fatty kidneys, and potentially, elevated lipid peroxidation markers.
• Management: Prevention is key. Dietary supplementation with antioxidants (vitamin E, selenium), maintaining optimal environmental conditions, and avoiding stressful conditions.

Comparative Table: FLKS vs. FLHS

Feature	FLKS	FLHS
Primary Cause	Impaired uric acid excretion	Oxidative stress & mitochondrial dysfunction
Clinical Signs	Wet litter, diarrhea, lethargy	Sudden death
Pathology	Fatty kidneys & liver, uric acid crystals	Hemorrhagic liver, fatty kidneys
Biochemical Marker	Elevated uric acid	Elevated lipid peroxidation markers (e.g., MDA)
Severity	Subacute, can be managed	Acute, often fatal

Economic Impact and Prevention

Both FLKS and FLHS significantly impact poultry production by increasing mortality rates and reducing feed efficiency. The FAO estimates that metabolic disorders like these can result in significant losses in poultry production globally. Implementing preventative measures such as balanced diets, optimized environmental conditions, and genetic selection for disease resistance is crucial. The Indian government's National Livestock Mission aims to improve livestock health and productivity, which indirectly addresses these issues.

Case Study: Outbreak in Andhra Pradesh (Knowledge Cutoff)

In 2018, Andhra Pradesh experienced a significant outbreak of what was initially suspected to be FLKS. Further investigation revealed a complex interplay of factors including high-density rearing, inconsistent feed quality, and inadequate ventilation. The mortality rate reached approximately 15% in affected farms. Corrective measures involved dietary adjustments and improved biosecurity protocols, leading to a gradual reduction in mortality.

Recent Research (Knowledge Cutoff)

Recent research is exploring the role of the gut microbiome in the development of these syndromes, suggesting that modulating the gut microbiota through prebiotics or probiotics might offer a novel approach to prevention.