Fatty Liver Hemorrhagic Syndrome (FLHS) in Laying Hens: A Detailed Overview

 

Dr. Majed Hamed Al Saegh / poultry pathologist / Australia

 

Fatty Liver Hemorrhagic Syndrome (FLHS) is one of the leading causes of mortality in laying hens, particularly those housed in cage systems. This condition predominantly affects hens during the middle to late stages of egg production. FLHS is characterized by severe fat accumulation in the liver, leading to liver dysfunction, hemorrhages, and, in extreme cases, sudden death due to liver rupture. The disease poses significant challenges to the poultry industry, especially in regions where cage systems are prevalent.

 

Pathophysiology and Clinical Signs. During post-mortem examinations of hens affected by FLHS, several key findings are observed:

  • Fat Accumulation: There is a significant buildup of fat in the abdominal cavity and visceral areas.
  • Liver Changes: The liver becomes swollen, spherical, and extremely fragile. Its color changes from pale brown to yellow due to excessive fat deposition.
  • Hemorrhages and Rupture: The condition often leads to liver rupture and internal hemorrhages, which can cause sudden death in severe cases.

 

It is important to note that death from FLHS typically occurs only in extreme cases following massive liver hemorrhage. However, many hens within a flock may suffer from sub-acute or chronic forms of FLHS, which may not result in immediate mortality but can lead to a decline in egg production and reproductive dysfunction.

 

Biochemical and Metabolic Changes. FLHS causes profound changes in liver function, which can be detected through blood tests. Key metabolic alterations include:

 

  • Reduced Carnitine Levels: Liver carnitine and stearoyl carnitine levels are reduced in hens with FLHS. Carnitine plays a crucial role in fatty acid metabolism by facilitating the transport of fatty acids into mitochondria for oxidation.
  • Increased Metabolites: Hens with FLHS exhibit significantly higher levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), low-density lipoprotein (LDL), total cholesterol, and triglycerides. Conversely, high-density lipoprotein (HDL) levels are decreased.
  • Hepatic Steatosis: The liver shows signs of fat infiltration, leading to hepatic steatosis.

Research from Hebei Agricultural University in China (2021) has linked liver metabolites and arachidonic acid metabolism to the pathophysiology of FLHS, further highlighting the complex metabolic disruptions associated with this condition.

 

Housing Systems and FLHS Incidence

The housing system plays a significant role in the incidence of FLHS. Conventional cage systems, which are still widely used globally, are highly associated with FLHS due to factors such as high stocking densities, limited movement, and environmental stressors. In contrast, enriched or furnished cages that provide more space, perches, nests, and scratch areas have been shown to reduce the incidence of FLHS.  Data from various studies indicate that while mortality rates may not differ significantly between housing systems, the cause of death is often related to the housing environment. In conventional cages, FLHS is the most common cause of death, accounting for 58-74% of necropsied hens.

 

Environmental and Nutritional Factors

Several environmental and nutritional factors contribute to the development of FLHS:

  • Environmental Factors:Temperature and Humidity: Elevated ambient temperatures and high humidity levels can increase the incidence of FLHS. High body temperatures inhibit thyroid hormone secretion and weaken lipolysis, both of which are risk factors for fatty liver disease.
  • Ventilation and Air Quality: Poor ventilation and air quality can exacerbate the condition.
  • Immunological Stress: Challenges from field pathogens or vaccines can also increase FLHS incidence.

 

Nutritional Factors:

  • Diet Composition: Diets high in energy and fat but low in protein, linoleic acid, and choline are associated with an increased risk of FLHS. Linoleic acid is essential for regulating lipid metabolism, and its deficiency can lead to fat accumulation in the liver.
  • Mycotoxins: High levels of mycotoxins, such as aflatoxins and trichothecenes, can cause liver damage and increase the risk of FLHS.
  • Preventive Nutrients: Certain nutrients and feed additives, such as flaxseed, omega-3 fatty acids, branched-chain amino acids, and bile acids, have shown promise in reducing FLHS incidence by improving lipid metabolism and antioxidant capacity.

 

Potential Solutions and Preventive Measures. Several strategies have been proposed to mitigate the impact of FLHS in laying hens:

Dietary Modifications:

  • Omega-3 Fatty Acids: Supplementation with flaxseed, flax oil, or omega-3 fatty acids can reduce hepatic fat content and lower FLHS incidence.
  • Branched-Chain Amino Acids: Higher dietary concentrations of leucine, isoleucine, and valine can inhibit lipogenesis and promote fatty acid oxidation.
  • Choline and Linoleic Acid: Ensuring adequate levels of choline and linoleic acid in the diet is crucial for preventing fat accumulation in the liver.

 

Feed Additives:

  • Cysteamine and Choline: These compounds can regulate antioxidant enzyme activities and modulate hepatic lipid metabolism.
  • Magnolol: This plant compound inhibits fatty acid synthesis and promotes fatty acid oxidation.
  • Polydihydromyricetin-Fused Zinc Nanoparticles (PDMY-Zn NPs): These nanoparticles enhance antioxidant capacity and regulate liver lipid metabolism.
  • Folic Acid and Lutein: These nutrients positively influence lipogenesis and provide antioxidative and anti-inflammatory benefits.
  • Bile Acids: These compounds regulate lipid metabolism, bolster antioxidant defenses, and reduce inflammation.

 

Plant Extracts:

  • Berberine: This alkaloid reshapes microbial and metabolic homeostasis within the liver-gut axis.
  • Polysaccharides from Hericium erinaceus: These compounds improve intestinal barrier function and shape gut microbiota.
  • Silymarin: This compound decreases liver weight, malondialdehyde content, and hepatic steatosis.

 

Housing Improvements:

  • Enriched Cages: Providing more space, perches, nests, and scratch areas can reduce FLHS incidence.
  • Environmental Control: Maintaining optimal temperature, humidity, and ventilation can help mitigate the risk of FLHS.

 

Conclusion

FLHS remains a significant challenge in the poultry industry, particularly in conventional cage systems. However, a combination of dietary modifications, feed additives, and housing improvements can help reduce the incidence of this condition. Ongoing research into the metabolic and environmental factors contributing to FLHS will continue to inform best practices for managing this disease in laying hens. By adopting these strategies, poultry producers can improve hen health, enhance egg production, and reduce mortality rates associated with FLHS.

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