Impact of Heat Stress on Poultry Health and Performance

Summary

Heat stress arises when ambient temperatures exceed the bird’s thermoneutral zone, provoking a cascade of physiological disturbances that undermine welfare, productivity and product quality. Exposure to elevated temperatures induces hyperthermia, leading to oxidative stress through overproduction of reactive oxygen species and impairment of mitochondrial function. Key consequences include suppressed feed intake, reduced weight gain, lower egg production, altered meat and egg quality, and compromised immune competence. At the cellular level, heat stress disrupts redox homeostasis, activates heat shock proteins and impairs intestinal barrier integrity, exacerbating systemic inflammation. The liver, central to lipid metabolism and detoxification, is especially vulnerable: oxidative damage in hepatocytes disrupts lipogenesis and energy supply. Poultry genetic lines with enhanced heat tolerance or modified genes (for example, naked-neck or frizzle) show variable resilience, indicating genetic interventions as one component of multi-pronged mitigation. Nutritional approaches—ranging from antioxidant supplementation, phytochemicals and trace minerals to nanoscale delivery systems—seek to restore antioxidant defences, stabilise intestinal function and preserve performance under thermal challenge. The global significance of this research spans food security, animal welfare and climate resilience in commercial and smallholder settings worldwide.

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Impact of Heat Stress on Poultry Health and Performance publication trend

The graph below shows the total number of articles in impact of heat stress on poultry health and performance across all publications each year (not limited to Nature Index journals).

Technical terms

Heat stress: A condition in which birds cannot dissipate sufficient body heat to maintain homeostasis, leading to hyperthermia and physiological disturbances.

Oxidative stress: An imbalance between the generation of reactive oxygen species and the capacity of antioxidant defences, resulting in cellular damage.

Reactive oxygen species (ROS): Chemically reactive molecules, such as superoxide and hydrogen peroxide, produced during normal metabolism but increased under stress.

Heat shock proteins (HSPs): A family of molecular chaperones induced by thermal stress that assist in protein folding and protect cells from damage.

Tight junctions: Intercellular protein complexes in the intestinal epithelium that regulate permeability and maintain barrier integrity.

References

  1. Biogenic Selenium Nanoparticles Synthesized with Alginate Oligosaccharides Alleviate Heat Stress-Induced Oxidative Damage to Organs in Broilers through Activating Nrf2-Mediated Anti-Oxidation and Anti-Ferroptosis Pathways. Antioxidants (2023).
  2. Association between heat stress and oxidative stress in poultry; mitochondrial dysfunction and dietary interventions with phytochemicals. Journal of Animal Science and Biotechnology (2016).
  3. Radical Response: Effects of Heat Stress-Induced Oxidative Stress on Lipid Metabolism in the Avian Liver. Antioxidants (2020).
  4. Effects of Dietary Betaine on Growth Performance, Digestive Function, Carcass Traits, and Meat Quality in Indigenous Yellow-Feathered Broilers under Long-Term Heat Stress. Animals (2019).
  5. Supplementation of Bacillus subtilis-based probiotic reduces heat stress-related behaviors and inflammatory response in broiler chickens1. Journal of Animal Science (2018).
  6. Effect of Heat Stress and Stocking Density on Growth Performance, Breast Meat Quality, and Intestinal Barrier Function in Broiler Chickens. Animals (2019).
  7. Differential Expression of Heat Shock Transcription Factors and Heat Shock Proteins after Acute and Chronic Heat Stress in Laying Chickens (Gallus gallus). PLOS ONE (2014).
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