How endotoxins aggravate broiler heat stress

Heat stress makes broiler chickens more susceptible to endotoxins, impacting performance and welfare.


Higher ambient temperatures in poultry housing have an influence on birds’ behavior, physiology and immune system, making broilers more susceptible to endotoxins with negative consequences on welfare and performance. Heat stress costs in the U.S. poultry industry are thought to be approximately US$128-165 million each year.

Heat stress impairs gut barrier function

In a healthy bird, tight junction proteins seal the spaces between intestinal epithelial cells, ensuring an intact gut barrier that helps to prevent pathogens or toxins from entering the blood stream (Figure 1a). However, during heat stress, tight junction proteins can be disrupted (Figure 1b), which allows pathogens or toxins to enter the circulatory system.


Heat stress increases a bird’s gut permeability two-fold, work conducted at the Biomin Research Center confirms.

Thirty-two birds at 28 days of age were either kept at thermoneutral conditions (23 C) or at heat stress conditions (36 C) for 10 hours. A marker molecule (FITC-Dextran) was administered orally and later measured in the blood to assess gut permeability. The gut permeability of the heat-stressed animals doubled compared with that of birds in thermoneutral conditions.


Endotoxins harm broilers and laying hens

Endotoxins, also known as lipopolysaccharides (LPS), are part of the outer membrane of the cell wall of gram-negative bacteria (e.g. Escherichia coli, Salmonella). LPS are released from bacterial cell walls by shedding or through bacterial lysis. There are many natural sources of endotoxins including air, dust, food, water and feces, but the major source is the gastrointestinal tract.

Poultry are exposed to LPS throughout their lives. In healthy birds, the intestinal and other epitheliums such as skin or lungs represent an effective barrier that prevents the passage of LPS into the bloodstream. Once there, however, endotoxins can elicit strong immune responses, weakening birds’ immune systems and impairing performance. Severely pronounced immune response can lead to septic shock.

LPS raise intestinal immune response during heat stress

A study was conducted at the Biomin Research Center to assess the influence of endotoxins on inflammation response of the intestine in heat-stressed birds.

The combination of heat stress and LPS led to an increase of the expression of various genes related to heat stress and inflammation (Table 1). The expression of heat shock protein (HSP70) was increased to 90-fold when the oral dose of LPS was applied. In addition, the cytokines interleukin 1beta and interleukin 6 — all indicative of inflammatory processes — showed a more prominent effect when both stressors were present.

Need for endotoxin control

The presence of endotoxins can cause birds to waste energy on activation of the immune system, leaving less energy available for growth and performance. This underscores the importance of proper endotoxin risk management. Table 2 highlights several ways to reduce the impact of heat stress and endotoxin contamination. When combined with good farm practice and the reduction of other stressors such as heat stress or mycotoxin contamination, the threat of endotoxins on bird performance can be eliminated. 

Dr Nicole Reisinger is a scientist at the Biomin Research Center.

Simone Schaumberger is a mycotoxin risk management product managers at Biomin.

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