Managing endotoxin risks in pigs

Endotoxins and their negative effects in animals

Lipopolysaccharides, also commonly known as endotoxins, are cell wall components of Gram-negative bacteria such as E. coli and Salmonella, which are released upon bacterial replication or death (lysis).  Lipopolysaccharides vary according to originating bacteria, being more or less harmful or toxic, according to variability happening in the O-specific polysaccharide chain. They also serve as a potential barrier to antimicrobials from entering the outer membrane of Gram-negative bacteria. Pigs are continuously exposed to lipopolysaccharides throughout their lives. While the main route for lipopolysaccharide exposure in pigs is the gastrointestinal tract, the concentration of endotoxins in the air and dust should not be overlooked: endotoxins are a major component of biological dust.

  In healthy animals, the intestinal epithelium and other epithelia such as that found on the skin or lungs, represent an effective barrier that prevents the passage of lipopolysaccharides into the bloodstream. Endotoxins can elicit strong immune responses, weakening immune systems and impairing performance. In the body of the animal, endotoxins cause an inflammatory cascade that increases a pig’s maintenance requirements (due to fever) that, coupled with anorexia, means less energy available for growth. Moreover, a severely pronounced immune response can lead to septic shock. Endotoxins also impair feed efficiency. A recent study of common challenges in pig farms reported a reduction in feed intake of 3% due to parasitic infections, 4.1% due to poor housing conditions, 10.2% due to digestive bacterial infections, 17.3% caused by respiratory diseases, 25.2% due to mycotoxicosis (mycotoxin-induced diseases) and 26.8% due to lipopolysaccharides (Figure 1).

Figure 1. Metabolic consequences of an activated immune system due to different challenges.

Prevention and management of endotoxin risks

In recent years, new concerns have emerged on nutritional, environmental and social factors that may disrupt the barrier function and/or increase exposure to lipopolysaccharides. The gut is the first line of defense against endotoxins and, if compromised due to nutrition, stress or metabolic state, endotoxin transport can increase, for example, heat stress, mycotoxins, inflammation, etc. In several livestock species, it is well established that a 1 to 2°C increase in body temperature causes the intestinal tight junction proteins to be affected, increasing intestinal permeability and allowing more lipopolysaccharides to enter the blood stream. High caloric and high fat diets increase serum endotoxin concentrations and induce acute low grade inflammation. Starvation depresses the expression and function of intestinal alkaline phosphatase (IAP), a brush–border enzyme that detoxifies lipopolysaccharides.

The Biomin solution for managing endotoxins

Mycofix is a state of the art, market leader product for the deactivation of mycotoxins, that utilises three strategies to provide a 360° counteraction:

  • adsorption
  • biotransformation
  • bioprotection

The product demonstrated efficacy against endotoxins as well, combining the strength of the only EU registered adsorbent existing on the market, with Biomin bioprotection mix: a combination of carefully selected plant and algae extracts that support the gastrointestinal tract, immune system and the liver. The performance of Mycofix on endotoxins was recently evaluated in two trials conducted at Iowa State University (USA) and at the Centre for Applied Animal Nutrition (CAN) in Austria. The aim of the trials was to evaluate the effects of Mycofix on endotoxin permeability and inflammation response in piglets under heat stress conditions. In the Iowa State University trial, 32 one-week post weaning gilts were assigned to two treatments: a control feed with no additive and a group where 2.5 kg of Mycofix per tonne of feed was included. The duration of the trial was 28 days. Several parameters were evaluated, including average daily weight gain and ileal endotoxin permeability (Figures 2 and 3).

In the second trial conducted at CAN, 36 piglets (21 days-old) were assigned to two treatments: a control diet with no additive; and a diet containing 2.5 kg of Mycofix per tonne of feed for 56 days. Several parameters were evaluated including performance (average daily weight gain in kg/d) over the whole feeding period, gut permeability during heat stress, measured via the sugar permeability assay (lactulose/rhamnose or L:R ratio), and endotoxin concentration (Units/mL) in the blood during heat stress (Figures 4, 5 and 6).

Figure 6. Endotoxin concentration in serum of pigs receiving either control feed or Mycofix on the first day of the heat stress.

Conclusion

Results of both trials demonstrate that Mycofix at a concentration of 2.5 kg per tonne of finished feed was able to counteract the negative effects of increased intestinal permeability induced by heat stress in weaning pigs; and to decrease endotoxin concentration in the blood. All results suggest a counteraction of the triggering effects by endotoxins, which lead to an increased performance during heat stress when Mycofix is used.

This article originally appeared in Asian Pork.

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