A constant antagonist: Consequences of endotoxins in animals

By Josep Garcia-Sirera (Toxins product manager)

All animal species are affected by gram-negative bacteria. Under normal circumstances, the bacteria are present in the gastrointestinal tract in equilibrium with other microorganisms. However, in situations of bacterial challenge—induced by stress, immunosuppression, etc.—the equilibrium can alter and cause an excess of gram-negative bacteria. During these imbalances, endotoxins are produced and released in the animal.

It is under circumstances of a high gram-negative to gram-positive bacteria ratio that endotoxins, also known as lipopolysac¬charides (LPS), can become a problem. An excess of LPS happens when there is a high turnover of gram-negative bacteria or a rapid destruction of gram-negative bacteria due to the use of antibiotics. An inflammatory pyrogen, lipopolysaccharides can trigger detrimental effects by stimulating an inflammatory reaction in the gastrointestinal tract and once absorbed, at other sites in the animal.

Overview of the endotoxin’s structure

What makes gram-negative bacteria differ from gram-positive bacteria is the structure of the cell envelope. Gram-positive bacteria have a cytoplasmic and a peptidoglycan outer membrane. In addition to these layers, gram-negative bacteria have an addion outer layer. The outer layer contains phospholipids, proteins, and LPS. This LPS consists of three elements: Lipid A (a hydrophobic component that is toxigenic), a core (an oligosaccharide), and O-antigen (hydrophilic component project¬ing into the extracellular space) (Figure 1).

Figure 1: Typical endotoxin structure. Lipid A is embedded in the outer membrane of gram-negative bacteria

Understanding endotoxin behavior

vThe mechanism of action is complex. Put simply, a lipopoly¬saccharide binds to a lipid-binding protein (LBP) to create the LPS/LBP complex that will eventually bind with Toll-like receptor-4 (TLR4). This triggers the signaling cascade for macrophage/endothelial cells to secrete pro-inflammatory cytokines and nitric oxide that lead to the characteristic “en-dotoxic shock” (Figure 2).

Figure 2: Lipopolysaccharides bind to lipid-binding protein and are car¬ried to Toll-like receptor-4 where it is then absorbed into the circulatory system via the microvilli and intestine cell lining

Presentation of endotoxic shock

Present in dust, feed, and feces, endotoxins are on every type of farm. However, different production species are not affected equally when it comes to an LPS. While it is well documented that all animals have receptors for LPS, the way an animal reacts to the presence of LPS varies greatly.

Poultry

Of production animals studied, poultry is the least affected by LPS. Their sensitivity to LPS action is much lower than swine or ruminants. The theory for this is due to differenc¬es in the TLR4 receptor. Utilizing the lock and key concept, the TLR4 activation site responsible for endotoxin action is slightly different from mammals, this could partly explain the lower effects of LPS in poultry. Though there is little research, some possible signs of endotoxins in poultry are fatty liver, reduced feed intake, wet litter, and decreased performance; be it laying rate and shell quality, growth, or reproduction.

Ruminants

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