As animal production becomes more and more sophisticated, previously unobserved factors that potentially hinder performance become a bigger issue. Intestinal commensal bacteria – bacteria that live together – fit this narrative.
Cell walls of nonpathogenic gram-negative bacteria are mostly lipopolysaccharides. Peptidoglycans (PGN), or murein, are primary components of gram-positive bacteria. In normal intestinal bacteria, neither class causes disease. But fragments of their cell walls which remain in the intestine as intestinal waste can push performance downward.
This is particularly the case with PGN – a thread that unites bacteria of virtually all types, regardless of species, type, or any other classification. While necessary for the survival of bacteria, PGN can snick away at bird performance and profits and not be noticed.
PGN is a massive polymer of amino acids (e.g., peptido-) and sugars (e.g.,-glycan) unique to bacterial cell walls. The carbohydrate or sugar constituents alternate from B-(1,4)-linked N-acetylglucosamine (NAG) to N-acetylmuramic acid (NAM) crosslinked by short peptides (Figure 1). Amino acids meld into a 2- or 3-dimensional lattice to reinforce and give strength. PGN provides the bacteria with structural support against osmotic pressure.
PGN undergoes constant growth and division in a manner similar to bone reconstruction in animals. As much as a 50% turnover of PGN occurs within one generation, according to researchers. This PGN remains in the spent growth media and probably mimics a similar phenomenon in the intestinal lumen.
In gram-positive (G+) bacteria, PGN is about 90% of the dry weight. (Figure 2). G+ bacteria predominate in the intestinal tract. In the turkey microbiome, for example, 77% of the microbes were G+ rods, while 14% were G-, and 9% were G+ cocci. In healthy swine, 71% of microbes were G+. This shows that G+ bacteria exist at a disproportionately higher level in the intestinal tract.
Natural bacterial cell death generates an abundant source of PGN in the intestine. In one study, 34% of total fresh fecal bacteria was classified as dead. In another, 32% of fresh fecal bacteria was dead, while an additional 20% was “injured.” And although G+ lactococci are resistant to gastric acidity (90 to 98% survival), only 10 to 30% survive the duodenum. In fact, 60% of the feces mass is comprised of bacteria.
And airborne PGN can be abundant in animal production facilities and grain processing plants. PGN carried on dust particles is common in swine farrowing and nursery production units. Repetitive exposure of these aerial organic dust particles can be debilitating to lung function in mice, according to Nebraska research.
When airborne sources are added to the G+ bacteria in the intestinal tract, where 90% of the cell wall is PGN and 30 to 35% of cells are dead, exposure to this cellular waste is quite high. It is this constant source of waste that can physically interfere with normal intestinal enzyme-substrate functions.
Intestinal mucous protects against potential pathogens and toxins, and impedes their entry into the blood stream. There has been a growing recognition that PGN and lipopolysaccharides act as intestinal antagonists and stimulate mucin secretion. This can adversely affect animal performance efficiency via the intestinal mucous barrier.
For example, about one-third of the amino acid content of mucin is threonine. The gastrointestinal requirement for most essential amino acids is 14 to 33% – but for threonine, this jumps to 61% for gut-related functions and mucin production. Swine research finds insufficient dietary threonine restricts intestinal mucin secretion.
Because mucin is essentially indigestible to the host, mucin represents a net nitrogen loss to the animal. Thus, excessive mucin synthesis and secretion fueled by antagonists like PGN is nutritionally costly.
The greatest threats to efficient and profitable animal performance are those that go unobserved. They allow stressors to secretly chip away at normal body processes, diverting nutrients away from growth and efficiency. Peptidoglycans fit this category.
05 September 2018
Aaron is a Corporate Science Fellow. He has a PhD in Animal Nutrition obtained from Aberdeen University, UK. Aaron has worked in commercial and academic innovation leadership roles since 2001, most recently as a Professor at the University of Sydney in Australia, joining the DSM innovation team in 2013. Aaron has published more than 200 peer-reviewed papers and book chapters and in addition to his role in DSM, is retained by Purdue University as an Adjunct Professor. In 2016 Aaron was awarded the Poultry Nutrition Research Award by the American Feed Industry Association and in 2019 the Life Mentor Award by the Poultry Science Association.
Nelson is an Enzyme Lead All Species, North America. He holds a PhD obtained at Clemson University.
Nelson held positions in technical service and technical marketing for enzymes, vitamins, and HyD within DSM. His expertise extends to growth promotants and amino acids from previous engagements. He currently is an adjunct professor at two universities in the U.S.
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