Location: Forage-animal Production Research
Title: How ruminant antibiotic growth promoters work and functional feeds as alternativesAuthor
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Submitted to: Meeting Proceedings
Publication Type: Proceedings Publication Acceptance Date: 9/13/2019 Publication Date: 9/13/2019 Citation: Flythe, M.D., Harlow, B.E. 2019. How ruminant antibiotic growth promoters work and functional feeds as alternatives. Meeting Proceedings. 1:25. Interpretive Summary: Technical Abstract: It is widely known that antibiotics have been used in ruminant feeds for non-clinical purposes, particularly for improved growth promotion and feed efficiency. However, there are misconceptions about how antibiotics can make cattle gain weight more rapidly (growth promotion) or gain at the same rate with less feed or less of a feed component (feed efficiency). It has been proposed that if an antibiotic improves the growth performance of an animal, then that animal must have had an undiagnosed infection, but that is incorrect. The growth of a health ruminant can be impacted by antibiotics and other antimicrobials. To understand how this works, we must examine the host-symbiont relationships between the animal and the microbiota that reside within it. The most distinctive feature of a ruminant is the specialized gastrointestinal tract that includes the rumen. The rumen is home to hundreds of microorganisms, including species from the bacteria, archaea, and eukarya, including both protozoa and fungi. It is key that the first enzymes that act on the feed are microbial, not mammalian. The combined metabolisms of this complex microbial ecosystem acts on almost all components of the plant tissue that the animal ingests. The fibrolytic microbiota, which ferment cellulose and other fiber, are possibly the most well known and most important guild (functional group). Ruminants, like other mammals do not produce enzymes to utilize cellulose, and it is only through the fibrolytic microbiota that ruminants can utilize the calories in fiber. Starch, simple sugars, lipids and protein are also fermented by different guilds of microbiota. In the Twentieth Century, the rumen was explored by the microbiologist Robert Hungate and his students. This group of researchers developed the methods to work with the cellulolytic bacteria, methanogens and the other strict anaerobes that inhabit the rumen, ruminant hindgut and the guts of other animals. The impetus for the research was, in fact, feed efficiency. Hungate noted that the metabolism of the rumen was complex, but it was largely fermentation. He hypothesized that rumen fermentation could be optimized, like any other industrial fermentation. Researchers have approached rumen optimization in a number of ways ranging from probiotic strain selection to animal genetic selection. Feed antibiotics have been among the most successful modulators of rumen fermentation, and it is through rumen activity that they work. Macrolydes and tetracyclines have been used in feed but let us focus on ionophores. The ionophore, monensin, was originally labeled as a coccidostat, but it is an antibiotic produced by the soil bacterium, Streptomyces cinnamonensis. Monensin acts on the cell membrane of sensitive bacteria, shuttling potassium and sodium ions down their respective concentration gradients. This activity leads to the loss of protonmotive force and depletion of intracellular potassium, which is necessary for cytokinesis in cell division. The spectrum of activity includes many protozoa, many Gram-positive and some Gram-negative species. Its activity against Streptococcus bovis can mitigate rumen acidosis to some degree. However, there are two other important activities that lead to growth promotion. Monensin inhibits methanogenesis which decreases methane loss. When methane is reduced, more carbon is retained in soluble products that are absorbed by the animal. Specifically, methane is an electron sink. When methanogens are inhibited alternate electron sinks, such as succinate and lactate are used. These latter metabolites are converted by other bacteria to propionate, which is nutritionally available to the host. Monensin also inhibits the proteolytic protozoa and hyper ammonia-producing bacteria (HAB) that convert feed amino acids into ammonia. When HAB are inhibited, more amino-nitrogen |
