For many years, the microbiota has been defined as a community of micro-organisms comprised of bacteria, archaea, protists, fungi and viruses.1,2 Intestinal microbiota can also be described as a typically complex mixture of bacterial groups that colonize a given area of a human or animal's gastrointestinal (GI) tract that has not been affected by medical intervention or disease.3,4
The digestive tract of a healthy chick is considered free from microorganisms at hatch. Afterwards microbial colonization evolves very quickly. At around 40 days in age, the microbiota becomes fully developed in birds and the bacteria can be categorized as commensal or pathogenic.5 The bacterial population within broilers is very diverse, comprised of over 900 species.6
The presence of bacterial pathogens within chicken microbiota becomes a crucial issue for both bird and human health.
Creating a healthy balance of bacteria provides a barrier against pathogen colonization and contributes to the overall well-being of the host. Microbiota produce metabolic substrates like vitamins and short-chain fatty acids to stimulate the immune system.8
· Improves host nutrition
· Reduces intestinal pathogen colonization
· Help with development of intestinal morphology
· Aid in immune function
Microbiota produce enzymes enabling the depolymerization of dietary polysaccharides.9 These enzymes are critical to the host animal's nutrition because broilers lack the genes to create enzymes that are necessary to facilitate this process. During the depolymerization of dietary polysaccharides, gut bacteria produce short-chain fatty acids (SCFAs). Common SCFAs produced are acetate, propionate and butyrate. Butyrate, or butyric acid, is the primary energy source of colonic epithelia and has been shown to be essential for homeostasis of colonocytes and development of gut villus morphology.9 Butyric acid can improve growth performance and carcass quality characteristics in chickens.10 Its also been stated that SCFAs can regulate intestinal blood flow, stimulate enterocyte growth and proliferation and mucin production in addition to affecting intestinal immune responses.11
Gut microbiota also contributes to the metabolism of nitrogen and dietary protein, which provides further amino acids for egg production, maintenance and growth.9 Gut microbiota in poultry may also create additional vitamin (especially B vitamins) supplies. Similar to bacterial proteins, most of the vitamins within gut bacteria are excreted in the faeces because they cannot be absorbed. However, coprophagic birds may benefit from this bacterial vitamin synthesis.
The gastrointestinal tract of a newly hatched chick is void of microorganisms but is colonized afterward by microorganisms present in the surrounding environment. This creates an opportunity for the enteric pathogens to attach to and breach the intestinal mucosal layer, causing infection in new hatchlings while there is an absence of a healthy gut microbiota.
A chicken gut generally maintains a proper balance of microbiota (based on its environment), but any disruption to the species can lead to the dramatic proliferation of pathogenic microbes like Eimeria, Campylobacter, etc.9
The establishment and maintenance of the microbiota before an infection occurs is essential to maintain bird health. The commensals, which comprise of a layer of dense and complex microbial communities along the GI tract, can also block the attachment and colonization of most invading enteric pathogens—this is called competitive exclusion. Some commensal bacteria act by producing secondary antibacterial substances called surfactants as a compound to inhibit pathogen growth.11
Gut microbiota play a critical role in intestinal development. Pathogens can also change intestinal morphology negatively. It has been suggested that the SCFAs produced by intestinal microbiota also increase enterocyte growth and proliferation.11 Gut microbiota also affects the intestinal morphology of poultry. Gnotobiotic birds, or birds colonized with a lower load of bacteria than in conventionally-raised birds, have an intestinal villus with shorter, shallower crypts.11
The intestinal tract is the largest immune organ in the body and is continuously exposed to a large variety of micro-organisms (commensal and pathogenic). The intestine has two contrasting tasks: nutrient absorption and prevent invasion of pathogen. The intestinal immune system consists of a mucosal layer (immunity), tightly interconnected intestinal epithelial cells (intestinal integrity), secreted soluble immunoglobulin A and antimicrobial peptides (immunity). Intestinal tight junctions are an interconnected part of immunity.
The mucosal layer consists of an outer layer where microorganisms can colonize and an inner, compact layer which repels bacteria. A beneficial microbial community plays a key role in maintaining normal physiological homeostasis, altering the immune system and influencing organ development and metabolism.12 As a component of the intestinal immune system, the mucus layer prevents intestinal microorganisms from entering the intestinal epithelium and serves as one of the first lines of protection against infection. Maintaining intestinal integrity via the formation and maintenance of intestinal tight junctions is the next line of defence for the body against pathogens.
The success of the broiler industry relies heavily on the effectiveness of feed conversion. Because feed is a huge factor in production costs (up to 70 percent), poor feed efficiency translates into significant economic losses.5 Mortality rates, decreased weight gain, increased time to slaughter, condemnations at slaughter and preventative treatments associated with diseases contribute to economic losses. Intestinal health is essential for maximizing the health, welfare and performance of poultry and swine. Livestock performance and poultry production can be optimized by managing the intestinal microbiota to prevent infections and promote animal health.
Kemin offers direct fed microbials (CLOSTAT®), encapsulated Butyric Acid (ButiPEARL™ ), and immune modulation (Aleta™) that can help support intestinal health by modulating intestinal microbiota, strengthening the intestinal barrier function and priming innate intestinal immunity.
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5Roberts, T., et al. 2015. New issues and science in broiler chicken intestinal health: Intestinal microbial composition, shifts, and impacts. World's Poultry Science Journal. 71:259-270.
6Apajalahti, J., et al. 2016. Interaction between chicken intestinal microbiota and protein digestion. Anim. Feed Sci. Tech. http://www.sciencedirect.com/science/journal/03778401?sdc=1.
7Wei. S., et al. 2013. Bacterial census of poultry intestinal microbiome. Poultry Science. 92:671-683.
8Ewing, M. W. 1997. The Living Gut. 2nd Edition. Nottingham University Press. Nottingham, U.K.
9Yeoman, C. J., et al. 2012. The microbiome of the chicken gastrointestinal tract. Animal Health Research Reviews. 13(1):89-99.
10Panda, et al. 2009. Effect of butyric acid on performance, gastrointestinal tract health and carcass characteristics in broiler chickens. Asian Aust. J. Anim. Sci. 22:1026-1031.
11Pan, D., Z. Yu. 2014. Intestinal microbiome of poultry and its interaction with host and diet. Gut Microbes. 5(1):108-119.
12Oakley, B. B., et al. 2014. The chicken gastrointestinal microbiome. FEMS Microbiol. Letters. 360:100-112.