Tech Forum Alert
An adequate supply of nutrients for any animal is dictated by the quality of feed ingested, level of gut development and enzyme secretion, allowing unhampered digestion and uptake. It is now well recognised that, in monogastric species as well as ruminants, there are important relationships between digestion, nutrient availability and the bacteria which populate the intestinal tract. The combination of these factors is implicit not only in the amounts of nutrients available for growth and maintaining body health and function, but also in the actual control of disease, especially in how these factors affect the opportunities for pathogenic invasion.
Changes in the use of bacteriocidal drugs linked to increased microbial resistance, such as antibiotic growth promoters, in regions such as the EU have brought these inter-relationships into sharp focus. In order to understand how to maintain or improve the function and health of the gut, it is essential first to understand its function.
Digestion of nutrients
Digestion of feed starts with the mechanical breakdown and acidification in the stomach, or gizzard in the case of birds. Hydrochloric acid is added at this point to initiate protein denaturation, and both grinding and HCl provide a defence against pathogens, by damaging bacterial cells. This effect can be exploited by using coarser-ground feeds with larger particles or adding whole grains (or grit to poultry feed) in the ration. The semi-digested feed moves from the duodenum into the jejunum, the major site of enzyme addition and digestive activity. Amylase and glucosidase enzymes attack starch and carbohydrates, whilst bile secretions emulsify fats, initiating their digestion by pancreatic lipase, and protease continue the breakdown of protein started in the gizzard. The duodenum contains densely packed villi, giving a highly absorptive surface that is very efficient for nutrient uptake across the gut wall into the blood supply. The duodenum is also the site where the acidified digesta is neutralised and stabilised to more neutral pH 6, ensuring optimal conditions for enzyme activity and reducing and damaging effects to unprotected tissue. Absorption efficiency slows as digesta moves into the ileum, where villi are less dense. At the end of the ileum, nutrients from a good quality diet will have been absorbed, leaving insoluble and fibrous compounds to pass to the lower gut for fermentation by beneficial bacteria, liberating vitamins and energy, before excretion. In poorly digested diets, nutrients will remain and be utilised by pathogenic bacteria.
At the end of the tract, caecal and colonic fermentation results in more energy in the form of volatile fatty acids (VFAs) being released, along with the generation of certain vitamins.
Development of intestinal microflora
The intestinal tract of a newly hatched chick is sterile, but starts to be colonised within a few hours of hatching. Complete colonisation of the intestine can take up to 6 weeks and is a fine balance between the all organisms present (Barnes et al., 1972), with initial ileal colonization including E. coli, Lactobacillus, Streptococcus and Enterococcus (Mead 2000). Colonisation of pig intestine occurs immediately after birth, led by coliforms, which are rapidly replaced with a complex mix of anaerobes (Van Kessel et al., 2004) The caeca is the main site of bacterial fermentation in monogastrics, as is the colon for nonavian species. Dominant bacteria in caeca are typically obligate anaerobes, reaching up to 1011 organisms/g of caecal content at 30 days of age in poultry (Barnes et al., 1972). Pig hindgut contains strict anaerobes, Lactobacilli, Enterobacteria and Streptococci (Simon et al.,2004).
One of the biggest problems in evaluating the composition of the microflora is the fact that 10-60% of bacterial species cannot be cultivated outside the intestine on conventional growth media. More recent advances in ribosomal RNA molecular techniques made it possible to detect a wide range of bacteria (Apajalahti 1999).
The microflora population depends very much on the balance between communities of organisms and the diet composition as the source of available substrates for micro-organisms. Despite this, it is possible to measure changes in bacterial products and numbers, e.g. Wagner and Thomas 1978, reported that the inclusion of rye significantly increased butyric acid concentration and gas production in the small intestine, most likely by a species of Clostridium.
It has been established (Sklan, 2004) that if the newly hatched chick has access to feed in the hatchery, its digestive development is greatly advanced. This leads to major benefits in caecal colonisation, enzyme secretion and nutrient uptake, culminating in improved growth by the end of the first week of life.
Within hours of hatching, enterocytes develop and elongate, increasing gut surface area, and villi crypts begin to form and cell count per crypt multiply, becoming well defined by 72 hours of age. Villi height increases two-fold in 48 h post-hatch, reaching a plateau at 6-8 days of age (duodenum) or 10 days (jejunum and ileum) in chicks. Total surface area increases in all gut areas until 72 h post-hatch.
There is increasing data showing that lack of access to feed post-hatch may retard the essential gut development vital for fuelling the growth required in the first weeks of age. Studies examining the effect of holding hatchlings without feed have shown that duodenal villus surface area is initially depressed in the absence of feed, recovering after 4 days, whereas in the jejunum villus surface area is still lower after 9 days. Chicks without access to feed show poor pancreatic secretion increases post-hatch. Rapid establishment of enzyme secretion is essential if the animal is to derive optimal nutrient uptake from feed, and also to control the flow of undigested material to the hindgut where it may act as a substrate for pathogenic bacteria.
Altering gut microflora
Supplementing feed with prophylactic antibiotics had the effect of reducing bacterial numbers in the digestive tract as a whole, which also limits the development of bacterial flora within the caeca. Research has shown that monogastric animals reared without antibiotic flora ('gnotobiotic') typically have up to 10% less energy from fermented VFAs than those raised with a normally developed flora. To establish a stable, complimentary microflora, bacterial populations must be primarily made up of beneficial or benign species, in suitable proportions, to promote optimal energy and vitamin production. This can be achieved by appropriate feed formulation in ingredients. This is particularly important after veterinary administration of therapeutic drugs to tackle disease situations, which can leave the animal without a stable microflora, and open to secondary infection.
Successful strategies to maintain cost effective poultry production include multiple components, if the balance between growth, gut health and bacterial resistance is to be maintained. The earlier an intervention/control program starts the better, since gut flora can be vertically transmitted (from parent to offspring). By preventing the establishment of unfavorable populations of organisms in the developing flora it is possible to eliminate the threat that such organisms pose during later periods of stress. The organisms derived from parent gut flora serve as the initial seed strain for the offspring normal flora and therefore, to a degree, determines the ability of the birds to resist colonization early on. Whether a producer is allowed or not to use antibiotics is becoming more irrelevant, as perceived antibiotic resistance increases, and more countries join the political ban on prophylactic feed supplementation.
Improved gut morphology (Dimitroglou and Davies, Univ. of Plymouth, UK)
Effect of Bio-Mos on gut morphology (UTAD 2003)
Apajalahti JHA (1999) World Poultry 15, 1-3.
Barnes EM, Mead GC, Barnum DA, Harry EG (1972) British Poultry Science 13, 311-26.
Mead GC (2000) In 'World Poultry Congress'. Montreal, Canada p. S3.5.02
Sklan, D (2004). In: Interfacing Immunity, Gut Health and Performance. Eds. L.A.Tucker &
J.A.Pickard. p. 9-33
Simon O, Vahjen W. and Taras, D. (2004) In: Interfacing Immunity, Gut Health and
Performance. Eds. L.A.Tucker & J.A.Pickard. p. 33-46
Van Kessel, A., Shirkey, T.W., Siggers, R.H., Drew, M.D. and Laarveld, B. (2004) in:
Interfacing Immunity, Gut Health and Performance. Eds. L.A.Tucker & J.A.Pickard. p. 47-59
Wagner DD, Thomas OP (1978) Poultry Science 57, 971-975
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