The biggest challenges facing the poultry industry today include disease prevention, particularly in the absence of antibiotics, and optimum nutrition, especially with regards to being able to incorporate novel/local ingredients into the diet. Interestingly these two are linked as much of the disease pressure that challenges current poultry production is enteric in its nature. Since the presence or absence of specific nutrients/antinutrients in the diet will influence the structure of the microbiome, it is clear that the diet has a role to play in the susceptibility of the animal to enteric and perhaps even systemic disease.
Feed enzymes play a role in moderating nutrient flow to the lower intestine by two mechanisms. The first is that they simply improve the digestibility of nutrients at the ileal level and as a result, there is less substrate remaining for the microbiota resident in the large intestine. A well-digested diet restricts nutrient supply to the large intestine which generally is considered beneficial if the goal is to minimise the risk of rapid increases in microbial populations. This is particularly true with regards to minimising the flow of undigested nitrogen into the large intestine as this not only provides the nutrients needed for many potential pathogens, but putrefaction of protein also yields undesirable amines, indoles, skatole and many other products which are damaging to the structure of the intestine. Thus the use of enzymes which improve the digestibility of amino acids should play a key role in the future nutrition of poultry. It is important to note, however, that the value of such products is maximised only when the matrices for each amino acid is employed and thus the total protein content of the diet reduced. In this way, performance of the animal is maintained, ie the digestible amino acid content of the diet is maintained, but with a diet which is lower in protein. By definition, such a strategy will reduce the flow of nitrogen into the large intestine and thus reduce the risk of a putrefactive fermentation. Almost all feed enzyme in use today, phytases, NSPases and proteases, can play a role in this regard, with phytases probably being the most under-utilised in terms of application of the benefits they bring in dietary formulations.
The second mechanism relates to the first but is likely specific to NSP’ases. Most species of bacteria that can putrefy proteins can ferment carbohydrates, and if both are available the preference is for the latter. If there are equal quantities of both, then the fermentable carbohydrate will quickly be consumed such that in the more distal regions of the intestine there will be proportionately more fermentable proteins. NSP’ases produce soluble fragments or oligo-saccharides from their action on cereal and oilseed meal cell wall material which are prebiotic in their nature. This means they are fermentable by the intestinal microbiota but neither digestible nor absorbed by the host animal. Since NSP’ases continue to work on the cell wall material in the digesta with passage through the small intestine, they continuously produce fermentable carbohydrates which replenish that consumed and ideally maintains an optimal fermentable carbohydrate: protein ratio. In this role, it is important that the NSP’ase is dosed sufficiently such that the optimum rate of oligomer production is achieved. Excessive dosage may be detrimental with some NSP’ases. Some enzymes may “over-process” the oligomers to simple sugars which are absorbed by the animal and are often excreted in the urine, causing litter moisture problems. Thus correct dosage is essential if such benefits are to be realised. In most commercial situations the recognition of the importance of correct dosage for phytases is real and apparent, whereas with NSP’ases, checking in feed activity regularly is not considered important. As we move forward into an era with fewer and fewer anti-microbial products, such a view will have to change.
Feed enzymes are by no means a panacea, but they should play a role in future antibiotic-free programmes along with other nutritional and managerial interventions.
Presented at the XXV Latin American Poultry Congress in Guadalajara, Mexico.
Hello, just was drawn to the discussion that I found has been interesting.
Indeed enzymes are working nearly immediately on a substrate that is constantly consumed by the animal, thus creating a prebiotic effect as an steady stage condition manner. In the case of wheat-based diets using the right enzyme will deliver not only the reduction of gut viscosity but also the continuous manufacturing of VFA linked to changes in microbiota population. What everyone is looking for extra butyrate production which has shown to be very beneficial in poultry production. Also with the right enzyme or combination of enzymes, similar effect can be obtained in corn-based diets.
Dear Jo, please keep in mind that feed enzymes are working immediately, very quickly. However, probiotics need some time to reach the necessary cell count. That's why it is necessary to wait some time to probiotic effect will be paralelly realized. Or synergic effect, I absolutely agree with Dr.Henk's opinion.
Hello Jo,
It is well documented that with wheat or barley diets our NSP-degrading enzymes reduce the gut viscosity to a level observed with non-viscous corn-based diets. When only tackling viscosity, there is no need for combinations with other products.
Viscosity is however not the only parameter that influences the microbial balance; also in corn diets, gut health and microbial balance remain issues to consider. In the animal gut, enzymes produce prebiotic substances in situ; thus enzymes are part of the solution. However, in line with the complexity of the microflora, combinations of products will result in a more consistent and higher level of performance.
Hello,
Fermentation and VFA production in the small intestine should be reduced because of competition with the host animal, while the same processes are welcome in the large intestine. Surely this aspect is a primary benefit in both poultry and swine as also starch and protein are lost for the host animal during small intestinal fermentation. Compared to poultry, pigs are indeed somewhat better utilizing VFA’s as a source of energy from large intestinal fermentation of fibrous material, but this aspect is of secondary importance compared to reducing small intestinal fermentation.
Before NSP degrading enzymes were available, viscosity inducing cereals such as wheat and barley simply were prohibited in broiler diets because of their disastrous impact, while such cereals were indeed more acceptable in pig diets. Viscosity reduction by NSP degrading enzymes shifts fermentation processes from small intestine to large intestine. The viscosity aspect remains a key issue on which Mike Bedford a.o. has performed groundbreaking work that remains highly appreciated (e.g.: Choct et al., 1996, British Poultry Science, 37: 609-621); in line with your comment, such literature indeed highlights a huge negative impact of small intestinal microflora on ME values. However, once the primary viscosity issue is remedied by the NSP-degrading enzymes, a further finetuning of the enzymes’ impact is in balancing the microflora by in vivo production of prebiotics. Such finetuning is the focus of the above communication.
So, while there are some species differences, the general concepts remain valid for all monogastric animals.
This is a very interesting discussion that really starts dealing with fundamental issues. Far too long, we have neglected the interaction between exogenous enzymes and microflora. So, thanks for this initiative.
Please allow me to add a few cents to the topic. Shouldn’t we make a distinction between nutrients that are beneficial to the host animal versus those that aren’t? • Glucose is a very good source of energy for the animal. Full hydrolysis of ß-glucans at an early stage in the small intestine should result in more glucose for the animal, thus reducing competition between animal and microflora for such glucose. • Galactose: upon absorption, animals readily transform galactose into glucose. What’s more: galactose and glucose are during lactation combined into a disaccharide called lactose. Similarly to ß-glucans, when hydrolyzing the Raffinose oligosaccharides in the proximal intestine, this results in more galactose and sucrose made available as an energy source for the animal, while simultaneously reducing microbial growth in the small intestine. • Mannose: is also metabolized within animal tissues, albeit somewhat less efficient compared to galactose. • Xylose: represents a huge contrast compared to the above-mentioned monosaccharides. Absorption from the gut is highly variable, while the fraction that is absorbed is excreted in unchanged form into the urine. Vertebrates don’t seem to be able to metabolize xylose.
Several studies show that xylose supplementation as such is counterproductive and leads to wet litter due to urinary secretion of xylose. The early days of xylanase supplementation also showed that we can overdose xylanase in animal feed (in contrast to current practices of phytase Superdosing). Is it a valid conclusion that xylanase dosing should be in line with what the microflora is able to consume? Are xylanases producing prebiotics within the animal gut, thus establishing a microflora population that transforms xylose-polymers into VFA’s which are more beneficial for the animal compared to the original xylose-chains? In other words: should xylan hydrolysis in the small intestine keep pace with microbial growth in order to avoid the negative impact of xylose absorption?
Mike, your comments would be appreciated. Anyhow, thanks again for this initiative.
Interesting. It seems perfectly logical to me that if you change the substrate flow into the caudal gut (by increasing the rate of digestion of e.g. starch and protein or altering the solubility or tertiary structure of NSP) the microbiome will rapidly adapt to this new ecology and reorient itself accordingly. However, I find it a little difficult to accept that the major mechanism of a xylanase on this 'microbiome axis' is to generate only minor quantities of short-chain xylo-oligomers which in turn signal the microbiome to generate their own xylanases (and equivalent) and degrade polymers directly. The reason for my slight hesitation there is that NSP polymers almost certainly will not enter the caecum and so must be degraded and solubilized in the small intestine. I wonder how likely it is that the ileal microbiome would have the time (not to mention the inclination!) to adequately degrade polymeric arabinoxylan using only their own digestive architecture? Caecal - perhaps... I guess it is possible and, as I say, it is very logical that changing the substrate flow into the hind gut will cause adaptation in the microbiome and that this, in turn, will influence product generation, pH, temperature etc. I just wonder how much xylo-oligomer generation (and subsequent fermentation) the resident microbiome would be really capable of vs. exogenous xylanase activity? Interesting.
Hi Rafael Yes, exactly. I suspect we are simply releasing oligosaccharides in such quantities that they cannot be quantitatively fermented to produce the increments in VFAs we see in the caeca, rather they act as a signal to the caecal microbiome to start producing their own xylanases/cellulases to digest the xylan fibre more effectively. Have a look at our abstract in this year's PSA meeting (Bedford and Apajalahti) where we show that the caecal microbiome from a xylanase fed broiler is far more capable of digesting wheat bran fibre, XOS and even xylose than the microbiome isolated from birds that have never been exposed to a xylanase. Regards Mike
Hi Rafael Great to hear from you and yes it is a long time!. You make an interesting point. Quantitatively the most untapped but potentially fermentable fibre source in the maturing bird (>14d of age) is xylan and to a lesser extent glucan. I used to think that the enzymes we were feeding quantitatively produced the prebiotics which were fermented in the caeca to offset the protein as discussed. But now I think from recent work we have been involved in that the NSPases we feed are releasing only minor amounts of oligosaccharides which are effectively signaling the microbiome to more aggressively directly attack the undigested fibre which is the polymer of the oligomeric signals we send. There are a few papers in process now (See Ribeiro et al in this months PSA) which allude to this effect. I also sort of cover it in BPS paper https://doi.org/10.1080/00071668.2018.1484074. So in short I would consider using an NSPase which directs the microbiome to attack the fibre fraction which forms the greatest fraction of the untapped potentially fermented fibre - to my mind this is mostly xylan but would be interested in comments!
