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Animal Health
Thursday, February 16, 2006 1:54:38 PM
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Elevating intestinal defense - the role of glycomics in maximising gut health

Peter Spring, Swiss College of Agriculture





Gut health remains a key contributor to maximal performance in young, growing animals. Studies in poultry, pigs and calves do show that during the first days, or months of life, diarrhoea is the most significant cause for disease and for effectuated treatments (Figure 1). The causative agents involve bacterial, viral and coccidial infections with E. coli and Clostrida being the predominant bacterial pathogens. In calves, digestive problems normally peak around 10 days of age. In piglets, particularly critical periods are observed between 5 and 14 days of life, during suckling, and then post weaning. With the global spread of Lawsonia intracellularis,infectious agents are challenging the pig producer throughout the production cycle of the growing and finishing pig. The immense economic losses due to intestinal diseases clearly justify strong measures to maximize gut health. Measures are also needed to guarantee the well being of the animals, and thus for the production of meat in accordance with animal right laws and modern consumer demands.



Prevention strategies for the neonate

Prevention strategies have to start before birth, as the neonate is at a particular risk to disease due to a lack of a complex micro flora and of a fully functioning immune system. Each production system must aim at a good quality day-old animal. It is important to regard the dam not only as a source for the genetic make up of the progeny and for its nutrition. The dam also provides the first passive immune protection and, in the case of the pig, through the fecal matter of the sow a major source of the bacterial make up that will colonize the progeny after birth. Good quality piglets should meet the following criteria:

    • Birth weight 90% > 1.2 kg
    • Maximum nutrient reserves
    • Short farrowing time to minimize stress
    • Stable body temperature to minimize losses of energy reserves
    • Quick initiation of suckling
    • Maximal and fast, high quality colostrum intake
    • Seeding of the GI microflora with little pathogens

Establishing the micro flora

Prevention strategies have to focus on minimizing contact of the animal with pathogens and on reducing pathogen multiplication within the digestive tract. Minimizing the contact with pathogens demands the development and enforcement of strict biosecurity systems. However, whatever measures are taken under commercial production conditions, contact with most common intestinal pathogens cannot be avoided. Minimizing pathogen multiplication in the animal must therefore be a key target in any nutrition and management program.


Two of the key allies in this process are the intestinal micro flora and the immune system of the animal. The micro flora offers a great deal of protection through competitive exclusion.



Collins and Carter (1978) did prove impressively the protective effect of a healthy gut micro flora (Figure 2). The LD 50 value for Salmonella enteritidis challenge went up from 5 to 5,000,000 germs due to the presence of the micro flora. At the time of hatch or birth, the digestive tract should be sterile, thus the micro flora is non-existent. Because invading pathogens can multiply quickly in a non-colonized gut, required infective doses are rather low during this life phase.


While a single salmonella organism can potentially colonize the gut of a newly hatched chick, the infective dose for an adult bird increases to 103 - 106 organisms, primarily because the adult bird has an established population of competing organisms referred to as "normal flora"  (Pivnick and Nurmi, 1982). The quick establishment of a normal flora can help in reducing the risk of early diarrhoea. The use of seeding cultures can help to speed up this process and lead to an early increase in gut protection.


Resistance to pathogen infection is clearly enhanced by dosing day-old chicks with flora from healthy adult birds provided adequate colonization occurs prior to pathogen challenge (Pivnick and Nurmi,1982; Fernandez et al., 2002). Competitive exclusion products are pathogen-free but yet undefined, meaning that not all bacterial species are well-characterized and minimal concentrations of individual species are not guaranteed. Many countries will just accept defined products for registration. Mathis and Hofacre (2000) have tested All-Lac XCL, a probiotic seeding culture in a Clostridium perfringens challenge trial. The culture was sprayed on the birds after hatching. The birds were later challenged with a high dose of C. perfringens leading to over 60 percent mortality due to Necrotic enteritis in the control grouped.


All-Lac XCL did cut mortality in half, thus offering a partial protection against the NE (Table 1).



Table 1. Effect of different feed additives on performance of broilers challenged with C.

perfringens (Mathis and Hofacre, 2000)

The piglet gut micro flora is strongly influenced by the micro flora of the sow, due to the consumption of considerable amounts of fecal material from the sow. Thus gut health of the sow is critical to a healthy piglet micro flora.


Minimising the immune gap

Initially the young animal is protected by immunoglobulins, which are transferred from the dam either through the egg, the placenta or the colostrum. As those antibodies will be diluted out within weeks and the development of the active immunity requires time, every young animal will face an "immune gap" with sub-optimal protection somewhere during the first weeks of life. This immune gap offers a window for pathogens to invade more easily (Figure 3). The immune gap cannot be avoided. However nutrition and management has to aim at keeping the window of risk as narrow as possible by maximizing uptake of passive immunity and favouring the build up of active immunity.

The pig placentation prevents the transplacental passage of immunoglobulins making the newborn piglet entirely dependent on antibodies in the colostrum.


Good colostrum quality, and early colostrum uptake are therefore essential for maximal protection of the day old piglet. The composition of the colostrum depends on many different factors. Some of the key factors involved are nutrition, genetics, body conditions, health status, immune status (e.g. vaccination) and age of the sow (Klobasa et al., 1987, King et al., 1993; Noblet und Etienne 1986; Jackson et al., 1995; Midgal 1991; Göransson 1990, Klaver et al., 1981).


As the gut is only capable, for a couple of hours after birth, to effectively take up Ig and because the colostrum quality drops quickly post partum, it is very important, that the piglet consumes sufficient and good quality colostrum as soon after birth as possible. Any means to enhance the Ig uptake can be very useful in enhancing disease resistance and with it, performance of the piglet. Different researchers investigated the effect of mannan oligosaccharide (Bio-Mos, Alltech Inc.) on colostral Ig concentrations in sows. Bio-Mos fed at 5 g/hd/d did enhance colostral Ig concentrations and with it, led to improved piglet weight gain and reduced pre-weaning mortality. (Table 2).



The exact mechanism of the improved performance seen in piglets nursing sows receiving Bio-Mos is not fully understood, but improved immune status of the piglets may provide an aid in performance by controlling sub-clinical problems. In addition Bio-Mos has been shown to reduce intestinal pathogen loads (Spring et al., 2000). Because the fecal matter of the sow is the primary inoculums to establish the micro flora in piglets, changes in the micro flora of the sow could also impact piglet performance.


Prevention strategies in the growing animal

While the micro flora is evolving towards a complex, mature system, the growing

animal is still at a particular risk to developing digestive upsets. The risk is increased by the immaturity of the immune system. The micro flora is much affected by the gut environment, the availability of fermentable nutrients, the presence of antimicrobial substances, the possibility to attach to the intestinal wall and by the immune protection (Figure 4). Those different control mechanisms have to be optimized in order to minimize the risk of intestinal disease.



In the past, much focus has been given to the use of antimicrobial substances. However, due to new market demands, regulatory rules and problems with resistance build up, any market will have to reduce its dependency on antimicrobial substances in the close future. This certainly will enhance the risk of intestinal infections. In order to avoid imbalances in the micro flora, other control mechanisms must be applied more stringently and more efficiently (Figure 5). Antibiotic growth promoters work primarily by reducing the microbial load in the intestine. In their absence, overall microbial growth must efficiently be controlled by limiting nutrient supply to the microbial population and by controlling the intestinal environment.


In addition, specific mechanisms should be applied to get more efficient control of pathogens. Mannan oligosaccharide has been shown both to control pathogen attachment and improve immune defense. By exploiting different control mechanisms as conventional tools they offer interesting additional value in nutritional programs.


Diet digestibility

Nutrient supply to the microbial population can best be limited by working with highly digestible diets. Diet digestibility can mainly be manipulated through three approaches:


1. Ingredient choice

2. Use of enzymes

3. Physical treatment (grinding, heat) of the diet.


Today the use of exogenous enzyme supplementation is almost standard in all pig and poultry feed. The efficacy of these enzymes to improve animal growth performance has been established in over 2500 publications (Rosen, 2003). Inclusion of xylanases and phytases significantly improves nutrient availability by depolymerising indigestible feed ingredients such as soluble NSP or phytate. As a result, nutrient digestibility by the host is significantly increased and bacterial population in the small intestine is reduced (Bedford, 2002).


Apajalahti, and Bedford (2000) suggested further that the depolymerisation of larger

arabinoxylans in wheat, with xylanase produced xylo-oligomers and xylose, could only be partially utilised by the microflora. Subsequently the total number of bacteria in the ileum was reduced by 60%. Enzymes can also help to reduce specific pathogens. Pluske (2001) showed that the incidence of Porcine intestinal spirochaetosis (PIS), swine dysentery (SD) and post weaning diarrhoea is closely related to the amount of indigestible starch and non-starch polysaccharides in the diet and the proliferation of pathogenic bacteria in the intestine.


Similarly, the use of poorly digestible protein sources alters the microflora and creates favourable condition in the intestine for the proliferation of pathogens. The microflora population depends very much on the balance between communities of organisms and the diet composition as the source of available substrates for microorganisms. The colonisation of potential pathogen is greatly reduced in animals fed highly digestible and a balanced diet according to their nutrient needs.



A second key approach to control overall bacterial growth is the control dietary buffering capacity by limiting phosphates and carbonates in the diet and by using organic acids. In order to limit phosphate levels, the use of microbial phytase has become standard in modern rations. Acids in form of Ca-salts allow to bring Ca into the diet while limiting carbonate addition. Acidification is a concept with is well proven, particularly in piglets after weaning when acidification capacity is still limited (Cranwell and Moughan, 1989) and the micro flora is undergoing profound changes to the abrupt change in diet. (Figure 6; Franklin et al., 2002; Mathew et al., 1996, Sileikiene et al., 2002).


Partanen und Mroz (Partanen and Mroz, 1999) have conducted a comprehensive Meta-Analyse on the effect of acids in piglet performance and concluded that acids do lead to a significant improvement in performance (Figure 7). However, as in any biological system, expected measured improvements in ADG were quite variable ranging from -58 g bis +106g).




Bio-Mos has been shown to have positive effects, not only in reproducing animals but also in young animals, due to its ability to block bacterial attachment and to strengthen the immune system, (Spring, 2003) Bio-Mos works with different mechanisms than conventional approaches to control intestinal pathogens and thus it can move existing prevention concepts to the next level. The relationship between the specific modes of action of MOS (Bio-Mos, Alltech Inc.) and the effects of animal growth performance and health under a range of conditions have been establish in numerous scientific publications. Hooge (2003) recently summarised over 45 broiler and turkey pen trials with Bio-Mos. The comparison trials were conducted around the globe under a variety of dietary and environmental conditions, with modern strains of broiler chickens (Arbor Acres, Avian, Cobb, Ross, Hybro) and market turkeys.


Final ages ranged from 25 to 49 days for broiler chickens and from 21 to 147 days for turkeys. In most cases, the experimental models included antibiotic control diets run side by side with negative control diets to compare each of these treatments with Bio-Mos -supplemented feeds. The pen trials were conducted on new litter, used litter, raised wire, or slatted floors. The levels of dietary Bio-Mos sometimes varied by trial and by feed phase, ranging from 0.05 to 0.40% (500 to 4,000 ppm). Body weight, feed conversion ratio, and mortality data were analyzed statistically as pairs of observations, using either negative control versus Bio-Mos or positive (antibiotic) control versus Bio-Mos treatments, by the Paired T-test.


In broilers, Bio-Mos led to significant improvements in weight gain, feed conversion and mortality compared to the negative control, (Table 3). When comparing performance with Bio-Mos to broilers fed diets containing AGPs, performance was similar, however, Bio-Mos-fed flocks showed lower mortality (Table 4). Current recommended optimal levels of Bio-Mos for broiler chicken feeds: 0.2%, 0 to 7 days; 0.1%, 7 to 21 days, and 0.05%, 21 to 42 days(or market).



Table 3. Effect of Bio-Mos on broiler performance and health compared to a negative control diet.


The meta-analysis of turkey data confirms the findings in broilers. Live performance results for antibiotic control and Bio-Mos diets were statistically similar (Table 5).



Prof. Jim Pettigrew and his group from the University of Illinois recently summarized the available literature on Bio-Mos and nursery pigs to date finding approximately 5% increase in ADG (Figure 8, Miquel et al., 2004).


This summary combines both research and field data with Bio-Mos inclusion levels between 1 to 4 kg/T. Based on his review, Prof. Pettigrew suggests a step-down program (3 kg/T in the pre-starter, 2 kg/T in the starter) to be the most cost-effective way to use Bio-Mos.



Figure 8. Effect of Bio-Mos on average daily gain in piglets (Miquel et al., 2004)



    • The beneficial micro flora and the immune system play key roles in controlling intestinal pathogens.
    • Prevention programs must start before birth aiming at maximizing the quality of the day old animal. Programs must focus on establishing a complex micro flora with a low pathogen load and on minimizing the immune gap.
    • As animal production will have to reduce its dependency on antibiotics, gut environment, availability of fermentable nutrients, control of bacterial and immune protection must be optimized.
    • Bio-Mos works through different mechanisms than conventional approaches thus offering an opportunity to move existing prevention concepts against intestinal pathogens to the next level.

Parameter Trial n P Age (days) AGP Bio-Mos Rel. Change (%)

Body weight, g 17 0.157 104.9 10.444 10.386 -0.56

FV 17 0.339 106.1 2.282 2.273 -0.39

Mortality, % 13 0.200 101.1 7.084 5.984 -15.5359Ko% Change in ADG


Figure 8. Effect of Bio-Mos on average daily gain in piglets (Miquel et al., 2004)



Collins, F. M., and P. B. Carter. 1978. Growth of salmonellae in orally infected germfree mice.

Infect. Immun. 21:41-47

Hofacre, C. L., T. Beacorn, S. Collett, and G. Mathis. 2003Using Competitive exclusion,

mannan-oligosaccharide and other intestinal products to control necrotic enteritis. J. Appl.

Poult. Res. 12:60-64'

Apajalahti, J., and Bedford, M. 2000. in World Poultry Congress, Vol. 21, pp. S3.5.03, WPSA,



Barac, I., D. Milic, T. Parker and N. Fuchs. 2002. Ucinak manan oligosacharida u prehrani

kamace na odlike prasadi. National feed conference. Opatia Cr, June 20-22.

Bedford, M. R. 2000. Animal Feed Science and Technology 86, 1-13.


Cranwell, P. D., and R. J. Moughan. 1989. Biological limitations imposed by the digestive

system to the growth performance of weaned pigs. In: Manipulation pig production, Werribee,

Australia. p 140-165


Fernandez, F., M. Hinton. B. van Gils. 2002. Dietary mannan oligosaccharide and their effect

on chicken caecal microflora in relation to Salmonella enteritidis colonization. Avian Pathol.



Franklin, A., A. G. Mathew, R. J. Vickers, and R. A. Clift. 2002. Characterization of microbial

populations and volatile fatty acid concentrations in the jejunum, ileum, and cecum of pigs

weaned at 17 vs 24 days of age. Journal of Animal Science 80: 2904-2910.


Göransson L., 1990. The effect of late pregnancy feed allowance on the composition of the

sow's colostrum and milk (sic). Acta Vet. Scand. 31:109-115


Hooge, D. 2004a. Meta-Analysis of Broiler Chicken Pen Trials Evaluating

Dietary Mannan Oligosaccharide, 1993-2003 Int. J. Poult. Sci. 3: 163-174.

Hooge, D. 2004b. Meta-Analysis of Turkey Pen Trials Evaluating Dietary Mannan

Oligosaccharide, 1993-2003. Int. J. Poult. Sci. 3: 179-188.


Jackson J.R., Hurley W.L., Easter R.A., Jensen A.H., Odle J., 1995. Effects of induced or

delayed parturition and supplemental dietary fat on colostrum and milk composition in sows.

J. Anim. Sci. 73:1906-1913


King R.H., Toner M.S., Dove H., Atwood C.S., Brown W.G., 1993. The response of first litter

sows to dietary protein level during lactation. J. Anim. Sci. 71:2457-2463


Klaver J., van Kempen G.J.M., de Lange P.G.B., Verstegen M.W.A., Boer H., 1981. Milk

composition and daily yield of different milk components as affected by sow condition and

lactation/feeding regimen. J.Anim. Sci. 52:1091-1097


Klobasa F., Werhan E., Butler J.E., 1987. Composition of sow milk during lactation. J. Anim.

Sci. 64:1458-1466


Mathew, A. G., M. A. Franklin, W. G. Upchurch, and S. E. Chattin. 1996. Effect of weaning

on ileal short-chain fatty acid concentrations in pigs. Nutrition Research 16: 1689-1698.

Maxwell, C. V., K. Ferrell, R. A. Dvorak, Z. B. Johnson, and M. E. Davis. 2003. Efficacy of

mannan oligosaccharide supplementation through late gestation and lactation on sow and

litter performance. J. Anim. Sci. 81 (Suppl. 2):69.


Mendal, P. 2004. Efficacy of addition of mannan-oligosaccharides (Bio-Mos) in sow and in

piglet diets. Final report: Trial code sows 2003. Imasde Agropecuaria, S.L., 28050 Madrid,

Spain (publication in preparation).


Midgal W., 1991. Chemical composition of colostrum and milk in sows fed diets

supplemented with animal fat. Wrld Rev. Anim. Prod. 26:11-15

Miguel, J. C., S. L. Rodriguez-Zas, and J. E. Pettigrew. 2004. Efficacy of a mannan

oligosaccharide (bio-mos) for improving nursery pig performance. Journal of Swine Health

Production 12: 296-307.Newman, K.E. 2001. Effect of mannan oligosaccharide on the

microflora and immunoglobulin status of sows and piglet performance. J. Anim. Sci.

79(Suppl. 1):189.


Noblet J., Etienne M., 1986. Effect of energy level in lactating sows on yield and composition

of milk and nutrient balance of piglets. J. Anim. Sci. 63:1888-1896

O'Quinn, P.R., D.W. Funderbunke and G.W. Tibbetts. 2001. Effect of dietary supplementation

of mannan oligosaccharide on sow and litter performance in a commercial production system.

J. Anim. Sci. 79(Suppl. 1):212.


Pivnick H. and E. Nurmi. 1982. The Nurmi concenpt and its role in the control of salmonella

in poultry. In R Davies (ed). Development in food microbiology. Essex, England. Applied

Science Publishers Ltd. 41-70.


Pluske, J. 2001. in Recent Advances in Animal Nutrition in Australia (Corbett, J. J., Ed.), Vol.

13, pp. 127-134, Animal Science, University of New England, Armidale.

Rosen, G. D. 2003. in 30th Annual Carolina Poultry Nutrition Conference, pp. 69-79.,

Carolina Feed Industry Association, Research Triangle Park, US.


Sileikiene, V. et al. 2002. Entwicklung der Duenndarmfunktion beim Ferkel waehrend der

Umstellung von der fluessigen and die feste Nahrungsform. Veterinarija ir Zootechnika 42:



Sileikiene, V. et al. 2002. Entwicklung der Duenndarmfunktion beim Ferkel waehrend der

Umstellung von der fluessigen and die feste Nahrungsform. Veterinarija ir Zootechnika 42:



Spring, P. (2003). "Intestinal Microflora and the Possibility to influence it with mannan

oligosaccharide." Praxis Veterinaria 51(1-2): 25-35.


Spring, P. e P. Geliot. 2003. Effetto di diete contenenti mannanoligosaccaridi sulle prestazioni

delle scrofe. Meeting Annuale della SIPAS, Salsomaggiore, It. March 27th and 28th.


Spring, P., C. Wenk, K.A. Dawson and K.E. Newman. 2000. The effects of dietary

mannanoligosaccharides on cecal parameters and the concentrations of enteric bacteria in the

ceca of salmonella-challenged broiler chicks. Poultry Sci. 79:205-211.

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