Prebiotics optimize poultry gut health

Prebiotics optimize poultry gut health

Feeding prebiotics to poultry supports nutrient utilization, maintains digestive function and enzyme activity, controls inflammation and reduces the gap between ideal and actual performance.

By ALEXIS KIERS*

*Dr. Alexis Kiers operates Kiers Consulting in Washington, D.C.

INCREASING restrictions on the use of antibiotics either as antibiotic growth promoters (AGPs) or as therapeutics are stressing that intestinal health may become the most important limitation to improving broiler productivity.

Legal restrictions are now in place in more than 40 countries and are expected in the U.S. in 2016, with China expected to follow shortly afterwards. On a more positive note, these restrictions, especially in the European Union, stimulated the search for alternative feed supplements to AGPs that provide similar performance improvements for the poultry industry, as well as other animal protein industries.

One of these compounds, the mannan-rich fraction of carbohydrate (MRF), has been the focus of considerable research during the past few years. Its beneficial effect on feed efficiency has been elucidated using both traditional and new techniques such as nutrigenomics.

 

What is MRF?

MRF belongs to the family of prebiotics. A prebiotic is defined as "a non-digestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon, thus improving host health" (Gibson and Roberfroid, 1995).

This definition has been somewhat expanded upon to include non-digestible functional carbohydrates that affect the gut ecophysiology through pathogen adsorption or immune modulation ("immunosaccharides").

In a previous article (Feedstuffs, Dec. 30, 2013), I evaluated new data that had become available on a second-generation, purified and more bioactive fraction of mannan sugars derived from a selected strain of Saccharomyces cerevisiae yeast using a proprietary process developed by Alltech. This natural MRF supports nutrient utilization, maintains digestive function and enzyme activity, controls inflammation and reduces the gap between ideal and actual performance (Hooge, 2013; Xiao et al., 2010).

These mechanisms have been confirmed using nutrigenomic data. Analyzing the nutrigenomic data led to a more concentrated bioactive feed additive that may be included in diets at lower inclusion rates for improved zootechnical performance observed under challenging field conditions.

The MRF (Actigen) has competitive advantages over traditional prebiotics in that it is traceable using a quantitative test to detect MRF in complete feed and that its consistency can be certified using a quick test to assess the activity of MRF. These provide unique assets — given the increasing requirements by the livestock industry for traceability and consistent product activity — over many compounds being offered as alternatives to AGPs.

 

General strategies

Effective use of feed additives to manage gut health is dependent upon understanding, to some degree, their mechanisms of action. Clearly, the modes of action of AGPs and their alternatives can differ considerably.

Low-level antibiotics work, in part, by decreasing the microbial load in the gut, resulting in a reduction in the energy and protein required to maintain and nourish the intestinal tissues.

Because the energy required to maintain the gut accounts for about 25% of the total basal metabolic needs of an animal (Croom et al., 2000), any reduction in gut tissue mass can have a significant impact on the amount of energy available for growth and caloric conversion efficiency.

The reduced microbial load in the gut by subtherapeutic levels of antibiotics also reduces immunological stress, resulting in more nutrients partitioned toward growth and production rather than toward mechanisms of disease resistance.

In contrast, most alternative compounds do not reduce overall microbial loads in the gut and, thus, will not promote growth by a mechanism similar to antibiotics. Instead, they alter the gut microflora profile by limiting the colonization of unfavorable bacteria while promoting the growth of more favorable species.

Consequently, alternatives to antibiotics promote gut health by several mechanisms, including altering the gut pH, maintaining protective gut mucins, selecting for beneficial intestinal organisms against pathogens, enhancing fermentation acids, enhancing nutrient uptake and increasing the humoral immune response. Strategic use of these alternative compounds will help optimize growth, provided that they are used in a manner that complements their modes of action.

 

Postprandial inflammation

Each meal leads to low-grade postprandial inflammation response in the small intestines (Figure 1), the magnitude of which is related to the caloric value, the glycemic index and specific components. If not properly regulated, postprandial inflammation could lead to unwanted consequences such as muscle catabolism, inappetite and predisposition to infections (Niewold, 2014).

One theory suggests that the growth promotion effect of subtherapeutic doses of antibiotics in poultry diets reduces the enteric microbial load, which consequently lowers the adverse effects of immunological stress by the bacteria and diminishes the level of inflammation in the intestine, which then increases energy efficiency and spares energy for growth and production (Niewold, 2007). It has been suggested that long-term activation of the innate immune system could lead to alterations in nutrient metabolism, therefore, by suppressing this pathway.

Bacitracin methylene disalicylate (BMD) could improve metabolism, leading to improved growth (Wolowczuk et al., 2008). Overstimulation of the host immune system by the resident microflora could impair the optimum growth and performance of the bird (Cook, 2000; Klasing, 1988).

In a recent study by Brennan et al. (2013), gene expression profiles from birds supplemented with BMD or MRF indicated similar down-regulation in the ubiquitination pathway. This specific pathway plays a major role in degradation of short-lived or regulatory proteins involved in different cellular processes, including antigen processing (Michalek et al., 1993) and mediation of the inflammatory response (Palombella et al., 1994). Therefore, this suggests that both BMD and MRF potentially decrease postprandial inflammation in the intestines.

Munyaka et al. (2012) similarly showed that MRF down-regulated expression of genes in the ileum and cecal tonsils, suggesting anti-inflammatory responses in broiler chickens. Lowering immunological stress seems to be one of the ways MRF improves feed efficiency in broiler chickens.

 

Gut morphology

Subtherapeutic levels of antibiotics in the diet have been shown to reduce the weight and length of the intestines (Viveros et al., 2011; Postma et al., 1999). A thinner intestinal epithelium in antibiotic-fed animals may enhance nutrient absorption (Miles et al., 2006; Visek et al., 1978) and reduce the metabolic demands of the gastrointestinal system.

Many publications reported that the dietary addition of mannan oligosaccharide (MOS) products improves gut health by increasing villi height (Baurhoo et al., 2007; Awad et al., 2009; Baurhoo et al., 2009). The change in gut morphology is thought to enhance the efficiency of digestion and absorption because a shortening of the villi height is believed to lead to decreased nutrient absorption and decreased performance (Xu et al., 2003).

Results from Brennan et al. (2013) showed that genes categorized by biological functions associated with protein synthesis, protein metabolism and cellular assembly and organization were down-regulated by MRF supplementation. These processes are required for cell growth and proliferation, and considering that the jejunum tissues were collected from birds with developed digestive tracts, this down-regulation may indicate that the intestinal cell turnover rate is slowed with MRF and, thus, potentially spares energy for growth and performance.

A study by Swick et al. (2013) investigated the efficacy of MRF as a replacement for zinc bacitracin and salinomycin using the necrotic enteritis challenge feeding study model. Additives did not completely protect birds from necrotic enteritis or coccidiosis lesions; however, MRF was as effective as zinc bacitracin and salinomycin in preventing a performance decline from the necrotic enteritis challenge.

The pattern of lesion scores was in line with the mode of action: zinc bacitracin being effective against the Gram-positive clostridia, salinomycin being specific against eimeria and MRF appearing to provide intestinal protection through alterations in goblet cells, mucin dynamics and gut integrity (Figure 2).

Mucins and glycoproteins associated with the intestinal brush border serve as a very important barrier and protect the delicate absorptive surface from the abrasive action of feedstuffs, bacterial colonization and toxins.

Mucin, which is produced by goblet cells, is secreted in response to the degree of insult on the absorptive surface of the gut. Dietary factors that result in increased mucus secretion may indirectly enhance an animal's ability to resist pathogen colonization. There is a complex balance between the gut ecosystem and intestinal mucins, and this balance can be altered by enteric health conditions and the diet.

Brennan et al. (2013) also showed that microarray results indicated that MRF increased the expression of MUC2, an important component of the protective mucosal barrier in the jejunum.

Another study (Mathis, 2014) assessed the feeding of MRF, BMD and NAT (a product containing a blend of organic minerals, plant extracts and yeast-derived MOS) on performance and reduction in necrotic enteritis of broilers subjected to a Clostridium perfringens challenge during a 42-day floor pen trial run on built-up litter.

All feed additives reduced the clinical effects of the C. perfringens challenge by significantly lowering necrotic enteritis mortality (MRF by 12%, NAT by 8% and BMD by 6%). Both the weight gain and feed conversion ratio performances on days 20, 35 and 42 for all birds given feed additives were significantly improved compared to the negative control treatment (Figure 3).

 

Conclusion

In response to consumer demands and government regulations, today's intensive animal agriculture industry must adapt to producing animals in a world without AGPs. The key to selecting the most cost-effective approach will depend on the production requirements of each company and the type of production challenges it faces.

Gene expression studies have given strong hints that MRF lowers the postprandial inflammation stress that increases energy preservation. This energy preservation translates into better feed efficiency and a growth promotion effect (Tables 1 and 2).

By providing protection of gut morphology through alterations in goblet cells, mucin dynamics and gut integrity, MRF enhances the efficiency of digestion and absorption during enteritis challenges. MRF has shown promise as a potential viable alternative to in-feed antimicrobials for the prevention of necrotic enteritis.

A more definitive understanding of the importance of dietary intervention in nutritional strategies for disease resistance and production efficiency will be gained by focusing on gene expression and functional genomics.

 

References

Awad, W.A., K. Ghareeb, S. Abdel-Raheem and J. Bohm. 2009. Effects of dietary inclusion of probiotic and synbiotic on growth performance, organ weights and intestinal histomorphology of broiler chickens. Poult. Sci. 88:49-56.

Baurhoo, B., P.R. Ferket and X. Zhao. 2009. Effects of diets containing different concentrations of mannan oligosaccharide or antibiotics on growth performance, intestinal development, cecal and litter microbial populations and carcass parameters of broilers. Poult. Sci. 88:2262-2272.

Baurhoo, B., L. Phillip and C.A. Ruiz-Feria. 2007. Effects of purified lignin and mannan oligosaccharides on intestinal integrity and microbial populations in the ceca and litter of broiler chickens. Poult. Sci. 86:1070-1078.

Brennan, K.M., D.E. Graugnard, R. Xiao, M.L. Spry, J.L. Pierce, B. Lumpkins and G.F. Mathis. 2013. Comparison of gene expression profiles of the jejunum of broilers supplemented with a yeast cell wall-derived mannan oligosaccharide versus bacitractin methylene disalicylate. Br. Poult. Sci. 54(2):238-246.

Cook, M.E. 2000. Interplay of management, microbes, genetics, immunity affects animal growth, development. Feedstuffs, Jan. 3. p. 11-12.

Croom, J., F.W. Edens and P.R. Ferket. 2000. The impact of nutrient digestion and absorption on poultry performance and health. Proceedings of the 27th annual Carolina Poultry Nutr. Conf. Carolina Feed Industry Assn., Research Triangle Park, Nov. 16. p. 65-73.

Gibson, G.R., and M.B. Roberfroid. 1995. Dietary modulation of the human colonic microbiota: Introducing the concept of prebiotics. J. Nutr. 125:1401-1412.

Hooge, D.M., A. Kiers and A. Connolly. 2013. Meta-analysis summary of broiler chicken trials with dietary Actigen (2009-2012). Intl. J. Poult. Sci. 12(1):1-8.

Klasing, K.C. 1988. Nutritional aspects of leukocytic cytokines. J. Nutr. 118:1436-1446.

Mathis, G., B. Lumpkins, T. Sefton and W.D. King. 2014. Actigen, Natustat or BMD administered in the feed for the reduction of necrotic enteritis caused by Clostridium perfringens in broiler chickens. Intl. Poult. Sci. Forum, Atlanta, Ga. Poster P27.

Michalek, M.T., E.P. Grant, C. Gramm, A.L. Goldberg and K.L. Rock. 1993. A role for the ubiquitin-dependent proteolytic pathway in MHC class I-restricted antigen presentation. Nature. 363:552-554.

Miles, R.D., G.D. Butcher, P.R. Henry and R.C. Littell 2006. Effect of antibiotic growth promoters on broiler performance, intestinal growth parameters and quantitative morphology. Poult. Sci. 85(3):476-485.

Munyaka, P.M., H. Echeverry, A. Yitbarek, G. Camelo-Jaimes, S. Sharif, W. Guenter, J.D. House and J.C. Rodriguez-Lecompte. 2012. Local and systemic innate immunity in broiler chickens supplemented with yeast-derived carbohydrates. Poult. Sci. 91:2164-2172.

Niewold, T.A. 2007. The non-antibiotic anti-inflammatory effect of antimicrobial growth promoters, the real mode of action? A hypothesis. Poult. Sci. 86:605-609.

Niewold, T.A. 2014. Gut health, intestinal immunity and performance. Proceedings of the Australian Poultry Sci. Symp. p. 73-77.

Palombella, V.J., O.J. Rando, A.L. Goldberg and T. Maniatis. 1994. The ubiquitin-proteasome pathway is required for processing the NF-kappa B1 precursor protein and the activation of NF-kappa B. Cell. 78:773-785.

Postma, J., P.R. Ferket, W.J. Croom and R.P. Kwakkel. 1999. Effect of virginiamycin on intestinal characteristics of turkeys. In: R.P. Kwakkel and J.P.M. Bos (eds.). Proceedings of the 12th European Symp. on Poultry Nutr. World's Poultry Science Assn., Dutch branch. Het Spelderholt, Beekbergen, Netherlands. p. 188.

Swick, R., S. M'Sadeq and A. Kocher. 2013. Use of Actigen as a tool to reduce the impact of necrotic enteritis in broilers. Intl. Poult. Sci. Forum, Atlanta, Ga.

Visek, W.J. 1978. The mode of growth promotion by antibiotics. J. Anim. Sci. 46:1447-1469.

Viveros, A., S. Chamorro, M. Pizarro, I. Arija, C. Centeno and A. Brenes. 2011. Effects of dietary polyphenol-rich grape products on intestinal microflora and gut morphology in broiler chicks. Poult. Sci. 90(3):566-578.

Wolowczuk, I., C. Verwaerde, O. Viltart, A. Delanoye, M. Delacre, B. Pot and C. Grangette. 2008. Feeding our immune system: Impact on metabolism. Clinical & Developmental Immunology. 639803.

Xiao, R., R.F. Power, D. Mallonee, C. Crowdus, T. Ao, J.L. Pierce and K.A. Dawson. 2010. Transcriptional signatures associated with biological functions of Bio-Mos and Actigen in broilers. Intl. Poult. Sci. Forum, Atlanta, Ga. Poster.

Xiao, R., R.F. Power, D. Mallonee, L. Spangler, K. Routt, K.M. Brennan, J.L. Pierce and K.A. Dawson. 2011. Gene expression study reveals the association of dietary supplementation of Actigen and the regulation of pathogen-influenced signaling pathways in broiler chickens. Poultry Science Assn. 100th Annual Meeting, St. Louis, Mo. Poster.

Xu, Z.R., C.H. Hu, M.S. Xia, X.A. Zhan and M.Q. Wang. 2003. Effects of dietary fructooligosaccharide on digestive enzyme activities, intestinal microflora and morphology of male broilers. Poult. Sci. 82:1030-1036.

Prebiotics optimize poultry gut health

 

1. Summary of live performance results from broiler chicken trials with AGP-supplemented positive control versus MRF-supplemented diets

Age,

MRF,

-Bodyweight, kg-

-FCR or F/G ratio-

-Mortality, %-

 

days1

g/mt2

AGP

MRF

AGP

MRF

AGP

MRF

Reference

42

400/2003

1.831

2.037

1.840

1.840

21.0

16.3

Hitech Hatch (2009)

42

800/400/200

2.530

2.501

1.843

1.852

4.17

4.46

Mathis (2009)

35

400/2004

1.652

1.636

1.502

1.513

4.87

4.95

Philippines (2009)

42

400

2.551

2.516

1.690

1.660

9.70

12.5

Kill et al. (2010)

42

400/200

2.551

2.552

1.690

1.660

9.70

11.5

Kill et al. (2010)

42

200

2.551

2.441

1.690

1.700

9.70

17.4

Kill et al. (2010)

38

882/441/2205

1.857

1.955

1.681

1.680

2.92

3.01

U.S. Integrator (2010)

42

400

2.468

2.478

1.750

1.750

6.95

4.07

Gernat (2011)

42

400/200

2.468

2.468

1.750

1.750

6.95

5.99

Gernat (2011)

42

200

2.468

2.451

1.750

1.770

6.95

4.46

Gernat (2011)

42

800/400/2006

2.124

2.134

1.803

1.784

3.85

4.77

Mathis (2011a)

52

400

2.900

2.865

1.807

1.820

4.00

3.80

Mathis (2011b)

42

800/400/200

3.430

3.437

1.720

1.708

6.39

3.89

Munyaka et al. (2011)

61

400/2007

4.300

4.377

1.980

2.004

2.33

2.39

N.C. A&T Res. (2011)

40.5

800/400/2008

2.939

2.758

1.869

1.791

6.15

2.85

Baynton (2012)

42

400

2.406

2.346

1.730

1.720

5.30

3.79

Guo et al. (2012)

42

800/400/2009

2.406

2.264

1.730

1.760

5.30

3.79

Guo et al. (2012)

52

800/2006

2.976

2.992

1.805

1.772

0.83

1.04

Mathis (2012)

35

800/400/20010

2.597

2.699

1.413

1.481

3.30

8.30

Swick et al. (2012)

37

800/400/20011

2.502

2.486

1.566

1.614

2.23

2.27

Chrystal & Owens (2012)

Comparisons (n)

 

20

20

20

20

20

20

 

Mean

 

2.575

2.570

1.731

1.731

6.13

6.08

 

P-value

 

0.771

0.889

0.935

 

 

 

 

Difference

 

-0.005

0

-0.05

 

 

 

 

Difference from AGP, %

-0.19

0

-0.82

 

 

 

 

 

1Average age was 42.73 days (number = 20).

2MRF in starter 0-21 days, grower 21-35 days and finisher 35-42 days, unless otherwise stated.

3MRF in starter and grower 0-24 days and finisher 24-42 days.

4MRF in starter 0-21 days and grower and finisher 21-35 days.

5MRF in starter 0-15 days, grower 15-28 days and finisher 28-38 days.

6MRF in starter 0-17 days, grower 7-31 days and finisher 31-52 days.

7MRF in starter 0-18 days and grower and finisher 18-61 days.

8MRF in pre-starter from about 0 to 7-10 days, starter to day 18-19, grower to day 30, then finisher to 40-41 days.

9MRF in starter 0-7 days, grower 7-21 days and finisher 21-42 days.

10Feed phase ages not given; mortality % from 0-32 days.

11MRF in starter, grower and finisher 1 and 2 feeds (ages not given).

 

2. Antibiotic programs used in obtaining broiler trial results presented in Table 1

Reference (Year)

Antibiotic

Inclusion rate by days of age (feeding phases)

Hitech Hatch Fresh (2009)

BMD

0-42 days at 350 g/mt

Mathis (2009)

BMD

0-21 days at 50 g/ton, 21-42 days at 25 g/ton

Philippines Field Trial (2009)

Avilamycin

0-28 days (approved 2.5-15 g/mt in Australia, e.g.)

Kill et al. (2010)

Avilamycin

0-42 days at 100 g/mt

U.S. Integrator (2010)

BMD

0-28 days (dose not stated)

Gernat (2011)

Zinc bacitracin

0-42 days (dose not stated)

Mathis (2011)

BMD

0-21 days at 50 g/ton, 21-42 days at 25 g/ton

Mathis (2011a)

BMD/virginiamycin

0-31 days: BMD at 50 g/ton; 31-52 days, virginiamycin at 20 g/ton

Munyaka et al. (2011)

BMD

0-42 days at 100 g/ton

N.C. A&T Research (2011)

BMD/virginiamycin

0-18 days, BMD at 50 g/ton; 18-35 days, BMD at 25 g/ton; 35-61 days, virginiamycin at 10 g/ton

Baynton (2012)

BMD

0-18/19 days, BMD at 110 g/mt, then at 55 g/mt to 40-41 days

Chrystal and Owens (2012)

Zinc bacitracin

0-35 days (adjusted to 37 days) at 100 mg/kg

Guo et al. (2012)

Chlortetracycline

0-42 days at 150 g/mt

Mathis (2012)

BMD/virginiamycin

0-31 days: BMD at 50 g/ton; 35-61 days: virginiamycin at 20 g/ton

Swick et al. (2012)

Zinc bacitracin

0-10 days at 100 mg/kg; 10-35 days at 50 mg/kg

 

Volume:86 Issue:20

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