Poultry nutrient- Managing the gut

Introduction

The impact of gastrointestinal disease ranges from erosive to catastrophic, and considerable time, effort and financial resources are devoted to limiting the risk and consequence of disease challenge. Intense breeding and selection programmes have provided birds with the genetic potential to perform in the face of disease challenge, while good biosecurity has reduced the risk and consequence of infectious disease. At the production level, capital investment in poultry housing and equipment, and best operating practices, have helped to limit environmental stress.

Ironically, relatively little effort has been directed at managing the ecology of the gastrointestinal tract, the very site of nutrient digestion and absorption. This neglect is in part due to ignorance, but perhaps more importantly, it stems from the success of in-feed antibiotics and anticoccidials in preventing enteric disease. In the absence of these in-feed antimicrobials the paradigm of gut health management has to change. Working with the forces of nature to control the ecology of the digestive tract is the only alternative. Although intestinal ecology is very complex, and, difficult to understand, the position is changing rapidly. Advanced molecular techniques are being used to characterise details of the gut flora at the cellular level, in the hopes that novel strategies to preserve gut health are revealed.

Managing Gut Health - form, function and flora

In the high volume low margin poultry industry the economic impact of low grade (subclinical) disease is commonly rate-limiting. Health and disease are, however, not mutually exclusive. Disease only measurably impacts performance once the aggregate of homeostatic stressors exceed the bird's coping mechanisms. The negative impact of any challenge is thus directly proportional to the prevailing level of stress. While low grade stress or sub-clinical disease may go unnoticed, it is frequently sufficient to preclude birds from achieving genetic potential. These subtle changes in flock health are signalled by a decline in flock uniformity, because the degree of stress experienced by each bird in a flock varies; flock uniformity is rapidly reduced and skewed by disease challenge (Collett, 2003; Klasing, 1998). Since flock uniformity is correlated with economic return, it serves as a very useful, sensitive and early indicator of changes in flock health.

Health tracking systems provide real time information which allows early detection and response to disease-challenge. There are, however, no clearly defined objective, visual indicators of low grade gastro-intestinal disease, that are closely correlated with bird productivity. Early detection, appraisal and response to overt disease remains an art. A thorough understanding of the complex ecology and epidemiology of disease in intensive production systems is essential. In order to predict the impact of gastrointestinal disease on performance, necropsy findings must be evaluated in conjunction with all other available information and not viewed as absolute. Each component of the digestive tract must be evaluated relative to form, function and microbial content.

The importance of early gut development cannot be over emphasized. The efficiency of digestion and absorption is directly proportional to the surface area and integrity of the intestinal epithelial lining. The epithelium, with its network of microfibers and intercellular tight junctions, make up the intestinal cytoskeleton which separates the host from the complex microenvironment of the enteron. A series of villi and microvilli adorn the epithelial surface, increasing the surface area by approximately 600 times. This intricate design allows the ebb and flow of copious amounts of water and the absorption of nutrients to occur on a continuous basis, while at the same time, preventing the microbial inhabitants and their toxic metabolites from gaining access to the body. The complex but harmonious relationship between the gut microbiota and the host, is crucial to normal function (Collier et al., 2003; Neish, 2002). Any breakdown in this highly evolved relationship, stimulates a protective response by the host, which involves a cascade of events causing inflammation and gastrointestinal disease.

The efficiency of nutrient assimilation hinges on the early establishment and maintenance of a favourable gut lumen environment. Colonization of the gut with pioneer bacteria species, that are able to modulate expression of genes in the gut epithelia to create favourable conditions for establishment of a stable and beneficial climax flora, should be the starting point of any gut health management program (Guarner and Malagelada, 2003; Hooper and Gordon, 2001).

Steps to control gut health should start at the parent flock level, since the first organisms to gain access to the hatchling gut originate from the parent. Vertical transmission of gut inhabitants (from parent to offspring) can be transovarial (inside the egg) or as a result of shell contamination. In the artificially clean hatchery environment, even low doses of beneficial bacteria can significantly improve resistance to pathogen colonization and artificial seeding of the gut at an early age has been shown to be beneficial (Chaing and Hseih, 1995; Edens et al., 1997; England et al., 1996; Fernandez et al., 2002; Fukata et al., 1991; Hofacre et al., 2003; Hofacre et al., 1998; Hofacre, 2003; La Ragione et al., 2004; Mohan et al., 1996; Owings et al., 1990).

The first organisms to colonize the gut determine the composition of the climax flora by creating the microenvironment necessary for complex microbial community architectural development (Hooper and Gordon, 2001). In addition to seeding the gut with the correct pioneer species, it is crucial to enhance their ability to proliferate, compete and colonize, so as to avoid pathogen proliferation. As colonization proceeds, organisms attach to one another and the epithelium, by a series of fibrils to form a tightly adherent mat over the gut surface (Giron et al., 2002). Pathogens are thereby precluded access to the epithelial surface and their ability to colonize is compromised by a process of competitive exclusion (Nurmi and Rantala, 1973). Microbe attachment to host cell docking sites on the intestinal epithelium is dependent on surface molecule structure and is the pivotal first step in the colonisation of the gut (Giron et al., 2002; Sharon and Lis, 1993; Stavric et al., 1987) . Since several gut pathogens recognise and attach to specific gut epithelia glycoproteins, products that mimic these docking sites are also useful in preventing attachment and reducing the risk of pathogen colonization (Finucane et al., 1999; Giron et al., 2002; Spring, 1996).

In-feed antibiotics have for the past 50 years been used to enhance feed efficiency by subtly changing the composition of the gut flora (Anderson et al., 2000; Collier et al., 2003; Lu et al., 2003; Rosen, 1996; Rosen, 1995). Weak organic acids can also be used to change gut flora community structure. As weak proton donors, they are able to escape inactivation in the proventriculus and gizzard, while their presence in the small intestine modifies microbial community composition by providing a competitive advantage to the acid tolerant organisms (Davidson, 2001; Ricke, 2003). Such manipulation of the microbiota has both short and long term implications.

Poultry production although cyclical in nature, should from a gut flora point of view, be viewed as a continuous system. Members of the gut microbial community surviving in litter residue are carried over from one cycle to the next, thus serving as the "seed stock" for the gut flora of the next placement (Lilijebjelke et al., 2003). In view of this, it is surprising that although there are literally thousands of growth-promotant trials demonstrating their efficacy, the literature is devoid of data showing the long-term effect of such programs. While in-feed antibiotics can alter the gut flora within a couple of weeks, it takes several grow-out cycles to change the house (litter) flora (Avellaneda et al., 2003; Idris et al., 2003; Lilijebjelke et al., 2003; Schildknect et al., 2003a,2003b). This is by no means a new concept, both rotation and shuttle programs have been used for decades to avoid the lack of response to in-feed antibiotics following their persistent use.

The realization that even minor changes in the microbial community composition can affect long term productivity (through incremental displacement and replacement of the house flora) has highlighted the significance of microbial community management. Attention to detail is more critical than ever. Mycotoxins, previously recognised for their host toxicity, also have strong antimicrobial properties and may, for example, affect long term productivity by altering the gut flora (Kubena et al., 2001; Swamy et al., 2002a; Swamy et al., 2002b). In such instances, mycotoxin binders may be useful in helping to preserve the stability of the microbiota, even when mycotoxin levels are low (Kubena et al., 2001; Swamy et al., 2002a; Swamy et al., 2002b).

The efficiency of nutrient assimilation is highly correlated with the functional surface area of the intestinal lining (Sklan, 2001). Inflammatory response at the gut interface has a direct impact on feed assimilation (intake, digestion and absorption) by compromising functional surface area. Irrespective of the initiating cause, disease process begins with an inflammatory response and it is the extent of this inflammatory response that determines its performance effect. An appropriate immune response limits the consequence of challenge, while an inadequate or excessive response depresses assimilation efficiency and productivity (Klasing, 1998; Klasing et al., 1987).

Once initiated, inflammation stimulates acute-phase protein synthesis in the liver which causes several behavioural, hormonal and metabolic perturbations, the ramifications of which range from negligible to dramatic (Klasing, 1998; Klasing and Johnstone, 1991). Local inflammatory response causes tissue damage, while systemic or fever response causes feed intake to decline, protein turnover to accelerate and a rapid transition into negative nitrogen balance (Collier et al., 2003; Klasing, 1998; Klasing et al., 1987). With systemic challenge, most (70%) of the negative impact on growth rate and feed efficiency is attributed to reduced feed intake, while the inefficiencies of catabolism and nutrient absorption account for the rest (30%) (Collier et al., 2003; Klasing, 1998; Klasing and Barnes, 1988; Klasing et al., 1987; Klipper et al., 2000). Low level antigen stimulation at the gut/ingesta interface, seldom results in systemic/fever response and is in fact essential for cellular homeostasis (Petrof et al., 2004; Sansonetti and Di Santo, 2007). Excessive pro-inflammatory mediator release can, however, damage host tissue, thereby causing localized inflammatory disease and reduced feed efficiency (Klasing, 1998; Klasing and Barnes, 1988; Klasing et al., 1987; Klipper et al., 2000,, 2001).

Antigen induced inflammation of the gut lining stimulates mucus secretion, increased paracellular permeability, and accelerated feed passage (peristalsis) (Collier et al., 2003; Cooper, 1984). The cascade of events that follows, is self perpetuating since increased permeability enhances toxin and antigen penetration which stimulates inflammation, and the resulting increase in mucus production attracts mucolytic species such as Clostridium perfringens, which produce tissue damaging cytotoxins (Collier et al., 2008; Collier et al., 2003).

The nature and extent of the inflammatory response is influenced by several nutritional factors. Dietary polyunsaturated fatty acids (PUFA) for example, indirectly determine the type of immune response that follows cell damage. Lipids incorporated into the cell membrane during growth and development are subsequently used as the substrate for immune system, communication molecule synthesis (Klasing, 1998; Korver and Klasing, 1995; Korver and Klasing, 1997). Cereal grains are high in linoleic acid (n-6 PUFA precursor for arachidonic acid) which favours the production of prostaglandins, leukotreins and thromboxanes, while fish oil is high in n-3 PUFA, which favours production of interleukin-1 and prostaglandin-E (Fritsche et al., 1991; Korver and Klasing, 1997).

Maternal antibodies provide crucial support to the maturing immune system of the hatchling, but early gastrointestinal defence is primarily dependent on the innate component of the immune system. During the first 3 days post hatch, the chick immune system learns to tolerate innocuous gut antigens. Gut barrier function matures by day 3 and oral exposure to ‘new' antigens after this is more likely to lead to an inappropriate immune response and negatively impact feed efficiency (Geyra et al., 2001; Klipper et al., 2001,, 2004; Uni et al., 2000; Uni et al., 1999). It may be advantageous to ensure that pre-starter rations contain the feed ingredients (antigens) necessary to ensure that the mature immune system is tolerant of these feed antigens after closure of gut barrier function.

Maternally derived antibodies also play a crucial role in guiding the development of the hatchling immune system. There is a fine line between tolerance and response. Maternal antibodies to hazardous/pathogenic antigens block development of tolerance thus enabling the developing immune system to differentiate potentially hazardous antigens from innocuous feed or commensal antigens (Klipper et al., 2004). Gut health management should start at the parent flock level (Fernandez et al., 2002).

The practice of maximising disease resistance is too costly for the modern poultry industry (Klasing, 1998). Immune stimulation needs careful evaluation since the cost of an exaggerated or inappropriate immune response is counterproductive in terms of feed efficiency (Collier et al., 2003; Grimble, 2001; Klasing, 1998; Klasing et al., 1987). Feed is the single largest input cost and as feed margin has declined, the cost driven poultry industry has shifted emphasis from disease resistance to disease resilience (Klasing, 1998).

While an excessive or inappropriate immune response erodes productivity by adversely affecting the feed conversion, an inadequate immune response usually results in increased flock mortality. Specific infectious diseases, nutritional deficiencies, toxicities and stress are all factors that can cause immune suppression and result in an inadequate immune response (Ferket et al., 1999; Ferket and Qureshi, 1992; Qureshi et al., 1998; Siegel, 1994; Surai, 2002; Swamy et al., 2002a; Swamy et al., 2002b; Sword et al., 1991).

It is possible to maintain productivity in the face of disease challenge by modulating the immune response. Stimulation of the protective antibody response enhances disease resistance and suppression of the acute phase/fever response preserves feed intake and bird performance (Collett, 2003; Collett and Dawson, 2001; Ferket et al., 2002; Klasing, 1998; Klasing et al., 1987; Parks et al., 2001; Savage et al., 1996). Both endogenous and exogenous anti-inflammatory agents help to maintain gut health by modulating the immune response so as to preserve the integrity of the gut lining and reduce the fever response (Choct et al., 2004; Ferket et al., 2002; Grimble, 2001; Kelly et al., 2004; Klasing, 1998; Korver et al., 1998; Korver et al., 1997; Parks et al., 2001; Surai, 2002; Sword et al., 1991).

Years of breeding and selection for growth rate have increased broiler appetite, daily feed intake, and feed passage rate. Interestingly, retention times for the small intestine have remained fairly constant while those for the proventriculus and gizzard have declined (Denbow, 2000; Washburn, 1991). This is probably because feed processing at the feed mill reduces the need for particle size reduction in the gizzard, while nutrient utilization is proportional to small intestine retention time. Protein digestion is, however, potentially compromised by short proventriculus/gizzard retention, since the conversion pepsinogen to pepsin is pH dependant (Denbow, 2000; Klipper et al., 2004; Sklan et al., 1975).

To adequately manage gut health the nutritionist should consider ingredient blend, in addition to nutrient specification, since ingredient characteristics such as viscosity, particle size, digestibility (starch), and lipid or protein content affect passage time (Bedford, 1996; Classen, 1996; Refstie et al., 1999; Sell et al., 1983; Sibbald, 1979; Weurding et al., 2001). Certain undesirable ingredient characteristics such as viscosity and non-digestible nutrient content can be countered with concomitant enzyme and/or osmolyte usage (Bedford, 2000; Cronje, 2007; Kettunen et al., 2001). Apart from the direct feed efficiency implication of reduced digestion and absorption, the through flow of undigested nutrients impacts downstream gut ecology (Gidenne, 1997). Undigested protein is strongly inflammatory and provides a competitive advantage to the proteolytic organisms, like Clostridium perfringens, in the caecae (Klipper et al., 2001,, 2004; Lillehoj and Trout, 1996). Potentially toxic compounds such as ammonia, amines, phenols and indoles, are generated by the proteolytic and ureolytic activity of the caecal flora on undigested nutrients that make their way through to the caecal pouches. These toxic compounds affect flora ecology (Gidenne, 1997) . The effect of this is likely more pronounced with soluble nutrients because liquids pass through the digestive tract 15% faster than solids (Klipper et al., 2004; Sklan et al., 1975; Sklan and Hurwitz, 1980).

The organisms of the lower gastrointestinal tract are normally kept in check by intense competition for a limited source of nutrients (Zinser and Kolter, 2004). Any factor that reduces digestion efficiency in the upper gastrointestinal tract or increases nitrogen turnover, could potentially alter caecal ecology. Urine (uric acid) and feed (undigested protein) nitrogen are used by caecal flora to synthesise microbial protein (Bjornhag and Sperber, 1977) and volatile fatty acids (VFA) formed during uric acid degradation, have antibacterial activity (Annison et al., 1968; Cherrington et al., 1990; Cherrington et al., 1991; Davidson, 2001; Sudo and Duke, 1980). Since caecal ecology is affected by protein through-flow, exogenous protein enzymes can be used to help stabilize caecal flora communities. The amount of protein nitrogen reaching the caeca can be further reduced if nutrient credit allocated permits a reduction in dietary protein (Schang and Azacona, 2003).

Conclusion

Strategies to improve gut health in commercial operations need to be cost effective, sustainable, farm specific and holistic. Intervention / product selection needs to be science based but practical and each intervention must address the specific objective for its inclusion. It is possible to enhance gut health and improve productivity by seeding of the hatchling gut with favorable flora, early modification of the gut environment to promote climax flora development, pathogen exclusion (competitive and selective), immune modulation, and ingredient/nutrient management.

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This presentation was given at the 9º Seminario de Actualización Avícola de AMEVEA, Entre Ríos, Argentina in September 2010. Engormix thank the author and the organizing committee for the contribution.