Prebiotic Feed Additives: Rationale and Use in Pigs

By John A. Patterson and presented at the 2005 Banff Pork - Disease has always been a critical issue in pig production, affecting not only animal health and well-being, but also the physical and economic health of the producer.
calendar icon 16 January 2006
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Prebiotic Feed Additives: Rationale and Use in Pigs - By John A. Patterson and presented at the 2005 Banff Pork - Disease has always been a critical issue in pig production, affecting not only animal health and well-being, but also the physical and economic health of the producer.

Growth promotant antibiotics have been fed to livestock since the 1940’s and have generally enhanced pig performance (Cromwell, 2000). Growth promotant antibiotics act by a variety of mechanisms to alter the intestinal microbiota, with subsequent direct and indirect effects on the pig (Anderson, et al., 2000, Gaskins et al., 2000). Enteric disease issues are coming to the forefront as governmental and public concerns about preharvest food safety and microbial antibiotic resistance increase. The European Union is phasing out use of growth promotant antibiotics and there is increasing pressure to do so in North America.

Thus, there is increasing interest in alternatives to growth promotant antibiotics. Fundamental to developing alternatives to growth promotant antibiotics is the enhancement of our understanding of defence systems used to inhibit pathogens, their interactions and regulation.

Host Defenses Against Infection

The pig’s defence against pathogens includes a combination of physical processes (gastric acidification, rapid transit through the small intestine), as well as the epithelial lining of the intestine, the mucosal immune system and the intestinal microbiota (Gaskins, et al., 2000, Mackie, et al., 1999). Effective defence against pathogens requires that all of these systems are functioning properly. Factors affecting these systems include genetics, pathogen load and stressors. We are just starting to learn about the extensive amount of cross talk between these systems (Deplancke and Gaskins, 2001, Hooper, et al., 2002, McCracken and Lorenz, 2001, Sonnenburg, et al., 2004, Xu and Gordon, 2003).

Symbiotic Microbiota

The microorganisms that are frequently associated with the majority of animals are called by a variety of names (normal, commensal, indigenous, symbiotic) and symbiotic will be used here. Opportunistic pathogens may be a small component of this microbiota, but only become pathogenic in response to specific environmental conditions. Studies using germ-free, gnotobiotic (colonized by selected bacterial species) and conventional animals clearly show that the symbiotic bacteria provide protection against enteric pathogens.

Although the intestinal microbiota is complex and the role of most of the bacteria in protecting the pig is not clear, bacterial species of the genera Lactobacillus and Bifidobacterium have been shown to provide protection against enteric infections. These two genera have also been shown to be suppressed when animals or humans are stressed. Recent research is unfolding a picture of how the symbiotic bacteria inhibit enteric pathogens and how they synergistically interact with the intestinal epithelium and mucosal immune system.

The intestinal tract is sterile at birth and undergoes a succession of bacterial populations before a stable microbial ecology is established. Facultative organisms, such as E. coli, initially colonize the intestinal tract. As the animal ages, the intestinal tract is subsequently colonized by relatively aerotolerant lactic acid bacteria (lactobacilli and bifidobacteria), bacteroides and other anaerobic bacteria (Mackie, et al., 1999, Tannock, 1997). The intestinal microbial community structure becomes increasingly complex after weaning and with time, the microbial community structure becomes relatively stable at the genus level. However, there is increasing evidence that the species composition within a genus is dynamic and varies between individual animals.

Thus, subtle changes in bacterial species may alter host resistance to pathogens. The microbial community structure is thought to be altered when the animal is stressed and this altered microbiota, along with altered epithelial and immune function, provide pathogens with an increased opportunity for colonization. Although the mechanisms of this decrease in bacterial resistance and specific microbial population changes involved are not known, lactobacilli and bifidobacterial populations have been shown to decrease in humans and these or similar beneficial populations may be decreased in pigs.

The symbiotic intestinal microbiota inhibit pathogens through a variety of mechanisms. The mechanism, or combination of mechanisms used depends upon the microbial species and the ecosystem within which they are residing.

Possible mechanisms are:

  • competition for nutrients
  • production of toxic conditions or compounds (low pH, fermentation acids, bacteriocins, etc.)
  • competition for binding sites on epithelial surfaces, or in the tightly adherent mucus layer
  • stimulation of the immune system

The intestinal microbiota are in highest numbers in the lumen of the intestinal tract, where competition for nutrients and production of toxic compounds would logically be important. The intestinal microbiota also colonize the mucus layer lining epithelial cells and thus competition for binding sites, in addition to competition for nutrients and production of toxic compounds may be important.

It is also most likely that the mucosally associated microorganisms are directly, or indirectly responsible for stimulating the immune system. Thus, manipulation of the microbiota in specific ecosystems influences the efficacy with which the symbiotic microbiota inhibits pathogens.

The symbiotic intestinal bacteria do not act alone to inhibit enteric pathogens, but act in concert with the intestinal epithelial barrier and the mucosal immune system. There are a number of management approaches that either enhance or suppress this alliance. However, understanding how they function is important in developing approaches to influence these defence systems.

Epithelial Tissues

The epithelial lining provides a physical barrier against entry of large molecules and microorganisms into the body proper. The morphology of the epithelial lining changes along the intestinal tract, but essentially consists of crypt regions (where cells are generated from stem cells) and apical or villi (depending upon location) regions, where cells have differentiated to perform different functions, and eventually die and are released into the lumen of the intestine. Cell turnover is rapid along the intestinal tract with cells being replaced every 3-5 days. Changes in epithelial tissue morphology alter nutrient absorption and defence against pathogen invasions.

Although it is well known that pathogens that attach to epithelial cells conscript the regulatory control of that cell, new information indicates that at least some species of the symbiotic microbiota that are in close association with the epithelium also influence activities of epithelial cells (Hooper, et al, 2002, Xu and Gordon, 2003). These changes in epithelial cell metabolism enhance colonization by those bacterial species and potentially enhance protection of the epithelial surface from colonization by pathogens. Thus, it is becoming increasingly clear that there is extensive cross-talk between the intestinal microbiota and epithelial cells.

Mucosal Immune System

The mucosal immune system is comprised of lymph nodes (mesenteric lymph nodes and Peyer’s Patches, located in the ileum) and diffuse lymphoid cells. The immune system has both innate and adaptive arms (Pickard et al., 2004). The innate system includes cells (macrophages, dendritic cells) that mount a non-specific response to the presence of any foreign antigen. The adaptive system has memory and once exposed to a pathogen, the adaptive system produces antibodies that are protective against subsequent infections by the same organism. Since the intestinal tract is constantly exposed to bacteria, it has to develop tolerance to the symbiotic bacteria and does so through a complex process.

The mucosal immune system develops tolerance to the indigenous microbiota and food antigens, resulting in an accumulation of IgA secreting B cells, T cells, macrophages and dendritic cells in the tissues lining the intestinal tract. In essence, the mucosal epithelium elicits a mild or controlled (Th1) inflammatory response to the symbiotic microbiota and a much more dramatic inflammatory response to pathogens. This allows the mucosal epithelium to respond more rapidly to pathogen challenge; however, it is expensive, from an energetic standpoint, to maintain this primed immune system in the absence of pathogen challenge (Anderson, et al. 2000). Good management practices can minimize pathogen load.


The mucosal epithelium is heavily innervated, with sympathetic and parasympathetic nerves influencing normal function of the intestinal system and mucosal tissues are exposed to hormonal action. When the animal is stressed, the hypothalamic-pituitary axis (HPA) responds by secretion of corticosteroids and direct neuronal stimulation of the mucosal tissues (Matteri, et al., 2000, Petrovsky, 2001). Thus, stress associated with production, including environmental, nutritional, weaning, transportation, and commingling suppress the pig’s ability to resist pathogens and increases the incidence of subclinical or clinical infection. Growth of some pathogenic bacteria is stimulated by addition of the stress hormones norepinephrine and epinephrine. This has been shown by growth in serum simulating medium and by increases in gram negative (E. coli) bacteria in the intestinal tracts of animals stimulated to release norepinephrine (Lyte, 2004). More information is needed on the interactions between the neuroendocrine response to stressors and regulation of pathogenic and symbiotic microbiota in the intestine.

Thus, there is extensive cross-talk between the various defence systems. These systems are effective in suppressing pathogens, and under normal conditions, few pigs become sick. Pigs that do become sick effectively control the infection. However, when the pig is challenged by environmental conditions that suppress one or all of these systems and when the pathogen load is high, then it becomes much more likely that an individual pig will become infected, the pig will become sicker and contribute to the pathogen load of pen mates and results in spread of the disease.

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Source: Paper presented during the 2005 Banff Pork Seminar Procedings

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