Without in-feed prophylactics --   antibiotics and coccidiostats --   the emphasis in poultry gut health management has to shift from working against to working with the intestinal microbial community (microbiota). This is commonly achieved through the use of pre- and probiotics.

The main microbiota mediated health risks are not limited to but include: separation of parent and offspring before hatch; all-in-all-out production systems; complete cleanout and disinfection; high feed intakes; high-protein diets; and high stocking densities.

By stabilizing the intestinal ecology, it is possible to ensure optimal intestinal integrity and thus bird performance. Attempts to accelerate the maturation and stability of the intestinal microbiota are most effective during a chick's initial development.

Even once established, however, the stability of the intestinal microbiota can be threatened by the intestinal health risks coming from intensive production, and these need to be addressed accordingly. Rehabilitation of the microbiota through pre- or probiotics should be considered after perturbation resulting from any dietary change or stress and following antibiotic therapy.

Intestinal ecology

The importance of early gut development cannot be overemphasized.

The efficiency of digestion and absorption is directly proportional to the intestinal surface area and integrity of the epithelial lining. The epithelium, with its microfibers and intercellular tight junctions, makes up the intestinal cytoskeleton, which separates the host from the complex microenvironment of the enteron. A series of villi and microvilli cover the epithelial surface, increasing its area by approximately 600 times.

This intricate design allows the ebb and flow of water and the absorption of nutrients on a continuous basis, while preventing the microbial inhabitants and their toxic metabolites from gaining access to the body.

Complex but harmonious relationship

The complex but harmonious relationship between the gut microbiota and the host is crucial to normal function. Any breakdown in this relationship stimulates a protective response by the host, involving a cascade of events causing inflammation and gastrointestinal disease.

Negative changes in the composition of the intestinal microbiota have been associated with deterioration in intestinal function as measured by feed conversion efficiency. Dysbacteriosis --   as it is commonly called in the poultry industry --   became common after the moratorium on in-feed antibiotics was introduced in the European Union.

Although poultry production systems are all-in-all-out, from a gut flora point of view, they are continuous.

Members of the gut microbial community surviving in-house are carried over from one cycle to the next and they serve as the seed stock for the gut flora of the next placement. While in-feed antibiotics can alter the gut flora within a couple of weeks, it takes several grow-out cycles to change the house flora.

Even minor changes in the composition of the microbial community can affect long-term productivity, hence the need for microbial community management. Attention to detail is more critical than ever.

The efficiency of nutrient assimilation hinges on the early establishment and maintenance of a favorable gut lumen environment.

In a drug-free production system, emphasis shifts from fighting unfavorable organisms with antibiotics to nurturing favorable organisms to ensure a favorable and stable intestinal ecology. In its simplest form, this involves:

  • Seeding the gut with favorable intestinal microbiota
  • Feeding these organisms to ensure rapid domination
  • Weeding out unfavorable organisms

Seeding the gut with favorable organisms

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.

Colonization of the gut, with bacteria species able to modulate the expression of genes in the gut epithelia to create favorable conditions for the establishment of a stable and beneficial climax flora, should be the starting point of any gut health management strategy.

Since the first organisms to gain access to the hatchling gut originate from the parent, controlling gut health should start at parent flock level. Vertical transmission of gut inhabitants can be inside the egg or as a result of shell contamination.

In the artificially clean hatchery environment, even low doses of beneficial bacteria can improve resistance to pathogen colonization, and artificial seeding of the gut at an early age can be beneficial.

Feeding the favorable organisms

In addition to seeding the gut with pioneer species, it is crucial to enhance their ability to proliferate, compete and colonize.

Weak organic acids can 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 such as the Lactobacilli and a competitive disadvantage to intolerant organisms such as the Clostridia, it is possible to guide the development of the microbiota. Such manipulation of the microbiota has both short- and long-term implications.

Weeding out unfavorable organisms

As colonization proceeds, organisms attach to one another and the epithelium to form a tightly adherent mat over the gut surface. Pathogens are thereby denied access to the epithelial surface, and their ability to colonize is compromised by competitive exclusion.

Microbe attachment to host cell products (mucus) and organism-specific docking sites on the intestinal epithelium is the pivotal first step in the colonization and infection of the gut. Since several gut pathogens recognize and attach to specific gut epithelia glycoproteins, products that mimic these docking sites are useful in preventing attachment and reducing pathogen colonization.

Pathogen-induced inflammation of the gut lining stimulates mucus secretion, increased paracellular permeability and accelerated feed passage. The cascade of events that follows is self-perpetuating. Increased permeability enhances toxin and antigen penetration, which stimulates inflammation. The resulting increase in mucus production attracts mucolytic species such as Clostridium perfringens, which produce tissue-damaging cytotoxin.

Dealing with coccidiosis

Currently, the only effective way to address the risk of a coccidiosis challenge in drug-free poultry production is by vaccination.

The coccidiosis vaccines available in the U.S. are not attenuated, so strictly speaking, the process of immunization is controlled exposure and not vaccination. This distinction is important. The only way to limit the extent of the reaction to controlled exposure is through dose control. Too high of a dose causes an exaggerated response and early (1-2 weeks) enteritis. Too low of a dose precludes the development of an adequate immune response, and clinical coccidiosis will develop at 3-4 weeks of age. Careful control of "vaccine" application is crucial.

Simple strategy

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.

Efforts to nurture and stabilize a favorable intestinal microbiota with alternative approaches have shown promise in addressing the negative impact of in-feed antibiotic removal.

While there are several opportunities and product options to achieve this, there are three simple interventions that have demonstrated particular promise. By seeding the hatchling gut with favorable organisms, feeding these organisms with an appropriate organic acid, and weeding out the unfavorable competitors with a type-1 fimbriae blocker, it is possible to improve performance. Coccidiosis control is a crucial component of any drug-free intestinal health management program.