Antibiotics have been used for decades as growth promoters in animal farming as a solution to promote better health and faster growth. Pigs supplemented with antibiotics in their feed require 10–15% less feed to achieve a desired level of growth. The meat obtained from antibiotic-fed animals is also of better quality with higher amount of protein and less amount of fat compared to that obtained from animals not supplemented with antibiotics. These growth responses are associated with improved nitrogen metabolism, including an increase in apparent nitrogen digestibility (+3.0%), increased nitrogen retention (+5.8%), and reduced nitrogen excretion (+10%) in pigs fed tylosin.

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These positive effects of AGPs on animal performance are coming from the depression of the intestinal flora. That leads us to postulate that gut bacteria, whether commensal or pathogenic, depress animal growth, either directly or indirectly, through their metabolic activities. Perhaps the best support of this hypothesis is the observation that oral antibiotics do not enhance the growth of germfree animals, while inoculating germfree animals with GI bacteria depresses growth.

The first assumption that comes to mind regarding the effectiveness of AGP is that antibiotics are affecting the pathogenic bacteria and promoting a better health of animals. But actually, the reasons behind AGPs mode of action are multiple. At least three other mechanisms have been proposed as explanations of antibiotic mediated growth enhancement:

Reduction of microbial use of nutrients

Most of the attention given to the pig intestinal microbiota has focused on the large intestine. Indeed, the large intestine (cecum and colon) is a major site of microbial colonization because of slow digesta turnover, and it is characterized by larger numbers of bacteria and relatively high short chain fatty acid (SCFA) concentrations. Microbial activity in the cecum and colon appears to benefit the host with estimates up to 5-20% of the pig’s total energy being provided by fermentation end-products.

However, the small intestine is the principal site of nutrient and energy absorption, and thus is the region in which bacterial activity is likely to have the greatest influence on the efficiency of growth.

Culture-based studies have shown that small intestinal bacteria tend to compete with the host for energy and amino acids. For example, as much as 6% of the net energy in pig diets can be lost due to bacterial utilization of glucose in the small intestine. Bacterial use of glucose to produce lactic acid reduces the energy available to the host epithelium. Lactic acid also enhances peristalsis, thus increasing the rate of nutrient transit through the intestine.

Reduction of growth-depressing microbial metabolites

Some bacteria called ‘proteolytic’ are responsible for the fermentation of some undigested peptides and amino acids to produce some potentially toxic metabolites such as ammonia, amines, phenols and sulfides. By depressing the overall bacteria population in the gut, AGPs will lead as well to a reduction of these toxic metabolites.

Reduction of bile conjugation

It has been demonstrated that bacteria in the small intestine are destroying a major part of the bile acids produced by the host pancreas. Gram-positive bacteria like lactobacillus, Enterococcus, Bifidobacterium and Clostridium are indeed producing an enzyme called BSH (bile salt hydrolases). The contributions of the lactobacilli to bile acid biotransformation in the intestine is demonstrated by evidence that ileal bile salt hydrolase activity in conventional mice is reduced 86% by the elimination of lactobacilli from the microbiota, and by greater than 98% when both lactobacilli and enterococci are eliminated. By deconjugating bile acids, these gram-positive bacteria are impairing lipid absorption and reduce animal growth performance.

Recently, some researchers have been exploring in-vitro the BSH inhibition properties of several additives. Indeed, if an additive could prevent the bacterial BSH to disactivate the host bile, that could help improvin lipid digestibility and absorption. Preliminary works showed that both Zinc and Copper are depressing the effect of BSH. That could be one of explanation behind the multiple mode of action of Zinc and Copper but more studies will be needed for confirmation.

Reduction of Mucus Layer

Most of bacteria present in the intestine have some mucolytic activities. They are literally eating up the mucus barrier resulting into a thinner wall. This aggression will oblige the enterocytes to build up their mucus layers and, in some cases, trigger a chronic inflammation, both defense mechanisms costing huge amount of energy for the hosts.

A clear difference between germfree and conventional animals is a thinner wall of the small intestine, with a reduction in connective tissue and lymphoid elements. Further, the rate of renewal of epithelial cells is slower in germfree animals, which may have a beneficial effect on basal energy expenditure and the efficiency of nutrient utilization.

- The Intestinal Microbiota is Competitive with the Host in the Small Intestine

but Cooperative in the Large Intestine –

When considering the elements developed above, it is essential to take some precautions when removing antibiotic from the diets, especially for young animals.

  1. Control gut flora and its negative effects by antimicrobial alternative such as zinc oxide and copper additives and probiotics

  2. Support fat emulsification and absorption by using effective emulsifiers

  3. Reduce the amount of indigestible protein and lower the dietary crude protein level by using good digestible protein sources, more synthetic amino acids

  4. Minimize gut stress by managing oxidative pressure and using solutions against mycotoxins