A preliminary study on the use of mannan oligosaccharides (MOS) in freshwater crayfish, Astacus leptodactylus Eschscholtz, 1823 juvenile diets

The ability of different enteric pathogens and coliforms to trigger agglutination of yeast cells (Saccharomyces cerevisiae, NCYC 1026) and a yeast cell wall preparation (MOS) was examined. Five of seven strains of Escherichia coli and 7 of 10 strains of Salmonella typhimurium and Salmonella enteritidis agglutinated MOS and Sac. cerevisiae cells. Strains of Salmonella choleraesuis, Salmonella pullorum, and Campylobacter did not lead to agglutination. Two strains that agglutinated MOS (S. typhimurium 29E and Salmonella dublin) and one nonagglutinating strain (S. typhimurium 27A) were selected as challenge organisms for in vivo studies in chicks under controlled conditions. In a series of three trials in which 3-d-old chicks were orally challenged with 10(4) cfu of S. typhimurium 29E, birds receiving 4,000 ppm of dietary MOS had reduced cecal S. typhimurium 29E concentrations (5.40 vs 4.01 log cfu/ g; P < 0.05) at Day 10. In a second series of three trials with S. dublin as challenge organism, the number of birds that tested salmonella positive in the ceca at Day 10 was less when MOS was part of the diet (90 vs 56%; P < 0.05). To test the effect of MOS on concentrations of bacteria that do not express Type 1 fimbriae, a challenge trial was conducted with S. typhimurium 27A. However, strain 27A did not colonize the birds sufficiently to evaluate whether MOS affected its cecal concentration. Mannanoligosaccharide did not significantly reduce the concentrations of cecal coliforms (P < 0.10) although they were numerically lower. It had no effect on cecal concentrations of lactobacilli, enterococci, anaerobic bacteria, lactate, volatile fatty acid, or cecal pH.

The intestinal microbiota, epithelium, and immune system provide resistance to enteric pathogens. Recent data suggest that resistance is not solely due to the sum of the components, but that cross-talk between these components is also involved in modulating this resistance. Inhibition of pathogens by the intestinal microbiota has been called bacterial antagonism, bacterial interference, barrier effect, colonization resistance, and competitive exclusion. Mechanisms by which the indigenous intestinal bacteria inhibit pathogens include competition for colonization sites, competition for nutrients, production of toxic compounds, or stimulation of the immune system. These mechanisms are not mutually exclusive, and inhibition may comprise one, several, or all of these mechanisms. Consumption of fermented foods has been associated with improved health, and lactic acid bacteria (lactobacilli and bifidobacteria) have been implicated as the causative agents for this improved health. Research over the last century has shown that lactic acid bacteria and certain other microorganisms can increase resistance to disease and that lactic acid bacteria can be enriched in the intestinal tract by feeding specific carbohydrates. Increased bacterial resistance to antibiotics in humans has caused an increase in public and governmental interest in eliminating sub-therapeutic use of antibiotics in livestock. An alternative approach to sub-therapeutic antibiotics in livestock is the use of probiotic microorganisms, prebiotic substrates that enrich certain bacterial populations, or synbiotic combinations of prebiotics and probiotics. Research is focused on identifying beneficial bacterial strains and substrates along with the conditions under which they are effective.