In contrast to the mode of action of most antibiotics and carbohydrate fermentation sources, MOS and possibly other oligosaccharides, serve as alternate attachment sites for Gram-negative pathogens, thereby preventing attachment onto enterocytes and subsequent enteric infection. Adherence of thepathogenic microbe to the enterocyte cell wall is thought to be a prerequisite for the onset of infection (Gibbons and Van Houte, 1975). For example, it has been shown that the organism Vibrio cholera is incapable of initiating disease unless it is able to attach to the cell wall, despite the presence of large numbers of bacteria present (Freter, 1969). Adhesion leads to bacterial growth, entrapment and formation of mixed colonies, the entrapment of nutrients for growth, the concentration of digestive enzymes and toxins onto enterocytes, and the possible prevention of antibody attachment to the pathogenic cell (Costerton et al., 1978). The cell wall of the yeast organism consists of carbohydrates and proteins in the form of chained and branched structures of glucose, mannose, and N-acetylglucosamine (Ballou, 1970). Mannanoligosaccharides, derived from mannans on yeast cell surfaces, act as high affinity ligands, offering a competitive binding site for the bacteria (Ofek et al., 1977). Pathogens with the mannose-specific Type-1 fimbriae adsorb to the MOS instead of attaching to intestinal epithelial cells and, therefore, move through the intestine without colonization. Newman (1994) reported that the presence of dietary MOS in the intestinal tract removed pathogenic bacteria that could attach to the lumen of the intestine in this manner. Mannose was shown by Oyofo et al. (1989a) to inhibit the in vitro attachment of Salmonella typhimurium to intestinal cells of the day old chicken. Then Oyofo et al. (1989b) provided evidence that dietary D-mannose was successful at inhibiting the intestinal colonization of Salmonella typhimurium in broilers. In an effort to confirm the inhibitory effects of MOS on pathogen colonization reported in previous research, Spring et al. (2000) screened different bacterial strains for their ability to agglutinate mannanoligosaccharides in yeast cell preparations (Saccharomyces cerevisiae, NCYC 1026). Five of seven strains of E. coli and 7 of 10 strains of Salmonella typhimurium and S. enteritidis agglutinated MOS and Sac. Cerevisiae cells. However, strains of
- choleraecuis, S. pullorum, and Campylobacter did not lead to agglutination. They also determined the effect of MOS on cecal fermentation parameters, cecal microflora, and enteric pathogen and coliform colonization in chicks. After 3-day old chicks were orally challenged with 104cfu of S. typhyimurium 29E and received 4000 ppm dietary MOS, cecal S. typhimurium29E concentrations decreased from 5.40 to 4.01 log cfu/g, P< 0.05) at day 10. A similar study using S. Dublin as the challenge pathogen resulted in a decrease in the number of positively infected birds by day 10 from 90% to 56% (P< 0.05). Dietary MOS supplementation also reduced the concentration of cecal coliforms, although less significantly (P < 0.10) as with the Salmonella challenges. Dietary MOS supplementation had no effect on cecal concentrations of lactobacilli, enterococci, anaerobic bacteria, lactate, volatile fatty acid, or cecal pH. The effects of hen age,
Escherichia coli, and dietary MOS and bambermycins on poult performance from 1 to 21 d were studied previously by Fairchild et al. (1999). Day-of-hatch BUTA (BIG-6) male poults were gavaged (1 mL) with 1 X 108cfu / mL E. coli composed of 4 serotypes or sterile carrier broth. A mixture of the same E. coli cultures was added to the drinking water (1 X 106cfu E. coli / mL drinking water) on a weekly basis to ensure a continuous bacterial challenge. Within each E. coli split plot treatment group, poults from hens of different ages (33 and 58 wk of age) were fed diets containing 1 kg MOS/ton feed) and 2 g bambermycins/ton feed, alone and in combination, in a randomized complete block design. One bird per pen (n=128) was randomly
chosen at 1 and 3 weeks of age for bacterial sampling of liver and intestinal tissue for coliforms, aerobic bacteria, and Lactobacillus spp. Individual body weights and feed consumption by pen were recorded weekly and poult mortality was recorded daily. Escherichia coliisolates from tissue samples were O stereotyped. Under E. coli challenge, dietary MOS and bambermycins improved (P< 0.05) poult body weight gains. When poults were not challenged with E. coli, dietary MOS improved (P< 0.05) poult growth during the second week, while dietary bambermycins Multi-State Poultry Meeting May 14-16, 2002 Peter R. Ferket improved (P< 0.05) poult growth through the third week. Cumulative 3-week body weight gains for unchallenged poults were improved (P< 0.05) by both MOS and bambermycins. Two of the four E. coli stereotypes administered were recovered in cultures of tissue samples. Several stereotypes were recovered that were not administered. This work demonstrates that dietary MOS can improve the overall performance of poults, especially when they are faced with an E. coli challenge, as well as traditionally used antibiotics. Improved performance has also been reported in turkeys receiving dietary MOS. Savage and Zakrzewska (1996) reported a significant increase in weight gain in Large White male poults fed a diet containing 0.11% MOS
