Review on the effects of potential prebiotics on controlling intestinal enteropathogens Salmonella and Escherichia coli in pig production

Catheter-associated urinary tract infections (CAUTIs) represent the most common type of nosocomial infection and are a major health concern due to the complications and frequent recurrence. These infections are often caused by Escherichia coli and Proteus mirabilis. Gram-negative bacterial species that cause CAUTIs express a number of virulence factors associated with adhesion, motility, biofilm formation, immunoavoidance, and nutrient acquisition as well as factors that cause damage to the host. These infections can be reduced by limiting catheter usage and ensuring that health care professionals correctly use closed-system Foley catheters. A number of novel approaches such as condom and suprapubic catheters, intermittent catheterization, new surfaces, catheters with antimicrobial agents, and probiotics have thus far met with limited success. While the diagnosis of symptomatic versus asymptomatic CAUTIs may be a contentious issue, it is generally agreed that once a catheterized patient is believed to have a symptomatic urinary tract infection, the catheter is removed if possible due to the high rate of relapse. Research focusing on the pathogenesis of CAUTIs will lead to a better understanding of the disease process and will subsequently lead to the development of new diagnosis, prevention, and treatment options.

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 ileal mucosa of Crohn disease (CD) patients is abnormally colonized by adherent-invasive E. coli (AIEC) that are able to adhere to and invade intestinal epithelial cells. Here, we show that CD-associated AIEC strains adhere to the brush border of primary ileal enterocytes isolated from CD patients but not controls without inflammatory bowel disease. AIEC adhesion is dependent on type 1 pili expression on the bacterial surface and on carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) expression on the apical surface of ileal epithelial cells. We report also that CEACAM6 acts as a receptor for AIEC adhesion and is abnormally expressed by ileal epithelial cells in CD patients. In addition, our in vitro studies show that there is increased CEACAM6 expression in cultured intestinal epithelial cells after IFN-gamma or TNF-alpha stimulation and after infection with AIEC bacteria, indicating that AIEC can promote its own colonization in CD patients.