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Ecological means of control of diarrhea.

In summary, altered intestinal ecology is very important in the pathogenesis of antibiotic-associated diarrhea and pseudomembranous colitis. Prevention of AAD has been demostrated with LactobacillusGG, Enterococcus SF68, and S. boulardii. While therapy with antibitics such as vancomycin or metranidazole is effective for PMC, relapse can occur and is difficult to treat. Antibiotics can be given, but another approach of restoring the normal colonic ecology may be more effective. Such therapy has included use of the nontoxigenic strains of C. difficile, rectal infusions of homologous feces or mixtures of bacteria, and oral administration of Lactobaccillus GG and the live yeast Saccharomyces boulardii. It is clear that many factors influence normal colonic homeostasis, including and individual's age, health, nutritions, medication, presence of gastrointentinal desease or surgery. The fetal flow is complex. Some factors related to C. difficile and disease production are known. For instance, only toxigenic strains cause disease, but rates of carrieage vary and not everyone with toxigenic strains of C. difficile will become ill. Studies of healthy volutenteers who took an oral cephalosporin antibiotic revealed that over 90% of them became colonized with C. difficile, and some excreted the organism for up to 26 days. Some volunteers had loose stools, but not was clinically ill[11]. Similary, neonates have a high rate of carriage of C. difficile and toxin (up to 60%), but usually are asymptomatic. Obviously, other factors besides presence of organism determine development of diseases. One such factor may the state of the immune system. In support of this are reports of recurrent C. difficile colitis in hypogammaglobulinemic children, and successful treatment of recurrent C. difficile colitis with intravenous gamma glubulin [51]. But recent studies of mucosal (secretory) IgA levels in C. difficile-associated diarrhea showed no clear-cut relaxationship of systemic or mucosol antibodies toxin A with the clinical course of C. Difficle infection [52] Other factors have not been explored, such as the influence of the diet. In addition, the intestinal flora may be allerted by bile acid production and/or pancreatics proteases.

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