Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diarrhea in children is often caused by enteropathogen infections that might benefit from early empirical antibiotic therapy. However, when the definition of the pathogen requires sophisticated laboratory studies, the etiology of enteritis is not known early in illness. Empirical therapy may be dangerous if the child is infected with a Shiga toxin-producing Escherichia coli (STEC) strain because antimicrobials may increase Shiga toxin (Stx) release, resulting in increased risk of microangiopathic hemolytic anemia with acute renal failure (hemolytic-uremic syndrome [HUS]) and death. There is a need for antimicrobials that would be effective against multiple bacterial enteropathogens yet not induce Stx release or increase the risk of HUS. Rifaximin has been evaluated in adults for treatment of bacterial enteritis and has a good record for safety and efficacy, but it has not been evaluated extensively in children with gastroenteritis. We therefore evaluated rifaximin's potential for phage induction, drug-induced bacteriolysis, and toxin release in 57 STEC strains (26 O157 and 31 non-O157 strains). Growth in ciprofloxacin, a known Stx phage inducer, caused bacteriolysis and release of toxin in 25/26 (96%) O157 strains and 15/31 (48%) non-O157 strains. In contrast, rifaximin did not induce phage replication or lysis in any strain. Toxin release in the presence of rifaximin was not different from release in the absence of antibiotic. Rifaximin, unlike many antibiotics used to treat pediatric gastroenteritis, does not induce phage-mediated bacteriolysis and Stx release.
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PMID:Rifaximin does not induce toxin production or phage-mediated lysis of Shiga toxin-producing Escherichia coli. 1752 59

Defining etiology of acute diarrhea is critical to disease therapy and prevention. In this review we look at recent developments in etiologic agents of acute diarrhea and advances in therapy and prevention of the illness. Newly appreciated agents include enterotoxigenic Bacteroides fragilis, Klebsiella oxytoca and Laribacter hongkongensis. Atypical enteropathogenic E. coli (EPEC) strains lacking the gene for epithelial attachment appear to be more important as causes of diarrhea than traditional EPEC strains. Enterotoxigenic E. coli and enteroaggregative E. coli diarrhea known to be important abroad, have recently been shown to occur in the United States. Non-O157:H7 strains of Shiga toxin-producing E. coli are increasing and infrequently are being sought. There is currently a serious epidemic of nosocomial diarrhea due to a fluoroquinolone-resistant and more virulent and difficult to treat strain of C. difficile. Rotavirus vaccine development should lead to reduction of infant gastroenteritis mortality in infants living in developing regions. Noroviruses produce outbreaks of water- and food-borne disease but show broad genetic diversity. Reduced osmolarity oral rehydration treatment (ORT) and recombinant human lactoferrin/lysozyme plus rice-based ORT effectively treat acute diarrhea. Probiotics were shown to be effective in preventing antibiotic associated- and C. difficile-diarrhea. Rifaximin prevents and azithromycin effectively treats travelers' diarrhea.
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PMID:Advances in defining etiology and new therapeutic approaches in acute diarrhea. 1782 22

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder with a multifactorial pathophysiology. The gut microbiota differs between patients with IBS and healthy individuals. After a bout of acute gastroenteritis, postinfection IBS may result in up to approximately 10% of those affected. Small intestinal bacterial overgrowth (SIBO) is more common in patients with IBS than in healthy individuals, and eradication of SIBO with systemic antibiotics has decreased symptoms of IBS in some patients with IBS and SIBO. The nonsystemic (i.e. low oral bioavailability) antibiotic rifaximin is indicated in the United States and Canada for the treatment of adults with IBS with diarrhea (IBS-D). The efficacy and safety of 2-week single and repeat courses of rifaximin have been demonstrated in randomized, placebo-controlled studies of adults with IBS. Rifaximin is widely thought to exert its beneficial clinical effects in IBS-D through manipulation of the gut microbiota. However, current studies indicate that rifaximin induces only modest effects on the gut microbiota of patients with IBS-D, suggesting that the efficacy of rifaximin may involve other mechanisms. Indeed, preclinical data reveal a potential role for rifaximin in the modulation of inflammatory cytokines and intestinal permeability, but these two findings have not yet been examined in the context of clinical studies. The mechanism of action of rifaximin in IBS is likely multifactorial, and further study is needed.
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PMID:Mechanism of action and therapeutic benefit of rifaximin in patients with irritable bowel syndrome: a narrative review. 3204 34