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The article discusses the recent changes and developments in the epidemiology of Clostridium difficile infection, which is a normal cause of colitis. The different approaches to management of this disease are reviewed.

Virtual colonoscopy can be as effective as traditional colonoscopy for detecting colorectal cancer and intestinal polyps that may become cancerous, according to a study published in 2003. If this can be confirmed, virtual colonoscopy could be used to screen all asymptomatic people 50 years old and older. Virtual colonoscopy uses three-dimensional CT scans, which takes less time and is less invasive than traditional colonoscopy.

We determined whether the cytoprotective heat shock protein HSP72 protects against the injurious effects of Clostridium difficile toxin A (TxA) on intestinal epithelial cells. Colonic epithelial Caco-2/bbe (C2) cells were stably transfected with HSP72 antisense (C2AS) or vector only (C2VC), resulting in low and high HSP72 expression, respectively. Measurements of epithelial barrier integrity, mitochondrial function, and apoptosis activation were assessed after TxA exposure. HSP72 and RhoA interactions were evaluated with immunoprecipitations. In C2AS cells, TxA was associated with a greater decrease in transepithelial resistance (TER), an increase in [[sup.3]H]mannitol flux, and increased dissociation of perijunctional actin. Although HSP72 binds RhoA, it failed to prevent RhoA glucosylation. TxA caused a more rapid decrease in ATP, release of cytochrome c, and activation of caspase-9 in C2AS cells. To determine whether ATP depletion decreases TER, we treated cells with antimycin A, which caused a decline in TER. We conclude that HSP72 may protect intestinal epithelial cells from TxA-mediated damage through several mechanisms, including actin stabilization, mitochondrial protection, and inhibition of apoptosis activation, but not by prevention of RhoA glucosylation. bacterial toxin; caspase; cytochrome c; heat shock proteins; transepithelial electrical resistance

Most chemotherapeutic drugs kill cancer cells by indirectly activating checkpoint-mediated apoptosis after creating nonselective damage to DNA or microtubules, which accounts for their toxicity toward normal cells. We seek to target cancer cells by directly activating checkpoint regulators without creating such damage. Here, we show that [beta]-lapachone selectively induces apoptosis in cancer cells without causing the death of nontransformed cells in culture. This unusual selectivity against cancer cells is preceded by activation of S-phase checkpoint and selective induction of E2F1, a regulator of checkpoint-mediated apoptosis. This study suggests direct checkpoint activation as a strategy against cancer.

A 17-year-old girl who developed fever, abdominal pain, and diarrhea three weeks after a cesarean delivery was found to have a Salmonella infection in her large intestine. The species was Salmonella newport, which is a common cause of food poisoning.

The role of reactive oxygen metabolites in the development of enteritis in rats induced by Clostridium difficile toxin A was investigated. Findings showed that intraluminal toxin A significantly increased hydroxyl radical and hydrogen peroxide production by ileal microsomes, which was inhibited by pretreatment with a reactive oxygen metabolite scavenger, superoxide dismutase or DMSO. On the other hand, mucosal xanthine oxidase increased only slightly following exposure to toxin A while allopurinol, an inhibitor of xanthine oxidase, did not affect toxin A-mediated intestinal responses.

Research suggests that human monocytes exposed to bacterium Clostridium difficile produce neutrophil chemoatractant blood factor interleukin-8. Experiments designed to assess the effects of Clostridium difficile toxins A and B on intestinal macrophages within rabbit ileum are described. Interleukin-8 concentration measurements in relation to toxin levels are reported.

The ability of epidermal growth factor (EGF) to prevent damage of colonic mucosa caused by Clostridium difficile toxins A and B was investigated. Cytotoxic activity of both toxins was tested against IMR-90 fibroblasts to determine the effect of EGF and the toxins on electrophysiology of the human colon. Results showed that administration of the tyrosine kinase inhibitor genistein attenuated the effect of EGF. Also, toxins A and B caused a decline in transepithelial resistance, suggesting toxin-induced damage of epithelial barrier integrity.

Experiment was conducted to compare the effects of interleukin-11 (rhIL-11) on rat ileal responses to two bacterial toxins, namely, C. difficile toxin A, which causes secretion and intestinal inflammation, and cholera toxin, which causes secretion without intestinal inflammation. The effects of rhIL-11 on toxin A-mediated responses in intestinal mast cells, lamina propria macrophages and peripheral blood monocytes were also evaluated. Results suggest that rhIL-11 blocks the intestinal release of inflammatory mediators from mucosal mast cells and intestinal macrophages.

The contribution of corticotropin releasing factor (CRF) and mast cells to stress-induced mucin release from rat colon was investigated using colonic mucosal explants. The results revealed that acute stress caused a marked increases in mast cell protease II, prostaglandin E2, mucin release, cyclooxygenase-2 mRNA, and fecal pellet output. It was suggested that mucin release was stimulated by the increase in CRF via activation of mast cells.

The disassembley of actin microfilaments is the primary mechanism by which cells respond to Clostridium difficule toxin B. The toxin is a proetin toxin associated with antibiotic related colitis. The disassembly reveals that the breakdown of the filaments occurs due to the calcium influx activated by Clostridium difficile toxin B.

Persistent diarrhea in children may be an indication of pseudomembranous colitis associated with Clostridium (C.) difficile toxin. Pseudomembranous colitis is an inflammation of the bowel mucous membranes with the formation of false membranes over ulcers. A 31-month-old girl was hospitalized after a two-week history of diarrhea, vomiting and dehydration, even after treatment with antibiotics. Her abdomen was distended and x-rays showed enlargement of several loops of the small bowel. She received fluids, electrolytes and antibiotics, but continued to have frequent loose, greenish stools that contained blood. A diagnostic test for C. difficile toxin was positive. She was treated with the antibiotics vancomycin, metronidazole and trimethoprim-sulfamethoxazole. An examination 15 days later showed abnormal fluid collection and yellow-white plaques. A biopsy specimen showed bowel lining cell death and formation of false membranes. The patient recovered after four weeks of treatment.

Pseudomembranous colitis is commonly caused by overgrowth of the bacterium Clostridium (C.) difficile after antibiotic therapy. Pseudomembranous colitis is inflammation of the mucous membrane of the colon characterized by the formation of false membranes, diarrhea, abdominal pain and fever. After antibiotic therapy, the colon membrane is susceptible to infection by C. difficile, which then produces toxins that cause diarrhea and other symptoms. C. difficile infections may occur as infection without symptoms, antibiotic-associated colitis without membrane formation, pseudomembranous colitis and sudden, life-threatening colitis. Diagnosis of C. difficile infections is by isolation of C. difficile toxins in the feces, but rapid antigen detection tests are also available. Discontinuation of antibiotic therapy will usually resolve minor infections. If symptoms are severe or persistent or if antibiotic therapy can not be discontinued, infections may be treated with metronidazole or vancomycin, which are antibacterial drugs.

Gastric mucus keeps the hydrochloric acid (HCl) secreted as a part of digestion from damaging the stomach's epithelium through viscous fingering. In vitro injection of HCl into mucin, a principal constituent of gastric mucus, produced these finger-shaped structures that result from the interaction of low-viscosity HCl with high-viscosity mucus. Acid-flow rate, pH and mucin levels also affect viscous fingering.