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At least 415 records · Page 23Linked to original sources
PubMed1996

Saccharomyces boulardii protease inhibits Clostridium difficile toxin A effects in the rat ileum.

Saccharomyces boulardii, a nonpathogenic yeast, is effective in treating some patients with Clostridium difficile diarrhea and colitis. We have previously reported that S. boulardii inhibits rat ileal secretion in response to C. difficile toxin A possibly by releasing a protease that digests the intestinal receptor for this toxin (C. Pothoulakis, C. P. Kelly, M. A. Joshi, N. Gao, C. J. O'Keane, I. Castagliuolo, and J. T. LaMont, Gastroenterology 104: 1108-1115, 1993). The aim of this study was to purify and characterize this protease. S. boulardii protease was partially purified by gel filtration on Sephadex G-50 and octyl-Sepharose. The effect of S. boulardii protease on rat ileal secretion, epithelial permeability, and morphology in response to toxin A was examined in rat ileal loops in vivo. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the purified S. boulardii protease revealed a major band at 54 kDa. Pretreatment of rat ileal brush border (BB) membranes with partially purified protease reduced specific toxin A receptor binding (by 26%). Partially purified protease digested the toxin A molecule and significantly reduced its binding to BB membranes in vitro (by 42%). Preincubation of toxin A with S. boulardii protease inhibited ileal secretion (46% inhibition, P < 0.01), mannitol permeability (74% inhibition, P < 0.01), and histologic damage caused by toxin A. Thus, S. boulardii protease inhibits the intestinal effects of C. difficile toxin A by proteolysis of the toxin and inhibition of toxin A binding to its BB receptor. Our results may be relevant to the mechanism by which S. boulardii exerts its protective effects in C. difficile infection in humans.

Animals↗
PubMed1999

Nucleotide and peptide sequences of the open reading frame encoding a truncated toxin A gene of Clostridium difficile strain CCUG 20309.

The open reading frame encoding a putative truncated toxin A gene of Clostridium difficile in strain CCUG 20309 (ATCC 8864), a strain that produces toxin B but not toxin A, was sequenced by cycle sequencing method. The coding region contains 2097 base pairs and has a GC content of 26.4%. The deduced polypeptide is 50 kDa and is generally hydrophilic. Although strain CCUG 20309 of C. difficile was reported not to produce toxin A, it is enterotoxic, an inherent property of toxin A in pathogenic strains of C. difficile. It therefore remains to be determined whether a truncated form of toxin A could actually be expressed from the open reading frame by this strain of C. difficile.

Amino Acid Sequence↗
PubMed1999

Antimicrobial susceptibility of Clostridium difficile by E test.

The in vitro inhibitory activity of 11 antimicrobials against 44 clinical isolates of Clostridium difficile was investigated. Minimum inhibitory concentrations (MICs) were determined using E test. Metronidazole (MIC90 0.38 microg/mL), teicoplanin (MIC90 0.75 microg/mL) and vancomycin (MIC90 1.0 microg/mL) were very active against the isolates examined, whereas, resistance to imipenem, cefoxitin, clindamycin and ciprofloxacin was found in most of the tested strains. We concluded that teicoplanin warrants clinical trials to determine its adequate dosage to treat C. difficile infection. The commonly used regimens to treat intra-abdominal and/or anaerobic infections (eg. imipenem, cefoxitin, clindamycin or ciprofloxacin) need special attention, while considering the side effects of C. difficile-associated diarrhea.

Ampicillin↗
PubMed2005

[Study on clostridium difficile-associated diarrhea suspected as nosocomial infection in urology ward].

Between June 2000 and January 2001, 11 patients were diagnosed with Clostridium diffcile (C. difficile)-associated diarrhea in the ward of urology at the Kakegawa Municipal Hospital. Of these 11 patients, 10 had exposure to antimicrobial agents, before the onset of diarrhea. All patients' stools were positive for C. difficile toxin A. After discotinuing antimicrobial agents with or without administering Vancomycin, they recovered from C. difficile-associated diarrhea. Between January 2001 and September 2002, 17 patients who were diagnosed with C. difficile-associated diarrhea in our hospital were classified into two types by PCR ribotyping. Therefore, we suspected a nosocomial outbreak of diarrhea caused by C. difficile.

Adult↗
PubMed1996

Clostridium difficile colitis--diagnosis and therapy.

Clostridium difficile is a Gram-positive bacillus which had been identified as the source of potent exotoxins: toxin A and toxin B. C. difficile infection usually follows antibiotic therapy and results from unrestrained growth of pathogenic strains of C. difficile in the colon. Typical clinical findings include: diarrhoea with blood and mucus, fever, abdominal pain, nausea, loss of body weight. In the past the diagnosis was based on positive result of stool culture but now several tests are available: latex-agglutination test, enzyme immunoassays and fluorescence-immunoenzymatic tests. Diagnostic methods enable quick and safe detection of C. difficile antigens or toxins and proper management. Poor susceptibility of C. difficile strains to common antibiotics hinders choosing the effective therapy.

Clostridioides difficile↗
PubMed2000

Treatment of Clostridium difficile-associated diarrhea and colitis.

Treatment of C. difficile diarrhea with metronidazole or vancomycin is highly effective at relieving symptoms. The high rate of diarrhea recurrence is concerning, but fortunately most patients respond to a second course of treatment. The problem of vancomycin resistance in hospital organisms has markedly reduced usage of this agent as a first-line treatment for C. difficile diarrhea, leaving metronidazole as the mainstay of treatment in the United States where teicoplanin and fusidic acid are not marketed. It is likely that any new antimicrobial agent used to treat C. difficile will be similarly plagued by a high rate of recurrence, presumably incurred as a result of disruption of normal bowel flora. There is a need for improved treatment and prevention of this increasingly frequent and debilitating nosocomial infection. Treatments that utilize passive antibodies, immunization, nontoxigenic C. difficile, or other forms of biotherapy may hold the key to improved treatment and prevention of C. difficile disease in the future. In the meantime, it behooves all practitioners to use antimicrobials judiciously in order to prevent as many cases of C. difficile diarrhea as possible.

Abdomen, Acute↗
PubMed2005

LuxS/autoinducer-2 quorum sensing molecule regulates transcriptional virulence gene expression in Clostridium difficile.

Toxigenic Clostridium difficile CCUG19126 produces the autoinducer-2 (AI-2) quorum sensing molecule that induces bioluminescence in Vibrio harveyi BB170 reporter strain. AI-2-containing cell-free supernatants from mid-log phase C. difficile and Escherichia coli DH5alpha expressing recombinant luxS(cd) upregulated the transcript levels of tcdA (7-10-fold), tcdB (4-6-fold), and tcdE (2-3-fold) in early-log C. difficile. In contrast, no induction occurred when cells were exposed to sterile medium or to cell-free supernatant from E. coli DH5alpha. AI-2 did not significantly increase the level of toxin A in early-log C. difficile. These results suggest that LuxS(cd)-dependent signaling regulates virulence gene expression at the transcriptional level in C. difficile.

Bacterial Proteins↗
PubMed2005

Subtyping of Clostridium difficile polymerase chain reaction (PCR) ribotype 001 by repetitive extragenic palindromic PCR genomic fingerprinting.

Fifty isolates of the most common UK strain of Clostridium difficile [polymerase chain reaction (PCR) ribotype 001] were analysed by three PCR-based typing methods in order to determine genomic diversity within this strain that may form the basis of a subtyping method. The three methods used were repetitive extragenic palindromic elements (REP), conserved repetitive DNA elements (BOX), and enterobacterial repetitive PCR intergenic consensus sequences (ERIC). The performance of each typing method was assessed by comparing powers of discrimination, typeability and reproducibility. All methods had satisfactory levels of typeability and reproducibility as determined by blind-coded repeats, but REP-PCR typing proved to be the most discriminatory method, yielding seven distinct amplicon profiles consisting of up to eight major bands. BOX-PCR generated between two and five major amplicons with four distinct BOX profiles. ERIC-PCR primers, however, could not discriminate between isolates. These results suggest that PCR ribotype 001 is not clonal in nature at present, and that REP-PCR subtyping methods offer promise to further our understanding of the epidemiology of C. difficile PCR ribotype 001 disease in UK hospitals.

Belgium↗