Article

Pseudomembranous colitis caused by a toxin A(-) B(+) strain of Clostridium difficile.

Department of Laboratory Medicine, University of Washington, Seattle, Washington 98195, USA.
Journal of Clinical Microbiology (Impact Factor: 4.07). 05/2000; 38(4):1696-7.
Source: PubMed

ABSTRACT We report a case of severe pseudomembranous colitis due to a toxin A(-) B(+) strain of Clostridium difficile in an immunosuppressed patient and discuss the implications for diagnostic testing in suspected C. difficile-associated diarrhea.

0 0
 · 
0 Bookmarks
 · 
127 Views
  • [show abstract] [hide abstract]
    ABSTRACT: Clostridium difficile infection (CDI) is considered to be the main cause of bacterial infectious diarrhea in nosocomial settings. Since the beginning of the new century a continuous rise in the incidence of severe CDI has been observed worldwide. Even though some CDI cases are not associated with previous antibiotic exposure, this remains as the principal risk factor for the development of CDI. The rate of recurrences represents perhaps one the most challenging aspect on the management of CDI. There are several microbiological tests available, but glutamate dehydrogenase antigen test can be selected as the first screening step in a diagnostic algorithm, with positive samples then confirmed using a toxin(s) test, to distinguish toxinogenic from nontoxinogenic CDI. Although metronidazole and vancomycin are and have been the mainstay treatment options for CDI, there are some unmet medical and therapeutical needs. Usually oral metronidazole is recommended for initial treatment of nonsevere CDI and vancomycin for treatment of severe disease. Fidaxomicin may be considered in patients who cannot tolerate vancomycin, although more data are needed. For treatment of a nonsevere initial recurrence of CDI, oral metronidazole should be used, but for treatment of subsequent recurrences or more severe cases fidaxomicin may be helpful.
    Expert Review of Anticancer Therapy 12/2012; 10(12):1405-23. · 3.22 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: The alarming emergence of hypervirulent strains of Clostridium difficile with increased toxin production, severity of disease, morbidity, and mortality emphasizes the need for a culture method that permits simultaneous isolation and detection of virulent strains. The C. difficile toxins A and B are critical virulence factors, and strains can either be toxin-producing (virulent) or non-toxin-producing (nonvirulent). Strains that are isolated from human infections generally produce either toxin A or toxin B or both. The methods currently available for culturing C. difficile do not differentiate strains that produce active toxins from strains that do not produce toxins or produce inactive toxins. As a result, the identification and isolation of toxin-producing strains from stool is currently a two-step process. First, the stool is plated on a selective medium, and then suspected colonies are analyzed for toxin production or the presence of the toxin genes. We describe here a novel selective and differential culture method, the Cdifftox plate assay, which combines in a single step the specific isolation of C. difficile strains and the detection of active toxin. This assay was developed based on our recent finding that the A and B toxins of C. difficile cleave chromogenic substrates that have stereochemical characteristics similar to their natural substrate, UDP-glucose. The Cdifftox plate assay is shown here to be extremely accurate (99.8% effective) in detecting toxin-producing strains through the analysis of 528 C. difficile isolates selected from 50 tissue culture cytotoxicity assay-positive clinical stool samples. The Cdifftox plate assay advances and improves the culture approach such that only C. difficile strains will grow on this agar, and virulent strains producing active toxins can be differentiated from nonvirulent strains, which do not produce active toxins. This new method reduces the time and effort required to isolate and confirm toxin-producing C. difficile strains.
    Journal of clinical microbiology 12/2011; 49(12):4219-24. · 4.16 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: Abstract Enterocyte turnover along with proper epithelial barrier function are crucial aspects of mucosal defense. Apoptosis is a highly regulated type of programmed cell death that allows for the homeostatic turnover of the epithelial layer. Recent studies have suggested that microbial modulation of enterocyte apoptosis can result in increased epithelial permeability, leading to gastrointestinal pathophysiology. In this review, we highlight key mechanisms and pathways via which various viral, bacterial and parasitic pathogens are able to modulate enterocyte apoptosis. We also discuss how these alterations to enterocyte apoptosis can result in the activation of chronic gastrointestinal disorders, such as allergies, irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). The role of proteinase-activated receptors in the pathogenesis of modulated apoptosis-induced pathogenesis is also discussed. Newly discovered processes, through which host epithelial cells may have evolved, rescue mechanisms from microbe-induced apoptosis are discussed. Together, these mechanisms are key to our ever-increasing understanding of host-microbe interactions in the gut.
    Critical Reviews in Microbiology 01/2013; · 5.07 Impact Factor

Full-text

View
0 Downloads
Available from

Ajit P Limaye