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: 3.99). 05/2000; 38(4):1696-7.
Source: PubMed


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.

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    • "Initially, toxin A was reported to be responsible for the disease (3). However, the role of toxin B has been reviewed and toxin B is now considered more important than toxin A, and possibly essential for virulence (3–6). Rapid diagnosis of this pathogen is decisive in allowing clinicians to prescribe the appropriate therapy and to take adequate measurement for controlling nosocomial spread. "
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    ABSTRACT: In this study, the prevalence of C. difficile, from patients with gastrointestinal complaints and its association with other enteropathogen microbes were investigated. Clostridium difficile is an important pathogen associated with outbreaks of pseudomembranous colitis and other intestinal disorders, such as diarrhea. Enterotoxin and cytotoxin (toxin A and toxin B) of C. difficile on the patient's stool samples were detected by a double sandwich enzyme-linked Immunosorbant assay technique using a commercial kit (Premier toxins A & B; Generic Assays, Inc., Germany). The microbial isolation and examination was done, according to the standard identification methods. Out of 356 individuals (57.6% male and 42.4% female) the results of C. difficile were positive for 19 patients (5.3%) and negative for 337 patients (94.6%) according to the results of C. difficile antigen kit. There was no association between the existence of C. difficile toxin and microbial population or antibiotic usage. This prevalence study clearly supports the hypothesis of a probable role of C.difficile in developing gastrointestinal complaints in patients with diarrhea. More studies are needed to evaluate the role of C. difficile in these diseases.
    Full-text · Article · Feb 2011 · Gastroenterology and hepatology from bed to bench
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    • "It has been suggested that TcdB-treated cells require activation of the pro-apoptotic factor RhoB, via TcdB inactivation of RhoA, in order to induce the associated C. difficile cytotoxicity (Genth et al., 2008). The cytopathic effects of TcdA and TcdB in tissue remain partially ambiguous, and the emergence of clinical isolates that are tcdB+ tcdA− but which result in clinical symptoms indistinguishable from tcdA+ tcdB+ strains suggest that both toxins are not absolutely required for a productive infection (Kato et al., 1998; Kuijper et al., 2001; Limaye et al., 2000). Recent work has indicated that C. difficile-induced apoptosis is due to TcdB inducing mitochondrial hyperpermeability via disruption of the mitochondrial membrane polarity, resulting in mitochondrial swelling, release of pro-apoptotic proteins and eventual lysis, all promoting progression of the host cell to apoptosis (Matarrese et al., 2007). "
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    ABSTRACT: Clostridium difficile is a leading cause of nosocomial infections, causing a spectrum of diseases ranging from diarrhoea to pseudomembranous colitis triggered by a range of virulence factors including C. difficile toxins A (TcdA) and B (TcdB). TcdA and TcdB are monoglucosyltransferases that irreversibly glycosylate small Rho GTPases, inhibiting their ability to interact with their effectors, guanine nucleotide exchange factors, and membrane partners, leading to disruption of downstream signalling pathways and cell death. In addition, TcdB targets the mitochondria, inducing the intrinsic apoptotic pathway resulting in TcdB-mediated apoptosis. Modulation of apoptosis is a common strategy used by infectious agents. Recently, we have shown that the enteropathogenic Escherichia coli (EPEC) type III secretion system effector NleH has a broad-range anti-apoptotic activity. In this study we examined the effects of NleH on cells challenged with TcdB. During infection with wild-type EPEC, NleH inhibited TcdB-induced apoptosis at both low and high toxin concentrations. Transfected nleH1 alone was sufficient to block TcdB-induced cell rounding, nuclear condensation, mitochondrial swelling and lysis, and activation of caspase-3. These results show that NleH acts via a global anti-apoptotic pathway.
    Full-text · Article · Mar 2010 · Microbiology
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    • "Clostridium difficile infection is the main cause of diarrhoea and colitis in hospitalized patients whose intestinal microbiota is altered due to the prescribed intake of antibiotics (Kelly et al., 1994b; Mylonakis et al., 2001). Clostridium difficile causes enteritis by releasing two exotoxins, toxin A and B, both of which have potent enterotoxicity in vitro and elicit intestinal secretion and inflammation in vivo (Kelly et al., 1994b; Alfa et al., 2000; Limaye et al., 2000; Savidge et al., 2003). Considerable mechanistic information is known about how toxin A exerts its effects. "
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    ABSTRACT: Clostridium difficile is responsible for a large proportion of nosocomial cases of antibiotic-associated diarrhoea and pseudomembranous colitis. The present study provides evidence that yeast, beef and pork extracts, ingredients commonly used to grow bacteria, can counteract C. difficile toxin A enterotoxicity in vitro and in vivo. In model intestinal epithelial cells the individual extracts could prevent the toxin A-induced decrease in epithelial barrier function and partially prevented actin disaggregation and cell rounding. Mice with ad libitum access to individual extracts for 1 week had almost complete reduction in toxin A-induced fluid secretion in intestinal loops. Concomitantly, the toxin A-induced expression of the essential proinflammatory mediator Cox-2 was normalized. Moreover this protective effect was also seen when mice received only two doses of extract by intragastric gavage within 1 week. These results show that yeast, beef and pork extracts have the potential to counteract the intestinal pathogenesis triggered by C. difficile toxin A.
    Full-text · Article · May 2009 · FEMS Microbiology Letters
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