Detection of toxin production in Clostridium difficile strains by three different methods

Yücesoy, Mine; McCoubrey, J.; Brown, Robert L.; Poxton, Ian R.

doi:10.1046/j.1469-0691.2002.00440.x

Cited by 12 publications

(13 citation statements)

References 25 publications

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“…Eradication of the responsible pathogen from the gastrointestinal tract and removal of toxins are the goal of any therapy. Obtaining a quick, accurate diagnosis is crucial, and therefore rapid detection assays for CD toxins should be used in all SORs presenting with diarrhea [18,19].…”

Section: Discussionmentioning

confidence: 99%

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Clostridium difficile Colitis in Solid Organ Transplantation—A Single-Center Experience

et al. 2007

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Clostridium difficile (CD) is one of the most common causes of diarrhea in solid organ transplantation (SOT). Between 1996 and 2005, a total of 2474 solid organ transplants were performed at our institution, of which 43 patients developed CD-associated diarrhea. There were 3 lung, 3 heart, 20 liver, 8 kidney-pancreas, 6 kidney, 1 composite tissue, and 2 multivisceral recipients. Onset of CD infection ranged from 5 to 2453 days posttransplant. All patients presented with abdominal pain and watery diarrhea. Toxins A and B were detected using rapid immunoassay or enzyme immunoassay. Treatment consisted of reduction of immunosuppression, fluid and electrolyte replacement, metronidazole (n=20), oral vancomycin (n=20), and a combination of metronidazole and vancomycin (n=2). Toxic megacolon was seen in five patients. Two of them had colonoscopic decompression, and the remaining three required colonic resection. One of these patients died due to multiorgan failure after cured CD enteritis. The remaining patients were discharged with well-functioning grafts and all are currently alive. CD colitis was a rare complication prior to 2000; 38 of the 43 cases occurred thereafter. We conclude that CD colitis represents a severe complication following SOT. Recently, a dramatic increase in the incidence of this complication has been observed. The development of life-threatening toxic megacolon must be considered in solid organ recipients.

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Section: Discussionmentioning

confidence: 99%

“…CD-associated diarrhea has been described in all types of SOT and after stem cell transplantation [10][11][12][13][14][15][16][17]. Rapid detection of enteric pathogens is essential in order to initiate timely treatment, since diarrhea during the early posttransplant period can cause severe secondary complications [18,19].…”

Section: Introductionmentioning

confidence: 99%

Clostridium difficile Colitis in Solid Organ Transplantation—A Single-Center Experience

et al. 2007

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“…Eradication of the responsible pathogen from the gastrointestinal tract and removal of toxins is the goal of any therapy. Obtaining a quick and accurate diagnosis is often difficult, as stool cultures can take up to 48 h. Sometimes, even repeated testing fails to identify pathogens 8,10,16 . Rapid detection assays should be applied in all SORs presenting with diarrhea, with the limitation that the sensitivity of tests for detecting CD toxins or proteins of RV in stool are often unsatisfactorily low.…”

Section: Discussionmentioning

confidence: 99%

Enterocolitis due to Simultaneous Infection with Rotavirus and Clostridium difficile in Adult and Pediatric Solid Organ Transplantation

Stelzmueller

Wiesmayr

Eller

et al. 2007

Journal of Gastrointestinal Surgery

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Diarrhea is a well-known complication of immunosuppression but is also frequently caused by pathogens such as Clostridium difficile (CD) and rotavirus (RV). Three adult and five pediatric solid organ recipients (SORs) developed diarrhea with simultaneous identification of CD and RV. Rotavirus was identified using an immunochromatografic- or enzyme-linked immunosorbent assay; CD was identified using a rapid immunoassay or enzyme immunoassay. One adult renal, one adult kidney-pancreas, one adult liver, and five pediatric liver recipients were affected. Onset of RV/CD infection ranged from 2 weeks to 4 years posttransplant. All patients presented with enterocolitis causing significant fluid and electrolyte loss. In adults, CD was treated with metronidazole and in children with oral vancomycin. RV infection was treated with fluid/electrolyte replacement. During diarrhea, a significant rise in tacrolimus serum level was noted. All patients cleared CD. One child developed recurrent episodes of RV infection and died from bacterial sepsis; the renal recipient died 6 months posttransplant from myocardial infarction. The remaining six patients are currently alive with well-functioning grafts. Simultaneous infection with CD and RV may lead to severe diarrhea in SORs. Both pathogens should be considered in SOR presenting with diarrhea.

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“…The cytotoxins (both toxins A and B) can be detected by bioassays using human fibroblasts, or more conveniently, by commercially available enzyme immunoassays. 64 The latter tests have been adopted by most hospital laboratories as a standard test to detect C. difficile cytotoxins. In patients with pseudomembranous colitis, the diagnosis can be confirmed by colonoscopy, which reveals yellowwhite, raised plaques, varying from 2 to 10 mm in size, over the mucosal surface, usually associated with patchy or diffuse colonic erythema.…”

Section: Clostridium Speciesmentioning

confidence: 99%

Bacterial hemorrhagic enterocolitis

2003

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Bacterial diarrhea can be classified into two clinical entities, noninflammatory diarrhea and inflammatory diarrhea syndromes. The latter type of diarrhea is characterized by bloody and puruloid mucus stool, and is often accompanied by fever, tenesmus, and severe abdominal pain. Pathogenic bacteria causing the inflammatory diarrhea syndrome include Salmonella, Vibrio, Shigella, enteroinvasive and enterohemorrhagic Escherichia coli, Campylobacter, Yersinia, Chlamydia, and Clostridium difficile. The pathologic changes in the inflammatory diarrhea syndrome range from a superficial exudative enterocolitis to a transmural enterocolitis with overt ulceration. This syndrome is also designated as bacterial hemorrhagic enterocolitis because of its usual manifestation by bloody diarrhea. The diagnostic approach needs information on the patient's age, travel history, epidemiological associations, sexual practice, and medical history, including usage of antibiotics. Bacterial information can be obtained by microscopic study, culture, and the identification of specific bacterial toxins. Flexible colonoscopy with biopsy is useful for the differentiation of bacterial hemorrhagic enterocolitis from idiopathic ulcerative colitis and ischemic colitis. Physicians should be familiar with the diagnostic modalities used to detect the specific pathogens causing hemorrhagic bacterial enterocolitis; namely, bacterial culture, serology, histology, and nucleic acid technologies.

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Detection of toxin production in Clostridium difficile strains by three different methods

Abstract: We can recommend the use of the Techlab A + B enzyme immunoassay for the detection of toxin production by C. difficile strains because of its high sensitivity and specificity, its ease of use, and its capability of detecting both A- and B-type toxins.

Cited by 12 publications

References 25 publications

Clostridium difficile Colitis in Solid Organ Transplantation—A Single-Center Experience

Clostridium difficile Colitis in Solid Organ Transplantation—A Single-Center Experience

Enterocolitis due to Simultaneous Infection with Rotavirus and Clostridium difficile in Adult and Pediatric Solid Organ Transplantation

Bacterial hemorrhagic enterocolitis

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