Clostridium difficile Infection

Abstract

The spore-forming anaerobe Clostridium difficile has become a serious enteropathogen. Changes in the composition of natural intestinal flora, mainly due to antibiotic therapy, permit its colonization of, and multiplication in, the colon. The disease is caused by (entero)toxin A and (cyto)toxin B, and infection ranges from asymptomatic carrier state and mild diarrhea to pseudomembranous colitis. The clinical diagnosis is made by observing inflammatory, sometimes bloody, diarrhea and by the colonoscopic detection of epithelial necrosis, ulceration, and, in the advanced state, pseudomembrane formation. The laboratory supports the diagnosis by detecting toxin A and/or B by an enzyme-linked immunoassay with high specificity, but sometimes less sensitivity than with the cytotoxin assay in tissue culture cells. Fecal leukocytes or fecal lactoferrin may be found. Culture for the isolation and identification of toxigenic C. difficile is time consuming but necessary for epidemiological studies. Polymerase chain reaction (PCR) tests have been tested for detection of the toxin B gene directly in stool. Therapy consists of stopping all systemic antibiotic treatment and the use of oral metronidazole or vancomycin. There may be more relapses after vancomycin therapy, and the increasing vancomycin resistance of Enterococcus is worrisome. Prevention, especially of nosocomial spread, requires isolation and enforced handwashing. For epidemiological studies, the bacteria can be typed by molecular DNA analyses, including PCR, protein electrophoresis, and immunological tests.

Six Rapid Tests for Direct Detection of Clostridium difficile and Its Toxins in Fecal Samples Compared with the Fibroblast Cytotoxicity Assay

“…However, these methods are nonspecific in that both toxigenic and nontoxigenic strains of C. difficile are identified. A latex agglutination toxin test and C. difficile PCR protocols have also been described but are not in widespread use (13,14). The current standard is the cytotoxin B assay (CBA).…”

“…These newer tests have been reported to approach the sensitivity of direct CBA, are specific, and offer significant advantages in terms of turn around time, cost, and ease of performance (14,17,22,28,29,33). In this study, we tested over 1,000 fecal samples to evaluate the performance of the following commercial IAs in comparison with direct CBA: Prima System Clostridium difficile Tox A (Prima A; Bartels Inc., now Trinity Biotech, Bray, Ireland) and VIDAS Clostridium difficile Tox A II (VIDAS A; bioMérieux Vitek, Inc., Hazelwood, Mo.…”

Isolation of Clostridium Difficile and Detection of A and B Toxins Encoding Genes

“…Antibiotic therapy is the most important risk factor for C. difficile colonization (22). In 2010, Wachter showed that every one in 100 hospitalized patients is diagnosed with this infection, and patients with C. difficile had a threefold increased risk of death during their hospitalization (23).…”

Antibiotikainduzierte Diarrhö und pseudomembranöse Enterokolitis

“…Seit der Anwendung von Breitbandantibiotika sind Clostridium difficile assoziierte Diarrhöen sowohl in der ambulanten Behandlung als auch als nosokomiale Infektion unter stationären Bedingungen vermehrt beobachtet worden [4].Clindamycin [37] und vor allem Cephalosporine der 2. und 3. Generation sind die häufig-sten Verursacher dieser Infektionen gefolgt von Penicillinen und Chinolonen [39,41,47,62,63].…”

“…Hall u. O`Toole [20] nannten dieses Bakterium "the difficult clostridium", weil es sehr langsam in den Kulturen heranwuchs und äußerst schwierig zu isolieren war.Es ist ein grampositives, anaerobes, sporenbildendes Bakterium,welches den menschlichen Dickdarm bei 3% der erwachsenen Bevölkerung und bis zu 50-70% von Neugeborenen der ersten 5 Monate asymptomatisch besiedelt [4,21,22],ohne eine Erkrankung auszulö-sen. Zu Nekrosen und Ulzerationen der Dickdarmschleimhaut mit Ausbildung von "Pseudomembranen" (⊡ Abb. Ätiologie,Therapie,Prognose und Prophylaxe dieser Erkrankung werden diskutiert.…”