Pseudomembranous colitis.

Ab, Price; Davies, David R.

doi:10.1136/jcp.30.1.1

Cited by 229 publications

(69 citation statements)

References 28 publications

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“…This finding is ofpotential importance, as it has variously been suggested that the intestinal lesions associated with pseudomembranous colitis in humans may be due to a primary endothelial effect (5) and that the toxin A effects on rabbit ileum are secondary to toxin-stimulated release of mediators from inflammatory cells (6). The most striking effect oftoxin A on Ts4 (17).…”

Section: Discussionmentioning

confidence: 99%

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Clostridium difficile toxin A perturbs cytoskeletal structure and tight junction permeability of cultured human intestinal epithelial monolayers.

Hecht¹,

Pothoulakis²,

LaMont³

et al. 1988

J. Clin. Invest.

372

209

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Toxin A of Clostridium difficile causes severe inflammatory enterocolitis in man and animals that appears to be mediated in part by acute inflammatory cells that migrate into the toxin A-exposed mucosa. To determine the direct effects of toxin A on intestinal epithelial permeability and structure in the absence of other modulating factors, we used cultured monolayers of a human intestinal epithelial cell line (T84). A toxin A concentration of 7 X 10-1 ,ug/ml (3 X i0-' M) nearly abolished monolayer transepithelial resistance within 6-8 h. This marked permeability defect occurred while the monolayers were still confluent. Dual sodium-mannitol flux studies localized the permeability defect to the intercellular tight junction. Cytotoxicity assays and morphological evaluation using Nomarski optics and electron microscopy failed to demonstrate any evidence of cell damage at the time the maximum resistance response was observed. Fluorescent staining for F actin, however, revealed a marked decrease in fluorescent intensity in toxin-treated monolayers versus controls. These data show that toxin A can directly affect the barrier function of this model intestinal epithelium and initially does so by selectively enhancing tight junction permeability. Furthermore, cytoskeletal structure is markedly altered over the same time course, although the integrity of individual cells is maintained. Because the cytoskeleton of intestinal epithelial cells is known to be capable of regulating tight junction permeability, we speculate that the above effects of toxin A on epithelial barrier function result from alterations of the cytoskeleton.

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Section: Discussionmentioning

confidence: 99%

“…is primarily affected by C. dificile toxins. Based on analysis of human rectal biopsies displaying pseudomembranous colitis in the early phase, Price and Davies (5) speculated that the initial target might be the endothelium lining the superficial capillary network. In this view, the epithelial effects would be a secondary event.…”

Section: Introductionmentioning

confidence: 99%

Clostridium difficile toxin A perturbs cytoskeletal structure and tight junction permeability of cultured human intestinal epithelial monolayers.

Hecht¹,

Pothoulakis²,

LaMont³

et al. 1988

J. Clin. Invest.

372

209

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“…Most cases of PMC are associated with antibiotic use, although 1–7% of cases of PMC have had no documented antibiotic exposure [34]. PMC has been reported in patients without antibiotic exposure who have insulin-dependent diabetes mellitus, hepatic and renal failure, malnutrition, cystic fibrosis or have had upper GI tract surgery [61].…”

Section: Risk Factorsmentioning

confidence: 99%

“…Ischemic colitis may also exhibit a yellow confluent pseudomembrane [30]. Histologic findings include epithelial necrosis, distended goblet cells, infiltration of the lamina propria with leukocytes, and plaques consisting of inflammatory cells, fibrin and mucin [10, 24, 34, 35](fig. 2a, b).…”

Section: Diagnosismentioning

confidence: 99%

Pseudomembranous Colitis: Causes and Cures

Surawicz

McFarland

1999

Digestion

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Clostridium difficile is the most common nosocomial pathogen of the gastrointestinal tract and has increased in frequency over time. Typical symptoms of C. difficile infection include diarrhea, which is usually nonbloody, or colitis associated with severe abdominal pain, fever and/or gross or occult blood in the stools. Pseudomembranous colitis (PMC), the severest form of this disease, occurs as a result of a severe inflammatory response to the C. difficile toxins. This review focuses on PMC, as this severe form is associated with the greatest medical concern. Diagnosis rests on detection of C. difficile in the stool, either by culture, tissue culture assay for cytotoxin B or detection of antigens in the stool by rapid enzyme immunoassays. Oral therapy with metronidazole 250 mg 4 times a day for 10 days is the recommended first-line therapy. Vancomycin is also effective, but its use must be limited to decrease the development of vancomycin-resistant organisms such as enterococci. Vancomycin (125–500 mg 4 times a day for 10 days) should be limited to those who cannot tolerate or have not responded to metronidazole, or when metronidazole use is contraindicated, as in the first trimester of pregnancy. A therapeutic response within a few days is usual. Recurrence of symptoms after antibiotics occurs in 20% of cases and is associated with persistence of C. difficile in the stools. Further recurrences then become more likely. Therapy with antibiotics in a pulsed or tapered regimen is often effective as are efforts to normalize the fecal flora. The yeast Saccharomyces boulardii has been proven in controlled trials to reduce recurrences when given as an adjunct to antibiotic therapy. Careful hand washing and environmental decontamination are necessary to prevent epidemics.

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“…Histologically, the pseudomembranes, composed of fibrin, mucus, epithelial and inflammatory cells appear as "clouds" rising from points of superficial ulcerations. The lesions have been termed "volcano" lesions appearing like an eruption above underlying glandular lesions [47] . In 22% of cases, pseudomembranes were visualized on endoscopy, but not present histologically [48] .…”

Section: Endoscopic Diagnosis Of CDImentioning

confidence: 99%

Clinical update for the diagnosis and treatment ofClostridium difficileinfection

Oldfield

Johnson

2014

WJGPT

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Clostridium difficile infection (CDI) presents a rapidly evolving challenge in the battle against hospitalacquired infections. Recent advances in CDI diagnosis and management include rapid changes in diagnostic approach with the introduction of newer tests, such as detection of glutamate dehydrogenase in stool and polymerase chain reaction to detect the gene for toxin production, which will soon revolutionize the diagnostic approach to CDI. New medications and multiple medical society guidelines have introduced changing concepts in the definitions of severity of CDI and the choice of therapeutic agents, while rapid expansion of data on the efficacy of fecal microbiota transplantation heralds a revolutionary change in the management of patients suffering multiple relapses of CDI. Through a comprehensive review of current medical literature, this article aims to offer an intensive review of the current state of CDI diagnosis, discuss the strengths and limitations of available laboratory tests, compare both current and future treatments options and offer recommendations for best practice strategies.

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Pseudomembranous colitis.

Cited by 229 publications

References 28 publications

Clostridium difficile toxin A perturbs cytoskeletal structure and tight junction permeability of cultured human intestinal epithelial monolayers.

Clostridium difficile toxin A perturbs cytoskeletal structure and tight junction permeability of cultured human intestinal epithelial monolayers.

Pseudomembranous Colitis: Causes and Cures

Clinical update for the diagnosis and treatment ofClostridium difficileinfection

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