Pseudomembranous Colitis: Presence of Clostridial Toxin

Larson, H Elliott; Ab, Price

doi:10.1016/s0140-6736(77)90363-4

Cited by 207 publications

(66 citation statements)

References 5 publications

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“…The authors also found that isolates of C. difficile produced a toxin that was detected in patients' stools. This observation correlated with an earlier finding indicating that toxin is produced in the intestinal tract in patients with antibiotic-associated diarrhea, although the source of this toxin had not been established (6,7). Other studies soon found that C. difficile causes PMC in hamsters if the animals are pretreated with clindamycin (8).…”

supporting

confidence: 82%

Variations in Virulence and Molecular Biology among Emerging Strains of Clostridium difficile

Hunt

Ballard

2013

Microbiol Mol Biol Rev

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SUMMARY Clostridium difficile is a Gram-positive, spore-forming organism which infects and colonizes the large intestine, produces potent toxins, triggers inflammation, and causes significant systemic complications. Treating C. difficile infection (CDI) has always been difficult, because the disease is both caused and resolved by antibiotic treatment. For three and a half decades, C. difficile has presented a treatment challenge to clinicians, and the situation took a turn for the worse about 10 years ago. An increase in epidemic outbreaks related to CDI was first noticed around 2003, and these outbreaks correlated with a sudden increase in the mortality rate of this illness. Further studies discovered that these changes in CDI epidemiology were associated with the rapid emergence of hypervirulent strains of C. difficile , now collectively referred to as NAP1/BI/027 strains. The discovery of new epidemic strains of C. difficile has provided a unique opportunity for retrospective and prospective studies that have sought to understand how these strains have essentially replaced more historical strains as a major cause of CDI. Moreover, detailed studies on the pathogenesis of NAP1/BI/027 strains are leading to new hypotheses on how this emerging strain causes severe disease and is more commonly associated with epidemics. In this review, we provide an overview of CDI, discuss critical mechanisms of C. difficile virulence, and explain how differences in virulence-associated factors between historical and newly emerging strains might explain the hypervirulence exhibited by this pathogen during the past decade.

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supporting

confidence: 82%

Variations in Virulence and Molecular Biology among Emerging Strains of Clostridium difficile

Hunt

Ballard

2013

Microbiol Mol Biol Rev

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“…Sterile fecal filtrates from patients receiving antibiotics also induced morphological changes, which could be neutralized by C. sordellii antiserum, in a variety of cultured mammalian cells (74,155). Further studies identified Clostridium difficile as the etiologic agent of pseudomembranous colitis in humans (25,101,156).…”

Section: Introductionmentioning

confidence: 99%

Clostridium difficile: clinical disease and diagnosis

1993

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Clostridium difficile is an opportunistic pathogen that causes a spectrum of disease ranging from antibiotic-associated diarrhea to pseudomembranous colitis. Although the disease was first described in 1893, the etiologic agent was not isolated and identified until 1978. Since clinical and pathological features of C. difficile-associated disease are not easily distinguished from those of other gastrointestinal diseases, including ulcerative colitis, chronic inflammatory bowel disease, and Crohn's disease, diagnostic methods have relied on either isolation and identification of the microorganism or direct detection of bacterial antigens or toxins in stool specimens. The current review focuses on the sensitivity, specificity, and practical use of several diagnostic tests, including methods for culture of the etiologic agent, cellular cytotoxicity assays, latex agglutination tests, enzyme immunoassay systems, counterimmunoelectrophoresis, fluorescent-antibody assays, and polymerase chain reactions.

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“…Clostridium dzficile has been shown to be the most important cause of antibiotic-associated pseudomembranous colitis and antibiotic-associated diarrhoea (Larson & Price, 1977;George at al., 1978;Bartlett et al, 1978). Resistance to antibiotics may also play a significant role in the development of the disease, as multiply resistant strains are often responsible for nosocomial outbreaks of C. dzficile-associated disease (Pierce et al, 1982;Wust et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Genetic analysis of a tetracycline resistance element from Clostridium difficile and its conjugal transfer to and from Bacillus subtilis

Mullany

Wilks

Lamb

et al. 1990

Journal of General Microbiology

104

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A tetracycline resistance (Tc') determinant from Closfridium &Bile strain 630 was cloned into the Escherichia coli plasmid vector pUC13. The resulting plasmid pPPM20, containing an insert of 3.4 kbp, was mapped and a 1.1 kbp SucI-Hind111 fragment wholly within the Tcr gene was identified. Dot-blot hybridization studies with the 1.1 kbp fragment showed that the Tcr gene belonged to hybridization class M. Tcr could be transferred between C. &mile strains and to Bacillus subtilis at a frequency of lo-' per donor cell. The element could be returned from B. subtilis to C. &@cik at a frequency of per donor cell. This is the first demonstration of C. &Wile acting as a recipient in intergeneric crosses. DNA from C. dzBcile transconjugants digested with EcoRV always has two hybridizing fragments of 9.5 and 11.0 kbp when probed with pPPM20. DNA from B. subtiZis transconjugants digested with EcoRV produced one hybridizing band of variable size when probed with pPPM20. The behaviour of the element was reminiscent of the conjugative transposons. Therefore we compared the element to the conjugative transpomn Tn916. The Him11 restriction maps of the two elements Mered and no hybridization was detected to oligonucleotides directed to the ends of Tn916. However, the elements do have some sequence homology, detected by hybridization analysis.

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Pseudomembranous Colitis: Presence of Clostridial Toxin

Cited by 207 publications

References 5 publications

Variations in Virulence and Molecular Biology among Emerging Strains of Clostridium difficile

Variations in Virulence and Molecular Biology among Emerging Strains of Clostridium difficile

Clostridium difficile: clinical disease and diagnosis

Genetic analysis of a tetracycline resistance element from Clostridium difficile and its conjugal transfer to and from Bacillus subtilis

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