Antibiotic-Associated Pseudomembranous Colitis: An Epidemiologic Investigation of a Cluster of Cases

Pierce, Phillip F.; Wilson, Robert H.; Silva, J.; Garagusi, Vincent F.; Rifkin, Gary D.; Fekety, Robert; Nunez-Montiel, O; Dowell, V. R.; Hughes, James M.

doi:10.1093/infdis/145.2.269

Cited by 102 publications

(29 citation statements)

References 11 publications

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“…In contrast, Pierce et al (19) failed to find differences in the rates of antibioticassociated colitis after the administration of several antibiotics, although the power of that study to detect significant differences likely was small. Quantitative risk estimations in humans are bedevilled by problems of sample size, uncertainties about how much and how often antibiotics are actually consumed, differences in routes of administration, use of combination antibiotic therapies, and ignorance about whether individuals have actually been exposed to C. diffcile in their environments.…”

mentioning

confidence: 85%

Quantitative study of antibiotic-induced susceptibility to Clostridium difficile enterocecitis in hamsters

Larson

Borriello

1990

Antimicrob Agents Chemother

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Commonly used antibiotics were compared for their ability to induce Clostridium difficile enterocecitis and death in hamsters. Susceptibility to infection with C. difficile was measured by calculating 50% lethal doses (in CFU) for hamsters for various intervals after antibiotic treatment. Infection occurred after very small doses of C. difficile were given to hamsters treated with clindamycin, ampicillin, flucloxacillin, and cefuroxime; there was little difference between the antibiotics in the degree of susceptibility that they induced. A large difference in the duration of susceptibility was observed, however, with susceptibility being temporary following ampicillin, flucloxacillin, and cefuroxime administration but long-lived following clindamycin administration. A larger dose of ampicillin, multiple doses of ampicillin, and a combination of antibiotics had comparatively small effects on the duration of susceptibility. C. dfficile growth and toxin production in in vitro suspensions of cecal contents were found to correlate closely with in vivo hamster infectivity. A persisting loss of colonization resistance following antibiotic treatment may be a type of postantibiotic effect. Although these results cannot be applied directly to humans, they suggest lines of further investigation into how antibiotics may differ in producing risks of C. difficile infection and pseudomembranous colitis in patients.Prior to the recognition that pseudomembranous colitis (PMC) was caused by Clostridium difficile, it was known to be a risk of antibiotic treatment, especially lincomycin and clindamycin (11). Discovery of the microbial pathogenesis of PMC (18) has permitted a more careful assessment of the relationship between antibiotic treatment and C. difficile infection (17). A large number of antibiotics have been found to facilitate infection in both animals and humans (2, 10).There has been suspicion that some antibiotics are more likely to result in C. difficile-associated disease than others. (17) were used in this study. Both strains produce toxins A and B. Antibiotic MICs were determined by a microdilution technique. For strain B-1 the MICs were as follows: clindamycin, 256 ,ug/ml; ampicillin, 0.5 ,ug/ml; flucloxacillin, 4 ,ug/ml; and cefuroxime, 128 ,ug/ml. Strain H-1 was inhibited by 0.13 ,ug of clindamycin per ml and 0.5 ,ug of ampicillin per ml. For inoculation of hamsters, a spore preparation was made from a 5-day Robertson cooked meat medium culture by using alcohol shock. The culture broth was centrifuged at 2,000 x g for 10 min, suspended in 5 ml of brain heart infusion (Difco Laboratories, Detroit, Mich.) with cysteine hydrochloride (BHIC; 0.5% [wt/vol]), mixed with 5 ml of 100% ethanol, held for 1 h at ambient temperature, and centrifuged again as described above. The pellet was washed once in BHIC and suspended in 5 ml of BHIC, and serial 10-fold dilutions in BHIC were prepared. The number of viable spores in the inocula was estimated by seeding 0.5 ml of diluted suspension on a blood agar plate (Difco), incub...

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mentioning

confidence: 85%

Quantitative study of antibiotic-induced susceptibility to Clostridium difficile enterocecitis in hamsters

Larson

Borriello

1990

Antimicrob Agents Chemother

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“…This is clinically important since proctoscopy alone may not detect these changes [10,17,21,65,68,[70][71][72]. Flexible sigmoidoscopy should be cautiously performed to confirm the diagnosis of PMC in all patients only exception is a toxic patient where high risk for perforation may exist as the disease progresses [52,[67][68][69][74][75][76][77]. Besides collecting tissue for culture assays or histology, decompression after assessment may be considor other inflammatory entities in patients with diarrhea, ered if abdominal distension is present [51,68,76,77].…”

Section: Endoscopymentioning

confidence: 99%

“…Other less important factors [19,21,136]. This may be secondary to the use of broadspectrum antibiotics in the treatment of frequent urogefor acquisition of C. difficile-associated disease include female sex, inflammatory bowel disease, gastrointestinal nital infections in women [2,74,123,136]. Secondly, inflammatory bowel disease is more common in females, manipulations, and renal disorders [2,3,46,53,107,111,[114][115][116].…”

Section: Endoscopymentioning

confidence: 99%

<i>Clostridium difficile </i>Infection: Risk Factors, Medical and Surgical Management

Klingler¹,

Metzger²,

Seelig³

et al. 2000

Dig Dis

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Background:Clostridium difficile has become recognized as a cause of nosocomial infection which may progress to a fulminant disease. Methods: Literature review using electronic literature research back to 1966 utilizing Medline and Current Contents. All publications on antibiotic-associated diarrhea, antibiotic-associated colitis, and pseudomembranous colitis as well as C. difficile infection were included. We addressed established and potential risk factors for C. difficile disease such as an impaired immune system and cost benefits of different diagnostic tests. An algorithm is outlined for diagnosis and both medical and surgical management of mild, moderate and severe C. difficile disease. Results: Diagnosis of C. difficile infection should be suspected in patients with diarrhea, who have received antibiotics within 2 months or whose symptoms started after hospitalization. A stool specimen should be tested for the presence of leukocytes and C. difficile toxins. If this is negative and symptoms persist, stool should be tested with ‘rapid’ enzyme immunoabsorbent and stool cytotoxin assays, which are the most cost-effective tests. Endoscopy and other imaging studies are reserved for severe and rapidly progressive courses. Oral metronidazole or vancomycin are the antibiotics of choice. Surgery is rarely required for selected patients refractory to medical treatment. The threshold for surgery in severe cases with risk factors including an impaired immune system should be low. Conclusion:C. difficile infection has been recognized with increased frequency as a nosocomial infection. Early diagnosis with immunoassays of the stool and prompt medical therapy have a high cure rate. Metronidazole has supplanted oral vancomycin as the drug of first choice for treating C. difficile infections.

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“…However, comparison of the rates of carriage must consider the method of culture (selective versus nonselective media) and the method of selection for healthy adults with no prior exposure to antimicrobial agents. Although the rate of spontaneous pseudomembranous colitis following antibiotic therapy is low, several clusters of cases have been reported (136,194,212,226,264).…”

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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Antibiotic-Associated Pseudomembranous Colitis: An Epidemiologic Investigation of a Cluster of Cases

Cited by 102 publications

References 11 publications

Quantitative study of antibiotic-induced susceptibility to Clostridium difficile enterocecitis in hamsters

Quantitative study of antibiotic-induced susceptibility to Clostridium difficile enterocecitis in hamsters

<i>Clostridium difficile </i>Infection: Risk Factors, Medical and Surgical Management

Clostridium difficile: clinical disease and diagnosis

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