Pseudomembranous Colitis 

  • Author: Jennifer A Curry, MD, MPH; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Sep 6, 2011
 

Background

Clostridium difficile is a spore-forming organism responsible for an infectious colitis that affects 1 of every 200 patients who are admitted to the hospital. Increasingly implicated as a significant cause of morbidity and mortality among hospitalized patients, C difficile colitis should also be recognized among outpatient populations. Prior antibiotic exposure remains the most significant risk factor for development of disease.

Several synonymous terms are used to refer to the spectrum of disease attributable to C difficile infections (CDI); these terms include C difficile –associated diarrhea (CDAD), antibiotic-associated colitis, C difficile colitis, and pseudomembranous colitis (PMC). C difficile is the primary pathogen of antibiotic-associated colitis and accounts for up to 25% of nosocomial antibiotic associated diarrhea.[1] Pseudomembranous colitis specifically describes the formation of a membranous exudate in the colon, which occurs in approximately 50% of cases of CDI. However, because endoscopy is now used less frequently in the evaluation of antibiotic-associated diarrhea, many articles reference this entity under the umbrella term of CDI. CDI, CDAD, PMC, and C difficile colitis essentially represent the same disease process; severity of the patient presentation dictates treatment.

An image depicting pseudomembranous colitis can be seen below.

Colonic pseudomembranes of pseudomembranous colitiColonic pseudomembranes of pseudomembranous colitis. Photographs courtesy of Eric M. Osgard, MD.

In 1893, Finney first reported pseudomembranous colitis in a patient who died after developing severe diarrhea after gastric surgery. Later, in the 1950s, both Staphylococcus aureus and Candida albicans were considered etiologic sources after isolation from the stools of affected patients. In 1977, C difficile and its toxins were established as the cause of antibiotic-associated colitis.

In the last decade, an increasing number of C difficile infections have been reported, and the proportion of cases complicated by severe outcomes has increased. This may be partially due to the spread of virulent clonal strains. In 2003, an outbreak in Quebec and 8 U.S. states received significant media attention. More than 80% of the isolates tested were of the same strain (designated PFGE NAP1, or PCR-ribotype 027), which was notable for the production of binary toxin and a deletion in the regulatory gene tcdC.[2, 3, 4] Multiple other outbreaks have been reported with other strains. The molecular epidemiology of C difficile in health care facilities is dynamic and incompletely understood.[5, 6]

Any antibiotic can increase the risk of C difficile disease, including metronidazole and vancomycin, which are used in the treatment of CDI. Disease has been reported following as little as one dose of antibiotic. Although the attributable risk has varied among studies, fluoroquinolones, macrolides, clindamycin, beta-lactam/beta-lactamase inhibitors, and all 3 generations of cephalosporins have consistently been shown to pose a significant risk for the development of CDI. Antineoplastic agents and proton pump inhibitors have also been associated with CDI.

The Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA) updated clinical practice guidelines regarding the diagnosis and management of Clostridium difficile infection in 2010.[7]

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Pathophysiology

C difficile is an anaerobic, toxigenic, spore-forming, gram-positive rod. The spores can survive for months on hospital environmental surfaces, and patients can remain asymptomatic carriers. The risk of colonization increases with length of hospital stay; nearly 20% of hospitalized patients have asymptomatic fecal colonization,[8] as opposed to the 1-3% rate in healthy community residents. Children under the age of 1 year have the highest rate of asymptomatic carriage, up to 60%.[9]

The use of antibiotics alters the normal bowel flora, predisposing to the overgrowth of C difficile and the production of its toxins. CDI results from the inflammatory reaction of the bowel wall to luminal toxins produced by C difficile. Continuation of inflammatory process can lead to formation of pseudomembranes, a mixture of inflammatory cells, fibrin, and bacterial and cellular components, which exudes from the bowel mucosa. Not all strains of C difficile are toxigenic.

Colonic pseudomembranes of pseudomembranous colitiColonic pseudomembranes of pseudomembranous colitis. Photographs courtesy of Eric M. Osgard, MD.

Toxigenic C difficile produces 2 similar large molecular weight toxins that disrupt the barrier function of the colonic mucosa.

Toxin A is an enterotoxin that binds to receptors in the bowel wall, leading to activation of the inflammatory cascade and disruption of the intercellular tight junctions, causing fluid secretion, mucosal injury, edema, and inflammation.

Toxin B is the primary cytotoxin responsible for C difficile infection. It appears to act as a cytoskeletal disruptor, leading to mucosal injury and further activation of the inflammatory cascade.

Binary toxin is a third toxin produced by a small percentage (about 5%) of C difficile isolates. It is similar in structure to the iota toxin of Clostridium perfringens. Binary toxin may be associated with increased disease severity, as well as with community-acquired disease.

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Epidemiology

Frequency

United States

Hospital admissions complicated by C difficile –associated disease almost doubled between 2000 and 2003, increasing from 0.27% to 0.51% of all hospital admissions in the United States. In elderly patients (age >65), the increased incidence was even more pronounced.[10] The reported incidence rate of C difficile infection in 2005 (84 per 100,000 patient-days) was two and a half times the 1996 rate (31 per 100,000).

In a recent study of community hospitals in the Duke Infection Control Outreach Network, C difficile infection surpassed MRSA as the leading cause of nosocomial infections (0.28 cases per 1000 patient days vs 0.23 cases per 1000 patient days).[11]

International

Canada and Europe have historically reported similar rates of CDI as those noted in the United States. A 2004 report from a large university center in Canada noted an increase in incidence from 35.6 cases per 100,000 patient-days in 1991 to 156.3 per 100,000 in 2003; among patients aged 65 years or older, the rate increased from 102 to 866.5 per 100,000. A follow-up study by the same group reported an overall incidence of 65 cases per 100,000 patient-days in 2005.[12]

Mortality/Morbidity

CDI causes a significant burden on the health care system. The costs associated with each hospitalized case of CDI were $3,699 in excess health care costs and 3.6 extra days of hospitalization, according to a report of short-stay hospitals in 2002.

Infection with toxigenic C difficile is a potentially life-threatening disease process. Historically, the attributable mortality of CDI has been less than 2% of cases.[13, 14] However, the more severe NAP1/BI/027 strain noted in outbreaks in Canada was associated with a 6.9% directly attributable 30-day mortality.

Significant morbidity can result from recurrent disease. Up to 25% of patients will experience at least one additional episode of disease

Age

Persons over the age of 65 are at higher risk for developing CDI and recurrent disease than younger persons. Increasing age is highly predictive of severe outcome or mortality.[15] Infants and children have high rates of asymptomatic carriage, but clinical disease is uncommon (4.0 cases per 1000 admissions).[16]

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Contributor Information and Disclosures
Author

Jennifer A Curry, MD, MPH  Attending Physician, Infectious Disease Clinic, Naval Medical Center Portsmouth; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences

Jennifer A Curry, MD, MPH is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Gary L Gorby, MD  Associate Professor, Departments of Internal Medicine and Medical Microbiology and Immunology, Division of Infectious Diseases, Creighton University School of Medicine; Associate Professor of Medicine, University of Nebraska Medical Center; Associate Chair, Omaha Veterans Affairs Medical Center

Gary L Gorby, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Joseph F John Jr, MD, FACP, FIDSA, FSHEA  Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgments

The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the U.S. government.

LCDR Jennifer Curry is a military service member. This work was prepared as part of official duties. Title 17 U.S.C. §105 provides that ‘Copyright protection under this title is not available for any work of the United States Government.’ Title 17 U.S.C. §101 defines a U.S. Government work as a work prepared by a military service member or employee of the U.S. Government as part of that person’s official duties.

Many thanks to Duane R Hospenthal, MD, PhD, Joseph Lee, MD, and Braden Hale, MD, MPH for their work on earlier versions of this topic.

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Colonic pseudomembranes of pseudomembranous colitis. Photographs courtesy of Eric M. Osgard, MD.
 
 
 
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