eMedicine Specialties > Infectious Diseases > Gastrointestinal Tract and Intra-abdominal Infections

Pseudomembranous Colitis

Author: Jennifer A Curry, MD, MPH, Staff Physician, Infectious Disease Clinic, Naval Medical Center Portsmouth
Coauthor(s): Braden R Hale, MD, MPH, Assistant Clinical Professor, Department of Internal Medicine, University of California at San Diego; Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Naval Medical Center at San Diego; Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, San Antonio Military Medical Center, Brooke Army Medical Center; Professor of Medicine, Uniformed Services University of the Health Sciences; Joseph Lee, MD, Staff Physician, Department of Medicine, Walter Reed Army Medical Center
Contributor Information and Disclosures

Updated: Aug 25, 2009

Introduction

Background

Clostridium difficile is a gram-positive 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; these terms include C difficile –associated diarrhea (CDAD), antibiotic-associated colitis, C difficile colitis, and pseudomembranous colitis (PMC). Pseudomembranous colitis specifically describes the formation of a membranous exudate in the colon, which occurs in approximately 50% of cases of CDAD. However, because endoscopy is now used less frequently to demonstrate pseudomembranes in the evaluation of CDAD, most recent journal articles reference this entity under the umbrella term of CDAD. The underlying management of the disease does not change based on classification. Although CDAD is inherently an antibiotic-associated diarrhea, the latter term is usually reserved for milder disease that is not caused by C difficile or its toxins.  

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.  

Any antibiotic can increase the risk of C difficile disease, including metronidazole and vancomycin, which are used in the treatment of CDAD. Disease has been reported following as little as one dose of antibiotic. Although the attributable relative 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 CDAD.

Recently, an increasing number of C difficile infections have been reported, and the proportion of cases complicated by severe outcomes has increased. This may be due to the spread of a particularly virulent clonal strain. In 2003, an outbreak in Quebec and 8 US states received significant media attention. More than 80% of the isolates tested were of the same strain, designated as pulsed-field gel electrophoresis NAP1, or polymerase chain reaction (PCR)–ribotype 027. This strain is notable for the presence of binary toxin and an 18–base pair (bp) deletion in the regulatory gene tcdC, which ordinarily downgrades toxin production.1,2,3

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, as opposed to the 1-3% rate in healthy community residents.  

The use of antibiotics alters the normal bowel flora, predisposing to the overgrowth of C difficile and the production of its toxins. Antineoplastic agents such as 5-fluorouracil, methotrexate, cisplatin, and cyclophosphamide have also been associated with CDAD.

CDAD 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 colit...

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

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Colonic pseudomembranes of pseudomembranous colit...

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

 

C difficile produces two similar large molecular weight toxins, which are unique among bacterial enterotoxins. Both disrupt the barrier function of the colonic mucosa.

  • Toxin A is an enterotoxin that binds to known receptors in the bowel wall. This process leads to activation of the inflammatory cascade, cytoskeletal derangements, and disruption of the intercellular tight junctions, causing fluid secretion, mucosal injury, edema, and inflammation.
  • Toxin B is a cytotoxin for which a receptor has not been found in the human bowel mucosa; however, this cytotoxin also appears to act as a cytoskeletal disruptor, leading to further mucosal injury. Toxin B may play a role in activating 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. The pathogenic role of binary toxin has not been fully elucidated.

Frequency

United States

The number of hospital admissions complicated by C difficile –associated disease has increased steadily over the last decade, increasing from 0.27% of all hospital admissions in the United States prior to 2000 to 0.51% of all hospital admissions in 2003.4

In elderly patients, the increased incidence is more pronounced; the most recent estimate of incidence in patients older than 65 years was 228 per 100,000 person-years.4  

The outpatient incidence of CDAD is significantly lower than the inpatient rate. The most recent estimates are 0.5-1 hospital admissions per 100,000 person-years; however, these rates may have also recently increased.

International

Canada and Europe have historically reported similar rates of CDAD as those noted in the United States. However, Canada has reported increased rates over the past decade. A 2004 report from a large university center in Canada noted an increase in incidence from 35.6 per 100,000 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.

Mortality/Morbidity

CDAD causes a significant burden on the health care system. The costs associated with each hospitalized case of CDAD 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. Patients who are not treated or in whom treatment is delayed may develop complications including fulminant toxic megacolon. The mortality rate in patients who develop complications is as high as 30%.

Significant morbidity can result from recurrent disease, which occurs in up to one third of patients.

Sex

Women are at higher risk for developing recurrent disease than men.

Age

Elderly persons are at higher risk for developing CDAD and recurrent disease than younger persons.

Clinical

History

The clinical course prior to development of C difficile –associated diarrhea (CDAD) typically contains a history of antibiotic exposure, risk factors for colonization, and alterations in host physiology.  

  • History of antibiotic exposure
    • CDAD symptoms typically develop 5-10 days after initiation of antibiotic therapy. However, they can develop after a single day of antibiotic use or can occur as late as 10 weeks after cessation. 
    • Some patients may develop CDAD without a clearly identified antibiotic exposure. 
    • Importantly, not all diarrhea cases following antibiotic use are due to C difficile. In fact, 70-80% of diarrhea following antibiotic use is due to changes in the osmotic pressure in the lumen after alteration of the bowel flora decreases the use and absorption of carbohydrates.
  • Colonization with C difficile
    • Generally, colonization occurs following ingestion of acid-resistant spores. 
    • In the hospital environment, the spores are common contaminants from patients who harbor C difficile. The organism can be transmitted via fomites or the hands of health care providers. 
    • Hospitalized patients and residents of long-term care facilities are at higher risk of colonization with C difficile. 
    • Although less common, colonization can occur in the outpatient setting.
  • Host factors that increase susceptibility to C difficile –associated diarrhea
    • Chronic debilitation critical illness 
    • Alteration in gut motility
      • Agents that affect the bowel, including enemas, stool softeners, and opioids, are identified as risk factors for disease development. 
      • Patients who have undergone abdominal surgery with subsequent ileus are also at increased risk.
    • Receipt of enteral tube feeds 
    • Use of proton pump inhibitors (These may increase the rate of successful colonization after oral ingestion; clinical studies have shown mixed results.)
    • Impaired humoral immunity (especially of the IgG subclasses) (This may increase the susceptibility to relapsing disease.) 
    • A common single nucleotide polymorphism (SNP) of the interleukin (IL)–8 gene promotor5

The clinical presentation of C difficile –associated disease can range from mild self-limited diarrhea to severe colitis with pseudomembrane formation complicated by development of toxic megacolon or colonic perforation. The classic presentation is cramping abdominal pain with profuse, mucoid, greenish, malodorous watery stools.

  • Clinical signs
    • Diarrhea: This is usually fairly mild, with 2-6 stools per day. However, persons with severe cases may have more than 20 stools per day.
    • Leukocytosis: Leukocytosis is found in 50-60% of patients. A WBC count of 12,000-20,000 103/μL with associated with minimal diarrhea and a lack of other presenting signs is a common hospital presentation. However, 30% of patients have a WBC count of more than 30,000 103/μL.
    • Fever: This affects 30-50% of patients.
    • Abdominal pain or cramping: This affects 20-33% of patients and may have various presentations. Sometimes generalized, diffuse, and cramping, it can also manifest as focal pain that mimics acute abdomen. Evidence of peritoneal signs should immediately raise suspicion for fulminant colitis and toxic megacolon.
    • Constipation with or without dyspepsia: This can be an atypical presentation.
    • Colitis can be present without accompanying diarrhea, particularly in patients with right-sided colonic involvement.
    • Toxic megacolon can complicate severe infection and can lead to bowel perforation.
    • Extraintestinal manifestations are rare and include the following:
      • Bacteremia, generally polymicrobial
      • Splenic abscess
      • Osteomyelitis
      • Reactive arthritis or tenosynovitis
    • Other findings include the following:
      • Nausea
      • Malaise
      • Anorexia
      • Hypoalbuminemia
      • Anasarca
      • Electrolyte disturbances
      • Occult colonic bleeding
      • Orthostatic due to dehydration

Physical

The diagnosis of CDAD relies primarily on an appropriate suggestive history. Physical examination findings may include fever, abdominal tenderness, and diarrhea. In cases of severe diarrhea, physical signs suggestive of dehydration (eg, dry mucous membranes, decreased skin turgor, orthostasis) may also be present.

Causes

C difficile –associated disease results from the action of toxins formed by the organism. Rarely, pseudomembranous colitis can be caused by other etiologies, such as Staphylococcus species or enterotoxigenic C perfringens, Campylobacter species, Listeria species, and Salmonella species.

More on Pseudomembranous Colitis

Overview: Pseudomembranous Colitis
Differential Diagnoses & Workup: Pseudomembranous Colitis
Treatment & Medication: Pseudomembranous Colitis
Follow-up: Pseudomembranous Colitis
Multimedia: Pseudomembranous Colitis
References
Further Reading
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Keywords

pseudomembranous colitis, PMC, antibiotic-associated colitis, antibiotic-associated diarrhea, Clostridium difficile colitis, C difficile colitis, C difficile diarrhea, Clostridium difficile diarrhea, Clostridium difficile –associated diarrhea, –associated diarrhea, CDAD, C difficile infection, pseudomembranes, antibiotic therapy, enterotoxin, cytotoxin, fulminant toxic megacolon, colonic perforation, transverse volvulus, binary toxin

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Contributor Information and Disclosures

Author

Jennifer A Curry, MD, MPH, Staff Physician, Infectious Disease Clinic, Naval Medical Center Portsmouth
Jennifer A Curry, MD, MPH is a member of the following medical societies: American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Braden R Hale, MD, MPH, Assistant Clinical Professor, Department of Internal Medicine, University of California at San Diego; Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Naval Medical Center at San Diego
Braden R Hale, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, San Antonio Military Medical Center, Brooke Army Medical Center; Professor of Medicine, Uniformed Services University of the Health Sciences
Duane R Hospenthal, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Society for Infectious Diseases, International Society of Travel Medicine, and Medical Mycology Society of the Americas
Disclosure: Nothing to disclose.

Joseph Lee, MD, Staff Physician, Department of Medicine, Walter Reed Army Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Gary L Gorby, MD, Program Director of Adult Infectious Diseases Fellowship, Associate Professor, Department of Internal Medicine, Division of Infectious Disease, St Joseph Medical Center, Creighton University School of Medicine
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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

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.

 
 
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