Pseudomembranous Colitis Workup

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

Laboratory Studies

Evaluation of C difficile infection primarily focuses on the detection of C difficile or its toxins in stool.[20, 7] The available testing modalities and their sensitivity/specificity may vary widely between laboratories.

  • In general, testing for C difficile should only be performed on unformed stools.
    • Testing of asymptomatic patients is not recommended (including as a test of cure)[7]
    • In the setting of an ileus, when stool is not obtainable, testing can be performed using a rectal swab.
  • Direct culture of C difficile from the stool provides the most sensitive diagnostic measure. This study is not commonly used clinically because of cost and turnaround time. However, with additional identification of toxigenic isolates, it has become the criterion standard against which other testing modalities are compared.
  • Cytotoxic assays are recommended over EIA for the diagnosis of C difficile.[7] Stool filtrate is mixed with mammalian tissue-culture cell lines and observed for cytopathic effect; turnaround time is roughly 48 hours. Cytotoxic assays are still only moderately sensitive in the detection of C difficile. For a single test, sensitivity ranges from 67-100% and specificity ranges from 85-100%.
  • Enzyme-linked immunosorbent assay (ELISA) techniques are used to detect the presence of toxin A and/or toxin B. A wide variety of these tests are commercially available. Reported sensitivities range from 63-99%, with specificities of 75-100%. Compared with cytotoxic assays, these tests are less expensive and yield quicker results but are less sensitive for the detection of C difficile.
    • Assays that detect both toxin A and B (rather than toxin A alone) are preferred, as an increasing number of circulating strains express only toxin B.
    • Stool samples should be refrigerated or frozen (depending on laboratory requirements) after collection if a delay in further processing is expected. The toxin may degrade to undetectable levels within 4 hours after collection if stored at room temperature
    • Newer EIA assays for glutamate dehydrogenase (GDH, C difficile common antigen) have been developed. Detection of GDH has fairly poor specificity for the toxin producing strains of C difficile that cause disease, but when used in conjunction with a toxin assay, it may greatly improve the negative predictive value of testing.
  • PCR technology can be used to detect the presence of toxins A or B; these tests are both sensitive and specific. PCR may eventually replace cytotoxic assays as the test of choice; however, it is not yet widely standardized. Several commercial PCR tests have received FDA approval.
  • Despite a relatively lack of sensitivity, repeated testing (ie, 3 samples) is no longer recommended. Studies have shown repeat samples add minimal utility and are not cost effective.[21, 22]
  • Other items to consider in the laboratory analysis include fecal leukocytes and fecal lactoferrin assays. These test lack specificity and have limited roles.
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Imaging Studies

  • Imaging studies do not aid in confirming the diagnosis of early or mild colitis.
  • In patients with severe disease, radiographic studies can aid in detecting complications (eg, toxic dilation, perforation). These studies may also be indicated to investigate other possible diagnoses.
  • CT scanning of the abdomen can be helpful by revealing the presence of bowel wall edema (>4 mm) and inflammation, particularly in cases involving the right colon; however, these findings are generally nonspecific. One retrospective study of CT scan findings showed an association between complicated CDI and both pleural effusion and colonic wall thickness of greater than 15 mm.[23]
  • Barium enema has no role in the diagnosis of early colitis and can be catastrophic in the setting of dilatation due to toxic megacolon or perforation.
  • Toxic megacolon is characterized radiographically by dilation of the transverse colon to greater than 6 cm and loss of colonic haustrations (possible “thumbprinting”).
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Procedures

  • Sigmoidoscopic examination
    • Pseudomembranes can be visualized in up to 50% of patients with CDI via endoscopic examination. Flexible sigmoidoscopy is sufficient in 90% of cases; few may require full colonoscopy.
    • In mild cases, pseudomembranes may not be grossly present, and diagnosis must be confirmed with biopsy.
    • The classic appearance of 2-mm to 10-mm raised yellow nodules is pathognomonic. These lesions are usually discrete but may become confluent plaques in more advanced cases. The pseudomembranes can be easily removed during endoscopy, revealing an erythematous inflamed mucosa.
    • Sigmoidoscopy is not routinely used in the diagnosis of CDI because of its invasiveness.
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Histologic Findings

Macroscopically, pseudomembranes are appreciated as patchy flecks of tan-to-black nodules, loosely adherent to the erythematous bowel wall with superficial erosions, punctate in mild forms, and more confluent in advanced disease.

Microscopically, the earliest sign is focal necrosis of surface epithelial cells in the glandular crypts, with neutrophilic infiltration and fibrin plugging of capillaries in the lamina propria and mucus hypersecretion in adjacent crypts. This leads to the formation of crypt abscesses. As the disease progresses, necrosis and denudation of the mucosa occurs with thrombosis of submucosal venules. The bowel wall inflammation tends to remain superficial; however, exposure of unprotected submucosa to the fecal stream can lead to global dysfunction of the colonic musculature and subsequent dilatation.

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Staging

Prospectively validated severity scores for patients with C difficile infection are lacking. The following criteria were used in the 2010 SHEA/ISDA clinical guidelines:

Mild-to-moderate disease

  • WBC count less than 15,000 cells/mL
  • Serum creatinine less than 1.5 times baseline

Severe disease

  • WBC greater than 15,000 cells/mL
  • Serum creatinine greater than 1.5 times baseline

Severe, complicated disease

  • Hypotension or shock
  • Ileus
  • Toxic megacolon

The clinical trail that demonstrated superiority of vancomycin for severe disease used 6 variables to characterize severe disease: age older than 60 years, temp higher than 38.3° C, albumin level below 2.5mg/dL, WBC greater than 15,000 cells/mL, evidence of pseudomembranous colitis, and ICU admission.[24]

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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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