Pseudomembranous Colitis Clinical Presentation

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

History

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

  • History of antibiotic exposure
    • Fluoroquinolones, macrolides, clindamycin, beta-lactam/beta-lactamase inhibitors, and all generations of cephalosporins have been most commonly associated with CDI.
      • All antibiotics, including those used to treat C difficile infection, can be associated with development of disease.
    • CDI 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 antibiotic cessation.
    • Both increased length of antimicrobial use and use of multiple antimicrobials increase the risk of CDI.
    • Some patients may develop CDI 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. Exposure to spores in soil, carriage by pets or other animals, and contaminated food or household contacts have all been implicated.[17]
  • Host factors that increase susceptibility to C difficile –associated diarrhea
    • Age greater than 65 years
    • Chronic debilitation or 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 ingestion.)
    • Cancer chemotherapeutic agents are associated with an increased risk of C difficile disease. This may be due to the antimicrobial activity of some of these agents or due to impaired immunity with neutropenia.
    • Impaired humoral immunity (especially of the IgG subclasses) may increase the susceptibility to relapsing disease.
    • HIV infection: C difficile infection has become one of the most common causes of infectious diarrhea in persons with HIV.[18]
    • Infections are being increasingly recognized in patients previously considered low risk, such as women in the peripartum state.

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 is usually fairly mild, with 3-6 stools per day. However, severe cases may have more than 20 stools per day.
    • Leukocytosis is found in 50-60% of patients. A patient who presents with a WBC count of 12,000-20,000 103/μL associated with minimal diarrhea and a lack of other presenting signs is common. However, 30% of patients have a WBC count of more than 30,000 103/μL.
    • Fever affects 30-50% of patients.
    • Abdominal pain or cramping affects 20-33% of patients and may have various presentations. Sometimes generalized, diffuse, or 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.
    • Other common findings include nausea, malaise, and anorexia.
    • Severe disease may lead to electrolyte disturbances, dehydration, hypotension, renal failure, sepsis, and death.
    • Constipation with or without dyspepsia is an atypical presentation, occurring in less than 1% of cases.[19]
    • 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
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Physical

The diagnosis of CDI 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.

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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.

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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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