Clostridium Difficile Colitis Clinical Presentation

  • Author: Faten N Aberra, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: May 18, 2012
 

History

C difficile colonization results in a wide spectrum of clinical conditions, including an asymptomatic carrier state, mild self-limited diarrhea, pseudomembranous colitis, and fulminant colitis.

Most patients develop diarrhea during or shortly after starting antibiotics. However, 25-40% of patients may not become symptomatic for as many as 10 weeks after completing antibiotic therapy.

Symptoms often include the following:

  • Mild-to-moderate watery diarrhea that is rarely bloody
  • Cramping abdominal pain
  • Anorexia
  • Malaise
  • Fever, especially in more severe cases
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Physical

Physical examination may reveal the following:

  • Fever
  • Dehydration
  • Lower abdominal tenderness
  • Rebound tenderness - Raises the possibility of colonic perforation and peritonitis
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Causes

C difficile colitis results from a disruption of the normal bacterial flora of the colon, colonization with C difficile, and release of toxins that cause mucosal inflammation and damage.

The chief risk factor for the disease is prior exposure to antibiotics. The most common antibiotics implicated in C difficile colitis include cephalosporins (especially second and third generation), ampicillin/amoxicillin, and clindamycin. Less commonly implicated antibiotics are the macrolides (ie, erythromycin, clarithromycin, azithromycin) and other penicillins.

Agents occasionally reported to cause the disease include aminoglycosides, fluoroquinolones, trimethoprim-sulfamethoxazole, metronidazole, chloramphenicol, tetracycline, imipenem, and meropenem. Even brief exposure to any single antibiotic can cause C difficile colitis. A prolonged antibiotic course or the use of 2 or more antibiotics increases the risk of disease. Even antibiotics traditionally used to treat C difficile colitis have been shown to cause disease.

Other risk factors include the following:

  • Advanced age (>60 y)
  • Hospitalization (particularly sharing a hospital room with an infected patient, intensive care unit stays, and prolonged hospital stays)

Rarer associations include the following:

  • Gastric acid suppressive therapy (proton pump inhibitors)
  • Antineoplastic agents, principally methotrexate
  • Hemolytic-uremic syndrome
  • Malignancies
  • Intestinal ischemia
  • Renal failure
  • Necrotizing enterocolitis
  • Hirschsprung disease
  • Inflammatory bowel disease
  • Nonsurgical gastrointestinal procedures, including nasogastic tubes

A US Food and Drug Administration (FDA) safety communication on February 8, 2012 described a possible association between the use of proton pump inhibitors (PPIs) and the development of Clostridium difficile –associated diarrhea (CDAD).[5] Data were collected from the FDA's Adverse Event Reporting System (AERS) and the medical literature for cases of CDAD in patients undergoing treatment with PPIs. Many of the adverse event reports involved patients who were elderly, had chronic and/or concomitant underlying medical conditions, or were taking broad-spectrum antibiotics that could have predisposed them to developing CDAD. The FDA also reviewed a total of 28 observational studies described in 26 publications. Of these studies, 23 showed a higher risk of C difficile infection or disease, including CDAD, associated with PPI exposure compared with no PPI exposure.

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Contributor Information and Disclosures
Author

Faten N Aberra, MD  Assistant Professor, Department of Medicine, Division of Gastroenterology, University of Pennsylvania School of Medicine

Faten N Aberra, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, Crohns and Colitis Foundation of America, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

Craig A Gronczewski, MD  Clinical Assistant Professor, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey; Consulting Staff, Princeton Medical Center; Consulting Staff, Robert Wood Johnson University Hospital

Craig A Gronczewski, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Jonathan P Katz, MD  Assistant Professor of Medicine, Department of Medicine, University of Pennsylvania School of Medicine

Jonathan P Katz, MD is a member of the following medical societies: American Gastroenterological Association and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Waqar A Qureshi, MD  Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

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

BS Anand, MD  Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

References

  1. CDC. Vital Signs: Preventing Clostridium difficile Infections. MMWR Morb Mortal Wkly Rep. Mar 9 2012;61:157-62. [Medline].

  2. Bauer MP, Notermans DW, van Benthem BH, et al. Clostridium difficile infection in Europe: a hospital-based survey. Lancet. Jan 1 2011;377(9759):63-73. [Medline].

  3. Centers for Disease Control and Prevention (CDC). Deaths from gastroenteritis double. Available at http://www.cdc.gov/media/releases/2012/p0314_gastroenteritis.html.

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  5. FDA Drug Safety Communication: Clostridium difficile-associated diarrhea can be associated with stomach acid drugs known as proton pump inhibitors (PPIs). US Food and Drug Administration. Available at http://www.fda.gov/Drugs/DrugSafety/ucm290510.htm. Accessed February 8, 2012.

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Endoscopic visualization of pseudomembranous colitis, a characteristic manifestation of full-blown Clostridium difficile colitis. Classic pseudomembranes are visible as raised yellow plaques ranging from 2-10 mm in diameter and scattered over the colorectal mucosa. Courtesy of Gregory Ginsberg, MD, University of Pennsylvania.
Colonic pseudomembranes of pseudomembranous colitis. Photographs courtesy of Eric M. Osgard, MD.
Gross pathology specimen from a case of pseudomembranous colitis revealing characteristic yellowish plaques.
Gross pathology specimen from a case of pseudomembranous colitis, again demonstrating characteristic yellowish plaques.
Frontal abdominal radiograph in a patient with proved pseudomembranous colitis. Note the nodular haustral thickening, most pronounced in the transverse colon.
Barium enema demonstrating typical serrated appearance of the barium column (resulting from trapped barium between the edematous mucosal folds and the plaquelike membranes of pseudomembranous colitis).
Axial CT scan of pseudomembranous colitis.
CT scan of pseudomembranous colitis.
Ultrasound image of pseudomembranous colitis.
 
 
 
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