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Clostridium Difficile Colitis Medication

  • Author: Faten N Aberra, MD; Chief Editor: BS Anand, MD  more...
Updated: Oct 13, 2015

Medication Summary

Pharmacologic therapy should be tailored according to the severity of C difficile infection (CDI). Treatment is not indicated for asymptomatic carriers. In very mild cases (ie, patients without fever, abdominal pain, or leukocytosis), in patients who do not have other comorbidities, cessation of causative antibiotics may be the only treatment necessary.

Approximately 15-25% of patients respond to conservative therapy, which allows for reconstitution of normal colonic flora and reduces the risk of relapse. Specific therapy aimed at eradicating C difficile is indicated if symptoms are persistent or if antibiotics cannot be discontinued safely.

Oral metronidazole and oral vancomycin have similar efficacy rates in treating diarrhea caused by C difficile in mild to moderate infection but not in severe disease. Whereas metronidazole is the recommended first-line treatment for mild to moderate disease without complications, vancomycin is recommended first-line therapy for severe infection or for patients with risk factors for adverse outcomes, such as advanced age, critical illness, overall debility, or inflammatory bowel disease (IBD). Vancomycin, rifaximin, and fidaxomicin are useful in recurrent or persistent cases.

The oral administration of these medications is the preferred route, because C difficile remains within the colonic lumen without invading the colonic mucosa. Vancomycin is poorly absorbed in the intestinal tract, thereby promoting high concentrations within the intestines while significantly reducing the prevalence of adverse systemic effects.

The Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA) recommend a regimen of metronidazole (500 mg PO TID for 10-14 days) as first-line therapy for mild to moderate disease without complications (lower cost and similar efficacy to PO vancomycin in these patients).[5] For patients who are unable to tolerate oral medication, intravenous metronidazole is effective.

A study by Louie et al compared vancomycin (125 mg PO QID) with fidaxomicin (200 mg PO BID).[50] The study showed that fidaxomicin therapy had a similar efficacy and resulted in a significantly lower rate of recurrence of CDI not associated with the epidemic North American Pulsed Field type 1 strains. Fidaxomicin was approved by the FDA in May 2011.

In another study, a review of 11 trials (1463 adult patients total) comparing metronidazole with vancomycin or another agent, combined agents, or placebo, neither vancomycin nor fidaxomicin were clearly superior for the initial treatment of CDI. One study in the review, however, showed CDI recurrence in only 15% of patients treated with fidaxomicin, compared with 25% of patients treated with vancomycin.[51]

As noted above, for severe cases, vancomycin (125 mg PO QID for 10 days) is the recommended first-line therapy. Higher dosing (250 mg PO [or per nasogastric tube] QID) may be used if poor absorption is possible due to situations such as ileus. Excretion of the drug into bile and exudation from the inflamed colon results in bactericidal levels in feces. Intravenous vancomycin is ineffective and should not be used for C difficile. The SHEA and IDSA recommend metronidazole (500 mg IV q8h) with vancomycin (500 mg PO QID and/or 500 mg PR q6h in 100 mL normal saline as a retention enema) for severe or complicated cases of CDI.[5]


Relapse occurs in 20-27% of patients treated with metronidazole or vancomycin. Most recurrences occur 3 days to 3 weeks after discontinuing antibiotic treatment. Once a patient has 1 relapse, the risk for a 2nd relapse is 45%.

Age greater than 65, severe underlying illnesses, and ongoing antibiotic treatments during C difficile therapy are all risk factors for recurrence. Recurrent infection tends to occur in patients who mount a poor host immune response to C difficile. Persistent disruption of the colonic microbial flora also confers an increased risk. Recurrent infection can result from reinfection of the same strain or a different strain of C difficile.

For the first relapse, the choice of antibiotic should be based on the severity of C difficile diarrhea/colitis. Mild symptoms of recurrence in patients who are otherwise well may be managed without further antibiotic therapy. Initial recurrence that is not severe can be treated with metronidazole. For subsequent recurrences, patients may benefit from vancomycin in a prolonged tapered and/or pulse regimen or fidaxomicin with or without probiotics. Rifaximin is also a potential option.


Probiotics are not recommended as a single agent for the treatment of active CDI owing to limited data supporting their benefit and a potential risk for septicemia.[5] Use of Saccharomyces boulardii and Lactobacillus species have shown mixed results in reducing the risk of CDI relapse. However, S boulardii has generated interest for the treatment of CDI, because it seems to inhibit the effects of toxins A and B on the human colonic mucosa.

Potential therapies

Rifaximin after treatment with vancomycin may reduce the risk of relapse, but rifaximin is not yet FDA approved for this indication.

Nitazoxanide, a medication used to treat parasites, has been shown to be as effective as vancomycin in a clinical trial for the treatment of C difficile.

A review of 10 clinical trials evaluating the treatment of an initial episode of CDI showed that nitazoxanide and teicoplanin did not demonstrate inferiority relative to vancomycin and metronidazole.[52] However, other antimicrobials, including rifampin, and the toxin-binding polymer tolevamer, did show inferiority compared with vancomycin and metronidazole.[52]

In contrast, in several clinical trials, 200 mg of oral fidaxomicin administered every 12 hours for 10 days was been found to be noninferior to 125 mg of oral vancomycin administered every 6 hours for 10 days for the treatment of C difficile.[53] There was no difference in cure rates based on C difficile disease severity. Symptomatic improvement can be expected within 2-3 days.

In a multicenter study including 1105 subjects with C difficile – associated diarrhea, 183 of whom had solid tumors or hematologic malignancies, fidaxomicin treatment was superior to vancomycin treatment in cancer patients, resulting in higher cure and sustained response rates for diarrhea, shorter time to resolution of diarrhea (TTROD), and fewer recurrences.[54, 55]

Cure rates for diarrhea in the study, which was conducted by Cornely et al, were lower overall in cancer patients than in others (79.2% vs 88.6%).[55] Whereas cure rates for noncancer patients were approximately the same with fidaxomicin as with vancomycin (88.5% vs 88.7%), those for cancer patients were higher with fidaxomicin than with vancomycin (85.1% vs 74.0%), though the difference was not statistically significant. Median TTRODs in noncancer patients were 54 hours with fidaxomicin and 58 hours with vancomycin; those in cancer patients were 74 and 123 hours, respectively.

In the same study, the risk of recurrence was approximately twice as high with vancomycin as with fidaxomicin, regardless of whether the patients had cancer or not, but because cure and recurrence outcomes were better with fidaxomicin than with vancomycin in cancer patients, the relative odds of sustained response at 28 days in these patients were more than 2.5-fold higher for fidaxomicin than for vancomycin.[55]

Intravenous immunoglobulin (IVIG), which contains C difficile antitoxin, has been reported as an effective adjunctive treatment for refractory and severe cases of C difficile colitis/diarrhea. In some individuals, a poor host immune response to C difficile may be a risk factor for lack of clearance of C difficile and may be the reason for the benefit of IVIG.

A review of the literature and a retrospective review of 21 of 1230 patients with CDI who received IVIG showed that conventional treatments were used for an average of 8 days before IVIG was administered.[56] All of the patients reviewed had radiologic pancolitis or clinical ileus. Following treatment with IVIG, 9 (43%) of the patients survived with resolution of their colitis, whereas 12 (57%) of the patients died. Patients who survived showed resolution of their symptoms after an average of 10 days (range, 2-20 d).[56]

Cholestyramine binds toxins A and B of C difficile, but the clinical experience of different investigators has shown marked variation in results. Cholestyramine binds vancomycin and should not be used concurrently with vancomycin therapy. Although not as effective as primary therapy for C difficile, the advantage of anion-binding resins is that they do not alter the colonic flora.

Other investigational therapies include the following:

  • Tolevamer: A toxin-binding polymer with no antimicrobial properties
  • The antibiotics ramoplanin and OPT-80 (poor intestinal absorption)
  • C difficile vaccination

Antibiotics, Other

Class Summary

The purpose of treatment is to eradicate C difficile infection (CDI) and/or promote restoration of normal colonic flora.

Metronidazole (Flagyl)


Metronidazole is recommended as the treatment of choice for mild to moderate cases of CDI. This agent provides effective therapy, with reported response rates from 95-100%. Its in vitro activity is bactericidal and dose dependent. Standard dosing has been shown to promote fecal concentrations capable of a 99.99% reduction of C difficile.

Metronidazole is relatively inexpensive. Intravenous (IV) metronidazole may be administered to those patients who cannot tolerate oral (PO) medications because of its potential to accumulate in the inflamed colon. However, the IV route is not as effective as the PO route.



Bacitracin inhibits the formation of major components of the bacterial cell wall and is bactericidal. This agent is used as an alternative therapy for CDI, but it is expensive and not as effective as metronidazole or vancomycin in clinical trials and is thus without sufficient data to warrant its use. Bacitracin is bitter and must be specially prepared in capsule form to prevent nausea. This agent is administered PO, and it is only negligibly absorbed from the gastrointestinal (GI) tract.



Class Summary

Oral vancomycin does not get absorbed and acts directly at the site of infection.

Vancomycin (Vancocin)


Vancomycin has excellent in vitro activity against C difficile. This agent kills the organism by inhibiting cell wall synthesis. Significant luminal levels after administration of PO vancomycin can be obtained because the drug is poorly absorbed from the GI tract. Its major disadvantage, however, is that it is relatively expensive.

Because of the cost and the concern over the emergence of vancomycin-resistant enterococci strains, this agent should be reserved for patients who cannot tolerate or do not respond to metronidazole, pregnant patients, and patients younger than 10 years.

Vancomycin is also preferred for severe cases and in patients who are high risk. Unlike IV metronidazole, IV vancomycin is not excreted into the GI lumen; therefore, it is difficult to deliver effective IV doses.



Class Summary

Fidaxomicin was approved in 2011 by the FDA for the treatment of C difficile -associated diarrhea in adults. This agent has a narrower antimicrobial spectrum and alters the gut microflora less than do metronidazole and vancomycin.

Fidaxomicin (Dificid)


Fidaxomicin is a macrolide antibiotic indicated for C difficile–associated diarrhea in adults. This agent is bactericidal against C difficile in vitro, inhibiting RNA synthesis by RNA polymerases.


Bile Acid Sequestrants

Class Summary

Bile acid sequestrants bind C difficile toxin and other proteins. Although not as effective as primary therapy for C difficile, the advantage of bile acid sequestrant therapy is that it does not alter the gut microflora.

Cholestyramine (Questran)


Cholestyramine is used to treat diarrhea associated with pseudomembranous colitis. This agent forms a nonabsorbable complex with bile acids in the intestine, which, in turn, inhibits enterohepatic reuptake of intestinal bile salts.

Note that cholestyramine binds vancomycin, which precludes combination therapy. This agent is available as a powder that must be mixed with water prior to ingestion. The efficacy of cholestyramine is inferior to that of metronidazole or vancomycin, but the drug may have a role under certain circumstances (eg, in patients who continue to relapse). This agent is not absorbed from the GI tract.

Contributor Information and Disclosures

Faten N Aberra, MD MSCE, Assistant Professor Of Medicine, Division of Gastroenterology, Hospital of the University of Pennsylvania, 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, Sigma Xi, Crohn's and Colitis Foundation of America

Disclosure: Nothing to disclose.


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, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

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, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.



The views expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the US 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 US Government as part of that person’s official duties.

Additional Contributors

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.

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.

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.

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

Disclosure: Nothing to disclose.

Duane R Hospenthal, MD, PhD, FACP, FIDSA Adjunct Professor of Medicine, Department of Medicine, University of Texas Health Science Center at San Antonio

Duane R Hospenthal, MD, PhD, FACP, FIDSA is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, 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 Human and Animal Mycology, International Society for Infectious Diseases,International Society of Travel Medicine, and Medical Mycology Society of the Americas

Disclosure: Nothing to disclose.

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.

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.

Joseph Lee, MD Staff Physician, Department of Medicine, Walter Reed Army Medical Center

Disclosure: Nothing to disclose.

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

  1. McDonald LC, Coignard B, Dubberke E, Song X, Horan T, Kutty PK. Recommendations for surveillance of Clostridium difficile-associated disease. Infect Control Hosp Epidemiol. 2007 Feb. 28(2):140-5. [Medline].

  2. Khanna S, Pardi DS, Aronson SL, et al. The epidemiology of community-acquired Clostridium difficile infection: a population-based study. Am J Gastroenterol. 2012 Jan. 107(1):89-95. [Medline]. [Full Text].

  3. Sloan LM, Duresko BJ, Gustafson DR, Rosenblatt JE. Comparison of real-time PCR for detection of the tcdC gene with four toxin immunoassays and culture in diagnosis of Clostridium difficile infection. J Clin Microbiol. 2008 Jun. 46(6):1996-2001. [Medline]. [Full Text].

  4. Grant TH, Rosen MP, Fidler JL, et al, for the Expert Panel on Gastrointestinal Imaging. ACR Appropriateness Criteria: acute abdominal pain and fever or suspected abdominal abscess. [online publication]. Reston, Va: American College of Radiology (ACR); 2008.

  5. Cohen SH, Gerding DN, Johnson S, et al. Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the society for healthcare epidemiology of America (SHEA) and the infectious diseases society of America (IDSA). Infect Control Hosp Epidemiol. 2010 May. 31(5):431-55. [Medline].

  6. Brandt LJ, Aroniadis OC, Mellow M, et al. Long-term follow-up of colonoscopic fecal microbiota transplant for recurrent Clostridium difficile infection. Am J Gastroenterol. 2012 Jul. 107(7):1079-87. [Medline].

  7. Laidman J. Fecal transfer proves potent clostridium difficile treatment. [serial online]. Medscape Medical News. Available at 2013 Jan 16; Accessed: July 23, 2013.

  8. van Nood E, Vrieze A, Nieuwdorp M, et al. Duodenal infusion of donor feces for recurrent Clostridium difficile. N Engl J Med. 2013 Jan 31. 368(5):407-15. [Medline].

  9. Ananthakrishnan AN. Clostridium difficile infection: epidemiology, risk factors and management. Nat Rev Gastroenterol Hepatol. 2011 Jan. 8(1):17-26. [Medline].

  10. Carroll KC, Bartlett JG. Biology of Clostridium difficile: implications for epidemiology and diagnosis. Annu Rev Microbiol. 2011. 65:501-21. [Medline].

  11. Pant C, Sferra TJ, Deshpande A, Minocha A. Clinical approach to severe Clostridium difficile infection: update for the hospital practitioner. Eur J Intern Med. 2011 Dec. 22(6):561-8. [Medline].

  12. Bingley PJ, Harding GM. Clostridium difficile colitis following treatment with metronidazole and vancomycin. Postgrad Med J. 1987 Nov. 63(745):993-4. [Medline]. [Full Text].

  13. US Food and Drug Administration. FDA Drug Safety Communication: Clostridium difficile-associated diarrhea can be associated with stomach acid drugs known as proton pump inhibitors (PPIs). Available at 2013 Feb 15; Accessed: July 23, 2013.

  14. Lowry F. Antidepressants linked to doubling of C difficile risk. Medscape Medical News. Available at 2013 May 7; Accessed: July 23, 2013.

  15. Rogers MA, Greene MT, Young VB, et al. Depression, antidepressant medications, and risk of Clostridium difficile infection. BMC Med. 2013 May 7. 11:121. [Medline]. [Full Text].

  16. Ananthakrishnan AN, Issa M, Binion DG. Clostridium difficile and inflammatory bowel disease. Gastroenterol Clin North Am. 2009 Dec. 38(4):711-28. [Medline].

  17. Garey KW, Jiang ZD, Ghantoji S, Tam VH, Arora V, Dupont HL. A common polymorphism in the interleukin-8 gene promoter is associated with an increased risk for recurrent Clostridium difficile infection. Clin Infect Dis. 2010 Dec 15. 51(12):1406-10. [Medline].

  18. Jiang ZD, DuPont HL, Garey K, et al. A common polymorphism in the interleukin 8 gene promoter is associated with Clostridium difficile diarrhea. Am J Gastroenterol. 2006 May. 101(5):1112-6. [Medline].

  19. Granlund Av, Beisvag V, Torp SH, et al. Activation of REG family proteins in colitis. Scand J Gastroenterol. 2011 Nov. 46(11):1316-23. [Medline]. [Full Text].

  20. Castagliuolo I, Riegler M, Pasha A, et al. Neurokinin-1 (NK-1) receptor is required in Clostridium difficile- induced enteritis. J Clin Invest. 1998 Apr 15. 101(8):1547-50. [Medline]. [Full Text].

  21. Na X, Kim H, Moyer MP, Pothoulakis C, LaMont JT. gp96 is a human colonocyte plasma membrane binding protein for Clostridium difficile toxin A. Infect Immun. 2008 Jul. 76(7):2862-71. [Medline]. [Full Text].

  22. Hasegawa M, Yamazaki T, Kamada N, et al. Nucleotide-binding oligomerization domain 1 mediates recognition of Clostridium difficile and induces neutrophil recruitment and protection against the pathogen. J Immunol. 2011 Apr 15. 186(8):4872-80. [Medline].

  23. Centers for Disease Control and Prevention. CDC vital signs: making health care safer. Stopping C. difficile infections. Available at 2012 Mar 6; Accessed: July 23, 2013.

  24. Centers for Disease Control and Prevention. Vital signs: preventing Clostridium difficile infections. MMWR Morb Mortal Wkly Rep. 2012 Mar 9. 61(9):157-62. [Medline].

  25. Wilcox MH, Mooney L, Bendall R, Settle CD, Fawley WN. A case-control study of community-associated Clostridium difficile infection. J Antimicrob Chemother. 2008 Aug. 62(2):388-96. [Medline].

  26. Dumyati G, Stevens V, Hannett GE, et al. Community-associated Clostridium difficile infections, Monroe County, New York, USA. Emerg Infect Dis. 2012 Mar. 18(3):392-400. [Medline]. [Full Text].

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

  28. Khanna S, Pardi DS. The growing incidence and severity of Clostridium difficile infection in inpatient and outpatient settings. Expert Rev Gastroenterol Hepatol. 2010 Aug. 4(4):409-16. [Medline].

  29. Nylund CM, Goudie A, Garza JM, Fairbrother G, Cohen MB. Clostridium difficile infection in hospitalized children in the United States. Arch Pediatr Adolesc Med. 2011 May. 165(5):451-7. [Medline].

  30. Johnson S. Recurrent Clostridium difficile infection: a review of risk factors, treatments, and outcomes. J Infect. 2009 Jun. 58(6):403-10. [Medline].

  31. Khanna S, Pardi DS, Aronson SL, Kammer PP, Baddour LM. Outcomes in community-acquired Clostridium difficile infection. Aliment Pharmacol Ther. 2012 Mar. 35(5):613-8. [Medline]. [Full Text].

  32. Loo VG, Poirier L, Miller MA, et al. A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality. N Engl J Med. 2005 Dec 8. 353(23):2442-9. [Medline].

  33. Ananthakrishnan AN, Guzman-Perez R, Gainer V, et al. Predictors of severe outcomes associated with Clostridium difficile infection in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2012 Apr. 35(7):789-95. [Medline]. [Full Text].

  34. Navaneethan U, Mukewar S, Venkatesh PG, Lopez R, Shen B. Clostridium difficile infection is associated with worse long term outcome in patients with ulcerative colitis. J Crohns Colitis. 2012 Apr. 6(3):330-6. [Medline].

  35. Sailhamer EA, Carson K, Chang Y, et al. Fulminant Clostridium difficile colitis: patterns of care and predictors of mortality. Arch Surg. 2009 May. 144(5):433-9; discussion 439-40. [Medline].

  36. Miller AT, Tabrizian P, Greenstein AJ, Dikman A, Byrn J, Divino C. Long-term follow-up of patients with fulminant Clostridium difficile colitis. J Gastrointest Surg. 2009 May. 13(5):956-9. [Medline].

  37. Khanna S, Pardi DS, Rosenblatt JE, Patel R, Kammer PP, Baddour LM. An evaluation of repeat stool testing for Clostridium difficile infection by polymerase chain reaction. J Clin Gastroenterol. 2012 Nov-Dec. 46(10):846-9. [Medline].

  38. El Feghaly RE, Stauber JL, Tarr PI, Haslam DB. Intestinal inflammatory biomarkers and outcome in pediatric Clostridium difficile infections. J Pediatr. 2013 Dec. 163(6):1697-1704.e2. [Medline].

  39. Debast SB, Bauer MP, Kuijper EJ. European Society of Clinical Microbiology and Infectious Diseases (ESCMID): update of the treatment guidance document for Clostridium difficile infection (CDI). Clin Microbiol Infect. 2013 Oct 5. [Medline].

  40. Barclay L. Guidelines: Antibiotics for all but very mild C difficile. Medscape Medical News. Available at 2013 Oct 30; Accessed: November 4, 2013.

  41. Fridkin S, Baggs J, Fagan R, et al. Vital signs: improving antibiotic use among hospitalized patients. MMWR Morb Mortal Wkly Rep. 2014 Mar 7. 63(9):194-200. [Medline]. [Full Text].

  42. Lowes R. CDC urges doctors to improve antibiotic prescribing. Medscape Medical News. March 4, 2014. [Full Text].

  43. Kling J. Low-dose vancomycin effective against C difficile. Medscape Medical News. Available at 2013 Sep 24; Accessed: October 21, 2013.

  44. Videlock EJ, Cremonini F. Meta-analysis: probiotics in antibiotic-associated diarrhoea. Aliment Pharmacol Ther. 2012 Jun. 35(12):1355-69. [Medline].

  45. Bakken JS, Borody T, Brandt LJ, et al. Treating Clostridium difficile infection with fecal microbiota transplantation. Clin Gastroenterol Hepatol. 2011 Dec. 9(12):1044-9. [Medline]. [Full Text].

  46. Hamilton MJ, Weingarden AR, Sadowsky MJ, Khoruts A. Standardized frozen preparation for transplantation of fecal microbiota for recurrent Clostridium difficile infection. Am J Gastroenterol. 2012 May. 107(5):761-7. [Medline].

  47. Kassam Z, Hundal R, Marshall JK, Lee CH. Fecal transplant via retention enema for refractory or recurrent Clostridium difficile infection. Arch Intern Med. 2012 Jan 23. 172(2):191-3. [Medline].

  48. Kling J. Fecal transplant an option even in the immunocompromised. Medscape Medical News. Available at 2013 Oct 16; Accessed: October 21, 2013.

  49. Gough E, Shaikh H, Manges AR. Systematic review of intestinal microbiota transplantation (fecal bacteriotherapy) for recurrent Clostridium difficile infection. Clin Infect Dis. 2011 Nov. 53(10):994-1002. [Medline].

  50. Louie TJ, Miller MA, Mullane KM, et al. Fidaxomicin versus vancomycin for Clostridium difficile infection. N Engl J Med. 2011 Feb 3. 364(5):422-31. [Medline].

  51. Drekonja DM, Butler M, MacDonald R, et al. Comparative effectiveness of Clostridium difficile treatments: a systematic review. Ann Intern Med. 2011 Dec 20. 155(12):839-47. [Medline].

  52. Venuto C, Butler M, Ashley ED, Brown J. Alternative therapies for Clostridium difficile infections. Pharmacotherapy. 2010 Dec. 30(12):1266-78. [Medline].

  53. Cornely OA, Crook DW, Esposito R, et al. Fidaxomicin versus vancomycin for infection with Clostridium difficile in Europe, Canada, and the USA: a double-blind, non-inferiority, randomised controlled trial. Lancet Infect Dis. 2012 Apr. 12(4):281-9. [Medline].

  54. Reuters Health. Fidaxomicin effective for C. difficile in cancer patients. Medscape Medical News. Available at 2013 May 30; Accessed: July 23, 2013.

  55. Cornely OA, Miller MA, Fantin B, Mullane K, Kean Y, Gorbach S. Resolution of Clostridium difficile-associated diarrhea in patients with cancer treated with fidaxomicin or vancomycin. J Clin Oncol. 2013 Jul 1. 31(19):2493-9. [Medline].

  56. Abougergi MS, Broor A, Cui W, Jaar BG. Intravenous immunoglobulin for the treatment of severe Clostridium difficile colitis: an observational study and review of the literature. J Hosp Med. 2010 Jan. 5(1):E1-9. [Medline].

  57. Bartlett JG. Pseudomembranous enterocolitis and antibiotic-associated colitis. Feldman M, Scharschmidt BF, Sleisenger MH, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia, Pa: WB Saunders Co; 1998. 1633-47.

  58. Cleary RK. Clostridium difficile-associated diarrhea and colitis: clinical manifestations, diagnosis, and treatment. Dis Colon Rectum. 1998 Nov. 41(11):1435-49. [Medline].

  59. Fekety R. Guidelines for the diagnosis and management of Clostridium difficile-associated diarrhea and colitis. American College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol. 1997 May. 92(5):739-50. [Medline].

  60. Gilbert DN, Moellering RC, Sande MA. Antimicrobial Therapy. The Sanford Guide to Antimicrobial Therapy. 30th ed. Hyde Park, Vt: 2000. 12.

  61. Guerrero DM, Chou C, Jury LA, Nerandzic MM, Cadnum JC, Donskey CJ. Clinical and infection control implications of Clostridium difficile infection with negative enzyme immunoassay for toxin. Clin Infect Dis. 2011 Aug 1. 53(3):287-90. [Medline].

  62. Johnson S, Gerding DN. Clostridium difficile--associated diarrhea. Clin Infect Dis. 1998 May. 26(5):1027-34; quiz 1035-6. [Medline].

  63. Jones EM, Kirkpatrick BL, Feeney R, Reeves DS, MacGowan AP. Hospital-acquired Clostridium difficile diarrhoea. Lancet. 1997 Apr 19. 349(9059):1176-7. [Medline].

  64. Kelly CP, LaMont JT. Clostridium difficile infection. Annu Rev Med. 1998. 49:375-90. [Medline].

  65. Kelly CP, LaMont JT. Clostridium difficile--more difficult than ever. N Engl J Med. 2008 Oct 30. 359(18):1932-40. [Medline].

  66. Kelly CP, Pothoulakis C, LaMont JT. Clostridium difficile colitis. N Engl J Med. 1994 Jan 27. 330(4):257-62. [Medline].

  67. Kolling GL, Wu M, Warren CA, et al. Lactic acid production by Streptococcus thermophilus alters Clostridium difficile infection and in vitro Toxin A production. Gut Microbes. 2012 Nov-Dec. 3(6):523-9. [Medline]. [Full Text].

  68. Lyerly DM, Wilkins TD. Clostridium difficile. Infections of the Gastrointestinal Tract. 1995. 867-891.

  69. McDonald CL, Gerding DN, Johnson S. "Clostridium difficile: Changing Diagnosis, Epidemiology, and Treatment" The content of this virtual lecture is derived from a satellite symposium presented on April 7, 2008, during the 18th Annual SHEA Scientific Meeting. Philadelphia, Pa:. Available at

  70. McFarland LV, Mulligan ME, Kwok RY, Stamm WE. Nosocomial acquisition of Clostridium difficile infection. N Engl J Med. 1989 Jan 26. 320(4):204-10. [Medline].

  71. Schneeweiss S, Korzenik J, Solomon DH, Canning C, Lee J, Bressler B. Infliximab and other immunomodulating drugs in patients with inflammatory bowel disease and the risk of serious bacterial infections. Aliment Pharmacol Ther. 2009 Aug. 30(3):253-64. [Medline].

  72. Sonnenberg A. Similar geographic variations of mortality and hospitalization associated with IBD and Clostridium difficile colitis. Inflamm Bowel Dis. 2010 Mar. 16(3):487-93. [Medline].

  73. Starr J. Clostridium difficile associated diarrhoea: diagnosis and treatment. BMJ. 2005 Sep 3. 331(7515):498-501. [Medline]. [Full Text].

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 to 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 the characteristic yellowish plaques.
Gross pathology specimen from a case of pseudomembranous colitis, again demonstrating the 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 the typical serrated appearance of the barium column (resulting from trapped barium between the edematous mucosal folds and the plaquelike membranes of pseudomembranous colitis).
Axial computed tomography scan of pseudomembranous colitis.
Computed tomography scan of pseudomembranous colitis.
Ultrasonographic image of pseudomembranous colitis.
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