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Educational Objectives

Educational Objectives. Discuss the pathophysiology of Clostridium difficile infection (CDI) as it relates to clinical disease Analyze elements which contribute to the economic burden of CDI Identify important risk factors for initial CDI and recurrence

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Educational Objectives

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  1. Educational Objectives • Discuss the pathophysiology of Clostridium difficile infection (CDI) as it relates to clinical disease • Analyze elements which contribute to the economic burden of CDI • Identify important risk factors for initial CDI and recurrence • Apply therapeutic strategies for improved patient outcomes • Implement methods to prevent CDI in high-risk patients

  2. CDI Overview: 60 Years of Research • Evolution of C. difficile knowledge over past 60 years • 1950: Staphylococcusenterocolitis (possibly some CDI) • 1974: “Clindamycin” colitis • 1978: C. difficile as agent of pseudomembranous colitis • 1981: Vancomycin approved by FDA for CDI • 1982: Metronidazole introduced for CDI • 1984: Enzyme immunoassays for CDI • 2000: Outbreak in Pittsburgh, PA • 2003: Outbreak in Quebec • 2005: Outbreaks throughout the US and localized in Europe • 2011: Fidaxomicin approved by the FDA for CDI

  3. CDI Overview • Spore-forming, anaerobic, gram-positive bacterium • Causes gastrointestinal infections resulting in diarrhea and colitis • Severity ranges from mild colitis to toxic megacolon and death • Leading cause of healthcare-associated infectious diarrhea in US • Rivals methicillin-resistant Staphylococcus aureus (MRSA) as the most common organism to cause healthcare-associated infections in US Gerding DN, et al. Infect Control Hosp Epidemiol. 1995;16:459-477. CDC. Fact Sheet, August 2004 (updated 7/22/05). McDonald LC, et al. Emerg Infect Dis. 2006;12:409-415.

  4. National Estimates of US Short-Stay Hospital Discharges with C. difficile as First-Listed or Any Diagnosis, National Inpatient Sample Any listed Primary Number of Discharges Year Elixhauser, A. (AHRQ), and Jhung, MA. (Centers for Disease Control and Prevention). Clostridium Difficile-Associated Disease in U.S. Hospitals, 1993–2005. HCUP Statistical Brief #50. April 2008. Agency for Healthcare Research and Quality, Rockville, MD. And unpublished data http://www.hcup-us.ahrq.gov/reports/statbriefs/sb50.pdf

  5. CDI Epidemiology • Severity of CDI appears to be increasing1-2 • Increased morbidity and mortality • Severe infection in “low-risk” populations1-3 • Emergence of novel, hypervirulent strain (BI/NAP1/027) now reported across the US, Canada, and Europe • Increased toxin production and sporulation may contribute to severe and widespread disease4,5 • Highly resistant to fluoroquinolones 1. McDonald LC, et al. Emerg Infect Dis. 2006;12(3):409-415. 2. Loo VG, et al. N Engl J Med. 2005;353:2442-2449. 3. Kuijper EJ, et al. Euro Surveill. 2007;12(6):E1-E2. 4. Tucker ME. http://www.ehospitalistnews.com/news/infectious-diseases/single-article/ic-difficilei-epidemic-still-poses-clinical- challenges/01e37c081f.html 5. Merrigan M, et al. J Bacteriol. 2010;192:4904-4911.

  6. Economic Burden of CDI 1. Kyne L, et al. Clin Infect Dis. 2002;34:346-353. 2. O’Brien JA, et al. Infect Control Hosp Epidemiol. 2007;28:1219-1227. 3. Dubberke ER, et al. Clin Infect Dis. 2008;46:497-504.

  7. CDI Pathophysiology • Primary virulence factors: • Toxin A (TcdA) • Toxin B (TcdB) • Toxins A and B are potent cytotoxic enzymes that damage the human colonic mucosa • Binary toxin (CDT) was previouslyidentified in ~6% of C. difficile isolates, but is present in all isolates of the hypervirulent strain • Role is unknown but may potentiate toxicity of TcdA and TcdB and lead to more severe disease • Denève C, et al. Int J Antimicrob Agents. 2009;33:S24-S28.

  8. Current Pathogenesis Model for C. difficile Infection (CDI) C. difficile acquisition C. difficile acquisition Asymptomatic C. difficile colonization Antimicrobial(s) CDI Hospitalization Acquisition of a toxigenic strain of C. difficile and failure to mount an anamnestic Toxin A IgG antibody response results in CDI. Johnson S, Gerding DN. Clin Infect Dis. 1998;26:1027-1036.Kyne L, et al. N Engl J Med. 2000;342:390-397.

  9. Risk Factors for Initial CDI • Classic risk factors: • Antibiotic therapy • Advanced age • Prolonged stay in healthcare facility • High severity of illness • Additional risk factors • Inflammatory bowel disease • Gastrointestinal surgery • Gastric acid suppression (PPIs) • Immunosuppression 1. Hookman P, Barkin, JS. World J Gastroenterol. 2009;15:1554-1580. 2. APIC. Guide to the Elimination of Clostridium difficile in Healthcare Settings. November 2008. 3. Makris AT, Gelone S. J Am Med Dir Assoc. 2007;8:290-299. 4. Cohen SH, et al. Infection Control and Hospital Epidemiology. 2010;31(5):431-455. 5. Goodhand JR, et al. Ailment Pharmacol Ther. 2011;33:428-441. 6. Aseeri M, et al. Am J Gastroenterol. 2008;103:2308-2313. 7. Schaier M, et al. Nephrol Dial Transplant. 2004;19:2432-2436.

  10. Identifying Patients at Risk for Recurrence and Poor Outcomes • Elderly • Administration of antibiotics after initial treatment of CDI • Prolonged hospitalization or stay in long-term care facility (LTCF) • Defective immune response to toxin A • Gastric acid suppression 1. Johnson S. J Infect. 2009;58:403-410. 2. Hookman P, Barkin JS. World J Gastroenterol. 2009;15(13):1554-1580. 3. Zilberberg M, et al. Crit Care Med. 2009;37:2583-2589. 4. Garey KW, et al. J Hosp Infect. 2008;70:298-304.

  11. CDI Recurrence by Age Group Pépin J, et al. Clin Infect Dis. 2005;40:1591-1597.

  12. Administration of Antibiotics After Initial CDI Therapy • Continued use of non-C. difficile antibiotic after diagnosis of CDI associated with an odds ratio of 4.23 (P<0.001) for recurrent disease1 • Time to resolution of diarrhea was also increased for patients who received concomitant antibiotics (CA) during treatment for CDI in two Phase 3 CDI trials of fidaxomicn vs. vancomycin2 -The recurrence rate was also increased significantly by receipt of CA during or after CDI treatment in this study 1. Garey KW, et al. J Hosp Infect. 2008;70:298-304. 2. Mullane KM, et al. Clin Infect Dis. 2011;53:440-447.

  13. Prolonged Hospitalization or Stay in LTCF • Risk related to transmission of C. difficile spores • Primary source healthcare workers • may carry C. difficile spores on their hands (not likely fecal carriers) • Environmental contamination secondary source • Up to 50% of LTCF residents and 40% of hospitalized patients have been found to be colonized with C. difficile or its toxin 1. McFarland LV, et al. N Engl J Med. 1989;320:204-210. 2. Bartlett JG, Gerding DN. Clin Infect Dis. 2008;46(Suppl 1):S12-S18. 3. Simor AE, et al. Infect Control Hosp Epidemiol. 2002;23:696-703. 4. Hookman P, Barkin JS. World J Gastroenterol. 2009;15:1554-1580.

  14. Defective immune response to toxin A Median serum concentrations of antibody against toxin A • Generation of an antibody response to toxin A is associated with protection against symptomatic disease and asymptomatic carriage of C. difficile • Following symptomatic infection, many individuals develop anti-toxin A and B antibodies • Inability to acquire immunity to toxin A increases risk for recurrent disease • Individuals with recurrent CDI mount poor anti-toxin responses Serum IgM Serum IgG 1. Giannasca PJ, Warny M. Vaccine. 2004;22:848-856. 2. Kyne L, et al. Lancet. 2001;357:189-193; with permission

  15. CDI Diagnostic Challenges

  16. CDI Diagnostic Challenges • Two- and three-step testing algorithms have been proposed • Initial screen: EIA for glutamate dehydrogenase • Confirmatory: Cell cytotoxicity assay (or culture) or polymerase chain reaction (PCR) • Results appear to differ based on the GDH kit used • Optimal universal strategy remains continuous source of debate 1. Hansen G, et al. Clin Laboratory News. 2010 July:10-13. 2. Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31(5):431-455.

  17. SHEA/IDSA 2010 Guidelines for Diagnosis • Testing for C. difficile or its toxins should be performed only on unformed stool (unless ileus is suspected)1 Brecher rule: “If it ain’t loose, it’s of no use”2 • Testing asymptomatic patients is not clinically useful1 • Test of cure is not recommended1 1.Cohen SH, et al. Infect Control Hosp Epidemiol.2010;31(5):431-455. 2. Dr. Stephen Brecher, verbal communication.

  18. SHEA/IDSA 2010 Guidelines for Diagnosis (Cont.) • EIA to detect toxin is a suboptimal alternative approach for diagnosis • 2-step testing can help to overcome low sensitivity of EIA toxin testing • More data on utility of PCR testing is necessary before it can be recommended for routine testing (consensus at time of Guidelines publication) • Repeat testing during same episode of diarrhea is not recommended Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31(5):431-455.

  19. Summary of C. difficile PCR Published Data Compared to Toxigenic Culture 1. Chapin KC, et al. J Mol Diagn. 2011;13:395-400. 2. Norén T, et al. J Clin Microbiol. 2011;49:710-711. 3. Kvach EJ, et al. J Clin Microbiol. 2010;48:109-114. 4. Novak-Weekley SM, et al. J Clin Microbiol. 2010;48(3):889-893. 5. Swindells J, et al. J Clin Microbiol. 2010;48 (2):606-608. Slide from Dr. Susan Novak-Weekley modified by Dr. Stephen Brecher

  20. Early Experience with PCR • CDI rates initially increase because of increased sensitivity (true prevalence detection) • Test volume goes down by 50% • Test materials cost offset by appropriate utilization of antibiotics and infection control protocols Belmares J, et al. SHEA 2011; Abstract #150.

  21. Basic Principles of CDI Therapy • Discontinue offending antimicrobial agent (if possible) • Send stool specimen for C. difficiletesting • Initiate CDI therapy either empirically or following confirmation of diagnosis • Pharmacotherapy • Vancomycin, Fidaxomicin (only FDA-approved treatments for CDI) • Metronidazole • Other • Supportive treatment • Monitor for symptom resolution and recurrence after treatment Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31(5):431-455.

  22. SHEA/IDSA Treatment Recommendations Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31(5):431-455.

  23. Additional Management of Severe, Complicated CDI • Prompt recognition of severe, complicated CDI and early surgical evaluation is critical* • Indications of severe, complicated disease course: • Elevated and rising white blood cell count (WBC) • Elevated serum creatinine (SCr) level • Elevated serum lactate • Clinical and/or radiographic evidence of severe ileus, impending toxic megacolon • Consider vancomycin per rectum if ileus is severe *Colectomy may be lifesaving, but is associated with increased risk of mortality if WBC is > 50,000 and lactate is >5 mg/dL 1. Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31(5):431-455. 2. Pépin J, et al. Dis Colon Rectum. 2009;52:400-405.

  24. Management of Recurrent CDI • CDI recurrence is a significant challenge • Rates of recurrent CDI: • 15-25% after first episode • 30-45% after first recurrence • 40-65% after two or more recurrences 1. Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31(5):431-455. 2. Johnson S. J Infect. 2009;58(6):403-410. 3. Pépin J, et al Clin Infect Dis2006;42:758–764.

  25. Multiple Recurrent CDI Several empirical approaches have been advocated but most have no controlled data1-3 Metronidazole should not be used beyond first recurrence or for prolonged course, ie, >14 days (concerns for hepatotoxicity and polyneuropathy)1-3 Uncontrolled data with vancomycin taper regimen4,5 Oral Vancomycin Taper 125 mg QID x 10-14 days 125 mg BID x 7 days 125 mg daily x 7 days 125 mg once every 2 days x 8 days 125 mg once every 3 days x 15 days 1. Aslam S, et al. Lancet Infect Dis. 2005;5:549-557. 2. McFarland LV, et al. Am J Gastroenterol. 2002:97:1769-1775. 3. McFarland LV, et al. JAMA. 1994;271:1913-1918. 4. Kyne L, Kelly CP. Gut. 2001;49:152-153. 5. Tedesco FJ, et al.Am J Gastroenterol. 1985;80:867-868.

  26. 65 year-old man with COPD hospitalized from 8/5 to 8/7/10 and treated for pneumonia with piperacillin/tazobactam, followed by oral moxifloxacin. Of note, patient was treated for C. difficileinfection (CDI) in 3/10. • Dx testing: 3/27/10: C. difficiletoxin A/B EIA= POSITIVE • 3/28/10: C. difficile toxin A/B EIA= POSITIVE • 3/28/10: C. difficile toxin A/B EIA= POSITIVE • Rx: Oral metronidazole 500 mg qid • (still on same regimen 4+ months later) • WHAT WOULD YOU SAY REGARDING CDI DIAGNOSTIC TESTING? • WHAT WOULD YOU RECOMMEND REGARDING CDI TREATMENT? Recurrent CDI Case

  27. Patient was readmitted the day after discharge (8/8/10) with new onset of diarrhea (4 watery stools, 1 episode of incontinence) and crampy abdominal pains. • Patient was still on moxifloxacin (metronidazole was discontinued on the day of his recent admission [8/5/10]). • Dx testing: • 8/8/10: C. difficiletoxin A/B EIA= NEGATIVE* • WHAT IS YOUR DIFFERENTIAL DIAGNOSIS? • WHAT EMPIRIC TREATMENT WOULD YOU START (IF ANY)? • *Additional information to be provided by faculty presenter Recurrent CDI Case (con’t)

  28. Newly Available CDI Therapy: Fidaxomicin • Rate of clinical cure with fidaxomicin non-inferior to that of vancomycin (phase 3 trial results) • Fidaxomicin associated with significantly lower rate of CDI recurrence & similar adverse event profile • Results of first phase 3 trial (nearly identical results from 2nd phase 3 trial): mITT=modified intent to treat PP=per protocol Louie TJ, et al. N Engl J Med. 2011;364:422-431; with permission.

  29. Newly Available CDI Therapy: Fidaxomicin • Approved by FDA on May 27, 2011 • Indication and dosing1 -Treatment of Clostridium difficile-associated diarrhea (aka, CDI) in adults (>18 years of age) -Recommended dose 200 mg orally twice daily for 10 days • Advantageous characteristics1,2 • Minimal systemic absorption • Bactericidal agent unrelated to agents used for treatment of systemic infections • Narrow spectrum (less collateral damage to host flora) • Challenges include • Which patients should receive fidaxomicin treatment? • Hospital formulary inclusion • Post approval monitoring for unanticipated side affects, evidence for resistance • Dificid [package insert]. San Diego, CA: Optimer Pharmaceuticals; 2011. • Tannock GW, et al. Microbiology. 2010;156(Pt11):3354-9.

  30. Alternative CDI Therapies: Probiotics • Adjunctive treatment for recurrent CDI • Randomized trials of Lactobacillus species failed to demonstrate benefit to prevent recurrent CDI • Saccharomyces boulardii for secondary prophylaxis was promising2,3 • “Confirmatory” trial failed to confirm • Overall no effect: 44% vs 47% recurrence (RR 0.91; 95% confidence interval 0.66 to 1.27)3 • subgroup analysis showed borderline benefit with S. boulardii and high dose vancomycin (p=0.05) • Reports of fungemia have been reported • More study needed for probiotics in primary prevention 1. Dendukuri N, et al. CMAJ. 2005;173:167-170. 2. Tung JM, et al. Can J Gastroenterol. 2009;23:817-821. 3. Surawicz CM, et al. Clin Infect Dis. 2000;31:1012-1017.

  31. Alternative CDI Therapies: Rifaximin(Not FDA Approved for CDI Treatment) • Rifaximin “chaser” therapy for multiple recurrent CDI episodes1 • Rifaximin 400 mg BID for 14 days immediately following last course of vancomycin • Seven of eight patients had no further diarrhea recurrence • Single case of rifaximin resistance with recurrent CDI after a second course of rifaximin • Follow up experience with 6 patients • 2 recurred, rifaximin resistance identified in one • Issues with resistance2 • Rifampin resistance observed in 36.8% of 470 recovered isolates and 81.5% of 205 epidemic clone isolates 1. Johnson S, et al. Clin Infect Dis. 2007;44:846-848. 2. Curry SR, et al. Clin Infect Dis. 2009;48:425-429. 3. Johnson S, et al. Anaerobe. 2009; 15:290-1

  32. Alternative CDI Therapies: Nitazoxanide (Not FDA Approved for CDI Treatment) Time to resolution of symptoms • May be effective in patients who failed treatment with metronidazole1 • 66% cure rate in 35 patients who failed treatment with metronidazole • Non-inferior to vancomycin in small study of 50 patients (Figure)2 • Initial response: • Vancomycin: 87% • Nitazoxanide: 94% • Similar time to complete resolution of symptoms P=0.55 1. Musher DM, et al. J Antimicrob Chemother. 2007;59:705-710. 2. Musher DM, et al. Clin Infec Dis. 2009;48:e41-e46; with permission.

  33. Alternative Adjunctive Therapies for Severe CDI(Not FDA Approved for CDI Treatment) • Tigecycline1-3 • Case reports and small case series with IV Tigecycline • Usually given in conjunction with other therapies for severe CDI • Intravenous Immunoglobulin4,5 • Several case series in severe CDI, but evidence for benefit is inconclusive 1. Lu CL, et al. Int J Antimicrob Agents. 2010;35:311-312. 2. Herpers BL, et al. Clin Infect Dis. 2009;48:1732-1735. 3. Kopterides P, et al. Anaesth Intensive Care. 2010;38:755-758. 4. Abougergi MS, et al. J Hosp Med. 2010;5:E1-E9. 5. O’Horo J, et al. Int J Infect Dis. 2009;13:663-667.

  34. Fecal Flora Restoration • Theory: Restoration of fecal flora restores colonization resistance • Data: • 1958 to 2000: 9 reports (68 patients); cure rate ~90%. • 2003: 18 patients; fecal filtrate (stool transplant); 1 of 16 survivors had a single subsequent recurrence; pre-treated with vancomycin and omeprazole; instilled through nasogastric tube. • Test donor for enteric pathogens, C. difficile, ova and parasites, HAV, HBV, HCV, HIV, RPR prior to transplanting stool. 1. Persky SE, Brandt LJ. Am J Gastroenterol. 2000;95:3283-3285. 2. Borody TJ. Am J Gastroenterol. 2000;95:3028-3029. 3. Palmer R. Nat Med. 2011;17:150-152.

  35. Potential Future CDI Therapies: Nontoxigenic C. difficile Non-toxigenic C. difficile prevented CDI in 87%-97% of hamsters • NontoxigenicC. difficile strains occur naturally • Natural asymptomatic C. difficile colonization (toxigenic or nontoxigenic) decreases risk of infection • NontoxigenicC. difficile can be administered orally as spores to provide protection against CDI • Mechanism by which nontoxigenicC. difficile prevents colonization by toxigenic strains not yet established • Human Phase 2 trials began in Q2 2011 M3, M23, T7 = non-toxigenic CD B1, J9, K14 = toxigenic CD 1. Gerding DN, Johnson S. Clin Infect Dis. 2010;51:1306-1313. 2. Sambol SP, et al. J Infect Dis. 2002;186:1781-1789; with permission

  36. Potential Future CDI Therapies: Monoclonal Antibodies(mAbs) • Recent study of mAbs in 200 CDI patients receiving metronidazole or vancomycin • Recurrence rates: • 7% in mAb group vs. 25% in placebo group Time to CDI recurrence Lowry I, et al. N Engl J Med. 2010;362:197-205; with permission.

  37. Prevention of CDI • Transmission between patients and healthcare professionals in hospitals is major source of C. difficile acquisition • Surveys report inconsistencies among infection control measures1 • Hand hygiene policies • Duration of isolation • Environmental cleaning practices • Antimicrobial stewardship programs • Potential future intervention of toxoid vaccine2 • APIC 2010 Clostridium difficile Pace of Progress Survey. Available at: http://www.apic.org/Content/NavigationMenu/ResearchFoundation/NationalCDiffPrevalanceStudy/CDI_Pace_of_Progress_Survey_Report.pdf • Foglia G, et al. Anarobe Society of Americas 2010; Abstract CD 1093.

  38. Minimize Transmission among Healthcare Personnel: Hand Hygiene • Appropriate hand hygiene – area of controversy • In routine settings, alcohol-based hand hygiene in conjunction with isolation precautions using gloves may be acceptable • In setting of outbreak or increased rates, consider washing hands with soap and water after caring for patients with C. difficile HCWs = healthcare workers. 1. Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31:431-455. 2. Dubberke ER, et al. Infect Control Hosp Epidemiol. 2008;29:S81-S92. 3. APIC Guide to the Elimination of Clostridium difficile in Healthcare Settings, Association for Professionals in Infection Control and Epidemiology, Inc. November 2008.

  39. WWS CWS WWA AHW AHR Efficacy of Hand Hygiene Methods for Removal of C. difficile Contamination from Hands Decrease in colony counts compared with no wash 2.5 WWS=warm water and soap CWS=cold water and soap WWA=warm water and antibacterial soap AHW=alcohol hand wipe AHR=alcohol hand rub 2 1.5 1 1.8 1.8 Decrease in colony counts (log CFU/mL) 1.4 0.5 ** ** * * 0.6 0 -0.1 -0.5 -1 Hand hygiene method * Different from AHR (P<0.05). ** Different from AHR and AHW (P<0.05). Oughton M, et al. Infect Control Hosp Epidemiol. 2009;30(10):939-944.

  40. Minimize Transmission Among Healthcare Personnel: Use of Gloves • Four wards randomized • Intervention • Education: gloves when handling body substances (stool, blood, urine) • Gloves placed at bedside • Significant reduction in CDI rate on glove wards P = 0.015 Johnson S, et al. Am J Med. 1990;88:137-140.

  41. Minimize Transmission Among Healthcare Personnel: Contact Precautions • Patients with CDI placed in private rooms when possible • Full barrier precautions (gown and gloves) for contact with CDI patient • Use of dedicated patient care items and equipment 1. Dubberke ER, et al. Infect Control Hosp Epidemiol. 2008;29:S81-S92. 2. Cohen SH, et al. Infect Control Hosp Epidemiol. 2010;31(5):431-455.

  42. Minimize Transmission from Environment: Disinfection • Use of sodium hypochlorite (at least 5,000 ppm available chlorine) for environmental contamination, during outbreak areas • Inconsistent efficacy in endemic settings • Areas in question: • Concentration of bleach? [Available chlorine: 5,000 ppm (1:10), 1,000 ppm, or 500ppm] • Where to clean? [CDI rooms only, all rooms, entire ward] • How frequent? [Daily or upon discharge] • How to implement? [Mix fresh daily, premixed, or prepackaged wipes; wipe or spray] Perez. J, et al. Am J Infect Control. 2005;33:320-325.

  43. Minimize Transmission by Environment: Bleach Disinfection Mayfield JL, et al. Clin Infect Dis. 2000;31:995-1000.

  44. Reduce Risk of CDI Acquisition: Antimicrobial Stewardship • Reduce use of “high risk” antimicrobials • Reduce unnecessary antimicrobial use • Effective in outbreak and non-outbreak settings 1. Valiquette L. Clin Infect Dis. 2007;45:S112-121; with permission. 2. Fowler S. J Antimicrob Chemother. 2007;59:990-995.

  45. Reduction in CDI after Bundle*(*enhanced isolation practices, laboratory notification procedures, coordination of infection control & environmental services activities) • CDI incidence decreased from 11.0 to 6.6 cases / 10,000 patient days (P<0.001) • Data on compliance with policies before or after bundle lacking • Unclear what parts of bundle were effective Abbett SK, et al. Infect Control Hosp Epidemiol. 2009; 30:1062-1069.

  46. CDI: Future Direction • Optimal diagnostic algorithm for CDI • Prompt recognition of severe CDI • Validation of risk-stratified treatment for CDI • CDI recurrence prevention and treatment • Expanding armamentarium for CDI (both antibiotic and non-antibiotic approaches) • Delineation of the most effective infection control measures—which aspects of the “CDI bundle” are important?

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