Clostridium difficile Infection: An Update on the Current State of Prevention

Transcription

1 Intermountain APIC and Qualis Health present I-APIC HAI Prevention Learning Network Webinar Series Clostridium difficile Infection An Update on the April 11, 2012 Ruth CarricoPhD RN FSHEA CIC Clostridium difficile Infection: An Update on the Current State of Prevention Associate Professor University of Louisville School of Public Health and Information Sciences and School of Medicine, Division of Infectious Diseases Louisville, KY 1

2 No disclosures relevant to this event CDI in Health Care Settings Clostridium difficile is the most common cause of healthcare- associated diarrhea in the United States with a special impact in long term care settings Clostridium difficile infection (CDI) now rivals MRSA infection as the most common healthcare-associated associated infection in many US healthcare facilities 2

3 CDI in Health Care Settings Recognize the microbiology, pathogenesis, and changing epidemiology of C. difficile and C. difficile Infection (CDI) Discuss current diagnostic and treatment approaches to C. difficile in healthcare settings Plan and implement appropriate C. difficile acquisition and transmission prevention strategies in healthcare settings CDI in Health Care Settings Microbiology & Epidemiology Pathogenesis Diagnosis & Treatment 4 Prevention 3

4 CDI in Health Care Settings Microbiology & Epidemiology Pathogenesis Diagnosis & Treatment 4 Prevention Microbiology & Epidemiology of CDI Genus: Clostridium Anaerobic, gram-positive, spore-forming bacilli Spores Vegetative forms Normal gastrointestinal flora Among the 90 known species, 30 are associated with human disease 4

5 Microbiology & Epidemiology of CDI Genus: Clostridium Anaerobic, gram-positive, spore-forming bacilli Spores Vegetative forms Normal gastrointestinal flora Among the 90 known species, 30 are associated with human disease Clostridial diseases mediated by toxins Spores Vegetative forms Toxin Microbiology & Epidemiology of CDI Clostridial diseases mediated by toxins Neurological Diseases Tetanus Botulism Clostridium tetani Clostridium botulinum 5

6 Microbiology & Epidemiology of CDI Clostridial diseases mediated by toxins Neurological Diseases Tetanus Botulism Clostridium tetani Clostridium botulinum Soft Tissue Diseases Gas gangrene Clostridium perfringes Microbiology & Epidemiology of CDI Clostridial diseases mediated by toxins Neurological Diseases Tetanus Botulism Clostridium tetani Clostridium botulinum Soft Tissue Diseases Gas gangrene Clostridium perfringes Enteric Diseases Neutropenic enterocolitis Pseudomembranous colitis Clostridium septicum Clostridium difficile 6

7 Microbiology & Epidemiology of CDI Clostridium difficile Environment Toxin A Spores Vegetative forms Toxin GI tract Toxin B Microbiology & Epidemiology of CDI Clostridium difficile Environment Toxin A Spores Vegetative forms Toxin GI tract Toxin B CDI 1. Germination of spores 2. Production of vegetative cells 3. Production of toxins 7

8 Microbiology & Epidemiology of CDI Risk Factors Previous antibiotic use is the predominant risk factor Chemotherapy Antibiotic Exposure Risk Factors Microbiology & Epidemiology of CDI Risk Factors Previous antibiotic use is the predominant risk factor Chemotherapy Antibiotic Exposure Risk Factors Hospitalization Admission to ICU Prolonged LOS Long term care LOS 8

9 Microbiology & Epidemiology of CDI Risk Factors Previous antibiotic use is the predominant risk factor Chemotherapy Antibiotic Exposure Risk Factors Hospitalization Admission to ICU Prolonged LOS Long term care LOS Advance Age >65 risk 20-fold Underlying disease Gastric acid? PPIs? Role of Immune Response: s with a poor immune response to C. difficile toxins are at increased risk of CDI 9

10 Microbiology & Epidemiology of CDI Emergence of a More Virulent Strain Categorization of C. difficile Toxin production Type of toxin Susceptibility Clinical response Non toxin producer Low toxin producer High toxin producer Highly toxigenic Toxin A & B Binary toxin Quinolone resistance response to therapy Increased Severity of CDI Microbiology & Epidemiology of CDI Emergence of a More Virulent Strain Categorization of C. difficile Toxin production Type of toxin Susceptibility Clinical response Non toxin producer Low toxin producer High toxin producer Highly toxigenic Toxin A & B Binary toxin Quinolone resistance response to therapy Epidemic Strain: North America PFGS type 1 NAP-1 NAP-1 NAP-1 NAP-1 Increased Severity of CDI 10

11 Microbiology & Epidemiology of CDI Increased Incidence & Severity of CDI Low toxin producer strain: Mild CDI Healthcare-Associated Diarrhea Abdominal Distension Hypervirulent NAP1/027 strain: Severe CDI Megacolon Septic Shock Perforation Colectomy Death within 30 days Increased Incidence & Severity of CDI Microbiology & Epidemiology of CDI Increased Severity of CDI 76 year-old white male in a long term care facility Episode of confusion, lethargy and hypotension Sent to hospital for urosepsis Treated with antibiotics and a short hospital stay Returned to long term care facility while completing antibiotic therapy Develops diarrhea Tested for C. difficile Toxin positive Age-related immunosenescence 11

12 New Terminology Useful in Understanding the Human Microbiome and Infection Control Flora plant life, as in flora and fauna Microbiota resident microbial communities Microbiome the collective genome of microbial communities Metagenomics whole genomic sequencing of microbiota, sometimes limited to sequences of DNA encoding16s ribosomal RNA (i.e. limited to species identification) Metabolomics chemical fingerprints --thanks to Dr. Cliff McDonald, CDC Microbiology & Epidemiology of CDI Increased Severity of CDI 76 year-old white male in a long term care facility Episode of confusion, lethargy and hypotension Sent to hospital for urosepsis Treated with antibiotics and a short hospital stay Returned to long term care facility while completing antibiotic therapy Develops diarrhea Tested for C. difficile Toxin positive Age-related immunosenescence Mild diseases Severe disease Recurrent/relapsing disease Recovery Death 12

13 CDI in Health Care Settings Microbiology & Epidemiology Pathogenesis Diagnosis & Treatment 4 Prevention Normal Colonic Microbiota & Mucosa Abnormal Flora & C diff Production of Toxins A & B Pseudomembranous Colitis 13

14 Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Production of Toxins A & B Pseudomembranous Colitis Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) Pseudomembranous Colitis 14

15 Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Normal colonic mucosa Pseudomembranes in areas of colonic mucosa Pseudomembranes entire colonic mucosa 15

16 Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) (-)C. diff (+)C. diff C. diff Colonization HCW (-) C diff Object 16

17 C. diff Colonization C diff spores can persist on hard surfaces for as long as 5 months HCW (-) C diff Object C diff is present in 50% of sites in rooms occupied by a patient with CDI and in 30% of sites in rooms occupied by asymptomatic carriers C. diff Colonization C diff spores can persist on hard surfaces for as long as 5 months HCW As levels of environmental contamination increase, so does the prevalence of C diff hand carriage among HCW (-) C diff Object C diff is present in 50% of sites in rooms occupied by a patient with CDI and in 30% of sites in rooms occupied by asymptomatic carriers 17

18 C. diff Colonization HCW As levels of environmental contamination increase, so does the prevalence of C diff hand carriage among HCW Reservoir of C diff (-) C diff C diff spores can persist on hard surfaces for as long as 5 months Object C diff is present in 50% of sites in rooms occupied by a patient with CDI and in 30% of sites in rooms occupied by asymptomatic carriers Hospitalization Colonization Rates Healthy adults:1-3% s 100% 5% 95% (-) C diff 18

19 Hospitalization Colonization Rates Healthy adults:1-3% s 100% 5% 95% (-) C diff 15% 80% (-) C diff Hospitalization Colonization Rates Healthy adults:1-3% s 100% 5% 95% (-) C diff 15% 80% 10% 5% (+) CDI (-) C diff 19

20 Hospitalization Colonization Rates Healthy adults:1-3% Carrier State Fecal excretors Environmental contamination 5% 10% s 100% 95% (-) C diff 15% 80% 5% (+) CDI (-) C diff Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) (-)C. diff (+)C. diff CDI 20

21 Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) (-)C. diff (+)C. diff CDI Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) (-)C. diff (+)C. diff CDI Changes in the gut environment may trigger germination Changes in normal microbiota alter the amount and ratio of bile derivatives Certain cholate (bile) derivatives and the AA glycine are co-germinants in transforming spores to vegetative cells 21

22 Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) (-)C. diff (+)C. diff CDI Antitoxin A Antibodies Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) (-)C. diff (+)C. diff CDI Asymptomatic carriers have high titers of antitoxin A IgG s with diarrhea have lower titers of antitoxin A IgG Variation in immune response may explain severity The ability of B cells to release immunoglobulins is dependent on CD4+ cells 22

23 First Step: C diff healthcare exposure Normal GI Microbiota First Step: C diff healthcare exposure Second Step: Collateral damage Normal GI Microbiota Disruption of GI Flora 23

24 First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Normal GI Microbiota Disruption of GI Flora First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Normal GI Microbiota Disruption of GI Flora Fulminant Colitis 24

25 First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Normal GI Microbiota Disruption of GI Flora Fulminant Colitis Death due to C diff First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Normal GI Microbiota Disruption of GI Flora Fulminant Colitis Death due to C diff Clinical Presentation Asymptomatic Asymptomatic Asymptomatic Diarrhea, nausea, fever, dehydration, anorexia, abdominal distention Leukocytosis Lethargy, fever, tachycardia, acute abdomen, paralytic ileus, SIRS 25

26 CDI in Health Care Settings Microbiology & Epidemiology Pathogenesis Diagnosis & Treatment 4 Prevention Diagnosis of CDI Risk Factors Diarrhea, abdominal cramps, fever, leukocytosis A. Clinical symptoms of CDI Diagnosis A+B or A+C B. Laboratory identification C. Visualization of PMC 26

27 Diagnosis of CDI Risk Factors Diarrhea, abdominal cramps, fever, leukocytosis A. Clinical symptoms of CDI Diagnosis A+B or A+C B. Laboratory identification C. Visualization of PMC Toxin A or toxin A/B ELISA (>100pg of toxin) & cell cytotoxicity assay PCR to detect the genes for toxin A, toxin B, and binary toxin Antigen test (glutamate dehydrogenase enzyme) is equivalent to culture Culture, isolation, and identification of toxigenic C diff strains Medical Treatment of CDI Non-Severe Disease 1. Initial Episode (Non-Severe) Oral Metronidazole (500mg q 8hs / 250 mg q 6hs) Oral Vancomycin ( 125mg q6hs) 2. Initial Relapse (Non-severe) Oral Metronidazole (500mg q 8hs / 250 mg q 6hs) Oral Vancomycin ( 125mg q6hs) 1. Initial Episode: Total of 10 to 14 days or 7 days after D/C ATB 2. Initial Relapse: Total of 10 to 14 days or 7 days after D/C ATB 27

28 Medical Treatment of CDI Non-Severe Disease 3. Subsequent Relapse (Non-severe) Oral Vancomycin ( 125mg q6hs) for 14 days Followed by Rifaximin 400mg bid for 14 days Probiotics for 3 weeks Oral Vancomycin ( 125mg q6hsfor 7 days) tapering dose 6 weeks Probiotics for 3 weeks Fidaxomicin FDA approved May 2011 DIFICID (Optimer Pharmaceuticals) Oral macrolide treatment for CDI in adults 18 and older First new antibacterial agent for CDI (proven or strongly suspected) in more than 25 years Non-inferior to vancomycin at the end of 10 day course (BI and non-bi strains) Superior to vancomycin when endpoint was prevention of recurrence (non-bi strains only) 28

29 Fidaxomicin 200 mg tablets given twice daily with or without food Minimal systemic absorption so not used to treat systemic (severe) disease No dose adjustments indicated for geriatric patients Laboratory interpretive criteria are available for microbiology lab Medical Treatment of CDI Severity of Disease Non-severe CDI versus Severe CDI WBC count > 20 Abnormal Creatinine Age > 65 Bowel movements > 10/day ICU Severe CDI Oral Vancomycin ( 500 mg q6hs) IV Metronidazole (500mg q 8hs) Ileus: Intracolonic Vancomycin 29

30 Medical Treatment of CDI Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Zar et al Clin Infect Dis 2007;45:302-7 Medical Treatment of CDI Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin There is no C diff resistant to metronidazole Oral Vancomycin may favor development of VRE Oral Vancomycin is more expensive than oral metronidazole 30

31 Medical Treatment of CDI Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins Medical Treatment of CDI Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin 31

32 Medical Treatment of CDI Normal Colonic Microbiota & Mucosa (Abnormal Microbiota) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin If antibiotics can not be discontinued, change to antibiotics with the lowest potential to produce CDI or the lowest potential for collateral damage Medical Treatment of CDI Antimicrobial Risk for CDI and Collateral Damage Antibiotic Imipenem, Meropenem, Ceftriaxone, Doripenem Pip-tazobactam, Cefepime, Moxi, Levo, Amp/sulbactam, Clinda Linezolid, Dapto, Aminoglycosides, Metronidazole, Vancomycin, Nafcillin, TMP/ZMX, Penicillin G Cephalosporins 1 st generation Tetracycline, Macrolides Risk

33 Medical Treatment of CDI Normal Colonic Flora & Mucosa (Abnormal Flora) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic 2. Probiotics Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin Medical Treatment of CDI Normal Colonic Flora & Mucosa (Abnormal Flora) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic 2. Probiotics Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin There is no conclusive evidence to support CDI therapy with probiotics Fungemia due to Saccharomyces cerevisiae and Saccharomyces boulardii 33

34 Medical Treatment of CDI Normal Colonic Flora & Mucosa (Abnormal Flora) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic 2. Probiotics / Prebiotics Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin Nutrients that facilitate the growth of normal colonic bacterial flora Medical Treatment of CDI Normal Colonic Flora & Mucosa (Abnormal Flora) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic 2. Probiotics 3. Stool transplant Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin 34

35 Medical Treatment of CDI Normal Colonic Flora & Mucosa (Abnormal Flora) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic 2. Probiotics 3. Stool transplant Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin The best approach to re-establish normal fecal flora Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin Stool transplant is the only successful strategy for patients with relapsing CDI To replace the need for adequate screening of stool donor: Synthetic stool Medical Treatment of CDI Normal Colonic Flora & Mucosa (Abnormal Flora) C diff Diarrhea (Toxins A & B) (Pseudomembranous) Return of Normal Flora 1. D/C inciting antibiotic 2. Probiotics 3. Stool transplant Antibacterial therapy 1. Oral Metronidazole 2. Oral Vancomycin Anti-toxin therapy 1. Anion-binding resins 2. IV Immunoglobulin Repeat stool toxin assays are NOT warranted following treatment 35

36 CDI in Health Care Settings Microbiology & Epidemiology Pathogenesis Diagnosis & Treatment 4 Prevention Prevention of CDI First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Normal GI Flora Disruption of GI Flora Fulminant Colitis Death due to C diff C diff Bundle 36

37 First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Prevention of CDI Normal GI Flora Disruption of GI Flora Fulminant Colitis Death due to C diff 1 C diff Bundle Infection Prevention Prevention Ingestion of the organism and its spores Strategies to Prevent First Step: Colonization HCW 4 1 (-) C diff 2 3 Object 37

38 Strategies to Prevent Improve identification HCW Improve hand hygiene First Step: Colonization 4 1 (-) C diff 2 3 Improve compliance with isolation Object Improve cleaning/ disinfection of surfaces Strategies to Prevent Improve identification HCW Improve hand hygiene 1 Alcohol-based hand sanitizers are highly effective against non-spore-forming organisms, but they do not kill C diff spores nor remove C diff from the hands First Step: Colonization 4 1 (-) C diff 2 3 Improve compliance with isolation Object Improve cleaning/ disinfection of surfaces 1 The most effective way to remove C diff spores from hands is through handwashing 38

39 Strategies to Prevent Improve identification HCW Improve hand hygiene 2 Only chlorine-based disinfectants and vaporized hydrogen peroxide are sporicidal First Step: Colonization 4 1 (-) C diff 2 3 Improve compliance with isolation Object Improve cleaning/ disinfection of surfaces 2 Commonly used hospital cleaning agents, such as quaternary ammoniumbased detergents, are not sporicidal and may in fact encourage sporulation Strategies to Prevent Improve identification HCW Improve hand hygiene 2 Only chlorine-based disinfectants and vaporized hydrogen peroxide are sporicidal First Step: Colonization 4 1 (-) C diff 2 3 Improve compliance with isolation Object Improve cleaning/ disinfection of surfaces 2 Commonly use hospital cleaning agents, such as quaternary ammoniumbased detergents, are not sporicidal and may in fact encourage sporulation 2 The use of 1:10 dilution of concentrated sodium hypochlorite (bleach) is recommended by the CDC during outbreaks of CDI 39

40 Strategies to Prevent Improve identification HCW Improve hand hygiene First Step: Colonization 4 1 (-) C diff Wearing gloves significantly reduces the spread of C diff Improve compliance with isolation Object Improve cleaning/ disinfection of surfaces Strategies to Prevent 4 Early identification and isolation of patients First Step: Colonization Improve identification 4 Decolonization? HCW Asymptomatic carriers are a potential source of transmission, Improve but they handdo not 1 (-) C diff 2 have a higher hygiene risk of developing CDI 4 3 Improve compliance with isolation Object Improve cleaning/ disinfection of surfaces 40

41 First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Prevention of CDI Normal GI Flora Disruption of GI Flora Fulminant Colitis Death due to C diff 1 2 C diff Bundle Infection Prevention Prophylaxis of Infection? Metro or Vanco when antibiotics are used: no evidence for routine clinical use Probiotics: No evidence for routine clinical use First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Prevention of CDI Normal GI Flora Disruption of GI Flora Fulminant Colitis Death due to C diff 1 2 C diff Bundle Infection Prevention Other Preventive Strategies? Areas of Research Probiotics: Genetically modified toxin-negative C diff Prevention of C diff spore germination C diff toxin-derived vaccine 41

42 Prevention of CDI First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Normal GI Flora Disruption of GI Flora Fulminant Colitis Death due to C diff C diff Bundle Infection Prevention Antimicrobial Stewardship Antimicrobial Stewardship Antimicrobial Stewardship Prevention of CDI First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Normal GI Flora Disruption of GI Flora Fulminant Colitis Death due to C diff C diff Bundle Infection Prevention Antimicrobial Stewardship Antimicrobial Stewardship Antimicrobial Stewardship 5 Optimal Surgical Treatment Total colectomy Optimal timing? 42

43 First Step: C diff healthcare exposure Second Step: Collateral damage Third Step: C diff toxin production Fourth Step: Toxin hyperproduction Fifth Step: Shock & Severe Sepsis Prevention of CDI Normal GI Flora Disruption of GI Flora Fulminant Colitis Death due to C diff C diff Bundle Infection Prevention Antimicrobial Stewardship Antimicrobial Stewardship Antimicrobial Stewardship 5 Optimal Surgical Treatment 6 Sentinel Event & Root Cause Analysis Resources APIC. Clostridium difficile Elimination Guide SHEA/IDSA Compendium of Recommendations. Infect Control Hosp Epidemiol 2008;29:S81 S92. Cohen SH, Gerding DN, Johnson S, Kelly CP, Loo VG, McDonald LC, Pepin J, Wilcox MH; Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by SHEA and IDSA. Infect Control Hosp Epidemiol May;31(5): Mayfield JL, Leet T, Miller J, et al. Environmental control to reduce transmission of Clostridium difficile. Clin Infect Dis 2000;31:

44 Save-the-Date: I-APIC HAI Series Antimicrobial Stewardship in Infection Prevention Wednesday, May 9, 1pm MT/12pm PT Julia Moody, MS SM(ASCP) Director, Infection Prevention, HCA Clinical Services Group APIC Antimicrobial Stewardship Task Force Co-Author, APIC Guide to the Elimination of MRSA Transmission in Hospital Settings Hand Hygiene Wednesday, June 13, 1pm MT/12pm PT Timothy Landers, CNP, PhD Assistant Professor, The Ohio State University College of Nursing 87 Contact Information Ruth Carrico Intermountain APIC Trish Heath, Education Lead Ginna Maggard, President Quality Improvement Organizations Jennifer Palagi Qualis Health, Idaho QIO Tina Schwien Qualis Health, Washington QIO Laurie Murray-Snyder Acumentra Health, Oregon QIO This material was prepared by Qualis Health, the Medicare Quality Improvement Organization for Idaho and Washington, under contract with the Centers for Medicare & Medicaid Services (CMS), an agency of the U.S. Department of Health and Human Services. The contents presented do not necessarily reflect CMS policy. ID/WA-C7-QH

45 Presentation Evaluation Will automaticallypop-up when you close out of presentation on your computer Share the evaluation link below with others attending with you, to capture their feedback Brief Survey Monkey: