CLOSTRIDIUM DIFFICILE: THE NEW HOSPITAL PLAGUE? - PowerPoint PPT Presentation

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CLOSTRIDIUM DIFFICILE: THE NEW HOSPITAL PLAGUE?

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  1. CLOSTRIDIUM DIFFICILE:THE NEW HOSPITAL PLAGUE? WHY IS CONTROL OF THIS DIARRHEA-CAUSING DISEASE MORE IMPORTANT NOW THAN EVER ? John L. Dyson RN, BSN MSN 621 Alverno College, Milwaukee, Wisconsin Last updated May 12, 2006 (enter by clicking on arrow to the right)

  2. Welcome… To navigate this tutorial, these tools are available: will move you FORWARD to the next page. will move you BACK one page. A highlighted area will move you to related articles, websites, or glossary definitions will RETURN you to the “click here” “TABLE OF CONTENTS”. Permission for use of information from this web-based tutorial must be obtained from the author at 4under1roof@sbcglobal.net. (Navigation symbols from Microsoft Office 2003)

  3. “CLICK” A SUBJECT BELOW TO LEARN MORE ABOUT… 1. PATHOPHYSIOLOGY OF C-DIFF 2..DISCOVERY OF C-DIFF. 3. GENETICS AND C-DIFF. 4. TREATMENT OF C-DIFF. 5. WHO IS AT RISK FOR COMPLICATIONS? 6. SYMPTOMS OF C-DIFF. 7. “THE ADVERSE EFFECTS OF CONTACT ISOLATION AND LONELINESS ON PATIENTS 8. REFERENCES (CLICKING ON “ ” WILL RETURN YOU HERE AT ANY TIME)

  4. HOW IS C-DIFFICILE SPREAD? (CLICK on YOUR ANSWER BELOW to CHOOSE) BY AN INHALED BACTERIUM? BY AN AIRBORNE VIRUS? BY THE FECAL/ORAL ROUTE? (sounds: Microsoft Office 2003)

  5. NO…. NOT AN INHALED BACTERIUM! …try again!! (click HERE to try again)

  6. NO… …IT’S NOT A VIRUS …try again!! (click HERE to try again)

  7. YES!!! …C-DIFFICILE IS A BACTERIUM IN THE FORM OF A SPORE! • It is transmitted by the fecal-oral route when shed in feces & released. • It can live up to 70 days in the environment!! Medical College of Wisconsin (2000) http://www.healthlink.mcw.edu/article/954992292.html)

  8. Pathophysiology of C-difficile Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (picture used with permission)

  9. Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (Picture used with permission)

  10. Pathophysiology of C-Difficile Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (picture used with permission)

  11. TWO STEPS OCCUR: Normal Flora must be disrupted (occurs with antibiotics). Clostridium difficile must be ingested. (These do not have to occur in this order) The Onset of Pseudomembraneous Colitis Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (picture used with permission)

  12. “SOME PATIENTS DEVELOP C-DIFF, WHILE OTHERS DO NOT…” “IT IS UNCLEAR WHY” THIS IS SO… Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (picture used with permission)

  13. ACTUAL ENDOSCOPY PICTURES: picture courtesy of Carol Hein, RN, MSN (used with permission)

  14. NO LONGER THE DISEASE OF THE ELDERLY AFFECTS: • ACUTE CARE PATIENTS • PEDIATRIC PATIENTS • TUBE-FED PATIENTS • HEALTHCARE WORKERS • FAMILIES

  15. WHICH OF THESE PRODUCES THE DIARRHEA SYMPTOMS OF C-DIFF? TOXINS “TD-1” AND “TD-2” TOXINS “A” AND “B” TOXINS “C” AND “DIFF”

  16. NO ! TRY ANSWERING AGAIN!

  17. YES… YOU GOT IT !! Sunenshine & McDonald (2006) (picture used with permission)

  18. HISTORY OF C-DIFF • FIRST ISOLATED IN THE 1930’S • NAMED “CLOSTRIDIUM DIFFICILE” DUE TO DIFFICULTY ISOLATING THE BACTERIUM SPORE. • SPORE CARRIES “TOXIN A” AND “TOXIN B”. • RESULTS IN “PSEUDOMEMBRENOUS COLITIS”- WHICH PRESENTS WITH THE DIARRHEA SEEN Conly (2001)

  19. WHEN IT WAS FIRST LINKED TO DISEASE IN 1978… THE C-DIFF BACTERIA WAS FOUND TO BE: • SPORE-FORMING • ANAEROBIC (REQUIRES NO OXYGEN TO SURVIVE) Sunenshine& McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf

  20. THERE ARE MORE THAN 3 MILLION C-DIFF CASES ANNUALLY IN THE U.S. • C-DIFF IS SEEN FOLLOWING LONGER- TERM ANTIBIOTIC THERAPY • THE DISEASE DESTROYS INTESTINAL MUCOSA, INFLAMING THE LARGE INTESTINE • THE RESULT: MUCOSY DIARRHEA Pothoulakis (2001) http://www.aboutibs.org/Publications/CDifficile.html. (picture: www.the-collective.net/~punxi/old/mompics, used with permission)

  21. SYMPTOMS: • MILD CASES: FREQUENT, FOUL SMELLING, WATERY STOOLS • MODERATE CASES: BLOODY, MUCOUSY DIARRHEA, ABDOMINAL CRAMPING- AND POSSIBLY AN ABNORMAL HEART RHYTHM (DUE TO AN ELECTROLYTE IMBALANCE) Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (picture, used with permission: www.cheshire-med.com/services/bugs/ecoli.html)

  22. THE RESULT: • SEVERE CASES: PSEUDOMEMBRANEOUS COLITIS, LEADING TO: TOXIC MEGACOLON …AND ULTIMATELY, . . . . DEATH!!!

  23. FULMINANT COLITIS • MOST SERIOUS COMPLICATION • OCCURS IN 3% OF PATIENTS • SEE: SEVERE LOWER ABDOMEN PAIN, DIARRHEA, HIGH FEVER WITH CHILLS, & RAPID HEART RATE • THIS OCCURS MOSTLY IN DEBILITATED, ELDERLY PATIENTS Pothoulakis (2001) http://www.aboutibs.org/Publications/CDifficile.html (picture: Microsoft Office 2003)

  24. PATIENT PRESENTATION • USUALLY HAVE HAD ANTIBIOTICS OR ANTINEOPLASTICS IN PAST 2 MONTHS • SOME COMMON ANTIBIOTICS THAT CONTRIBUTE TO C-DIFF INCLUDE: • AMPICILLIN • AMOXACILLIN • CEPHALOSPORINS • CLINDAMYCIN Pothoulakis (2001) http://www.aboutibs.org/Publications/CDifficile.html (picture: Microsoft Office 2003)

  25. TOP 4 CAUSES OF CROSS-CONTAMINATION # 4. TOILETS # 3. TELEPHONES # 2. STETHOSCOPES picture: http://funtavern.com/pictures/gp-germs.jpg (used with permission)

  26. THE NUMBER ONE REASON:(click the picture) (picture: Microsoft Office 2003)

  27. CAREGIVER HANDS!!!

  28. DID YOU KNOW….? • C-DIFF SPORES HAVE A LIFE EXPECTANCY OF UP TO 70 DAYS ? • SPORES ARE RESISTANT TO DISINFECTANTS AND STANDARD CLEANING SOLUTIONS BY HOUSEKEEPING ? • ALCOHOL-BASED “PUMP” SANITIZERS DO NOT KILL THE SPORE? Medical College of Wisconsin (2000) http://healthlink.mcw.edu/article/954992292.html

  29. THE RESULT… • LONGER HOSPITALIZATIONS • CHRONIC DIARRHEA IN SOME ELDERLY • SERIOUS / LIFE THREATENING DISEASE Stelfox, Bates, & Redelmeier (2003)

  30. THE C-DIFF GENOMIC PATHOGENOCITY LOCUS- Identified as “Toxin A” & “Toxin B” (Also known as tcdA and tcdB)- A number after the locus identifies the mutation site (IE: tcdB1470)Rupnik, Dupuy, et. al. (2005)http://jmm.sgmjournals.org/cgi/content/full/54/2/113#F13

  31. Toxin “A” & the Neurokinin-1 Receptor STUDIES WITH LABORATORY MICE HAVE SHOWN: • TOXIN “A” BINDS TO THE NEUROKININ-1 (NK-1) RECEPTOR IN THE INTESTINAL LINING. • THE FAMILY OF Rho PROTEINS (PROTEINS INVOLVED IN CELLULAR FUNCTION) IS INACTIVATED. • THE ACTIN MICROFILAMENTS (PROTEIN FILAMENTS PROVIDING MECHANICAL SUPPORT FOR THE CELL) BECOME DISAGGREGATED. Castagliuolo, Riegler, Pasha, et. Al. (1998). “Actin Microfilaments” definition obtained from: en.wikipedia.org. (picture: Microsoft Office 2003)

  32. A COMPLEX CASCADE EFFECT • Toxin “A” stimulates production of “Substance P”, a neuropeptide affecting the Central Nervous System and causes nausea, pain, and can serve as a vasodilator. • Enteric (intestinal) Nerves are affected. • Macrophages (infection-fighting cells) and Leukocytes. Castagliuolo, Riegler, Pasha, et. al (1998) (picture: Microsoft Office 2003)

  33. EMBRYONIC STEM CELL RESEARCH IN MICE SHOWS… • REMOVING Substance “P”, causing a deficiency of NK-1 DIMINISHED the inflammatory changes leading to Clostridium difficile when Toxin “A” was administered. • This supports a direct cause-effect relationship!! Castagliuolo, Riegler, Pasha, et. al. (1998) (picture: Microsoft Office 2003)

  34. TO SUMMARIZE THE GENETICS PROCESS: • Toxin “A” binds to the Neurokinin-1 (NK-1) receptors of the intestinal linings. • Rho Proteins become inactivated & Actin Microfilaments become disaggregated, essentially breaking down the cell. • Toxin “A” stimulates Substance“P”, causing nausea, pain, & vasodilation. • Macrophages and Leukocytes complete the inflammatory intestinal lining damage. • Toxin “A” needs Substance “P” in a cause- effect relationship, or damage is diminished.

  35. ENTER: The NEW C-diff Strain ! NAP 1 (North American pulsed-field gel electrophoresis type 1) FOUND IN OUTBREAKS IN NORTH AMERICA AND EUROPE! • Produces 16x MORE Toxin “A”, 23x MORE Toxin B”, and a third “BINARY TOXIN” (whose significance is not yet known). • Resistant to GATIFLOXACIN & MOXIFLOXACIN (historical C-diff strains are not). • POSSIBLY due to a deletion in a negative regulatory gene. Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf

  36. C-DIFF AND GENETICS:A SUMMARY • C-diff occurs in the clinical and natural environment. • C-diff is a nosocomial pathogen. • C-diff (as yet) has no specifically identified gene site. • Genetics has helped ID the toxins to diagnose C-Diff, but no specific genes are known to CAUSE it ! Farrow, Lyras, & Rood (2001) http://mic.sgmjournals.org/cgi/content/abstract/147/10/2717

  37. GLOSSARY • TOXIC MEGACOLON: A grave complication of ulcerative colitis resulting in perforation of the colon, septicemia and death. • Click HERE to return

  38. ANTIBIOTICS CAUSE IT…ANTIBIOTICS TREAT IT !! IN THE PAST IT WAS TREATED WITH: • INTRAVENOUS AND ORAL METRONIZADOLE (INEXPENSIVE) • ORAL VANCOMYCIN (COSTLY)Colorado Department of Public Health and Environment, (1999) http://www.cdphe.state.co.us/hf/cdiff99.htm (picture: Microsoft Office 2003)

  39. The Latest Treatment Recommended: Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (table from article used with permission)

  40. WHEN THE DIARRHEA GOES AWAY….IT IS CONSIDERED RESOLVED…BUT…

  41. IT CAN COME BACK! • 12% - 24% HAVE A SECOND C-DIFF OCCURANCE WITHIN 2 MONTHS. • 48% - 56% ARE ACTUALLY REINFECTED WITH A DIFFERENT STRAIN OF C-DIFF. • PATIENTS WITH TWO OR MORE EPISODES HAVE A 50% - 65% RISK OF RE-OCCURANCE. Sunenshine & McDonald (2006) www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_CCJM02_06.pdf (picture: Microsoft Office 2003)

  42. WHO IS SUSCEPTIBLE ??

  43. EVERYONE!

  44. THOSE MOST SUSCEPTIBLE… ASYMPTOMATIC C-Difficile Colonization is present in: • Up to 3 % of healthy adults • As many as 50 % of infants “The major risk factor for C. difficile infection is antibiotic usage” Oguz, Uysal, Dasdemir, Oskovi, & Vidinlisan (2001) (picture: Microsoft Office 2003)

  45. HIGHEST RISK GROUPS: • OLDER PATIENTS • CHRONIC RENAL FAILURE PATIENTS • PATIENTS WITH NASOGASTRIC FEEDING TUBES • PATIENTS WITH A C-DIFF HISTORY THIS IS DUE TO “PHYSIOLOGICAL AND FUNCTIONAL CHANGES OF THE GUT”, WHICH “ARE OFTEN ACCOMPANIED BY AN INCREASED INCIDENCE OF GASTROINTESTINAL INFECTIONS” (picture: Microsoft Office 2003)

  46. PATIENTS IN ISOLATION 3.9 ROOM ENTRIES/HOUR. 2.1 MEAN CONTACTS/HR BY A REGISTERED NURSE. 4.5 MINUTES OF ACTUAL HEALTHCARE WORKER INTERVENTION TIME PER OCCURANCE. Kirkland & Weinstein (1999) PATIENTS NOT IN ISOLATION 7.9 ROOM ENTRIES/HOUR. 4.2 MEAN CONTACTS/HR BY A REGISTERED NURSE. 2.8 MINUTES OF ACTUAL HEALTHCARE WORKER INTERVENTION TIME PER OCCURANCE. “ADVERSE EFFECTS OF CONTACT ISOLATION” (picture: Microsoft Office 2003)

  47. “HOSPITAL PATIENTS IN ISOLATION RECEIVE INFERIOR CARE, STUDY SAYS” • ISOLATED PATIENTS NOT GIVEN MEALS OR MEDICATIONS ON TIME • CALL LIGHT RESPONSE NOT PROMPT • HIGHER INCIDENCE OF FALLS & BEDSORES • PATIENT/CAREGIVER BARRIERS CREATED Bakalopoulos (2003) http://www.thevarsity.ca.

  48. “PSYCHOLOGICAL EFFECTS OF SOURCE ISOLATION” • ISOLATED PATIENTS EXPERIENCE FREQUENT MOOD DISTURBANCES. • CONSISTENT USE OF VERBAL & WRITTEN INSTRUCTIONS FOR PATIENTS SEEMS TO MINIMIZE THEIR VERBALIZED FEELINGS OF ISOLATION FROM THE GENERAL PUBLIC ACTIVITIES Rees, Davies, Birchall, & Price (2000)

  49. Sunenshine & McDonald (2006) (picture from article used with permission)

  50. Sunenshine & McDonald (2006) (picture from article used with permission)