Presentation is loading. Please wait.

Presentation is loading. Please wait.

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.

Similar presentations


Presentation on theme: "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."— Presentation transcript:

1

2 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)

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

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

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

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

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

8 YES!!! …C-DIFFICILE IS A BACTERIUM IN THE FORM OF A SPORE! It is transmitted by the fecal-oral It is transmitted by the fecal-oral route when shed in feces & released. route when shed in feces & released. It can live up to 70 days in the environment!! It can live up to 70 days in the environment!! Medical College of Wisconsin (2000)

9 Pathophysiology of C-difficile Sunenshine & McDonald (2006) (picture used with permission)

10 Sunenshine & McDonald (2006) (Picture used with permission)

11 Pathophysiology of C-Difficile Sunenshine & McDonald (2006) (picture used with permission)

12 The Onset of Pseudomembraneous Colitis TWO STEPS OCCUR: 1.Normal Flora must be disrupted (occurs with antibiotics). 2.Clostridium difficile must be ingested. (These do not have to occur in this order) Sunenshine & McDonald (2006) (picture used with permission)

13 “SOME PATIENTS DEVELOP C-DIFF, WHILE OTHERS DO NOT…” “IT IS UNCLEAR WHY” THIS IS SO… Sunenshine & McDonald (2006) (picture used with permission)

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

15 NO LONGER THE DISEASE OF THE ELDERLY AFFECTS: ACUTE CARE PATIENTSACUTE CARE PATIENTS PEDIATRIC PATIENTS PEDIATRIC PATIENTS TUBE-FED PATIENTS TUBE-FED PATIENTS HEALTHCARE WORKERS HEALTHCARE WORKERS FAMILIES FAMILIES

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

17 NO ! TRY ANSWERING AGAIN!

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

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

20 WHEN IT WAS FIRST LINKED TO DISEASE IN 1978… THE C-DIFF BACTERIA WAS FOUND TO BE: THE C-DIFF BACTERIA WAS FOUND TO BE: SPORE-FORMINGSPORE-FORMING ANAEROBIC (REQUIRES NO OXYGEN TO SURVIVE)ANAEROBIC (REQUIRES NO OXYGEN TO SURVIVE) Sunenshine& McDonald (2006)

21 THERE ARE MORE THAN 3 MILLION C-DIFF CASES ANNUALLY IN THE U.S.THERE ARE MORE THAN 3 MILLION C-DIFF CASES ANNUALLY IN THE U.S. C-DIFF IS SEEN FOLLOWING LONGER- TERM ANTIBIOTIC THERAPYC-DIFF IS SEEN FOLLOWING LONGER- TERM ANTIBIOTIC THERAPY THE DISEASE DESTROYS INTESTINAL MUCOSA, INFLAMING THE LARGE INTESTINETHE DISEASE DESTROYS INTESTINAL MUCOSA, INFLAMING THE LARGE INTESTINE THE RESULT: MUCOSYTHE RESULT: MUCOSY DIARRHEA DIARRHEA Pothoulakis (2001) Pothoulakis (2001) (picture: (picture: used with permission) used with permission)

22 SYMPTOMS: MILD CASES: FREQUENT, FOULMILD CASES: FREQUENT, FOUL SMELLING, WATERY STOOLS SMELLING, WATERY STOOLS MODERATE CASES: BLOODY, MUCOUSY DIARRHEA, ABDOMINAL CRAMPING- AND POSSIBLY AN ABNORMAL HEART RHYTHM (DUE TO AN ELECTROLYTE IMBALANCE)MODERATE CASES: BLOODY, MUCOUSY DIARRHEA, ABDOMINAL CRAMPING- AND POSSIBLY AN ABNORMAL HEART RHYTHM (DUE TO AN ELECTROLYTE IMBALANCE) Sunenshine & McDonald (2006) (picture, used with permission:

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

24 FULMINANT COLITIS MOST SERIOUS COMPLICATIONMOST SERIOUS COMPLICATION OCCURS IN 3% OF PATIENTSOCCURS IN 3% OF PATIENTS SEE: SEVERE LOWER ABDOMEN PAIN, DIARRHEA, HIGH FEVER WITH CHILLS, & RAPID HEART RATESEE: SEVERE LOWER ABDOMEN PAIN, DIARRHEA, HIGH FEVER WITH CHILLS, & RAPID HEART RATE THIS OCCURS MOSTLYTHIS OCCURS MOSTLY IN DEBILITATED, IN DEBILITATED, ELDERLY PATIENTS ELDERLY PATIENTS Pothoulakis (2001) Pothoulakis (2001) (picture: Microsoft Office 2003) (picture: Microsoft Office 2003)

25 PATIENT PRESENTATION USUALLY HAVE HAD ANTIBIOTICS OR ANTINEOPLASTICS IN PAST 2 MONTHSUSUALLY HAVE HAD ANTIBIOTICS OR ANTINEOPLASTICS IN PAST 2 MONTHS SOME COMMON ANTIBIOTICS THAT CONTRIBUTE TO C-DIFF INCLUDE:SOME COMMON ANTIBIOTICS THAT CONTRIBUTE TO C-DIFF INCLUDE: 1.AMPICILLIN 2.AMOXACILLIN 3.CEPHALOSPORINS 4.CLINDAMYCIN Pothoulakis (2001) Pothoulakis (2001) (picture: Microsoft Office 2003) (picture: Microsoft Office 2003)

26 TOP 4 CAUSES OF CROSS-CONTAMINATION # 4. TOILETS # 4. TOILETS # 3. TELEPHONES # 3. TELEPHONES # 2. STETHOSCOPES # 2. STETHOSCOPES picture: picture: (used with permission) (used with permission)

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

28 CAREGIVER HANDS!!!

29 DID YOU KNOW….? C-DIFF SPORES HAVE A LIFE EXPECTANCY OF UP TO 70 DAYS ?C-DIFF SPORES HAVE A LIFE EXPECTANCY OF UP TO 70 DAYS ? SPORES ARE RESISTANT TO DISINFECTANTS AND STANDARD CLEANING SOLUTIONS BY HOUSEKEEPING ?SPORES ARE RESISTANT TO DISINFECTANTS AND STANDARD CLEANING SOLUTIONS BY HOUSEKEEPING ? ALCOHOL-BASED “PUMP” SANITIZERSALCOHOL-BASED “PUMP” SANITIZERS DO NOT KILL THE SPORE? DO NOT KILL THE SPORE? Medical College of Wisconsin (2000) Medical College of Wisconsin (2000)

30 THE RESULT… LONGER HOSPITALIZATIONSLONGER HOSPITALIZATIONS CHRONIC DIARRHEA IN SOME ELDERLYCHRONIC DIARRHEA IN SOME ELDERLY SERIOUS / LIFE THREATENING DISEASESERIOUS / LIFE THREATENING DISEASE Stelfox, Bates, & Redelmeier (2003) Stelfox, Bates, & Redelmeier (2003)

31 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: tcdB 1470 ) Rupnik, Dupuy, et. al. (2005) 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: tcdB 1470 ) Rupnik, Dupuy, et. al. (2005)

32 Toxin “A” & the Neurokinin-1 Receptor STUDIES WITH LABORATORY MICE HAVE SHOWN: 1.TOXIN “A” BINDS TO THE NEUROKININ-1 (NK-1) RECEPTOR IN THE INTESTINAL LINING. 2.THE FAMILY OF Rho PROTEINS (PROTEINS INVOLVED IN CELLULAR FUNCTION) IS INACTIVATED. 3.THE ACTIN MICROFILAMENTS (PROTEIN FILAMENTS PROVIDING MECHANICAL SUPPORT FOR THE CELL) BECOME DISAGGREGATED. Castagliuolo, Riegler, Pasha, et. Al. (1998). Castagliuolo, Riegler, Pasha, et. Al. (1998). “Actin Microfilaments” definition obtained from: en.wikipedia.org. “Actin Microfilaments” definition obtained from: en.wikipedia.org. (picture: Microsoft Office 2003)

33 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.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.Enteric (intestinal) Nerves are affected. Macrophages (infection-fighting cells) and Leukocytes.Macrophages (infection-fighting cells) and Leukocytes. Castagliuolo, Riegler, Pasha, et. al (1998) Castagliuolo, Riegler, Pasha, et. al (1998) (picture: Microsoft Office 2003)

34 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.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!!This supports a direct cause-effect relationship!! Castagliuolo, Riegler, Pasha, et. al. (1998) Castagliuolo, Riegler, Pasha, et. al. (1998) (picture: Microsoft Office 2003)

35 TO SUMMARIZE THE GENETICS PROCESS: 1.Toxin “A” binds to the Neurokinin-1 (NK-1) receptors of the intestinal linings. 2.Rho Proteins become inactivated & Actin Microfilaments become disaggregated, essentially breaking down the cell. 3.Toxin “A” stimulates Substance “P”, causing nausea, pain, & vasodilation. 4.Macrophages and Leukocytes complete the inflammatory intestinal lining damage. 5.Toxin “A” needs Substance “P” in a cause- effect relationship, or damage is diminished. effect relationship, or damage is diminished.

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

37 C-DIFF AND GENETICS: A SUMMARY C-diff occurs in the clinical and natural environment.C-diff occurs in the clinical and natural environment. C-diff is a nosocomial pathogen.C-diff is a nosocomial pathogen. C-diff (as yet) has no specifically identified gene site.C-diff (as yet) has no specifically identified gene site. Genetics has helped ID the toxins to diagnoseGenetics has helped ID the toxins to diagnose C-Diff, but no specific genes are known to CAUSE it ! C-Diff, but no specific genes are known to CAUSE it ! Farrow, Lyras, & Rood (2001) Farrow, Lyras, & Rood (2001)

38 GLOSSARY TOXIC MEGACOLON: A grave complication of ulcerative colitis resulting in perforation of the colon, septicemia and death.TOXIC MEGACOLON: A grave complication of ulcerative colitis resulting in perforation of the colon, septicemia and death. Click HERE to returnClick HERE to returnHERE

39 ANTIBIOTICS CAUSE IT… ANTIBIOTICS TREAT IT !! IN THE PAST IT WAS TREATED WITH: INTRAVENOUS ANDINTRAVENOUS AND ORAL METRONIZADOLE ORAL METRONIZADOLE (INEXPENSIVE) (INEXPENSIVE) ORAL VANCOMYCIN (COSTLY) Colorado Department of Public Health and Environment, (1999)ORAL VANCOMYCIN (COSTLY) Colorado Department of Public Health and Environment, (1999) (picture: Microsoft Office 2003)

40 The Latest Treatment Recommended: Sunenshine & McDonald (2006) (table from article used with permission)

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

42 IT CAN COME BACK! 12% - 24% HAVE A SECOND C-DIFF OCCURANCE WITHIN 2 MONTHS.12% - 24% HAVE A SECOND C-DIFF OCCURANCE WITHIN 2 MONTHS. 48% - 56% ARE ACTUALLY REINFECTED WITH A DIFFERENT STRAIN OF C-DIFF.48% - 56% ARE ACTUALLY REINFECTED WITH A DIFFERENT STRAIN OF C-DIFF. PATIENTS WITH TWO OR MORE EPISODESPATIENTS WITH TWO OR MORE EPISODES HAVE A 50% - 65% RISK OF RE-OCCURANCE. HAVE A 50% - 65% RISK OF RE-OCCURANCE. Sunenshine & McDonald (2006) (picture: Microsoft Office 2003)

43 WHO IS SUSCEPTIBLE ??

44 EVERYONE!

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

46 HIGHEST RISK GROUPS: Tal, Gurevich, et. al. (2002) Tal, Gurevich, et. al. (2002) OLDER PATIENTSOLDER PATIENTS CHRONIC RENAL FAILURE PATIENTSCHRONIC RENAL FAILURE PATIENTS PATIENTS WITH NASOGASTRIC FEEDING TUBESPATIENTS WITH NASOGASTRIC FEEDING TUBES PATIENTS WITH A C- DIFF HISTORYPATIENTS WITH A C- DIFF HISTORY THIS IS DUE TO “PHYSIOLOGICAL AND FUNCTIONAL CHANGES OF AND FUNCTIONAL CHANGES OF THE GUT”, WHICH “ARE OFTEN ACCOMPANIED BY AN INCREASED INCIDENCE OF GASTROINTESTINAL INFECTIONS” ACCOMPANIED BY AN INCREASED INCIDENCE OF GASTROINTESTINAL INFECTIONS” (picture: Microsoft Office 2003)

47 “ADVERSE EFFECTS OF CONTACT ISOLATION” PATIENTS IN ISOLATION PATIENTS IN ISOLATION 3.9 ROOM ENTRIES/HOUR.3.9 ROOM ENTRIES/HOUR. 2.1 MEAN CONTACTS/HR2.1 MEAN CONTACTS/HR BY A REGISTERED NURSE. BY A REGISTERED NURSE. 4.5 MINUTES OF ACTUAL HEALTHCARE WORKER INTERVENTION TIME PER4.5 MINUTES OF ACTUAL HEALTHCARE WORKER INTERVENTION TIME PER OCCURANCE. OCCURANCE. Kirkland & Weinstein (1999) 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. (picture: Microsoft Office 2003)

48 ISOLATED PATIENTS NOT GIVEN MEALS OR MEDICATIONS ON TIMEISOLATED PATIENTS NOT GIVEN MEALS OR MEDICATIONS ON TIME CALL LIGHT RESPONSE NOT PROMPTCALL LIGHT RESPONSE NOT PROMPT HIGHER INCIDENCE OF FALLS & BEDSORESHIGHER INCIDENCE OF FALLS & BEDSORES PATIENT/CAREGIVER BARRIERS CREATEDPATIENT/CAREGIVER BARRIERS CREATED Bakalopoulos (2003) Bakalopoulos (2003) “HOSPITAL PATIENTS IN ISOLATION RECEIVE INFERIOR CARE, STUDY SAYS”

49 “PSYCHOLOGICAL EFFECTS OF SOURCE ISOLATION” ISOLATED PATIENTS EXPERIENCE FREQUENT MOOD DISTURBANCES.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 ACTIVITIESCONSISTENT 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) Rees, Davies, Birchall, & Price (2000)

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

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

52 REFERENCES Bakalopoulos, P. (2003). Hospital Patients in Isolation Receive Inferior Care, Says Study. The Varsity-Science. Retrieved February 28, 2006 from (“Search” title of article; then free sign-in is required to view article.) Varsity-Science. Retrieved February 28, 2006 from (“Search” title of article; then free sign-in is required to view article.)http://www.thevarsity.ca Castagliuolo, I., Riegler, M., Pasha, A., Nikulasson, S., Lu, B., Gerard, C., Gerard, N.P. & Pothoulakis, C. (1998). Neurokinin-1 (NK-1) Receptor Is Required in Clostridium Pothoulakis, C. (1998). Neurokinin-1 (NK-1) Receptor Is Required in Clostridium difficile-induced Enteritis. Journal of Clinical Investigations, 101, 8, difficile-induced Enteritis. Journal of Clinical Investigations, 101, 8, Colorado Department of Public Health and Environment. (1999). Management of Clostridium difficile-Associated diarrhea: Guidelines for Long Term Care and Clostridium difficile-Associated diarrhea: Guidelines for Long Term Care and Rehabilitation Facilities. Retrieved February 28, 2006 from: Rehabilitation Facilities. Retrieved February 28, 2006 from: Conly, J.M. (2000) Clostridium difficile-Associated Diarrhea - The New Scourge of the Health Care Facility. The Canadian Journal of Infectious Diseases & Medical Microbiology, 11, 1. Farrow, K.A., Lyras, D. & Rood, J.I. (2001). Genomic Analysis of the Erythromycin Resistance Element Tn5398 From Clostridium difficile. Retrieved electronically March 1, 2006 from: Tn5398 From Clostridium difficile. Retrieved electronically March 1, 2006 from:

53 REFERENCES Kirkland, K.B. & Weinstein, J.M. (1999). Adverse Effects of Contact Isolation. Lancet, 354, Medical College of Wisconsin. (2000). Clostridium Difficile. Retrieved February 28, 2006 from: Microsoft Office Clip Art, Animation, Sounds Oguz, F., Uysal, G., Dasdemir, S., Oskovi, H, & Vidinlisan, S. (2001). The Role of Clostridium difficile in Childhood Nosocomial Diarrhea. Scandinavian Journal of Infectious Disease, 33, 10, Clostridium difficile in Childhood Nosocomial Diarrhea. Scandinavian Journal of Infectious Disease, 33, 10, Pothoulakis, C. (2001). Clostridium Difficile Infection. Participate. Retrieved March 1, 2006 from: Rees, J., Davies, H.R., Birchall, C. & Price, J. (2000). Psychological Effects of Source Isolation Nursing (2): Patient Satisfaction. Nursing Standard, 14, )

54 REFERENCES Rupnik, M., Dupuy, B. et al. (2005). Revised Nomenclature of Clostridium difficile Toxins and Associated Genes. Journal of Medical Microbiology, 54, Retrieved March 1, 2006 from: ttp://jmm.sgmjournals.org/cgi/content/full/54/2/113#F13 Stelfox, H.T., Bates, D.W. & Redelmeier, D.A. (2003) Safety of Patients Isolated for Infection Control. Journal of the American Medical Association, 290, Sunenshine, R.H. & McDonald, L.C. (2006). Clostridium difficile-associated disease: New challenges from an established pathogen. Cleveland Clinic Journal of Medicine, 73, 2. Retrieved April 10, 2006 from: Tal, S., Gurevich, A., et al. (2002). Risk Factors for Recurrence of Clostridium difficile- Associated Diarrhea in the Elderly. Scandanavian Journal of Infectious Disease, 34, 8,


Download ppt "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."

Similar presentations


Ads by Google