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 UPTODATE 
 American College of Gastroenterology 
 210 Update by Society for Healthcare 
Epidemiology of America (SHEA ) and the 
Infectious Diseases Society of America 
 Center for Infectious Disease 
 CGH Guidelines
The Patient 
 HTN 
 AF 
 CCF 
 Osteoporosis 
 TIA 
 Dementia 
 Depression 
 Iron deficiency 
anemia 
 Gout 
 Recurrent admission for 
UTI, 
 Gout attacks 
 1/2014 : Pneumonia 
 -Augmentin 
 Chlarithromycin 
 3/24/2014: Pneumonia 
 Rocephine & Doxycyciine 
 Moxifloxacin 
 10/4/2014 : Gastroenteritis 
 Ceftriaxone 
 Augmentin
Course in the Wards 
 Gastroenteritis with Dehydration 
 IV fluids 
 IV Rocephine shifted to Augmentin 
 AKI and Hypernatremia 
 Deconditioning
Course in the Wards 
 Gastroenteritis likely antibiotic related 
 Cd toxin not detected 
 Antibiotics discontinued 
 Diarrhea resolved 
 Delirium likely stroke disease 
 Poor Oral intake 
 Depression 
 Worsening Dementia 
 NGT was inserted
Course in the Wards 
 Recurrence of diarrhea 
 CD toxin : 
 CD PCR : Positive 
 Metronidazole 500 mg per NGT 6 hourly 
 Vancomycin 250mg per NGT q6hourly
Epidemiology
Clostridium Difficile 
 Anerobic gram positive 
spore forming, toxin 
producing bacillus 
 Exists in spores and 
vegetative forms 
 causative pathogen for 
antibiotic associated 
diarrhea and colitis 
NAP1/B1/027 – 
virulent strain
How C. Difficile Spreads 
L.S.W . 96/female, went to doctor, diagnosed with Pneumonia, given antibiotics that put 
her at risk of developing antibiotic related diarrhea 
1 ½ month later : admitted to Pneumonia, given another course of antibiotics. A health 
care worker forgetting to wash hands /wear gloves after attending to a C. D. Infected 
patient next to her bed, infecting patient 
At Rehab facility – with no strict contact precaution. L.S.W. developed diarrhea, CD toxin 
was not tested at that time. health care worker attends to her, infects another patient 
Few days later, persistence of diarrhea, retested for CD, which turns out to be positive. 
Was given proper antiobitiotics, with resolution of diarrhea

Clostridium difficile 
Pathonegesis 
FROM THE FOLLOWING ARTICLE: 
Clostridium difficile infection: new developments in epidemiology and pathogenesis 
Maja Rupnik, Mark H. Wilcox & Dale N. Gerding 
Nature Reviews Microbiology 7, 526-536 (July 2009)
Risk factors 
Antibiotics 
Hospitalization 
Advanced age 
Severe illness 
Gastric acid suppression 
Enteral feeding 
Gastroentrointestinal conditions & procedures 
Obesity 
Cancer chemotheray 
Hematopoetic transplantation 
Antidepressant
Factors contributing to the development of Clostridium difficile colonization and 
diarrhea [adapted, with permission, from Johnson S, Gerding DN. Clostridium difficile-associated 
diarrhea. Clin Infect Dis 1998;26:1027-36, published by the University of Chicago Press, Infectious 
Diseases Society of America; 1998]. Photo: Lianne Friesen and Nicholas Woolridge
Antimicrobial agents that may 
induce Clostridium difficile 
diarrhea and colitis 
Frequently 
associate 
Occasionally 
associated 
Rarely 
associated 
Fluoquinolones Macrolides Aminoglycosides 
Clindamycin Trimethoprim Tetracyclines 
Penicillins sulfonamides Chloramphenicol 
Cephalosphorins Metonidazole 
Vancomycin
Clinical Manifestations and 
Diagnosis 
Carrier 
state 
Diarrhea 
and colitis 
Pseudomem 
branous 
colitis 
Recurrent 
disease : 
relapse vs 
reinfection 
Fulminant 
colitis
Clinical Manifestations 
 96% of patients with symptoms had 
received antimicrobials with 14 days 
before the onset of diarrhea 
 Symptoms begin soon after colonization 
( median time onset 2-3 days ) 
 Fever, cramping, abdominal discomfort 
and peripheral leukocytosis are common 
 Arthritis, bacteremia 
 Unexplained Leukocytosis
Diagnosis 
Presence of moderate to severe diarrhea or 
ileus 
And either 
A stool positive for C. Difficile toxins or 
toxigeneic c. Dificile 
Endoscopic or histologic findings of 
pseudomembranous colitis
Diagnostics Tests 
Only stools from patient with diarrhea should be tested for 
CD 
• ( strong recommendation, High Quality evidence ) 
NAAT ( PCR are superior to toxins A & B EIA testing as a 
standard diagnostic test for CDI 
• (strong recommedation, moderate quality evidence ) 
Glutamate Dehydrogenase can be used in 2 to 3 step 
screening algorithms with subsequent toxin A and B EIA 
testing, but the sensitivity of such is lower than NAATS 
• ( strong recommendation, moderate quality evidence )
Diagnostic testing 
Repeat testing should be discourage 
• Strong recommendation, moderate quality evidence 
Testing for cure should not be done 
• ( strong recommendation, moderate quality evidence ) 
Stool culture is most sensitive and essential in 
epidemiologic studies 
• ( good evidence to support recommendation)
Other Methodologies 
Sigmoidoscopy or colonoscopy 
• Detects pseudomembranous colitis in 51-55% of 
CDI cases 
Histopathology 
Abdominal CT SCAN – facilitate diagnosis, 
but not sensitive nor specific
CDI Severity Scoring System 
Severity criteria 
Mild to moderate Diarrhea + s/s not meeting severe or 
complicated criteria 
Severe Disease <3g/dl + 1 of the ff: 
WBC >15,000 cells/mm3, abdominal 
tenderness 
Severe and 
Complicated disease 
Any of the following attributable to CDI 
Admission to ICU 
Hypotension +/- vasopressors 
Fever >38.5 C 
Ileus or significant abdominal distention 
Mental status chnages 
WBC >35,0000or <2,000 
Recurrent CDI Recurrent within 8 weeks of completion of 
therapy
Factors to Consider Before 
Treating 
AGE 
Peak 
White cell 
count 
Peak 
serum 
creatinine
Treatment 
• Metronidazole 500mg TDS or 250mg QDS for 10-14 
days 
• Vancomycin 125mg orally QDS 10-14 days. 
Mild 
disease 
• Vancomycin500mg 4x/day + metronidazole 500mg every 
8 hours IV 
• If complete ileus : add rectal vancomycin 
Severe 
disease 
• If symptoms is mild, conservative management may be 
appropriate 
• If antibiotics are needed, repeat treatment as in initial 
episode 
• Alternative : Fidaxomicin 200mg BD x 10 days 
First 
Relapse
Treatment 
• Tapering and pulsed vancomycin 
with or without probiotics 
• 125mg QDS for 7-14 days 
• 125 TDS x 7 days 
• 125 once x 7 days 
• 125mg orally every other day for 7 
days 
• 125mg orally every 3 days x 14 days 
• Alternative : Fidaxomicin 200mg 
orally BD x 10days 
Second 
Relapse
Treatment 
• Fidaxomicin 200mg 
Orally BD x 10 days 
• Alternative : 
vancomycin 125mg 
QDS x 14 days 
followede by rifiximim 
400mg BD x 14 days 
Subsequent 
relapse
Fidoximicin 
 Macrolide, bactericidal 
 Narrower antimicrobial spectrum than 
Metronidazole & vancomycin 
 3RCT : in non severe C. Difficile , clinical 
cure rates with vacomycin were similar 
 Recurrence is less often among patients 
with non NAP1 strain ( 10 vs 28 % )
Probiotics 
 May be effective for prevention and 
treatment 
 Alteration of intestinal flora 
 Antimicrobrial activity 
 Intestinal barrier protection 
 immunomodulation 
 Administration consist only of regimens 
with demonstrated efficacy 
 Dosage of >10 billion CFU per day 
 A cocrane review: insufficient evidence to 
recommend as adjunct in treatment
RICE WATER 
Rice water and diarrhoea 
The advantage of using rice water is that rice is cooked 
daily in South East Asia. 
WHO photograph by Dr Gramiccia In South East Asia, rice is 
prepared in two ways - to produce either dry, cooked rice or, 
with extra water, rice porridge. This leaves a fluid (rice water) 
on top of the cooked rice grains. 
Professor Wong Hock Boon, a paediatrician working in 
Singapore, has been using rice water to rehydrate babies for 
several years. If the babies are bottle-fed rice water is given 
exclusively for the first 24 hours of treatment - breastfeeding 
can continue as normal (1). 
Professor Wong and his colleagues have found that many 
babies who have not responded to other rehydration solutions 
respond well to rice water. If diarrhoea starts again with the 
re-introduction of milk, extra rice water is given with additional 
rice porridge. Older babies are sometimes given rice porridge 
alone.
Treatment 
 Antimotility Agents and Opoids 
 Associated with increase risk of toxic 
megacolon 
 IVIG 
 No effective immunotherapy is currently 
available 
 Does not a tole a s sole therapy for RCDI 
 May be helpful in patient with 
hypogammaglobulimenia
Colectomy 
 Consider in severely ill patients 
 Monitoring serum lactate and White cell 
may be helpful in prompting a decision 
to operate
Fecal Microbiota 
Transplantation 
 Patient selection 
 Severe and Recurrent C. Difficile infection 
 Cure rates 81-94% in patients with 
recurrent disease 
 Response within 24h to 12 days 
 Only method capable of providing 
durable implantation of probiotics 
 Route of administration : 
 Colonoscopy, nasogastric, enema
Prognosis 
 Mild disease, may recover without 
specific therapy 
 Debilitating and can last for several 
weeks 
 20-27% treated for first episode , 
relapse after successful completing the 
antibiotics , 3days -3week after 
treatment 
 65%- relapse rate with patient with 2 or 
more relapses
Infection Control, & Prevention 
 A hospital – based infection contol program 
can help decrease the incidence of CDI 
 Routine screening for C. Difficile in 
hospitalized patients without diarrhea is not 
recommended and asymptomatic carriers 
should not be treated 
 Antibiotic stewardship is recommended to 
reduce the risk of CDI
Infection Control and 
Prevention 
 Gloves and gowns upon entry to a room 
 Emphasize compliance with practice of 
hand hygiene 
 Hand wash with soap and water after 
caring for or contacting patient with CDI 
 Accommodate patients with CDI in 
private room with contact precaution
Environmental Cleaning and 
Disinfection 
 Identification and removal of environmental 
sources of C. Dificille including 
 replacement of electronic rectal thermometers 
with disposable, can reduce the incidence of CDI 
 Use chlorine-containing cleaning agents or 
other sporicidal agents 
 to address environmental contamination in area 
 associated with increased rates CDI
Prognosis 
 Adverse outcomes 
 Treatment failure 
 Severe or severe complicated infection 
 Sepsis 
 Need for admission to ICU 
 Need for colectomy 
 Increase length of hospital stay 
 Need for hospitalization for community acquired 
CDI 
 Mortality 4.2-6.9%
Differential Diagnosis 
 Osmotic diarrhea 
 
 Antibiotics alter colonic microflora 
 Impaired carbohydrate fermentation 
 Increased osmotic concentration in 
colonic lumen
Prevention strategies 
 Early detection and isolation 
 Rapid implementation of contact precautions 
 Vigilant screening for new onset diarrhea in 
patients at risk and rapid and accurate 
testing 
 Contact precaution
Prevention and strategies 
 Hand Hygiene 
 Healthcare personel should hand wash 
hands with soap and water 
 Alcohol based hand rub does NOT eradicate 
C. Difficile spores 
 Adherance to gloves is also important
clostridium Diarrhea

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clostridium Diarrhea

  • 1.
  • 2.  UPTODATE  American College of Gastroenterology  210 Update by Society for Healthcare Epidemiology of America (SHEA ) and the Infectious Diseases Society of America  Center for Infectious Disease  CGH Guidelines
  • 3.
  • 4. The Patient  HTN  AF  CCF  Osteoporosis  TIA  Dementia  Depression  Iron deficiency anemia  Gout  Recurrent admission for UTI,  Gout attacks  1/2014 : Pneumonia  -Augmentin  Chlarithromycin  3/24/2014: Pneumonia  Rocephine & Doxycyciine  Moxifloxacin  10/4/2014 : Gastroenteritis  Ceftriaxone  Augmentin
  • 5. Course in the Wards  Gastroenteritis with Dehydration  IV fluids  IV Rocephine shifted to Augmentin  AKI and Hypernatremia  Deconditioning
  • 6. Course in the Wards  Gastroenteritis likely antibiotic related  Cd toxin not detected  Antibiotics discontinued  Diarrhea resolved  Delirium likely stroke disease  Poor Oral intake  Depression  Worsening Dementia  NGT was inserted
  • 7. Course in the Wards  Recurrence of diarrhea  CD toxin :  CD PCR : Positive  Metronidazole 500 mg per NGT 6 hourly  Vancomycin 250mg per NGT q6hourly
  • 8.
  • 10. Clostridium Difficile  Anerobic gram positive spore forming, toxin producing bacillus  Exists in spores and vegetative forms  causative pathogen for antibiotic associated diarrhea and colitis NAP1/B1/027 – virulent strain
  • 11. How C. Difficile Spreads L.S.W . 96/female, went to doctor, diagnosed with Pneumonia, given antibiotics that put her at risk of developing antibiotic related diarrhea 1 ½ month later : admitted to Pneumonia, given another course of antibiotics. A health care worker forgetting to wash hands /wear gloves after attending to a C. D. Infected patient next to her bed, infecting patient At Rehab facility – with no strict contact precaution. L.S.W. developed diarrhea, CD toxin was not tested at that time. health care worker attends to her, infects another patient Few days later, persistence of diarrhea, retested for CD, which turns out to be positive. Was given proper antiobitiotics, with resolution of diarrhea
  • 12.
  • 13.
  • 14. Clostridium difficile Pathonegesis FROM THE FOLLOWING ARTICLE: Clostridium difficile infection: new developments in epidemiology and pathogenesis Maja Rupnik, Mark H. Wilcox & Dale N. Gerding Nature Reviews Microbiology 7, 526-536 (July 2009)
  • 15. Risk factors Antibiotics Hospitalization Advanced age Severe illness Gastric acid suppression Enteral feeding Gastroentrointestinal conditions & procedures Obesity Cancer chemotheray Hematopoetic transplantation Antidepressant
  • 16. Factors contributing to the development of Clostridium difficile colonization and diarrhea [adapted, with permission, from Johnson S, Gerding DN. Clostridium difficile-associated diarrhea. Clin Infect Dis 1998;26:1027-36, published by the University of Chicago Press, Infectious Diseases Society of America; 1998]. Photo: Lianne Friesen and Nicholas Woolridge
  • 17. Antimicrobial agents that may induce Clostridium difficile diarrhea and colitis Frequently associate Occasionally associated Rarely associated Fluoquinolones Macrolides Aminoglycosides Clindamycin Trimethoprim Tetracyclines Penicillins sulfonamides Chloramphenicol Cephalosphorins Metonidazole Vancomycin
  • 18. Clinical Manifestations and Diagnosis Carrier state Diarrhea and colitis Pseudomem branous colitis Recurrent disease : relapse vs reinfection Fulminant colitis
  • 19. Clinical Manifestations  96% of patients with symptoms had received antimicrobials with 14 days before the onset of diarrhea  Symptoms begin soon after colonization ( median time onset 2-3 days )  Fever, cramping, abdominal discomfort and peripheral leukocytosis are common  Arthritis, bacteremia  Unexplained Leukocytosis
  • 20. Diagnosis Presence of moderate to severe diarrhea or ileus And either A stool positive for C. Difficile toxins or toxigeneic c. Dificile Endoscopic or histologic findings of pseudomembranous colitis
  • 21. Diagnostics Tests Only stools from patient with diarrhea should be tested for CD • ( strong recommendation, High Quality evidence ) NAAT ( PCR are superior to toxins A & B EIA testing as a standard diagnostic test for CDI • (strong recommedation, moderate quality evidence ) Glutamate Dehydrogenase can be used in 2 to 3 step screening algorithms with subsequent toxin A and B EIA testing, but the sensitivity of such is lower than NAATS • ( strong recommendation, moderate quality evidence )
  • 22. Diagnostic testing Repeat testing should be discourage • Strong recommendation, moderate quality evidence Testing for cure should not be done • ( strong recommendation, moderate quality evidence ) Stool culture is most sensitive and essential in epidemiologic studies • ( good evidence to support recommendation)
  • 23. Other Methodologies Sigmoidoscopy or colonoscopy • Detects pseudomembranous colitis in 51-55% of CDI cases Histopathology Abdominal CT SCAN – facilitate diagnosis, but not sensitive nor specific
  • 24.
  • 25.
  • 26. CDI Severity Scoring System Severity criteria Mild to moderate Diarrhea + s/s not meeting severe or complicated criteria Severe Disease <3g/dl + 1 of the ff: WBC >15,000 cells/mm3, abdominal tenderness Severe and Complicated disease Any of the following attributable to CDI Admission to ICU Hypotension +/- vasopressors Fever >38.5 C Ileus or significant abdominal distention Mental status chnages WBC >35,0000or <2,000 Recurrent CDI Recurrent within 8 weeks of completion of therapy
  • 27. Factors to Consider Before Treating AGE Peak White cell count Peak serum creatinine
  • 28. Treatment • Metronidazole 500mg TDS or 250mg QDS for 10-14 days • Vancomycin 125mg orally QDS 10-14 days. Mild disease • Vancomycin500mg 4x/day + metronidazole 500mg every 8 hours IV • If complete ileus : add rectal vancomycin Severe disease • If symptoms is mild, conservative management may be appropriate • If antibiotics are needed, repeat treatment as in initial episode • Alternative : Fidaxomicin 200mg BD x 10 days First Relapse
  • 29. Treatment • Tapering and pulsed vancomycin with or without probiotics • 125mg QDS for 7-14 days • 125 TDS x 7 days • 125 once x 7 days • 125mg orally every other day for 7 days • 125mg orally every 3 days x 14 days • Alternative : Fidaxomicin 200mg orally BD x 10days Second Relapse
  • 30. Treatment • Fidaxomicin 200mg Orally BD x 10 days • Alternative : vancomycin 125mg QDS x 14 days followede by rifiximim 400mg BD x 14 days Subsequent relapse
  • 31. Fidoximicin  Macrolide, bactericidal  Narrower antimicrobial spectrum than Metronidazole & vancomycin  3RCT : in non severe C. Difficile , clinical cure rates with vacomycin were similar  Recurrence is less often among patients with non NAP1 strain ( 10 vs 28 % )
  • 32. Probiotics  May be effective for prevention and treatment  Alteration of intestinal flora  Antimicrobrial activity  Intestinal barrier protection  immunomodulation  Administration consist only of regimens with demonstrated efficacy  Dosage of >10 billion CFU per day  A cocrane review: insufficient evidence to recommend as adjunct in treatment
  • 33. RICE WATER Rice water and diarrhoea The advantage of using rice water is that rice is cooked daily in South East Asia. WHO photograph by Dr Gramiccia In South East Asia, rice is prepared in two ways - to produce either dry, cooked rice or, with extra water, rice porridge. This leaves a fluid (rice water) on top of the cooked rice grains. Professor Wong Hock Boon, a paediatrician working in Singapore, has been using rice water to rehydrate babies for several years. If the babies are bottle-fed rice water is given exclusively for the first 24 hours of treatment - breastfeeding can continue as normal (1). Professor Wong and his colleagues have found that many babies who have not responded to other rehydration solutions respond well to rice water. If diarrhoea starts again with the re-introduction of milk, extra rice water is given with additional rice porridge. Older babies are sometimes given rice porridge alone.
  • 34. Treatment  Antimotility Agents and Opoids  Associated with increase risk of toxic megacolon  IVIG  No effective immunotherapy is currently available  Does not a tole a s sole therapy for RCDI  May be helpful in patient with hypogammaglobulimenia
  • 35. Colectomy  Consider in severely ill patients  Monitoring serum lactate and White cell may be helpful in prompting a decision to operate
  • 36.
  • 37. Fecal Microbiota Transplantation  Patient selection  Severe and Recurrent C. Difficile infection  Cure rates 81-94% in patients with recurrent disease  Response within 24h to 12 days  Only method capable of providing durable implantation of probiotics  Route of administration :  Colonoscopy, nasogastric, enema
  • 38. Prognosis  Mild disease, may recover without specific therapy  Debilitating and can last for several weeks  20-27% treated for first episode , relapse after successful completing the antibiotics , 3days -3week after treatment  65%- relapse rate with patient with 2 or more relapses
  • 39. Infection Control, & Prevention  A hospital – based infection contol program can help decrease the incidence of CDI  Routine screening for C. Difficile in hospitalized patients without diarrhea is not recommended and asymptomatic carriers should not be treated  Antibiotic stewardship is recommended to reduce the risk of CDI
  • 40. Infection Control and Prevention  Gloves and gowns upon entry to a room  Emphasize compliance with practice of hand hygiene  Hand wash with soap and water after caring for or contacting patient with CDI  Accommodate patients with CDI in private room with contact precaution
  • 41. Environmental Cleaning and Disinfection  Identification and removal of environmental sources of C. Dificille including  replacement of electronic rectal thermometers with disposable, can reduce the incidence of CDI  Use chlorine-containing cleaning agents or other sporicidal agents  to address environmental contamination in area  associated with increased rates CDI
  • 42. Prognosis  Adverse outcomes  Treatment failure  Severe or severe complicated infection  Sepsis  Need for admission to ICU  Need for colectomy  Increase length of hospital stay  Need for hospitalization for community acquired CDI  Mortality 4.2-6.9%
  • 43.
  • 44.
  • 45.
  • 46.
  • 47. Differential Diagnosis  Osmotic diarrhea   Antibiotics alter colonic microflora  Impaired carbohydrate fermentation  Increased osmotic concentration in colonic lumen
  • 48. Prevention strategies  Early detection and isolation  Rapid implementation of contact precautions  Vigilant screening for new onset diarrhea in patients at risk and rapid and accurate testing  Contact precaution
  • 49. Prevention and strategies  Hand Hygiene  Healthcare personel should hand wash hands with soap and water  Alcohol based hand rub does NOT eradicate C. Difficile spores  Adherance to gloves is also important

Hinweis der Redaktion

  1. Places a high burden to our health care system A leading cause of hospital associated GI illness Forms heat resistant spores that can persist in the environment for several months to years. Ill briefly discuss a case And ill present a the guidelines in the management , prevention and control
  2. Presented with fever after last discharge in March 2014, associated with lethragy and poor appetite 5 days prior to admission , she had episodes of watery stools 2 x perday
  3. Trial of antidepressant given
  4. More common in elderly Increase in overall incidence Transmission : person to person contact Fecal oral route Principally occuring within inpatient occuring facility shed on
  5. 30 % of hospitalized patients who have antibiotic associated diarrhea will have CDI
  6. Patients are exposed to C. difficile spores through contact with the hospital environment or health care workers. After taking an antibiotic, they develop CDI if they acquire a toxigenic C. difficile strain and fail to mount an anamnestic serum immunoglobulin G (IgG) antibody response to toxin A (ToxA; also known as TcdA)64; if they can mount an antibody response they become asymptomatically colonized with C. difficile. If they acquire a non-toxigenic C. difficile strain, they also become asymptomatically colonized. Colonized patients have been shown to be protected from CDI126.
  7. Patients are resistant to CDI if their normal gut flora is not disrupted by antibiotics (a). Once antibiotic treatment starts, infection with a C. difficile strain that is resistant to the antibiotic is more likely while the antibiotic is being administered owing to the presence of the antibiotic in the gut (b). When the antibiotic treatment stops, the levels of the antibiotic in the gut diminish rapidly, but the microflora remains disturbed for a variable period of time (indicated by the break in the graph), depending on the antibiotic given (c). During this time, patients can be infected with either resistant or susceptible C. difficile. Finally, after the microflora recovers, colonization resistance to C. difficile is restored (d).
  8. C. difficile colonizes the intestine (colon) after disruption of the normal intestinal flora. To what extent adhesion and biofilm production are involved in the pathogenesis of C. difficile is unknown; in the schematic, bacterial cells are shown as free cells and attached to host cells. Toxigenic strains produce toxin A and toxin B (TcdA and TcdB). TcdA binds to the apical side of the cell and, after internalization, causes cytoskeletal changes that result in disruption of tight junctions and loosening of the epithelial barrier, in cell death or in the production of inflammatory mediators that attract neutrophils. Disruption of tight junctions enables both TcdA and TcdB to cross the epithelium. TcdB binds preferentially to the basolateral cell membrane. Both toxins are cytotoxic and induce the release of various immunomodulatory mediators from epithelial cells, phagocytes and mast cells, resulting in inflammation and the accumulation of neutrophils. In an animal model, TcdB was shown to have a tropism for cardiac tissue, which would require that TcdB enter the bloodstream.
  9. A history of treatment with antibiotics or antineoplastic within the previous 8 weeks is present in majority of cases. 2 related studies documented an incresed risk of CDI in adults taking antidepressant mirtazipine and fluoxetine
  10. Among cephalosporins : the 2nd and third gens have increased risk A brief exposure to any single antibiotic can cause C. Difficile colitis. Aprolonged antibiotics course or the use of 2 or more antibiotics increased the risk of disease. Vancomycin and metronidazole have been shown to cause disease
  11. water diarrhea – cardinal symptom of CDI The clinical mnaifestations of infection with toxin producing strains of c. Difficele range from Asymptomatic carrier state to fulminant disease with toxic megacolon. Several studies have showned that 50 % of hospital patients colonize C. Dificile are symptomless carries, possibly reflecting the natural immunity.
  12. The presence of diarrhea is defined as passage of 3 or more unformed stools in 24 or fewer consecutive hours. Same criteria is use to diagnose recurrent CDI.
  13. Whta are the best testing stragegies to diagnose CDI in the clinical laboratory and what are the acceptable options? PCr is an excellent confirmatory test Data on LAMP testing is not yet sufficient to recommend it Few published data on the performance of one of the 3 and 4, Metaanalysis of three PCR assays, indicate that they have similar sensitivities of the a specificities of 90% and 95%, rspectively
  14. Pseudomembaranous colitis can only be diagnosed by direct visualization of pseudomembranes on lower Gastrointestinal endoscopy or by histopathology
  15. Three factors may indicate a severe or complicate course and should be considered when initiating a therapy. The influence of greater age probably reflects a senecnese of the immune response against C. Dificile and its toxins the greater age has been consistently related to adverse outcomes. Leukocytosis likely reflects the severity of colonic inflammation, complications are more common in patients with leukocytosis of 15,000 or higher. The course of disease is sometimes catastrophic in patients with leukocytosis of > 50,000 or higher An elevated creatinine may indicate severe diarrhea with subsequent dehydration or inadequate renal perfusion.
  16. Consider in severely ill patients Monitoring serum lactate and White cell may be helpful in propting a decision to operate lactate Lactate of 5mmol/Land wcc of 50,000 have been associated with greatly increased perioperative mortality. If surgical managemnt is necessary, perform subtotal colectomy with preservation of rectum
  17. Antibiotics are the bigger risk factors for CDI, numerous studies have shown that restriction of the most common offending antimicrobials is effective in CDI prevention. Minimizing the frequency and duration of antimicrobial therapy and the number of antimicrobial agents prescribes to reduce CDI
  18. Measures for Health Care Workers, Visitors, Patient