Clostridium Difficile Infection(CDI).pptx

Clostridium Difficile Infection signs symptoms and management

1. Clostridium Difficile Infection(CDI)

2. OBJECTIVES: Introduction. Microbiology and Pathophysiology. Transmission. Risk factor. Clinical manifestation. Diagnosis. Treatment.

3. INTRODUCTION

4. CDI: Clostridioides   difficile  infection (CDI) is one of the most common hospital-acquired infections and is an increasingly frequent cause of morbidity and mortality among older adult hospitalized patients. CDI is also increasingly diagnosed in younger patients and in the community. 

5. C. difficile  colonizes the human intestinal tract after the normal gut flora has been disrupted (frequently in association with antibiotic therapy) and it is the causative organism of antibiotic-associated colitis including pseudomembranous colitis.

6. MICROBIOLOGY AND PATHOPHYSIOLOGY

7. C. difficile  is an anaerobic gram-positive, spore-forming, toxin-producing bacillus first described in 1935. It was named "difficult clostridium" because of difficulty related to its isolation and growth on conventional media.

8.   C. difficile  can exist in spore and vegetative forms. Outside the colon, it survives in spore form; spores are resistant to heat, acid, and antibiotics. Once spores are in the intestine, they convert to their fully functional vegetative, toxin-producing forms and become susceptible to killing by antimicrobial agents.

9. Toxins:   C. difficile  releases two potent exotoxins that mediate colitis and diarrhea: toxin A and toxin B. The organism is rarely invasive, and nontoxigenic strains do not cause CDI.

10.   C. difficile  toxins contain a series of contiguous repeated units at the carboxyl terminus. For toxin A, this region is important for toxin A carbohydrate receptor binding to facilitate intracellular transport as well as for antibody binding in enzyme-linked immunosorbent assays.

11. In vivo, stool toxin levels correlate with disease severity Toxin A (enterotoxin) causes inflammation leading to intestinal fluid secretion and mucosal injury Toxin B (cytotoxin) is a major factor for the virulence of  C. difficile  and its 10 times more potent than toxin A on a molar basis for mediating colonic mucosal damage.

12. Pathogenesis of Clostridioides difficil e diarrhea:

13. TRANSMISSION

14. Patients with  C. difficile  carriage are a reservoir for environmental contamination in the presence or absence of clinical infection.   C difficile  is highly transmissible via the fecal-oral route by ingestion of spores. The organism can be cultured readily from the hospital environment, including items and inert surfaces in patient rooms as well as the hands, clothing, and stethoscopes of health care workers.

15. RISK FACTORS

16. Antibiotic use is the most widely recognized and modifiable risk factor for CDI. Other established risk factors include: advanced age and severe comorbid illness. Hospitalizatio n and gastric acid suppression. enteral feeding and gastrointestinal surgery. Obesity or Cirrhosis. inflammatory bowel disease. cancer chemotherapy ( may be related to the antimicrobial effect of chemotherapeutic agents and/or their immunosuppressive effects ).

17. Risk factors for recurrent CDI include: age >65 years, severe underlying medical disorders, need for ongoing therapy with concomitant antibiotics during treatment for CDI. serum creatinine ≥1.2 mg/dL, and lack of an antibody-mediated immune response to  C. difficile  toxins especially toxin B.

18. Risk factors for complications associated with CDI: abnormal blood tests: (white blood cell count <4000 cells/ microL or ≥20,000 cells/ microL , albumin <25 g/L, blood urea nitrogen >7 mmol/L, and C-reactive protein ≥150 mg/L), and abnormal vital signs (heart rate >90/minute, respiratory rate >20/minute) perforation, toxic megacolon, colectomy, admission to intensive care unit, death, include older age CDI can also occur in the absence of any risk factors.

19. CLINCAL MANIFISTATION

20. CDI can cause a spectrum of manifestations ranging from an asymptomatic carriage to fulminant disease with toxic megacolon 1- Asymptomatic carriage :  Asymptomatic individuals do not warrant screening for  C. difficile  carriage, and individuals with asymptomatic carriage of  C. difficile  do not warrant treatment or contact precautions. Its occurs in up to 20 percent of hospitalized adults; these patients shed  C. difficile  in stool but do not have diarrhea or other clinical symptoms.

21. 2-Nonsevere disease:    Watery diarrhea (≥3 loose stools in 24 hours) is the cardinal symptom of CDI. Other manifestations include lower abdominal pain and cramping, low-grade fever, nausea, and anorexia Diarrhea may be associated with mucus or occult blood, but melena or hematochezia are rare.

22. 3-Severe disease: Clinical manifestations of severe colitis include diarrhea, lower quadrant or diffuse abdominal pain, abdominal distention, fever, hypovolemia, lactic acidosis, hypoalbuminemia, elevated creatinine concentration, and marked leukocytosis. Criteria proposed for severe CDI (based on expert opinion) include white blood cell count >15,000 cells/ microL or serum creatinine ≥1.5 mg/dL; prospectively validated severity scores for CDI are needed. Peripheral eosinopenia has also been proposed as an indicator of CDI severity .

23. 4-Fulminant colitis: previously referred to as severe, complicated CDI, may be characterized by hypotension or shock, ileus, or megacolon. Severe hypotension progressing to multisystem organ failure may occur in the setting of fulminant CDI and/or in the setting of bowel perforation with peritonitis.

24. Megacolon should be suspected in patients with severe systemic toxicity together with radiographic evidence of large bowel dilatation (>7 cm diameter in the colon and/or >12 cm diameter in the cecum). Megacolon may be complicated by bowel perforation; manifestations include abdominal rigidity, involuntary guarding, diminished bowel sounds, rebound tenderness, and severe localized tenderness in the left or right lower quadrants; abdominal radiographs may demonstrate free abdominal air

25. 5- Unusual presentations:   Unusual manifestations of  C. difficile  infection include protein-losing enteropathy and extracolonic involvement.

26. A- Protein-losing enteropathy: Inflammation of the bowel wall allows leakage of albumin into the lumen, causing colonic loss of albumin with inadequate compensatory hepatic synthesis. As a result, serum albumin levels may drop below 2.0 g/dL (20 g/L). Ascites and peripheral edema may be observed. The protein losing enteropathy responds to appropriate medical therapy of the infection.

27. B-Extracolonic involvement: Rare cases of  C. difficile  appendicitis, small bowel enteritis, and extraintestinal involvement have been described. Appendicitis due to CDI has been described in a few case reports. Small bowel involvement with  C. difficile  enteritis is rare but may occur in older adults and/or patients with multiple comorbidities.

28. In some cases, patients have had prior colectomy with ileostomy; manifestations may include increased ileostomy output, and it may be possible to visualize pseudomembranous (raised white or tan plaques attached to epithelium) on the exposed ileal mucosa at the stoma. Such patients may be at increased risk for fulminant disease with a high mortality rate.

29. DIAGNOSIS

30. TREATMENT

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