Pseudomembranous colitis is an inflammatory condition of the colon primarily associated with Clostridium difficile infection, often following antibiotic use. It is characterized by yellow-white plaques on the mucosa, with symptoms ranging from mild diarrhea to severe abdominal pain and can lead to complications like toxic megacolon. Diagnosis typically involves patient history and specific tests, with treatment focusing on stopping antibiotics and using oral vancomycin or metronidazole.

1. PSEUDOMEMBRANOUS COLITIS
INFECTIOUS DISEASES
OMOREGIE IYOBOSA SONIA
KYIV MEDICAL UNIVERSITY (KMU

2. Pseudomembranous Colitis
Pseudomembranous colitis is an inflammatory condition of the colon characterized by
elevated yellow-white plaques that coalesce to form pseudomembranes on the
mucosa.
Its manifestation of severe colonic disease that is usually associated with Clostridium
difficile infection, but can be caused by a number of different etiologies.
It is also more frequently related with ischemic disease, obstruction, sepsis, uremia,
and heavy metal poisoning
Other causes maybe :
Bacterial i.e
Clostridium ramosum
Escherichia coli
Staphylococcus aurus

3. • Parastitic :Entamoeba histolytica, Schitosoma mansoni
• Other colitis : Behcet’s disease, collagenous colitis, inflamatory bowel
dieseases e.t.c
• C. difficile – an anaerobic organism and toxin producing gram postive
rod with the ability to form spores. Causative agent od diarrhea and
as the primary cause of antibiotic associated colitis.
• C difficile is a component of the normal intestinal flora of a small
percentage of healthy adults and of a relatively large percentage of
healthy neonates. It also may be found in the environment, especially
in hospitals.
• Patients treated with clindamycin have a higher incidence of C
difficile disease, but most cases are found in patients treated with
other antibiotics because of the more widespread use of these
agents.

4. Pathogenesis
• C difficile disease is caused by the overgrowth of the organism in the
intestinal tract, primarily in the colon.
• The organism appears unable to compete successfully in the normal
intestinal ecosystem, but can compete when normal flora are disturbed
by antibiotics, allowing overgrowth of C difficile.
• This organism then replicates and secretes two toxins. Toxin A is an
enterotoxin that causes fluid accumulation in the bowel, and it is a weak
cytotoxin for most mammalian cells; toxin B is a potent cytotoxin.
• In the intestinal tract, toxin A damages villous tips and brush border
membranes, and may result complete in erosion of the mucosa. This
tissue damage causes a viscous hemorrhagic fluid response.
• oxin B exerts its pathogenic effect following dissemination through a
damaged gut wall to extraintestinal organs

5. Clinical Presentation of Clostidium Difficile
• Varying from asymptomatic carrier to patient with PMC, fulminant
Colitis and toxic mega colon.
• Clinical symptoms of C difficile disease vary widely from mild diarrhea
to severe abdominal pain accompanied by fever (typically >101°F) and
severe weakness.
• Diarrhea is watery and usually nonbloody (Fig. 18-4), but
approximately 5 to 10% of patients have bloody diarrhea
• Fecal material typically contains excess mucus, and pus or blood.
• Hypoalbuminemia and leukocytosis.
• In pseudomembranous colitis, possibly including intestinal
perforation and toxic megacolon.

6. • leukocytic infiltrate into the lamina propria accompanied by
elaboration of a mixture of fibrin, mucus, and leukocytes, which can
form gray, white, or yellow patches on the mucosa.
• Pseudomembranes develop, hence the name.
• Pseudomembranes usually develop after 2-10 days of antibiotic
treatment, but they may appear 1-2 weeks after all antibiotic therapy
has stopped.
• C difficile is now considered a major cause of diarrhea in hospitals and
nursing homes.

7. Diagnosis
• History of patient which may include taking antibiotics in the last 4-6
weeks
• Non specific : cbc, glucose , ecg, ultrasound, Copogram , urea test,
kidney function test
• Specific : Cytotoxicity test (gold standard) from fecal extract, stool
culture, rapid latex agglutination test, also most common is enzyme
linked immunoassays can detect both toxin A and B.
• Colonoscopy- Histological biopsy

8. Treatment
• Stop offending antibiotics
• Rehydration therapy
• Oral Vancomycin (gold standard)
• Metronidazole