
By Kelvin Dodzi Kumah
Pseudomembranous colitis (PMC) is a serious colonic disease which can occur when antibiotics or other agents disrupt the normal colonic flora. The severity of illness ranges from benign diarrhea to PMC.

The earliest description of PMC was in 1893 when a young woman died following gastric surgery. After surgery, she developed diarrhea, which became bloody, and she died shortly thereafter. Her postoperative care had included alcohol enemas. In this case, which clearly antedated the use of antibiotics, risk factors for altered colonic flora included the enemas as well as surgery of the gastrointestinal (GI) tract.
In the preantibiotic era, PMC was associated with ischemic cardiovascular insufficiency, colonic obstructions, heavy metal intoxications, sepsis, shock and uremia. In the 1950s, the etiology of PMC was thought to be Staphylococcus aureus, but since 15±30% of normal healthy adults were also colonized, its role in PMC was disputed.
SYMPTOMS AND COMPLICATION
Symptoms
● Watery diarrhea (99%)
● Fever (29%)
● Abdominal pain or cramping (33%)
● Leukocytosis (61%)
● When PMC is severe or does not respond to therapy, complications can occur. In a study of 48 cases of PMC, complications included hypokalemia (37%), renal failure (27%) and hypoproteinemia (50%). Late-onset complications of PMC have been reported and include acute oligoarthritis and hemolytic-uremic syndrome.
PATHOPHYSIOLOGY

The intake of broad spectrum antibiotics tends to reduce the “colonization resistance” of the intestinal flora. Due to this, there is an overgrowth of the bacteria (Clostridium difficile, a spore-forming anaerobic bacteria).

C.dificile after colonization begins to secrete toxins(i.e toxin A and toxin B) which bind to receptors on the surface of the enterocytes.
After adhesion, the toxins are internalized by endocytosis. Once inside the cell, the toxins inactivate a guanine-nucleotide-binding protein called rho A, leading to the disaggregation of F actin. Rho is involved in maintaining the cytoskeleton structure within the cell. The consequence of cytoskeleton disruption is cellular rounding which widens the tight junctions between enterocytes leading to fluid loss and diarrhea.
TREATMENT
Antimicrobial Therapy
The initial evaluation should assess the level of hydration and severity of illness. It may be reasonable to treat for presumptive C. difficile infection in anyone who develops diarrhea in the hospital, in some cases of chronic diarrhea, or when symptoms worsen or progress, or in anyone who has had a prior history of C. difficile disease. The two most commonly used antibiotics to treat C. difficile disease are metronidazole and vancomycin. The recommended dose for metronidazole is 250 mg 4 times a day for 10 days, and for vancomycin it is 125±500 mg 4 times a day for 10 days


