• This segment of colon has been opened longitudinally.

• Tan tellow plaque-like pseudomembranes (black arrow) form on top of ulcerated red mucosa (green arrow) .

•The etiology of PMC in the preantibiotic era associated with a variety of conditions is unknown

•Currently, most cases of PMC are associated with antibiotic use and overgrowth of the commensal anaerobe C.difficile

•Antibiotic associated C.difficile PMC does not appear to arise in antibiotic resistant strains of C.difficile

•Antibiotic disturbance of the normal anaerobic gut flora appears to allow overgrowth of toxigenic strains of C.difficile

•The clinical and pathologic effects are caused by the production of Toxin A and Toxin B by C.difficile

•Toxin A is mildly cytopathic but induces large fluid shifts and mucosal inflammation. Toxin B is intensely cytopathic

•The incidence of C.difficile colonization is 2-3% in a normal healthy population

•The presence of C.difficile colonization, presence of C.difficile toxin in stool and the incidence of PMC also increase with age

•The antibiotics most commonly associated with C.difficile PMC are: Ampicillin or Amoxicillin, Clindamycin, and the Cephalosporins

•Asymptomatic C.difficile carriers, bedpans, toilets and floors have been implicated in nosocomial mini-epidemics of PMC

•Most cases of PMC are associated with antibiotic use, with 2/3rds of patients experiencing watery diarrhea during therapy and 1/3rd afterwards

•Other frequent symptoms are abdominal pain, left lower quadrant tenderness, low grade fever and occasionally signs of sepsis

•While PMC in the preantibiotic era was often a fulminating disease, most current cases are associated with antibiotic use, are diagnosed early in the course of the disease and are cured with appropriate antibiotic therapy

•Relapses occur in 20% of cases

•The lesions of Pseudomembranous Enterocolitis(PMC) when secondary to antibiotic usage with C.difficile toxin production are usually restricted to the colon, with non-antibiotic associated cases often involving the small intestine

•Early lesions appear as discrete plaques of yellow white exudate <10mm separated by normal or mildly hyperemic mucosa

•Lesions may progress to form an exudative membrane covering most of the surface of the colon

•Rarely, severe untreated cases progress to broad ulceration of the mucosal surface

•The earliest lesion is punctate necrosis of the surface epithelium with an overlying accumulation of fibrin, polys, mucous and necrotic epithelial cells(summit lesion). The lamina propria adjoining the area of necrosis has an infiltrate of polys and eosinophils

•The second stage lesion has necrosis of superficial crypts with a heavier infiltrate of polys and a plaquelike pseudomembrane of polys, fibrin and cellular debris which is plastered against the mucosal surface

•The hallmark of most lesions is their involvement of the superficial mucosa only

•Rarely, progressive necrosis of deeper layers of the mucosa occur producing deep denuding ulcerations

• Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 795

• Sleisenger MH, Fordtran JS. Gastrointestinal disease. 5th ed. Philadelphia: Saunders, 1993, pp. 1174-1189

• Current literature from PubMed at National Library of Medicine