Histologically, which findings help differentiate infectious colitis and NSAID-associated colitis?
• Infectious colitis on histologic examination shows acute inflammation in the lamina propria with cryptitis, crypt abscesses, and lack of prominent chronic inflammatory infiltrate or basal plasmacytosis (as seen in IBD). Chronic architectural changes may not be pronounced. Causative organisms include Escherichia coli O157:H7, Salmonella, Shigella, Clostridium, Campylobacter, Yersinia, cytomegalovirus colitis, amebic colitis, and histoplasmosis. Granulomas can be seen in tuberculosis, Yersinia pseudotuberculosis, and Chlamydia infections.
Intestinal spirochetosis shows organisms on the luminal surface that may not cause an active inflammatory response or injury in the mucosa. These anaerobic organisms belong to Brachyspira spp.
• NSAID-associated colitis changes are patchy, may involve any part of the colon, and histologically include focal active colitis, erosions and ulcers, increased apoptosis in crypts, and diaphragm strictures. Diaphragm-like strictures are formed as a result of repeated injury and repair and are seen microscopically as mucosal and submucosal fibrosis. These may cause luminal narrowing and occasionally serosal strictures. Thickened subepithelial collagen layer in longstanding cases has been associated with NSAIDs that can be confused with collagenous colitis and requires correlation with clinical history and endoscopic findings.