Mycobacterium tuberculosis
Extrapulmonary tuberculosis (EPTB) accounts for about 20% of cases in immunocompetent patients and 50% of cases in HIV-positive individuals; intestinal TB (ITB) is the sixth most prevalent form of EPTB. Bovine TB (Mycobacterium bovis), caused by contaminated dairy products, is a rare cause of ITB that exists where pasteurization practices are lacking.
ITB develops most commonly after ingesting infected sputum in cases of active pulmonary TB. Prior to effective therapy, up to 70% of TB cases developed ITB via this route. Other routes include hematogenous spread or contiguous spread from adjacent organs. The ileocecal area and jejunoileum are the most common sites involved because of high densities of lymphoid aggregates and physiologic stasis. In studies, the ileocecal region has been involved in about 90% of ITB cases [9].
ITB is thought to arise by the same pathophysiologic sequence as pulmonary TB; initial infection of macrophages followed by multiplication, subsequent caseation necrosis, and host inflammatory response. The intestinal lesions can be ulcerative (most common), hypertrophic or ulcerohypertrophic, or fibrous. With chronic inflammation, the ileal wall may become stenotic or fibrotic with stricture formation or may form masses (tuberculomas) leading to intestinal obstruction or perforation. Rarely, ITB presents with malabsorption and a protein-losing enteropathy.
Symptoms include fever, night sweats, abdominal pain, a palpable mass, altered bowel habits, and/or bleeding [10••, 11•]. Because symptoms are nonspecific and about 70% of ITB cases have a normal chest radiograph, clinicians must have a high suspicion for diagnosis. Several disease processes, as described in this review, resemble TB ileitis. A notoriously difficult dilemma is to differentiate ITB from CD, especially in geographic regions where both diseases are prevalent. Features that favor ITB are high fevers in the absence of an intra-abdominal abscess, lack of perianal disease, and shorter duration of symptoms [12]. Serologic tests such as anti-Saccharomyces cerevisiae antibodies (ASCA) do not reliably discriminate between ITB and CD [13].
Contrast-enhanced CT, MRI, and ultrasound may aid in differentiating ITB from CD. Findings supportive of ITB in the ileocecal region include asymmetric wall thickening and enlarged necrotic lymph nodes [14]. In CD, wall thickening is usually symmetric and concentric, with fibrofatty proliferation of the mesentery known as “creeping fat.”
Endoscopic features of ITB are similar to CD; both may have ulcerations, pseudopolyps, luminal narrowing, strictures, and nodularity of the ileocecal valve [15••]. As in CD, ITB may involve any part of the gastrointestinal (GI) tract but the esophagus, stomach, rectosigmoid, and anal canal are much less commonly affected. In a recent study, clinical parameters more common in CD were anorectal lesions, longitudinal ulcers, aphthous ulcers, and a cobblestone appearance that involved fewer than four segments; a patulous ileocecal valve, transverse ulcers, and pseudopolyps were observed more frequently in patients with ITB [16].
It can be challenging to diagnose ITB on endoscopic biopsy. The typical caseating granulomas and acid-fast bacilli (AFB) stained by Ziehl-Neelsen are present in less than 30% of cases. PCR may provide a rapid diagnosis, but endoscopic biopsy material has sensitivities of only 40% to 75% [17]. A positive TB culture remains the gold standard, but diagnosis may be delayed (3-8 weeks). Apart from finding AFB, differentiating ITB and CD can be difficult. Histologic features encountered more frequently in ITB are granulomas that are confluent, larger (> 200 µm), and multiple in number (> 5 per section) [18].