Gastrointestinal Tuberculosis Imaging 

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Each year, tuberculosis (TB) results in the death of 3 million people globally. In 2000-2020, an estimated 1 billion people will be infected, 200 million people will become sick, and 35 million will die from TB, if control is not strengthened. Radiologic features and pathologic correlation to the pattern of tuberculous infection in the GI tract is discussed in this article (see the images below). Overall, one third of the world’s population is infected with the TB bacillus, but not all infected individuals have clinical disease. ^[1]  The bacteria cause the disease when the immune system is weakened, as in older patients and in patients who are HIV positive. The control of TB has been challenging because of the natural history of the disease and the varying pattern in which it manifests in different groups.

GI TB is a major health problem in many underdeveloped countries. A recent significant increase has occurred in developed countries, especially in association with HIV infection. Global migration and immigration have also contributed to the increase in developed countries. In 2015, Germany reported a 29% increase in cases of TB almost exclusively due to emigration. ^[2]  In the United Kingdom, a retrspective study of intestinal TB in London found 93% of patients had emigrated from TB‐endemic areas (Indian subcontinent: 88%, Africa: 9%). ^[3]

Autopsies of patients with pulmonary TB before the era of effective treatment demonstrated intestinal involvement in 55-90% of fatal cases. The previously noted frequent association between pulmonary TB and intestinal TB no longer prevails, and only a minority of patients (< 50%) with abdominal TB now have abnormal chest radiographic findings. However, approximately 20-25% of patients with GI TB have pulmonary TB. Any part of the GI system may be infected, although the ileum and colon are common sites.

On gross pathologic examination, intestinal TB can be classified into 3 categories:

The ulcerative form of TB is seen in approximately 60% of patients. Multiple superficial ulcers are largely confined to the epithelial surface. This is considered a highly active form of the disease, with the long axis of the ulcers perpendicular to the long axis of the bowel.

The hypertrophic form is seen in approximately 10% of patients and consists of thickening of the bowel wall with scarring; fibrosis; and a rigid, masslike appearance that mimics that of a carcinoma.

The ulcerohypertrophic form is a subtype seen in 30% of patients. These patients have a combination of features of the ulcerative and hypertrophic forms.

Tripathi and Amarapurkar studied 110 cases of GI TB to identify the morphologic spectrum of the disease, and according to the authors, an important finding was the coexistence of different types of granulomas. In a significant number of cases, granulomas were seen in a submucosal location, and the predominant type of inflammation in the lamina propria was lymphoplasmacytic. On gross examination, in addition to the typical TB lesions, intestinal perforation was seen with higher frequency, and ischemic bowel was also identified. Morphologic patterns of caseating, noncaseating, confluent, discrete, and suppurative granulomas were identified on histopathology. ^[4]

According to a study by Lin et al, principal comorbidities associated with lower GI tract TB are type II diabetes mellitus (23%) and alcoholism (23%). Of the 30 patients followed, 22 had radiographic findings suggestive of pulmonary tuberculosis, of which 13 were confirmed by culture. Diagnostic yield of mycobacterial cultures of stool or sputum was approximately 50%, a rate comparable to that of histologic studies of colonoscopic or surgical biopsies. Multidrug-resistant TB was present in 4 of the patients, 2 of whom had alcoholism. The 1-year mortality was 20%, but mortality was 50% in patients with multidrug resistance. ^[5]

In a study by Park et al, 6 months of therapy was found to be as effective as 9 months of therapy in patients with intestinal TB. The authors note that shorter-duration therapy may have the added benefits of reduced cost and increased patient compliance ^[6]

For patient education information, see the Bacterial and Viral Infections Center, as well as Tuberculosis.

Esophageal TB is rare, usually occurring because of spread from TB in the thorax either from mediastinal nodes, the lungs, or the spine. ^[7] Esophageal TB is the least common site of TB in the GI tract. Dysphagia and retrosternal pain indicate esophageal involvement, with ulcerations just above the tracheal bifurcation. ^[8] A rare granular form of TB occurs in miliary spread of primary TB.

Common radiologic features include deep ulceration, intramural dissection, and fistula formation, especially in patients with AIDS. The ulceration can mimic esophageal malignancy with nodularity of the mucosa on barium examination. Mass and sinus tract formation can be better appreciated by using CT to assess extent of mediastinal involvement.

Endoscopic ultrasound findings include asymmetrical thickening of the esophageal wall with loss of the wall stratification, as well as loss of fat planes with right pulmonary artery. ^[8]

Biopsy of the ulcerated mucosa reveals epithelioid granulomas.

Stomach and duodenal involvement by TB is rare because of (1) the sparsity of lymphoid tissue in the upper GI tract, (2) the high acidity of peptic secretions, and (3) the rapid passage of ingested organisms into small bowel. Symptoms of stomach and duodenal involvement include abdominal pain and upper GI bleeding. Nausea and vomiting is a feature when gastritis and outlet obstruction are present.

Gastric TB may show multiple large, deep ulcers in the stomach, most frequently on the lesser curvature of the antrum or in the pyloric region. Scarring from ulcers leads to diffuse antral narrowing, resulting in gastric outlet obstruction. The stomach may be diffusely involved and show irregular contour, simulating a linitis plastica of primary scirrhous carcinoma of the stomach. Multiple fistulous tracks may develop as the disease advances (see the image below). ^[9]

Duodenal involvement is seen with diffuse mucosal fold thickening, ulcers, or stricture formation or is complicated by fistulae. Simultaneous involvement of the pylorus and duodenum is a feature but is nonspecific for TB, because this feature is also seen in Crohn disease, lymphoma, and carcinoma.

Clinical features of intestinal TB include abdominal pain, weight loss, anemia, and fever with night sweats. Patients may present with symptoms of obstruction, right iliac fossa pain, or a palpable mass in the right iliac fossa. Hemorrhage and perforation are recognized complications of intestinal TB, although free perforation is less frequent than in Crohn disease. ^[10]

Malabsorption may be caused by obstruction that leads to bacterial overgrowth, a variant of stagnant loop syndrome. Involvement of the mesenteric lymphatic system, known as tabes mesenterica, may retard chylomicron removal because of lymphatic obstruction and result in malabsorption (see the image below).

The ileum is more commonly involved than the jejunum. Ileocecal involvement is seen in 80-90% of patients with GI TB. This feature is attributed to the abundance of lymphoid tissue (Peyer patches) in the distal and terminal ileum.

Proximal small intestinal disease is seen more commonly with Mycobacterium avium complex (MAC) infection, predominantly infection involving the jejunum. Intestinal obstruction may be partial or complete with TB. Segmental involvement usually is in a stenotic form.

Early changes on barium examinations reveal nodular thickening of mucosal folds, with loss of symmetry in the fold pattern (see the image below). As with Crohn disease, deep fissures, sinus tracts, enterocutaneous fistulae, and perforation can occur, although less commonly. A cobblestone appearance of the mucosa is a feature seen in Crohn disease that is not seen in TB. Ulceration may be demonstrated on double-contrast examinations, typically perpendicular to the long axis of the bowel; these heal with the formation of short annular strictures. Because of persistent irritability from inflammation in the terminal ileum, rapid emptying of that segment may occur (Stierlin sign). The ileocecal angle is obliterated with a widely patent ileocecal valve. ^{[11, 12, 13, 14]}

Characteristic ultrasonographic (US) features that indicate early changes of TB have been described. US features suggestive of intestinal TB are mesenteric thickness of 15 mm or more and an increase in the mesenteric echogenicity (from fat deposition) combined with mesenteric lymphadenopathy. However, these features also may be seen on sonograms in patients with Crohn disease; therefore, they become less specific for TB in a Western population.

Radiologic features of intestinal TB in HIV-infected patients are similar to those in other patients (see the images below). ^[15] The ileocecal region is the most common site of involvement, with thickening of the ileocecal valve, adjacent ileum, and colonic wall.

CT scans show mesenteric lymphadenopathy with a hypoattenuating center suggestive of necrosis. Distinguishing M tuberculosis from MAC infections in patients with AIDS may be possible. Diffuse jejunal wall thickening and enlarged soft-tissue–attenuating lymph nodes with hepatosplenomegaly suggest disseminated MAC infection, whereas focal abdominal lesions with low-attenuating lymph nodes suggest disseminated M tuberculosis. MAC infection is also called pseudo-Whipple disease because of the diffuse mucosal fold thickening in the jejunum and histiocytic aggregates infected with MAC that stain positive with periodic acid–Schiff testing.

Abdominal lymphadenopathy in intestinal TB may be demonstrated with US and CT. The distribution of lymphadenopathy is sometimes difficult to differentiate from lymphoma. Contrast-enhanced CT may be useful in differentiating lymphomas from TB. Mesenteric lymph nodes are involved more often in disseminated TB (80%) and in nondisseminated TB (52%) than in patients with untreated Hodgkin disease (6%). ^{[16, 17, 18]}

MR enterography allows concurrent evaluation of luminal integrity, mural abnormality, and both extraluminal and extraintestinal extent of the disease process. ^[1]

Colonic TB is most often associated with ileal TB. The involvement is segmental and especially involves the right colon. Symptoms include weight loss, fever, and pain in the right iliac fossa, with a palpable mass and diarrhea.

A small-bowel barium study is the main radiographic method for the evaluation of intestinal TB in regions of the world where the disease is endemic. However, because peritonitis is common in GI TB, abdominal CT may be performed as a preferred examination, which nearly always suggests the diagnosis in the presence of necrotic lymph nodes or changes suggestive of TB peritonitis. The CT features suggestive of abdominal TB include irregular soft-tissue densities in the omentum, low-attenuating masses surrounded by thick solid rims, low-attenuating necrotic nodes, disorganized appearance of soft-tissue densities, high-attenuating ascitic fluid and bowel loops forming poorly defined masses, and a multiloculated appearance after the intravenous administration of iodinated contrast material. ^[19]

Radiologic features include a combination of narrowing, deep ulceration, and mucosal granulation producing nodularity and inflammatory polyps. Less common findings are aphthous ulcers and a diffuse colitis. Changes are usually noted in the ascending and transverse colon. Bowel contour may be lost with asymmetry simulating Crohn disease. When a short segment is involved, the strictures are hourglass-shaped rather than the apple-core deformity associated with carcinoma. In some cases, they may be indistinguishable.

The ileum empties into a deformed cone-shaped cecum at right angles with hypertrophy of the ileocecal valve (Fleischner sign). Fistulae and sinuses may occur but are rare. The cecum may be pulled upward with fibrosis.

Differentiating Crohn disease from TB before treatment is initiated is important, as steroid therapy can be catastrophic in patients with undiagnosed TB. CT demonstrates colonic wall thickening with spiculations, transmural fibrosis, and lymphadenopathy.  The presence of necrotic lymph nodes excludes a Crohn disease diagnosis, while findings of wall stratification, comb sign, and fibrofatty proliferation suggest Crohn disease. ^[20]  If doubt exists and if imaging findings cannot definitively differentiate GI TB from Crohn disease and other inflammatory disorders, laparoscopy with a targeted biopsy is currently considered the most rapid and specific method for diagnosing GI TB.

TB is a well-recognized cause of rectal stricture in the Asian population. Isolated rectal involvement is rare and may be mistaken for rectal malignancy.

The measurement of ascitic fluid adenosine deaminase levels is a major advance in the diagnosis of tuberculous peritonitis, which should be considered when dealing with exudative ascites. Laparoscopic biopsy samples from the peritoneum should be stained for acid-fast bacilli (AFB), and cultures should be obtained. Where laparoscopy is not available, percutaneous peritoneal biopsy and diagnostic ascitic tap (if ascites are present) for microbiologic and biochemical examination should suffice. Peritoneal biopsy is also helpful in nonascitic cases. Findings are positive in 42% of patients with abdominal TB.

The most common site of GI TB is the ileocecal region, if the area can be reached with a flexible endoscope. A rapid diagnosis can be achieved if smear or culture results are positive or if caseating granulomas are seen in biopsy samples. In countries where GI TB is endemic, a therapeutic trial of antituberculosis treatment may be justified if the clinical picture is compatible with TB.

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Stojkovic M, Müller J, Junghanss T, Weber TF. Radiological Diagnoses in the Context of Emigration: Infectious diseases. Rofo. 2018 Feb. 190 (2):121-133. [Medline]. [Full Text].

Kentley J, Ooi JL, Potter J, Tiberi S, O’Shaughnessy T, Langmead L, et al. Intestinal tuberculosis: a diagnostic challenge. Trop Med Int Health. 2017 Aug. 22 (8):994-999. [Medline]. [Full Text].

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Lin PY, Wang JY, Hsueh PR, Lee LN, Hsiao CH, Yu CJ, et al. Lower gastrointestinal tract tuberculosis: an important but neglected disease. Int J Colorectal Dis. 2009 Oct. 24(10):1175-80. [Medline].

Park SH, Yang SK, Yang DH, Kim KJ, Yoon SM, Choe JW, et al. Prospective randomized trial of six-month versus nine-month therapy for intestinal tuberculosis. Antimicrob Agents Chemother. 2009 Oct. 53(10):4167-71. [Medline]. [Full Text].

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Limsrivilai J, Shreiner AB, Pongpaibul A, Laohapand C, Boonanuwat R, Pausawasdi N, et al. Meta-Analytic Bayesian Model For Differentiating Intestinal Tuberculosis from Crohn’s Disease. Am J Gastroenterol. 2017 Mar. 112 (3):415-427. [Medline]. [Full Text].

Mahesh Kumar Neelala Anand, MBBS, DNB, FRCR Consultant Interventional Radiologist, Department of Radiology, Mediclinic Middle East Hospitals, UAE; Previous Consultant Interventional Radiologist and Clinical Director of Radiology, Pennine Acute Hospitals NHS Trust, UK

Mahesh Kumar Neelala Anand, MBBS, DNB, FRCR is a member of the following medical societies: British Society of Gastroenterology, British Society of Interventional Radiology, Cardiovascular and Interventional Radiological Society of Europe, European Society of Gastrointestinal and Abdominal Radiology, Indian Radiological and Imaging Association, Radiological Society of North America, Royal College of Radiologists

Disclosure: Nothing to disclose.

Jinna Jagan Mohan Reddy, MBBS, MD Radiologist, Clinical Imaging Department, Mafraq Hospital

Disclosure: Nothing to disclose.

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR Consultant Radiologist and Honorary Professor, North Manchester General Hospital Pennine Acute NHS Trust, UK

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR is a member of the following medical societies: American Association for the Advancement of Science, American Institute of Ultrasound in Medicine, British Medical Association, Royal College of Physicians and Surgeons of the United States, British Society of Interventional Radiology, Royal College of Physicians, Royal College of Radiologists, Royal College of Surgeons of England

Disclosure: Nothing to disclose.

Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand

Disclosure: Nothing to disclose.

Spencer B Gay, MD Professor of Radiology, Department of Radiology and Medical Imaging, University of Virginia School of Medicine

Disclosure: Nothing to disclose.

Eugene C Lin, MD Attending Radiologist, Teaching Coordinator for Cardiac Imaging, Radiology Residency Program, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine

Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, Society of Nuclear Medicine and Molecular Imaging

Disclosure: Nothing to disclose.

Zahir Amin, MD, MBBS, MRCP, FRCR Consulting Staff, Department of Imaging, University College Hospital, UK

Zahir Amin, MD, MBBS, MRCP, FRCR is a member of the following medical societies: British Institute of Radiology, British Medical Association, Royal College of Radiologists

Disclosure: Nothing to disclose.

Gastrointestinal Tuberculosis Imaging 

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