You are in: eMedicine Specialties > Radiology > GASTROINTESTINAL Tuberculosis, GastrointestinalArticle Last Updated: Jan 19, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 9
  Author: Mahesh Kumar Neelala Anand, MBBS, DNB, FRCR, Clinical Director, Consultant Radiologist, Department of Radiology, Pennine Acute Hospitals NHS Trust, Manchester, UK Mahesh Kumar Neelala Anand is a member of the following medical societies: British Medical Association, Radiological Society of North America, and Royal College of Radiologists Coauthor(s): Jinna Jagan Mohan Reddy, MBBS, Consultant, Department of MRI, Mafraq Hospital, India; Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia Editors: Zahir Amin, MD, MBBS, MRCP, FRCR, Consulting Staff, Department of Imaging, University College Hospital, UK; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Spencer B Gay, MD, Professor of Radiology, Director of Body Computed Tomography, Department of Radiology, University of Virginia Health Sciences Center; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center Author and Editor Disclosure Synonyms and related keywords: mycobacterial infection in gastrointestinal tract, Koch infection, TB, gastrointestinal TB, GI TB, pulmonary tuberculosis, pulmonary TB, Mycobacterium tuberculosis, M tuberculosis, esophageal TB, gastric TB, duodenal TB, intestinal TB, mycobacterium avium intracellulare, mycobacterium avium complex INTRODUCTIONSection 2 of 9
  Background: 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. Overall, one third of the world's population is infected with the TB bacillus, but not all infected individuals have clinical disease. 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. 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. Radiologic features and pathologic correlation to the pattern of tuberculous infection in the GI tract is discussed in this article. For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center. Also, see eMedicine's patient education article Tuberculosis. Pathophysiology: Pathogen and routes of spread The TB pathogen is Mycobacterium tuberculosis. Other mycobacterial species that simulate TB are M bovis, M avium, and M intracellulare. Routes of GI infection include the following: (1) spread by means of the ingestion of infected sputum, in patients with active pulmonary TB and especially in patients with pulmonary cavitation and positive sputum smears; (2) spread through a hematogenous route from tuberculous focus in the lung to submucosal lymph nodes; and (3) local spread from surrounding organs involved by primary tuberculous infection (eg, renal TB causing fistulas into the duodenum or mediastinal TB lymphadenopathy involving the esophagus). Pathologic findings Pathologically GI TB is characterized by inflammation and fibrosis of the bowel wall and the regional lymph nodes. Mucosal ulceration results from necrosis of Peyer patches, lymph follicles, and vascular thrombosis. At this stage of the disease, the changes are reversible and healing without scarring is possible. As the disease progresses, the ulceration becomes confluent, and extensive fibrosis leads to bowel wall thickening, fibrosis, and pseudotumoral mass lesions. Strictures and fistulae formation may occur. The serosal surface may show nodular masses of tubercles. The mucosa is inflamed with hyperemia and edema similar to that observed in Crohn disease. In some cases, aphthous ulcers may be seen in the colon. Caseation may not always be seen in the granuloma, especially in the mucosa, but it is almost always seen in the regional lymph nodes. On gross pathologic examination, intestinal TB can be classified into 3 categories:
Frequency:
Race: More than two thirds reported TB cases occur in racial and ethnic minorities.
Age: TB can occur in persons of any age, although it is more common in children and in older persons whose immune systems are weak. TB can be seen in any age group that is immunocompromised. Clinical Details: GI TB involves any part of the gut, although the ileum and colon are common sites. Nonspecific symptoms such as weight loss and abdominal pain are present in 80-90% of patients with intestinal TB. Nausea and vomiting may occur in patients with intestinal obstruction. Approximately one third of patients report constipation. In HIV-infected patients, TB tends to occur earlier than other AIDS-defining opportunistic infections when the CD4 cell count is in the range of 150-350 cells per microliter. Laboratory tests may reveal anemia and a normal WBC count. Tuberculin skin-test results are negative in most patients with primary intestinal TB. A positive test does not indicate active disease. ESOPHAGEAL TBSection 3 of 9
Clinical features Esophageal TB is rare, usually occurring because of spread from TB in the thorax either from mediastinal nodes, the lungs, or the spine. 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. A rare granular form of TB occurs in miliary spread of primary TB. Radiologic features 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. Other diagnostic studies Biopsy of the ulcerated mucosa reveals epithelioid granulomas. GASTRIC AND DUODENAL TBSection 4 of 9
Clinical features 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. Radiologic features Gastric TB may show multiple large and 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. 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. INTESTINAL TBSection 5 of 9
Clinical features 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. 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. 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 M avium-intracellulare (MAI) complex infection, predominantly infection involving the jejunum. Intestinal obstruction may be partial or complete with TB. Segmental involvement usually is in a stenotic form. Radiologic features Early changes on barium examinations reveal nodular thickening of mucosal folds, with loss of symmetry in the fold pattern. 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. 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 other patients. 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 MAI complex infections in patients with AIDS may be possible. Diffuse jejunal wall thickening and enlarged soft-tissue–attenuating lymph nodes with hepatosplenomegaly suggest disseminated MAI complex infection, whereas focal abdominal lesions with low-attenuating lymph nodes suggest disseminated M tuberculosis. MAI complex infection is also called pseudo-Whipple disease because of the diffuse mucosal fold thickening in the jejunum and histiocytic aggregates infected with MAI 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%). COLONIC TBSection 6 of 9
Clinical features Colonic TB most often is 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. Radiologic features 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. 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. 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. Other diagnostic studies 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. DIFFERENTIALSSection 7 of 9
Non-Hodgkin lymphoma is one of the most common neoplasms of the small intestine, accounting for approximately 40% of primary malignant neoplasms. Some conditions predispose a person to secondary intestinal lymphoma; these include celia The differential diagnosis of TB includes Crohn disease, non-Hodgkin lymphoma, yersiniosis, South American blastomycosis, and anisakiasis. The valvulae conniventes thickens with intraluminal and extraluminal mass causing filling defects. The bowel may reveal focal aneurysmal dilatations without association of a stricture and is characteristic of lymphoma, but the feature Yersiniosis is an infection caused by Yersinia enterocolitica, a gram-negative bacillus. The appearance of yersiniosis in the small bowel mimics TB, largely with involvement of the terminal ileum. However, yersiniosis may be difficult MULTIMEDIASection 8 of 9
REFERENCESSection 9 of 9
Tuberculosis, Gastrointestinal excerpt Article Last Updated: Jan 19, 2007 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
