Tuberculosis, Gastrointestinal

Author: Mahesh Kumar Neelala Anand, MBBS, DNB, FRCR; Chief Editor: Eugene C Lin, MD more...

Updated: Nov 30, 2009

Overview
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.

Chest radiograph reveals calcified hilar tuberculous lymphadenitis.

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 Barium study shows marked narrowing of the body of stomach, which was proven to be gastric tuberculosis.

Recent studies

Because gastrointestinal TB is often difficult to differentiate from other intestinal inflammatory lesions, Tripathi and
Amarapurkar studied 110 cases of GI TB to identify the morphologic spectrum of the disease. The diagnosis of GI TB
in this study was based on the presence of acid-fast bacilli on histology, caseating or noncaseating epithelioid cell
granulomas, evidence of TB at other sites, and complete response to antituberculous therapy. 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. 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.[1]

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.[2]

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[3]

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.

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 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:

1. 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.
2. 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.
3. The ulcerohypertrophic form is a subtype seen in 30% of patients. These patients have a combination of
features of the ulcerative and hypertrophic forms.

Demographics

Frequency

In the US: After a decades-long decrease in TB cases, the disease has now re-emerged as a serious national
problem. Between 1985 and 1993, the number of new TB cases increased by 14% as a result of the following:
the combination of TB and HIV disease (an immunocompromised state predisposes an individual to TB
infection), immigration from countries where TB is common, deterioration of the health care infrastructure, and
outbreaks of multidrug-resistant TB. An estimated 10-15 million people are infected with M tuberculosis. Only
4% of persons with HIV develop TB. In persons co-infected with TB and HIV, the risk of TB disease may be
more than 100 times greater than for persons with TB infection alone.
Internationally: The burden of TB worldwide is emphasized by the fact that nearly 1% of the world's
population is newly infected with TB each year. Nearly 3 million TB cases per year occur in Southeast Asia.
Each year, more than 250,000 TB cases occur in Eastern Europe. TB accounts for approximately 15% of AIDS
deaths worldwide. In Africa, HIV is the single most important factor determining the increased incidence of TB
in the last 10 years. Approximately 43% of persons who are HIV-infected develop TB in developing countries.

Race

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 More than two thirds reported TB cases occur in racial and ethnic minorities.

The disease is more common in developing countries and among racial and ethnic minorities of the West.
Compared with non-Hispanic whites, Asians are 10 times more likely to have TB; blacks are 8 times more likely
to have TB; and Hispanic Native Americans and Alaskan natives are 5 times more likely to have the disease.

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.[4, 5]

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 Tuberculosis
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 Tuberculosis

Clinical features

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 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.

Barium examination reveals a long stricture of the duodenum caused by tuberculosis.

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 Tuberculosis
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.

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 Delayed image from follow-through series shows a collapsed colon and markedly distended long segment of ileum from chronic
obstruction. This may represent tabes mesenterica.

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.[6, 7, 8]

Crohn disease. The radiologic pattern shows cobblestoning of the mucosal surface characteristic of Crohn disease. This is not a feature
of tuberculosis.

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

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 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.

Barium meal follow-through series reveals gross dilatation of distal ileal segments in this British-born patient of Asian origin with
malabsorption. He had visited Pakistan once 15 years ago. Lymphoid masses found at surgery were proven to be intestinal tuberculosis.

CT scan of the abdomen in a patient with AIDS shows edematous jejunal loops and extensive lymphadenopathy, which was proven to be
a Mycobacterium avium intracellulare infection.

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 CT scan in an HIV-positive patient with intra-abdominal tuberculosis (TB) shows ascites, marked omental thickening in both flanks, and
stranding in the mesentery. Courtesy of Zahir Amin, MD.

Plain radiograph of abdomen with diffuse calcified mesenteric lymphadenopathy in a patient with tuberculosis.

Barium meal follow-through series reveals gross dilatation of distal ileal segments in this British-born patient of Asian origin with
malabsorption. He had visited Pakistan once 15 years ago. Lymphoid masses found at surgery were proven to be intestinal tuberculosis.

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 Tuberculosis
Clinical features

Colonic TB most often is associated with ileal TB. The involvement is segmental and especially involves the right

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 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.

Differential Diagnosis
Non-Hodgkin lymphoma is one of the most common neoplasms of the small intestine, accounting for

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 approximately 40% of primary malignant neoplasms.
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.
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.

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