Enteritis Tuberculosa

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Official reprint from UpToDate www.uptodate.com ©2015 UpToDate

AuthorsLouis-Michel Wong Kee Song, MD,FRCP(C)Norman E Marcon, MD, FRCP(C)

Section EditorStephen B Calderwood, MD

Deputy EditorElinor L Baron, MD, DTMH

Tuberculous enteritis

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jul 2015. | This topic last updated: Apr 15, 2015.

INTRODUCTION — Extrapulmonary tuberculosis (TB) affects approximately 20 percent of TB cases in immunocompetent individuals and 50 percent of

cases in HIV-infected patients. Tuberculous enteritis is a form of extrapulmonary TB that can involve any aspect of the gastrointestinal tract. It accounts for

1 to 3 percent of TB worldwide [1] and represents the sixth most frequent form of extrapulmonary TB (after lymphatic, genitourinary, bone and joint, miliary,

and meningeal tuberculosis) [2]. The epidemiology of tuberculous enteritis varies widely around the globe, influenced in part by age, sex, socioeconomic

factors, immune status, and Mycobacterium tuberculosis genotype [3]. Young adults, primarily women, are mostly affected in regions like Pakistan,

Turkey, and West Africa, whereas a lower disease incidence but similar or greater numbers of male patients are reported in studies from China, Singapore,

India, and the United Kingdom [3].

Prior to antituberculous therapy, gastrointestinal involvement was observed in 55 to 90 percent of patients with active pulmonary TB but since has been

observed in approximately 25 percent of cases [4].

Issues related to gastrointestinal TB will be reviewed here; issues related to other aspects of extrapulmonary TB are discussed separately. (See "Clinical

manifestations, diagnosis, and treatment of extrapulmonary and miliary tuberculosis".)

PATHOGENESIS — The pathogenesis of tuberculous enteritis has been attributed to four mechanisms [5-7]:

The ileocecal region is the most common site of intestinal involvement. The affinity of M. tuberculosis for this site may be due to the relative stasis and

abundant lymphoid tissue in this region. The organism penetrates the mucosa and localizes in the submucosal lymphoid tissue, where it initiates an

inflammatory reaction with subsequent lymphangitis, endarteritis, granuloma formation, caseation necrosis, mucosal ulceration, and scarring.

The macroscopic appearance of the intestinal lesions can be categorized as follows [5]:

®

®

Swallowing infected sputum●

Hematogenous spread from active pulmonary or miliary tuberculosis (TB)●

Ingestion of contaminated milk or food●

Contiguous spread from adjacent organs●

Ulcerative (60 percent), characterized by multiple superficial ulcers typically in a transverse/circumferential orientation relative to the long axis of the

gut lumen

●

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CLINICAL MANIFESTATIONS — The symptoms and signs of tuberculous enteritis are relatively vague and nonspecific. The presentation can be acute,

chronic, or acute-on-chronic with a chronic presentation of weeks to months being most common. As a result, the diagnosis of ileocecal tuberculosis (TB)

can be difficult and requires a high index of suspicion, especially in high-risk groups.

Symptoms — Nonspecific chronic abdominal pain is the most common symptom, occurring in 80 to 90 percent of patients. Anorexia, fatigue, fever, night

sweats, weight loss, diarrhea, constipation, or blood in the stool may be present. A palpable right lower quadrant abdominal mass is present in 25 to 50

percent of patients [5,6]. The presence of ascites may help to distinguish ileocecal TB from Crohn disease, since ascites is uncommon in Crohn disease.

Fistula and intestinal stricture may occur. Bowel obstruction is the most common complication and may be due to progressive stricture or adhesions [8-

10].

Laboratory tests — Routine laboratory tests demonstrate mild anemia and increased sedimentation rate in 50 to 80 percent of patients [7]. The white

blood count is usually normal.

A tuberculin skin test is positive in the majority of patients with intestinal TB but is of limited value because it does not differentiate between active disease

and previous sensitization by contact or vaccination [7]. Similarly, a positive interferon gamma release assay may be observed but cannot be used to

distinguish between latent and active disease. (See "Diagnosis of latent tuberculosis infection (tuberculosis screening) in HIV-uninfected adults", section

on 'Tuberculin skin test' and "Interferon-gamma release assays for diagnosis of latent tuberculosis infection".)

Imaging — Oral and intravenous contrast-enhanced computed tomography (CT) is the most helpful imaging modality to assess intraluminal and

extraluminal pathology and extent of disease [11-13]. The most common CT finding is concentric mural thickening of the ileocecal region, with or without

proximal intestinal dilatation (image 1). Occasionally, asymmetric thickening of the medial cecal wall is seen. Characteristic lymphadenopathy with

hypodense centers, representing caseous liquefaction, may be present in the adjacent mesentery. Findings more suggestive of TB than Crohn disease

include mural thickening with contiguous ileocecal valve involvement and hypodense lymph nodes with peripheral enhancement in the mesentery and

retroperitoneum.

Abdominal radiograph findings are generally nonspecific. Small bowel follow-through or barium enema may demonstrate mucosal ulcerations and

strictures, a deformed cecum, and/or a gaping and incompetent ileocecal valve (image 2).

DIAGNOSIS

General principles — A presumptive diagnosis of tuberculous enteritis can be made in the setting of known active pulmonary tuberculosis (TB; and/or

revealing chest radiograph), together with clinical, endoscopic, and/or radiographic findings suggestive of intestinal TB. However, chest radiographs are

positive (for active or healed TB) in less than 50 percent of patients [14-16].

Definitive diagnosis is based on a combination of histology and culture of biopsy material; these can establish the diagnosis in up to 80 percent of patients

[17]. Colonoscopy with biopsy is the most useful nonoperative diagnostic procedure to obtain material for histology and culture [14-16,18-20]. In regions

Hypertrophic (10 percent), characterized by scarring, fibrosis, and pseudotumor lesions●

Ulcerohypertrophic (30 percent), characterized by an inflammatory mass around the ileocecal valve with thickened and ulcerated intestinal walls. The

ulcerohypertrophic form is more commonly observed in ileocecal disease than with TB involving other segments of the gastrointestinal tract.

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where available, a polymerase chain reaction (PCR) of biopsy specimens can facilitate diagnosis, since it has higher sensitivity than routine culture, and

results can be obtained within 48 hours [3,21]. Biopsy is also useful for investigation of the diseases that compose the differential diagnosis of TB enteritis.

In the setting of ileocecal TB, endoscopic fine needle aspiration for cytology may be positive even if the biopsy is negative [22]. (See 'Colonoscopy' below

and 'Differential diagnosis' below.)

Colonoscopy — Colonoscopic findings of ileocecal TB may include ulcers, strictures, nodules, pseudopolyps, fibrous bands, fistulas, and/or deformed

ileocecal valves [23]. The main differential diagnosis at endoscopy is Crohn disease (CD). (See 'Differential diagnosis' below.)

The endoscopic finding of aphthous ulcers with normal surrounding mucosa, linear ulcers, or the presence of cobblestoning favors the diagnosis of CD;

these lesions are rarely seen with TB. However, diffusely inflamed mucosa may be seen with severe inflammation due to CD. Ulcers due to TB tend to be

circumferential (picture 1) and are usually surrounded by inflamed mucosa. A patulous valve with surrounding heaped-up folds or a destroyed valve with a

fish mouth opening is more likely to be caused by TB than CD (picture 2).

TB granulomas are often submucosal; CD granulomas are typically mucosal, though submucosal granulomas may also be seen [24]. Therefore, deep

endoscopic biopsies should be taken from ulcers and their margins. Care must be taken to avoid perforation in the setting of significant inflammation or

deep ulcerations.

A TB isolation mask should be worn by all individuals in the endoscopy suite when a colonoscopy is performed on a patient for whom there is suspicion of

intestinal TB.

Histopathology — Granulomas associated with TB tend to be large and confluent, often with caseation necrosis. Ulcers are lined by aggregate epithelioid

histiocytes, and disproportionate submucosal inflammation is seen. In contrast, granulomas associated with CD are infrequent, small, nonconfluent, and

noncaseating. CD is also characterized by focally enhanced colitis and a high prevalence of chronic inflammation in endoscopically normal-appearing

areas [25].

Typical histologic features of TB such as caseation granulomas and positive acid-fast stain are found in less than 33 percent of cases [15,23]. Some

histologic features that help differentiate TB enteritis from other etiologies include confluent granulomas, granulomas >400 micrometers in diameter, more

than five granulomas in biopsies from one segment, and granulomas located in the submucosa or granulation tissue [26].

Differential diagnosis — The differential diagnosis of ileocecal TB includes CD, actinomycosis, histoplasmosis, amebiasis, yersiniosis, typhlitis,

lymphoma, colon cancer, mucoceles, and drug-induced lesions (such as lesions due to nonsteroidal antiinflammatory drugs) [27].

Biopsy for culture and histopathology evaluation can be useful to definitively distinguish between these entities. The differentiation between CD and

tuberculous enteritis is becoming increasingly important with the reemergence of TB in Western countries in the wake of the AIDS epidemic, migration

from developing countries, and the emergence of CD in Asian countries, possibly as a result of Westernization [28].

This distinction is also of utmost importance because the use of steroids or antitumor necrosis factor drugs in the setting of an incorrect diagnosis of CD

may have disastrous consequences in patients with TB enteritis [7,11]. However, there can be marked overlap between the features of CD and intestinal

TB, making the differentiation between the two conditions difficult. A combination of clinical, radiographic, endoscopic, and biopsy findings are used to

distinguish between them (table 1) [13,28-32].

In one multivariate analysis involving 106 patients (53 with CD and 53 with intestinal TB), the presence of blood in stool, weight loss, focally enhanced

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colitis, and involvement of the sigmoid colon were the most important clinical features in differentiating CD from intestinal TB [29]. In another study involving

43 patients with confirmed diagnosis of intestinal TB and 53 patients with CD, the most important clinical features to differentiate CD from intestinal TB

were night sweats, longitudinal ulcers, and granulomas [33].

Clinical approach with uncertain diagnosis — The diagnosis of tuberculous enteritis can be difficult to establish. For situations in which there is a high

index of suspicion based on clinical, radiographic, and endoscopic findings (in the absence of histological and/or microbiologic confirmation), many favor

empiric initiation of antituberculous therapy [6,14-16,19,34]. Patients with tuberculous enteritis generally demonstrate clinical improvement within two

weeks on empiric therapy [35] and, in one study, colonoscopic follow-up after two to three months of anti-TB therapy showed complete healing of active

ulcers and erosions [36]. In the absence of clinical response, surgical exploration may be warranted to evaluate for alternative diagnoses such as Crohn

disease, lymphoma, or malignancy [7].

Similarly, for situations in which the index of suspicion for tuberculous enteritis is moderate or low and the diagnostic approach described above is

unrevealing, laparoscopic exploration and possible laparotomy may be warranted to evaluate for alternative diagnoses.

MANAGEMENT — The management of intestinal tuberculosis (TB) depends upon the acuity of presentation and associated complications. In the

presence of closed loop bowel obstruction, intestinal ischemia, bowel perforation, massive bleeding, or peritonitis, emergent surgical exploration with

targeted treatment is warranted [6,7,17]. Subsequently, antituberculous therapy should be initiated once the patient has stabilized from the operation. In

the subacute setting, initiation of antituberculous therapy can result in a relatively prompt clinical response with improvement of symptoms in less than two

weeks [37]. However, cases of worsening of strictures due to scar tissue formation have been reported.

In general, the medical treatment of tuberculous enteritis is similar to treatment of pulmonary TB [7], with conventional antituberculous chemotherapy

(RIPE: rifampicin, isoniazid, pyrazinamide, and ethambutol) for two months, followed by rifampicin plus isoniazid (RI) for an additional four to seven

months. Most countries adhere to the World Health Organization guidelines of directly observed treatment, short course (DOTS) given on a daily or thrice-

weekly basis. In one prospective, randomized trial, both DOTS (RIPE thrice weekly for two months followed by RI thrice weekly for four months) and daily

chemotherapy (RIPE for two months followed by RI for seven months) were equally effective at healing ileocecal and colonic tuberculosis in 79 and 75

percent of patients, respectively [35]. The initiation of therapy, modification of the drug regimen based on drug susceptibility testing, and monitoring of

therapy and drug toxicity are discussed in detail separately. (See "Treatment of pulmonary tuberculosis in HIV-uninfected patients".)

Patients with low-grade obstruction and fistulas may respond to antituberculous therapy, and most with mild to moderate intestinal strictures can be

managed nonoperatively. Bowel obstruction is the most common complication and may be due to progressive stricture or adhesions [10]. Healing in the

setting of antituberculous therapy can also result in symptomatic scarring. Those with multiple and/or severe strictures are less likely to respond to

medical therapy, and surgical resection may be required for high-grade obstruction. (See "Overview of enteric fistulas" and "Overview of management of

mechanical small bowel obstruction in adults".)

The surgical resection should be conservative; in some cases, multiple strictures of the small bowel may be amenable to strictureplasty to avoid major

resection [17]. Bypass surgery for obstructing lesions should be avoided because of complications related to blind loop syndrome. Colonoscopic balloon

dilation may be an alternative to surgery; it may be used to manage symptomatic short ileal strictures, although experience with this technique is limited

[38].

SUMMARY

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REFERENCES

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Tuberculous enteritis can develop via swallowing infected sputum, hematogenous spread, ingestion of contaminated milk or food, and/or contiguous

spread from adjacent organs. The ileocecal region is the most common site of intestinal involvement of tuberculosis (TB), likely due to the relative

stasis and abundant lymphoid tissue in this region. (See 'Pathogenesis' above.)

●

The clinical manifestations of tuberculous enteritis are relatively vague and nonspecific. Chronic abdominal pain is common. Anorexia, fatigue, fever,

night sweats, weight loss, diarrhea, constipation, or blood in the stool may be present. A palpable right lower quadrant abdominal mass may be

observed. Ascites may be present. (See 'Clinical manifestations' above.)

●

A presumptive diagnosis of tuberculous enteritis can be made in the setting of known active pulmonary TB (and/or revealing chest radiograph),

together with clinical, endoscopic, and/or radiographic findings suggestive of intestinal TB. Definitive diagnosis is based on a combination of histology

and culture of biopsy material. (See 'General principles' above.)

●

Colonoscopy with biopsy is the most useful nonoperative diagnostic procedure to obtain material for histology and culture. Colonoscopic findings of

ileocecal TB may include ulcers, strictures, nodules, pseudopolyps, fibrous bands, fistulas, and/or deformed ileocecal valves. (See 'Colonoscopy'

above.)

●

Computed tomography (CT) is the most helpful imaging modality to assess intraluminal and extraluminal pathology and extent of disease. The most

common CT finding is concentric mural thickening of the ileocecal region, with or without proximal intestinal dilatation. (See 'Imaging' above.)

●

The differential diagnosis of ileocecal TB includes Crohn disease, actinomycosis, histoplasmosis, amebiasis, yersiniosis, typhlitis, lymphoma, colon

cancer, mucoceles, and drug-induced lesions. Biopsy for culture and histopathology evaluation is the most useful tool to distinguish between these

entities. (See 'Differential diagnosis' above.)

●

For situations in which there is high index of suspicion for tuberculous enteritis based on clinical, radiographic, and endoscopic findings (in the

absence of histological and/or microbiologic confirmation), initiation of empiric antituberculous therapy is appropriate. Lack of clinical improvement

after two weeks of empiric therapy should prompt reassessment; laparoscopic exploration and/or laparotomy for further evaluation of alternative

diagnoses may be needed. For situations in which there is moderate or low index of suspicion for tuberculous enteritis, early laparotomy may be

warranted for evaluation of alternative diagnoses before determination regarding empiric antituberculous therapy. (See 'Clinical approach with

uncertain diagnosis' above.)

●

In general, treatment of tuberculous enteritis is similar to treatment of pulmonary TB. Surgery is warranted for patients with complications such as

perforation, massive bleeding, and/or high-grade obstruction. (See 'Management' above and "Treatment of pulmonary tuberculosis in HIV-uninfected

patients".)

●

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21. Anand BS, Schneider FE, El-Zaatari FA, et al. Diagnosis of intestinal tuberculosis by polymerase chain reaction on endoscopic biopsy specimens.Am J Gastroenterol 1994; 89:2248.

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24. Kirsch R, Pentecost M, Hall Pde M, et al. Role of colonoscopic biopsy in distinguishing between Crohn's disease and intestinal tuberculosis. J ClinPathol 2006; 59:840.

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26. Pulimood AB, Peter S, Ramakrishna B, et al. Segmental colonoscopic biopsies in the differentiation of ileocolic tuberculosis from Crohn's disease. JGastroenterol Hepatol 2005; 20:688.

27. Dilauro S, Crum-Cianflone NF. Ileitis: when it is not Crohn's disease. Curr Gastroenterol Rep 2010; 12:249.

28. Lee YJ, Yang SK, Byeon JS, et al. Analysis of colonoscopic findings in the differential diagnosis between intestinal tuberculosis and Crohn'sdisease. Endoscopy 2006; 38:592.

29. Makharia GK, Srivastava S, Das P, et al. Clinical, endoscopic, and histological differentiations between Crohn's disease and intestinal tuberculosis.Am J Gastroenterol 2010; 105:642.

30. Gabellec MM, Panzanelli P, Sassoè-Pognetto M, Lledo PM. Synapse-specific localization of vesicular glutamate transporters in the rat olfactorybulb. Eur J Neurosci 2007; 25:1373.

31. Li X, Liu X, Zou Y, et al. Predictors of clinical and endoscopic findings in differentiating Crohn's disease from intestinal tuberculosis. Dig Dis Sci2011; 56:188.

32. Pulimood AB, Amarapurkar DN, Ghoshal U, et al. Differentiation of Crohn's disease from intestinal tuberculosis in India in 2010. World JGastroenterol 2011; 17:433.

33. Yu H, Liu Y, Wang Y, et al. Clinical, endoscopic and histological differentiations between Crohn's disease and intestinal tuberculosis. Digestion2012; 85:202.

34. Wagner TE, Huseby ES, Huseby JS. Exacerbation of Mycobacterium tuberculosis enteritis masquerading as Crohn's disease after treatment with atumor necrosis factor-alpha inhibitor. Am J Med 2002; 112:67.

35. Tony J, Sunilkumar K, Thomas V. Randomized controlled trial of DOTS versus conventional regime for treatment of ileocecal and colonictuberculosis. Indian J Gastroenterol 2008; 27:19.

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GRAPHICS

Tuberculous enteritis - computed tomography

Contrast-enhanced computed tomography of histologically proven ileocecal

tuberculosis showing thickened terminal ileum (black arrow), ileocecal valve (red

arrow), and cecum (white arrow) with enlarged necrotic ileocecal lymph nodes

(yellow arrows).

Courtesy of Sudhakar Venkatesh, MD.

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Tuberculous enteritis - barium enema

Double contrast barium enema demonstrates ileocecal valve region. The cecum is fibrotic

and contracted (red arrow), the ileocecal valve is irregular, narrowed, gaping, and

incompetent (green arrow), and the terminal ileum appears to empty directly into the

ascending colon (Stierlin's sign; region of green arrow). Note the diffuse ulcerations in

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the ascending colon (orange arrows) and the lymphoid follic les in the terminal ileum (blue

arrows).

Reproduced with permission from: Eisenberg RL. An atlas of differential diagnosis, 4th Edition,

Lippincott Williams & Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams & Wilkins.

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Ascending colon tuberculous enteritis

(A) Colonoscopic view of circumferential ulcers involving the cecum and

ascending colon due to tuberculosis.

(B) Colonoscopic view of longitudinal ulcers (arrows) involving the ascending

colon due to Crohn disease.

Courtesy of Harshad Devarbhavi, MD (image A) and Louis M. Wong Kee Song, MD

(image B).

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Ileocecal tuberculous enteritis

Colonoscopic views of histologically confirmed ileocecal tuberculosis with

ulcerations (A) and destroyed ileocecal valve (B and C).

Courtesy of Harshad Devarbhavi, MD.

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Features that help distinguish between Crohn disease and intestinal tuberculosis

Crohn disease Intestinal tuberculosis

Clinical

manifestations

Perianal disease High-swinging fever (>38.5°C) in absence of intraabdominal

abscess

Evidence of pulmonary TB on chest radiograph

Radiographic

findings (CT/MRI)

Symmetrical bowel wall thickening

Mesenteric fibrofatty proliferation

(creeping fat)

Mesenteric vascular engorgement

(comb sign)

Small homogenous pericecal lymph

nodes

Asymmetrical bowel wall thickening

Inflammatory mass centered around the cecum and

enveloping the terminal ileum

Large mesenteric nodes with necrotic centers

Ascites

Endoscopic

findings

Longitudinal ulcers

Aphthous ulcers

Cobblestoned mucosa

Preservation of ileocecal valve

Multiple skip lesions

Anorectal lesions

Transverse ulcers

Hypertrophic mucosa

Scars/fibrous bands/inflammatory polyps

Gaping/destruction of ileocecal valve

Hyperemic nodules

Histopathologic

findings

Single granulomas

Architectural distortion distant from

granulomatous inflammation

Caseating granulomas or positive acid-fast bacilli staining*

Confluent (≥5/biopsy) and large (diameter >200

micrometers) granulomas; submucosal granulomas

Ulcers lined by epithelioid histiocytes

Disproportionate submucosal inflammation

TB: tuberculosis; CT: computed tomography; MRI: magnetic resonance imaging.

* Features pathognomonic for intestinal TB but present in <30 percent of cases; no single variable described above is absolutely

specific for either condition otherwise.

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Disclosures: Louis-Michel Wong Kee Song, MD, FRCP(C) Nothing to disclose. Norman E Marcon, MD, FRCP(C) Nothing to disclose.Stephen B Calderwood, MD Patent Holder: Vaccine Technologies Inc. [Vaccines (Cholera vaccines)]. Equity Ow nership/Stock Options:Pulmatrix [Inhaled antimicrobials]; PharmAthene [Anthrax (Anti-protective antigen monoclonal antibody)]. Elinor L Baron, MD, DTMH Nothing todisclose.

Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are addressed by vetting through amulti-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content isrequired of all authors and must conform to UpToDate standards of evidence.

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