Enteritis Tuberculosa

8/17/2015
Tuberculous enteritis
Official reprint from UpToDate

www.uptodate.com 2015 UpToDate
Authors
Louis-Michel Wong Kee Song, MD,
FRCP(C)
Norman E Marcon, MD, FRCP(C)
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH
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]:
Swallowing infected sputum

Hematogenous spread from active pulmonary or miliary tuberculosis (TB)
Ingestion of contaminated milk or food
Contiguous spread from adjacent organs
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]:
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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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.
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 [810].
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
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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 thriceweekly 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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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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2. Dasgupta A, Singh N, Bhatia A. Abdominal tuberculosis: a histopathological study with special reference to intestinal perforation and mesenteric
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8. Petrosyan M, Mason RJ. Tuberculous enteritis presenting as small-bowel obstruction. Clin Gastroenterol Hepatol 2006; 4:xxiii.
9. Garca-Daz RA, Ruiz-Gmez JL, Rodrguez-Sanjuan JC, et al. Perforation of the colon caused by intestinal tuberculosis. Dis Colon Rectum 2006;
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10. Ha HK, Ko GY, Yu ES, et al. Intestinal tuberculosis with abdominal complications: radiologic and pathologic features. Abdom Imaging 1999; 24:32.
11. Balthazar EJ, Gordon R, Hulnick D. Ileocecal tuberculosis: CT and radiologic evaluation. AJR Am J Roentgenol 1990; 154:499.
12. Suri S, Gupta S, Suri R. Computed tomography in abdominal tuberculosis. Br J Radiol 1999; 72:92.
13. Almadi MA, Ghosh S, Aljebreen AM. Differentiating intestinal tuberculosis from Crohn's disease: a diagnostic challenge. Am J Gastroenterol 2009;
104:1003.
14. Bhargava DK, Kushwaha AK, Dasarathy S, et al. Endoscopic diagnosis of segmental colonic tuberculosis. Gastrointest Endosc 1992; 38:571.
15. Shah S, Thomas V, Mathan M, et al. Colonoscopic study of 50 patients with colonic tuberculosis. Gut 1992; 33:347.
16. Misra SP, Misra V, Dwivedi M, Gupta SC. Colonic tuberculosis: clinical features, endoscopic appearance and management. J Gastroenterol Hepatol
1999; 14:723.
17. Aston NO. Abdominal tuberculosis. World J Surg 1997; 21:492.
18. Kalvaria I, Kottler RE, Marks IN. The role of colonoscopy in the diagnosis of tuberculosis. J Clin Gastroenterol 1988; 10:516.
19. Singh V, Kumar P, Kamal J, et al. Clinicocolonoscopic profile of colonic tuberculosis. Am J Gastroenterol 1996; 91:565.
20. Kim KM, Lee A, Choi KY, et al. Intestinal tuberculosis: clinicopathologic analysis and diagnosis by endoscopic biopsy. Am J Gastroenterol 1998;
93:606.
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.
22. Kochhar R, Rajwanshi A, Goenka MK, et al. Colonoscopic fine needle aspiration cytology in the diagnosis of ileocecal tuberculosis. Am J
Gastroenterol 1991; 86:102.
23. Alvares JF, Devarbhavi H, Makhija P, et al. Clinical, colonoscopic, and histological profile of colonic tuberculosis in a tertiary hospital. Endoscopy
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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 Clin
Pathol 2006; 59:840.
25. Pulimood AB, Ramakrishna BS, Kurian G, et al. Endoscopic mucosal biopsies are useful in distinguishing granulomatous colitis due to Crohn's
disease from tuberculosis. Gut 1999; 45:537.
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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. J
Gastroenterol 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's
disease. 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, Sasso-Pognetto M, Lledo PM. Synapse-specific localization of vesicular glutamate transporters in the rat olfactory
bulb. 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 Sci
2011; 56:188.
32. Pulimood AB, Amarapurkar DN, Ghoshal U, et al. Differentiation of Crohn's disease from intestinal tuberculosis in India in 2010. World J
Gastroenterol 2011; 17:433.
33. Yu H, Liu Y, Wang Y, et al. Clinical, endoscopic and histological differentiations between Crohn's disease and intestinal tuberculosis. Digestion
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34. Wagner TE, Huseby ES, Huseby JS. Exacerbation of Mycobacterium tuberculosis enteritis masquerading as Crohn's disease after treatment with a
tumor 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 colonic
tuberculosis. Indian J Gastroenterol 2008; 27:19.
36. Park YS, Jun DW, Kim SH, et al. Colonoscopy evaluation after short-term anti-tuberculosis treatment in nonspecific ulcers on the ileocecal area.
World J Gastroenterol 2008; 14:5051.
37. Giouleme O, Paschos P, Katsaros M, et al. Intestinal tuberculosis: a diagnostic challenge--case report and review of the literature. Eur J
Gastroenterol Hepatol 2011; 23:1074.
38. Bhasin DK, Sharma BC, Dhavan S, et al. Endoscopic balloon dilation of ileal stricture due to tuberculosis. Endoscopy 1998; 30:S44.
Topic 2688 Version 12.0
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GRAPHICS
Tuberculous enteritis - computed tomography
Contrast-enhanc ed c omputed tomography of histologic ally proven ileoc ec al

tuberc ulosis showing thic kened terminal ileum (blac k arrow), ileoc ec al valve (red
arrow), and c ec um (white arrow) with enlarged nec rotic ileoc ec al lymph nodes
(yellow arrows).
Courtesy of Sudhakar Venkatesh, MD.
Graphic 83833 Version 1.0
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Tuberculous enteritis - barium enema
Double c ontrast barium enema demonstrates ileoc ec al valve region. The c ec um is fibrotic
and c ontrac ted (red arrow), the ileoc ec al valve is irregular, narrowed, gaping, and
inc ompetent (green arrow), and the terminal ileum appears to empty direc tly into the
asc ending c olon (Stierlin's sign; region of green arrow). Note the diffuse ulc erations in
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the asc ending c olon (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.
http://www.uptodate.com.wdg.biblio.udg.mx:2048/contents/tuberculous-enteritis?topicKey=ID%2F2688&elapsedTimeMs=0&source=search_result&searchTerm=extrapulmonary+tuberculosis&selectedTitle=6%7E
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Ascending colon tuberculous enteritis
(A) Colonosc opic view of c irc umferential ulc ers involving the c ec um and
asc ending c olon due to tuberc ulosis.
(B) Colonosc opic view of longitudinal ulc ers (arrows) involving the asc ending
c olon 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
Colonosc opic views of histologic ally c onfirmed ileoc ec al tuberc ulosis with
ulc erations (A) and destroyed ileoc ec al 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
Clinical
manifestations
Perianal disease
Intestinal tuberculosis
High-swinging fever (>38.5C) in absence of intraabdominal
abscess
Evidence of pulmonary TB on chest radiograph
Radiographic
Symmetrical bowel wall thickening
Asymmetrical bowel wall thickening
findings (CT/MRI)
Mesenteric fibrofatty proliferation
Inflammatory mass centered around the cecum and
(creeping fat)
enveloping the terminal ileum
Mesenteric vascular engorgement
Large mesenteric nodes with necrotic centers
(comb sign)
Ascites
Small homogenous pericecal lymph

nodes
Endoscopic
findings
Longitudinal ulcers
Transverse ulcers
Aphthous ulcers
Hypertrophic mucosa
Cobblestoned mucosa
Scars/fibrous bands/inflammatory polyps
Preservation of ileocecal valve
Gaping/destruction of ileocecal valve
Multiple skip lesions
Hyperemic nodules
Anorectal lesions
Histopathologic
Single granulomas
Caseating granulomas or positive acid-fast bacilli staining*
findings
Architectural distortion distant from
Confluent (5/biopsy) and large (diameter >200
granulomatous inflammation
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
Disclosures: Louis-Michel Wong Kee Song, MD, FRCP(C) Nothing to disclose. Norm an E Marcon, MD, FRCP(C) Nothing to disclose.
Stephen B Calderw ood, 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 to
disclose.
Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a
multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
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Official reprint from UpToDate

Swallowing infected sputum

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

vasculopathy. J Lab Physicians 2009; 1:56.

Contrast-enhanc ed c omputed tomography of histologic ally proven ileoc ec al

Tuberculous enteritis - barium enema

Ascending colon tuberculous enteritis

Ileocecal tuberculous enteritis

Symmetrical bowel wall thickening

Asymmetrical bowel wall thickening

Mesenteric fibrofatty proliferation

Inflammatory mass centered around the cecum and

enveloping the terminal ileum

Mesenteric vascular engorgement

Large mesenteric nodes with necrotic centers

Small homogenous pericecal lymph

Scars/fibrous bands/inflammatory polyps

Preservation of ileocecal valve

Gaping/destruction of ileocecal valve

Multiple skip lesions

Caseating granulomas or positive acid-fast bacilli staining*

Architectural distortion distant from

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

micrometers) granulomas; submucosal granulomas

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

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