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Abdominal Tuberculosis
Introduction
Abdominal tuberculosis (TB) involves the following sites singly or in combination: gastrointestinal tract, peritoneum, visceral organs, and intra-abdominal lymph nodes. As a form of extrapulmonary TB (EXPTB), abdominal TB can occur in the presence or absence of active pulmonary TB. Abdominal TB is relatively rare, representing 1% to 3% of global TB cases, and the rate varies worldwide as a function of overall EXPTB rates within geographic locations.[1] Abdominal TB estimates range from approximately 13% of the EXPTB cases in India to 6% of the EXPTB cases in the United States.[2][3] Diagnosis is challenging and often delayed due to its nonspecific presentation. Abdominal TB responds well to standard antituberculous drugs when diagnosed early, with surgery only required in cases that develop complications (eg, strictures or obstruction) or that are unresponsive to medical therapy. High clinical suspicion, early initiation of antituberculous therapy, and involvement of an interprofessional team are necessary for reducing morbidity and mortality.
Etiology
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Etiology
The Mycobacterium tuberculosis complex consists of several closely related mycobacteria species that are the etiology of abdominal TB. See StatPearls companion resource, "Tuberculosis Overview," for more information on the microbiology and etiology of tuberculosis. Abdominal TB can occur in several ways, including:
- Sputum ingestion by a patient with active pulmonary disease from Mycobacterium tuberculosis
- Hematogenous spread from a distant focus
- Lymphatic spread through infected lymph nodes
- Direct extension from a contiguous site
- Ingestion of milk products infected with Mycobacterium bovis (particularly seen with consumption of raw milk) [4]
Some authors have classified abdominal TB into 2 types: a primary form due to the direct ingestion of M. bovis and a secondary form due to the spread of infection from active pulmonary disease.[5]
The terminal ileum, ileocaecal valve, and peritoneum are the abdominal sites most commonly involved due to factors specific to these regions, including a narrow lumen, relatively increased physiological stasis, minimal digestive activity, and abundant lymphatic tissue that can take up tubercle bacilli.[5][6][7] From the gastrointestinal tract, the TB bacilli can gain entry into the portal and hepatic artery circulation and infect abdominal solid organs (eg liver, spleen, and pancreas). Hematogenous and lymphatic spread from a distant organ can also lead to infection at abdominal sites. Direct extension of infection to the peritoneum can result from gastrointestinal sites, as well as infected adnexa and paraspinal muscle.[8]
Epidemiology
EXPTB accounts for about 12% of all TB cases, of which abdominal TB accounts for 6% to 13%.[9] Between 6% to 38% of patients with abdominal TB may have concomitant pulmonary TB.[10][11] Abdominal TB is more commonly seen in populations with lower socioeconomic status.[3][9]
Abdominal Tuberculosis Risk Factors
Risk factors for abdominal TB are similar to those for EXPTB. Factors that increase the risk of abdominal TB include:
- Individuals living with HIV
- Individuals receiving immunosuppressive therapy [3][12]
- Female gender
- End-stage renal disease
- Cirrhosis
- Diabetes [13][14][15]
In industrialized countries, the majority of abdominal TB cases occur in HIV-TB coinfected persons and immigrants from high TB endemic areas. In the latter population, TB reactivation is the most common mechanism of disease.[16]
Pathophysiology
TB is capable of infecting any organ. Abdominal TB can involve sites from the oral cavity to the anus. Primary abdominal TB can result from ingestion of sputum or unpasteurized milk containing the organism. Secondary abdominal TB can occur via lymphatic and hematogenous spread from a distant organ or contiguous spread from an infected organ within the abdominal cavity. Abdominal TB may result from either progressive primary disease or latent infection and is most commonly located in the intestine and peritoneum.[17] Nonspecific symptoms, including fever, malaise, weight loss, change in bowel habits, and abdominal pain, are characteristic of abdominal TB.
Oral Tuberculosis
TB involving the oral cavity is rare. The mandible, buccal mucosa, lips, gingiva, and tongue can be involved with lesions that appear as painless or painful ulcers, nodules, fissures, and granulomas. The lesions can be of acute or chronic onset. Biopsy, acid-fast staining, polymerase chain reaction (PCR), and culture are required to establish the diagnosis.[18]
Esophageal Tuberculosis
Esophageal TB is rare. Contiguous spread from tuberculous mediastinal adenopathy is the most common pathophysiologic mechanism, whereas primary esophageal TB is exceedingly rare. Clinical features mimic those of esophageal cancer, with progressive dysphagia as a common characteristic. Nodular and ulcerative lesions are typical findings. Biopsied lesions typically show caseating and noncaseating granulomas. Acid-fast staining, PCR, and culture of biopsied tissues should be performed.[19]
Gastric and Gastroduodenal Tuberculosis
Gastric and gastroduodenal TB are rare, likely due to a combination of protective effects of gastric acid, relative paucity of lymphoid tissue, and rapid transit of stomach contents. Anorexia, weight loss, and gastric outlet obstruction are common clinical manifestations. Additionally, ulcerative and hypertrophic lesions can be seen by endoscopy. Pyloric stenosis may develop in the late stage of the disease. Lymphadenopathy can result in extrinsic compression of the duodenum.[15][8]
Tuberculosis of the Small and Large Intestine
The ileocecal region and terminal ileum are common sites of abdominal TB due to the abundance of lymphoid tissue and relatively slow transit time of contents. The following 4 major forms have been reported:
- Ulcerative: The most common form is the ulcerative type, usually presenting with superficial transverse ulcers and is most likely to be seen in the small intestine.
- Hypertrophic: This form occurs as a hyperplastic reaction around the ulcer, producing an inflammatory mass. The hypertrophic form is more likely to be seen in the cecum.
- Ulcero-hypertrophic: A combination of ulcerative and hypertrophic forms may occur.
- Fibrous stricture: Abdominal TB may lead to fibrosis and stricture formation, resulting in intestinal obstruction.[11][20]
Bowel obstruction is a common complication. Bowel perforation may occur. Intestinal TB and Crohn's disease have similar clinical, radiologic, endoscopic, and histologic features. Diagnosis is established based on endoscopic biopsies demonstrating the presence of organisms by stains, PCR, or culture.[8][15][21]
Rectal and Anal Tuberculosis
Rectal and anal TB are rare. Hematochezia is a common symptom, though mucosal ulcers, hypertrophic ulcers, abscesses, and strictures may also be present. Diagnosis is based on the presence of mycobacteria identified by histology, PCR, or culture.[22][3]
Visceral Organ Tuberculosis
Infection of visceral organs can occur, including the liver, gall bladder, spleen, pancreas, kidneys, and adnexa. Lymphohematogenous dissemination and contiguous spread of the bacteria between intraabdominal organs are pathophysiologic mechanisms.[20] Nonspecific symptoms, including fever, malaise, weight loss, abdominal pain, jaundice, and ascites, contribute to delayed diagnosis. Imaging studies will often demonstrate small miliary nodules due to disseminated disease. Less frequently, isolated lesions representing tubercular abscesses may be seen.[23]
Peritoneal Tuberculosis
Peritoneal TB often occurs with other forms of abdominal TB and develops after the rupture of necrotic mesenteric lymph nodes or by contiguous organ involvement. Reactivation of latent TB is the most common pathophysiologic mechanism of the disease. Chronic ascites in the absence of liver disease are the most frequent manifestation.[24] The ascitic fluid may be free, loculated, fibrotic, or a combination of these features. Bowel loops may become adherent, and peritoneal nodules may be present.[23]
Histopathology
TB infection of GI tract tissues often demonstrates the presence of submucosal caseating and noncaseating granuloma, cellular inflammation, and lymphatic hyperplasia. The identification of acid-fast bacilli by Ziehl-Neelsen staining is likely a function of the microscopist's time spent and experience due to the infection's paucibacillary nature. Abdominal TB morphology and histology characteristics on histologic exam can mimic Crohn's disease.[25] The presence of caseating granuloma, confluent granuloma, and ulcers lined by histiocytes are features that are more specifically indicative of abdominal TB. In addition, granuloma involving intraabdominal lymph nodes in the absence of intestinal inflammation is suggestive of TB.[17]
TB-infected hepatic tissue may demonstrate the presence of caseating and noncaseating granulomas. However, granulomatous hepatitis notably has a broad range of differential diagnoses.[15] The sensitivity of AFB stains is operator-dependent; the relatively low sensitivity reflects the paucibacillary nature of the infection.
History and Physical
Clinical History
Abdominal TB often occurs in the absence of a history of TB. A family history or known exposure may not be evident in all patients, and a high index of suspicion is required to make a timely diagnosis. Occasionally, it can occur coincident with the onset of active pulmonary TB.[15] Nonspecific constitutional symptoms of fever, malaise, anorexia, weight loss, epigastric pain, nausea, vomiting, abdominal pain, and change in bowel habits are common and contribute to delays in diagnosis. Given the variety of organs that can be involved singly or in combination, the symptoms and signs of abdominal tuberculosis can vary. The onset of illness is often indolent.[3][26]
Physical Examination
Abdominal tenderness, ascites, organomegaly, jaundice, and an abdominal mass are signs that may be found on physical exam. Obstructive symptoms and signs can develop due to strictures, extrinsic compression from contiguous inflammation, or adenopathy.[17] Fever of unknown origin may be the only symptom, adding to the challenge of establishing a diagnosis. None of the signs, symptoms, or physical findings are pathognomonic. (Please refer to the Pathophysiology section for more information on the characteristics of abdominal TB related to specific anatomic sites of infection).
Evaluation
General Laboratory Evaluation
Patients with symptomatic abdominal TB frequently are anemic, hypoalbuminic, and have elevated C-reactive protein (CRP) levels.[27] CRP, erythrocyte sedimentation rate (ESR), and fecal calprotectin may be useful surrogate markers to monitor healing while on antituberculosis treatment (ATT).[28] Analysis of ascitic fluid can be valuable in suggesting a diagnosis. Ascitic fluid due to TB peritonitis typically contains high protein concentrations and lymphocytosis. Moreover, the analysis of ascitic fluid cytology and cultures can help exclude other causes of peritonitis. Chest radiography should be performed to evaluate patients for evidence of active and latent pulmonary TB.
Mycobacterium-Specific Testing
See StatPearls companion resource, "Tuberculosis Overview," for more information on the approach to TB evaluation. The following are some recommended TB-specific laboratory studies:
- Abdominal TB is a paucibacillary disease.[29] AFB stains and cultures have low sensitivity and high specificity; PCR may provide greater sensitivity.[30]
- Tuberculin skin tests and interferon-gamma release assays (IGRA) may be false-negative and are not useful in establishing a diagnosis of active TB.[31]
- Elevated adenosine deaminase (ADA) levels in peritoneal fluid are a good diagnostic marker and support a diagnosis of peritoneal TB.[32][17]
- The value of IGRA in peritoneal fluid has not been established.[17]
- Polymerase chain reaction (PCR) testing for M. tuberculosis on clinical specimens can be used as an adjunct for initial diagnosis but should not be used for follow-up. This is because it cannot differentiate between living and dead M. tuberculosis. Thus, it can remain positive even after the completion of successful anti-TB treatment.[33] It may be useful in distinguishing intestinal TB from Crohn's disease.[34] Multiplex PCRs that detect multiple TB genes have been found to have higher sensitivity and specificity and may also help differentiate TB from Crohn's disease.[35][36]
- The World Health Organization (WHO) recommends a test that amplifies genomic DNA by PCR assay for the diagnosis of TB, with results provided within 2 hours. It combines a nested PCR technique with automated amplification that detects M. tuberculosis and rifampicin resistance genes. Rifampicin resistance is a surrogate marker for potential resistance to other anti-TB antibiotics.
Imaging Studies
Computed tomography scan
Computed tomography (CT) scan is the modality of choice in evaluating the extent and type of abdominal TB.[37] Intestinal TB may have the appearance of asymmetric wall thickening of the terminal ileum, cecum, or ileocecal valves associated with necrotic lymph nodes. After chronic inflammation, the cecum may appear small and irregular due to fibrosis and stenosis. Solid-organ involvement manifests as multiple small hypoattenuating nodules on the surface and throughout the parenchyma.[38] Peritoneal fluid has high protein and cellular content, creating areas of high attenuation on CT imaging. Other characteristics of peritoneal TB may include plastic/fibrous type, which is seen as mesenteric, and peritoneal thickening with loculated ascites. The nodular or dry form of TB peritonitis is characterized by mesenteric nodular thickening and fibrous adhesions with a carcinomatosis appearance.[39] CT-guided aspiration or biopsy can obtain cells and tissue specimens for analysis.
Ultrasound
Ultrasound is frequently the initial modality used for the evaluation of abdominal TB and can identify peritoneal and bowel wall thickening, ascites, and adenopathy. Ultrasound-guided aspiration and assisted laparoscopic biopsy may help in the diagnosis.[40][41]
Laparoscopic Evaluation
Laparoscopy can be used to obtain specimens and to visualize tissues. The presence of peritoneal thickening, small light-yellow tubercles, and fibroadhesive stranding on the surface of the tissues is suggestive of TB. However, laparoscopy is associated with risks of bleeding and bowel perforation.[17]
Gastroenterology Procedures
Colonoscopy may detect asymptomatic cases when performed for other reasons.[42] Biopsies obtained by colonoscopy have been reported to have as high as 80% diagnostic accuracy. The yield from culture has been reported to be higher when multiple tissue biopsies are obtained during colonoscopy.[43] The ileocecal region is a commonly involved site for abdominal TB. While not pathognomonic for TB, certain morphological features can help distinguish it from Crohn's disease.[17]
Therapeutic Trials
In some cases, when diagnostic testing is inconclusive, but clinical suspicion is high, patients are started empirically on ATT. Response to ATT is proposed as a criterion for diagnosing abdominal TB.[28][44] The accuracy of therapeutic trials, as reported in different studies, has varied between 16% and 29%.[45][29] Response to therapy occurs rapidly, usually within 2 weeks.
Treatment / Management
Medical Therapy
A standard 4-drug regimen consisting of isoniazid, rifampicin, pyrazinamide, and ethambutol is recommended. These 4 drugs are used 3 times a week for the first 2 months, followed by isoniazid and rifampin for an additional 4 months.[46] Healing of intestinal ulcers can be seen as early as the end of the initiation phase of therapy (2 months).[44] See StatPearls companion resource, "Tuberculosis Overview," for more information on the approach to treatment.(B3)
Most treatment guidelines recommend a 6-month course of anti-TB therapy for luminal TB. Prospective, randomized controlled studies and a Cochrane systematic review have confirmed good cure rates with 6 months of therapy instead of 9 months, with the added benefits of reduced cost and increased compliance.[47][48] However, prolonged therapy may be needed when a concern for disseminated disease is present.[49][50] Thus, each patient should be evaluated individually. Consultation with an expert in infectious diseases is recommended.(A1)
Response to therapy occurs by mucosal healing. However, strictures, polyps, and hypertrophic lesions may persist.[44] Additionally, an obstruction may worsen during therapy due to healing and scar formation.[51] The role of adjunctive corticosteroids has not been established at this time.[17](B3)
Endoscopic Intervention
Endoscopic balloon dilatation has been used to manage ileal and duodenal strictures.[52][53](B3)
Surgical Therapy
Surgery may be needed for complications, eg, obstruction, perforation, and fistulation.[54] Surgical options are categorized into the following 3 main broad groups:
- Bypassing of involved bowel segments: Entero-enterostomy and ileo-transverse colostomy procedures are not routinely done as they are usually complicated by blind loop syndrome, fistula formation, and recurrent disease in the remaining segments.
- Radical resection of involved segments: Tuberculous bowel perforations are usually treated with resection of involved segments and primary anastomosis. This can be combined with effective anti-TB antibiotics to eradicate the disease. However, these surgeries are often hindered by the malnourished status of most patients, making them poor surgical candidates.
- Conservative surgeries: Procedures, eg, strictureplasty, may be considered for strictures that cause more than 50% luminal compromise. Surgery may also be needed in patients with persistent strictures while receiving ATT, as well as those with multiple strictures who are less likely to respond to the antibiotics.[46][47][55]
Differential Diagnosis
Abdominal TB is known as "the great mimicker," reported to mimic esophageal cancer, esophageal ulcers, gastric ulcers, gastric cancer, colorectal cancer, hepatic abscess, hepatic granulomatosis, and malignancies.[56][57] Moreover, abdominal TB can be clinically indistinguishable from spontaneous bacterial peritonitis, appendicitis, colitis, acute cholecystitis, and necrotizing fasciitis.[58][59][60] Other infectious etiologies can cause caseating granulomas, and noncaseating granulomas can occur with sarcoidosis and berylliosis.[3] TB lesions may be enhanced with CT contrast media and demonstrate radioactive uptake with positron emission tomography.[61]
Differentiation from Crohn's Disease
Intestinal TB and Crohn's disease are granulomatous diseases with similar clinical, radiological, endoscopic, and histologic features.[62] Distinguishing between these conditions can be difficult, and misdiagnoses have been reported.[63] Both TB skin tests and IGRAs are of limited value in helping to establish a diagnosis. Numerous studies have attempted to develop criteria to help distinguish between intestinal TB and Crohn's disease with limited success.[21] While there can be differences in endoscopic and histologic morphology between TB and Crohn's disease lesions, much overlap exists.
A definitive diagnosis is established based on the microbiological results, and multiple biopsies are recommended on that basis. The sensitivity of AFB smears is very low in abdominal TB specimens; thus, a negative stain cannot be relied upon to exclude a diagnosis. The sensitivity of cultures ranges from 7% to 79%. The sensitivity of PCR analysis depends on the gene sequences used in the assay.[30] Using a multiplex assay can increase the sensitivity and identify the presence of resistance genes. When a definitive diagnosis cannot be established, it may be necessary to resort to less-than-optimal options and administer a trial of anti-TB antibiotics. Initiating immune-modulating drugs as an empiric trial is not advised. In countries with high TB endemicity, excluding abdominal TB is recommended before the initiation of therapy for Crohn's disease.[21]
Prognosis
Untreated abdominal TB has a 6% to 20% mortality rate and may lead to complications that require surgical intervention. When identified early, abdominal TB has an excellent response to ATT.[64]
Complications
Multiple complications due to abdominal TB have been reported, including:
- Upper and lower gastrointestinal bleeding
- Fistula occurring at different sites
- Obstruction of the gastrointestinal lumen
- Stricture formation
- Intussusception
- Perforation
- Anemia
- Malnutrition, malabsorption, weight loss [65][66][67][68][69]
Complications can result from adverse reactions to ATT. See StatPearls companion resource, "Tuberculosis Overview," for more information on complications associated with ATT.
Deterrence and Patient Education
Abdominal TB poses a diagnostic challenge as it typically presents with nonspecific clinical and radiologic features. The diagnosis is often delayed due to its vague presentation, resulting in various complications. A high index of clinical suspicion and appropriate use of various investigative modalities can aid in early diagnosis, reducing associated morbidity and mortality. Abdominal TB is rarely seen in industrialized countries and, therefore, is frequently overlooked. Adherence to ATT is a challenge for most patients. Educating patients about the risks of nonadherence to therapy is most important.
Enhancing Healthcare Team Outcomes
Managing abdominal tuberculosis (TB) requires a comprehensive, interprofessional approach to ensure patient-centered care, safety, and optimal outcomes. Clinicians must cultivate the skill of recognizing TB risk factors during routine patient evaluations, especially when presented with nonspecific symptoms like abdominal pain and constitutional illness. A high index of suspicion is critical, given the rarity of abdominal TB in many regions and its ability to mimic other conditions. Early coordination with infectious disease experts is strongly encouraged to guide the diagnostic and therapeutic process. Additionally, because abdominal TB can affect multiple anatomic locations, close collaboration with specialists such as gastroenterologists, clinical microbiologists, and pathologists is essential for accurate diagnosis and effective management.
Pharmacists play a key role in optimizing medication safety, managing drug interactions, and monitoring for resistance to antituberculous drugs, while public health nurses and primary care practitioners are critical for ensuring adherence to treatment regimens through patient education and follow-up. Effective communication across these disciplines enhances team performance and prevents delays in diagnosis or treatment. By fostering a culture of care coordination, the healthcare team can reduce morbidity, improve patient safety, and achieve better long-term outcomes for individuals with abdominal TB.
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