This page includes the following topics and synonyms: Gastrointestinal Tuberculosis, Tuberculous Enteritis. Gastrointestinal tuberculosis (also known as tuberculous enteritis) is caused by infection with the organism Mycobacterium tuberculosis and may be seen with or . The diagnosis of extrapulmonary tuberculosis can be elusive, Tuberculous enteritis can result from swallowing of infected sputum, ingestion.

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In the s, after a steady decline during tubeculosa decades, there was a resurgence in the rate of tuberculosis in the United States that coincided with the acquired immunodeficiency syndrome epidemic. Disease patterns since have changed, with a higher incidence of disseminated and extrapulmonary disease now found.

Extrapulmonary sites of infection commonly include lymph nodes, pleura, and osteoarticular areas, although any organ can be involved.

The diagnosis of extrapulmonary tuberculosis can be elusive, necessitating a high index of suspicion. Physicians should obtain a thorough history focusing on risk behaviors for human immunodeficiency virus HIV infection and tuberculosis.

Antituberculous therapy can minimize morbidity and mortality but may need to be initiated empirically. A negative smear for acid-fast bacillus, a lack of granulomas on histopathology, and failure to culture Mycobacterium tuberculosis do not exclude the diagnosis. Novel diagnostic modalities such as adenosine deaminase levels and polymerase chain reaction can be useful in certain forms of extrapulmonary tuberculosis.

In general, the same regimens are used to treat pulmonary and extrapulmonary tuberculosis, and responses to antituberculous therapy are similar in patients with HIV infection and in those without. Treatment duration may need to be extended for central nervous system and skeletal tuberculosis, depending on drug resistance, and in patients who have a delayed or incomplete response. Adjunctive corticosteroids may be beneficial in patients with tuberculous meningitis, tuberculous pericarditis, or miliary tuberculosis with refractory hypoxemia.

From until there was a resurgence of tuberculosis in the United States that coincided with the epidemic of acquired immunodeficiency syndrome AIDS. All patients with tuberculosis should have counseling and testing for HIV infection. All confirmed cases of active tuberculosis should be reported to the local health department. Dnteritis corticosteroid enteritiss is recommended, based on limited evidence, in patients with tuberculous meningitis or pericarditis, and in miliary tuberculosis with refractory hypoxemia.

Patients should be monitored using directly observed therapy whenever feasible to ensure compliance and prevent emergence of drug resistance. Patients with pulmonary or laryngeal tuberculosis should be placed in respiratory isolation until they are no ehteritis infectious. For information about neteritis SORT evidence rating system, see page or https: Extrapulmonary involvement can be seen in more than 50 percent of patients with concurrent AIDS and tuberculosis.

Response to antituberculous therapy is favorable and similar to that of patients without HIV infection, although adverse drug reactions occur more commonly in those with HIV infection.

It is unclear whether patients with HIV infection have a higher risk of relapse. Infectious disease consultation is advisable given complex drug-drug interactions and the risk of paradoxical response or immune reconstitution. Clinical clues that should prompt suspicion of extrapulmonary tuberculosis are listed in Table 1.

Patients with suspected tuberculosis should have appropriate specimens sent for acid-fast bacillus AFB staining, mycobacterial culture, and histology. Hospitalization is not necessary for tuberculosis to be diagnosed unless clinically indicated.

Hospitalized patients in whom infectious i. The local health department should be notified of all confirmed cases of tuberculosis. Exudative pleural effusion with lymphocyte predominance, negative bacterial cultures, and pleural thickening. Unexplained pericardial effusion, constrictive pericarditis, or pericardial calcification. A six- to nine-month regimen two months of isoniazid [INH], rifampin [Rifadin], pyrazinamide, and ethambutol [Myambutol], followed by four to seven months of isoniazid and rifampin is recommended as initial therapy tuerculosa all forms of extrapulmonary tuberculosis unless the organisms are known or strongly suspected to be resistant to the first-line drugs.


Extended therapy also may be required for patients with bone and joint tuberculosis, delayed treatment response, or drug resistance.

Adjunctive corticosteroids may be useful in patients who have tuberculous meningitis, tuberculous pericarditis, or miliary tuberculosis with refractory hypoxemia.

Directly observed therapy is strongly recommended to encourage medication compliance. Lymphadenitis is the most commonly occurring form of extrapulmonary tuberculosis. Cervical adenopathy is most common, but inguinal, axillary, mesenteric, mediastinal, and intramammary involvement all have been described.

Patients without HIV infection typically present with chronic, nontender lymphadenopathy. If untreated, the nodes become fluctuant and drain spontaneously with sinus tract formation. Computed tomographic scan of the neck reveals a heterogeneous mass in the right posterior cervical space arrow with central necrosis. Most patients have a positive tuberculin skin test result and a normal result on chest radiography.

During antituberculous therapy see Principles of Managementaffected nodes may enlarge or new nodes may appear, representing an immune response to killed mycobacteria. A similar phenomenon in patients with HIV infection who begin concurrent antiretroviral therapy is a result of immune reconstitution.

Lymph node excision usually is not indicated. When lymph nodes are fluctuant and ready to drain, aspiration or incision and drainage appear to be beneficial. In the United States, pleural tuberculosis accounts for about 5 percent of all tuberculosis cases. Pleural tuberculosis often is an acute illness with cough, pleuritic chest pain, fever, or dyspnea. Chest radiography tubercuolsa reveals a small to moderate, unilateral pleural effusion; about tuberculoza percent of patients have associated pulmonary lesions.

Pleural thickening of more than 1 cm is seen in most instances. Computed tomographic scan showing loculated pleural fluid tubegculosa pleural thickening arrow in the right chest with associated right lower lobe atelectasis.

Pleural fluid is exudative with a lymphocyte predominance i. Pleural fluid glucose and pH can be low or normal. AFB smears of pleural fluid are seldom positive 5 percent of cases unless the patient has tubercculosa empyema.

Pleural fluid cultures for M. Biochemical markers such as adenosine deaminase, interferon gamma, and lysozyme in the pleural fluid can be useful. In one study, 20 a high level of adenosine deaminase greater than 47 U per L [ nkat per L] was seen in 99 percent of tuberculous effusions.

In countries with a low prevalence of tuberculosis, such as the United States, a normal or low level of pleural fluid adenosine deaminase has a high negative predictive value and can be used to exclude tuberculous pleurisy. Tuberculous pleurisy responds well to medical therapy, with resorption of pleural fluid in six to 12 weeks. The effusion may resolve without therapy, but tuberculosis later recurs.

Rare complications include bronchopleural fistula, empyema, and fibrothorax. Bone and joint tuberculosis may account for up to 35 percent of cases of extrapulmonary tuberculosis. Skeletal tuberculosis most often involves the spine, followed by tuberculous arthritis in weight-bearing joints and extraspinal tuberculous osteomyelitis.

Infection begins in the anteroinferior aspect of the vertebral body with destruction of entreitis intervertebral disc and adjacent vertebrae Figure 3. The resulting anterior wedging and angulation of adjacent vertebral bodies with disc space obliteration are responsible for the palpable spinal prominence gibbus and a classic radiographic appearance.

Paraspinal and psoas abscesses can develop, with extensions to the surface or adjacent tissues Figure 4. Patients present with local pain, constitutional symptoms, or tuberculoda secondary to cord compression.

Magnetic resonance imaging of the spine revealing osteomyelitis involving T10 and T11 vertebral bodies and disc space A; arrow and an adjacent multiloculated paravertebral abscess B; arrow. Computed tomographic scan of the abdomen showing a left iliopsoas abscess arrow that likely originated from tuberculous osteomyelitis involving the T12, L1, tuberculoea L2 vertebrae. Articular tuberculosis is a slowly progressive mono-arthritis of the hip or knee.


Gastrointestinal tuberculosis | Radiology Reference Article |

Presentation is indolent with pain, joint swelling, and decreased range of motion. Draining sinuses and abscesses are seen in chronic cases. Systemic symptoms usually are absent. Radiographic changes are nonspecific and include soft tissue swelling, juxta-articular osteopenia, joint space narrowing, and subchondral erosions Figure 5.

Radiograph of the right knee showing a large effusion, osteopenia, joint space narrowing, and lucencies in the distal femur. Extraspinal tuberculous osteomyelitis often presents with local pain and can involve any bone. Involvement of adjacent structures may result in complications such as carpal tunnel syndrome, tenosynovitis, and facial palsy. Chest radiography shows pulmonary disease in one half of patients with osteoarticular tuberculosis, but active pulmonary disease is uncommon.

To establish the diagnosis of skeletal or articular tuberculosis, a high index of suspicion is critical. Physicians should consider skeletal tuberculosis in patients with an indolent clinical course manifesting as osteomyelitis involving the thoracic spine or monoarticular septic arthritis with negative bacterial cultures.

Arthrocentesis with mycobacterial cultures of synovial fluid yields positive results in up to 80 percent of patients with tuberculous arthritis. Synovial biopsy also may be diagnostic caseating granulomas on histology or positive mycobacterial culture. Surgery may be necessary to drain abscesses, debride infected tissue, or stabilize the spine and relieve spinal cord compression.

Central nervous system tuberculosis includes tuberculous meningitis the most common presentationintracranial tuberculomas, and spinal tuberculous arachnoiditis. Meningitis results from intense inflammation following rupture of a subependymal tubercle into the subarachnoid space.

Cranial vasculitis may lead to focal neurologic deficits.

Extrapulmonary Tuberculosis: An Overview

Hypersensitivity to tuberculoproteins may cause meningismus and typical cerebrospinal fluid CSF findings. Cerebral edema causes impairment of consciousness, seizures, and raised intracranial tubedculosa, whereas tuberculomas can manifest as space-occupying lesions. An initial phase of malaise, headache, fever, tyberculosa personality change is followed in two to three weeks by protracted headache, meningismus, vomiting, confusion, and focal neurologic findings.

If untreated, mental status deteriorates into stupor or coma. Convulsions can occur at all stages of the illness. A high index of suspicion is necessary for timely diagnosis and prompt initiation of therapy. CSF protein levels range from to mg per dL 1, to 5, mg per L and can be extremely high 2 to 6 g per dL [20 to 60 g per L]with xanthochromia in the presence of subarachnoid block.

CSF glucose concentration usually is ebteritis than 45 mg per dL 2.

AFB smears on CSF are positive in 10 to 90 percent of patients; sensitivity can be improved if large volumes of CSF from multiple lumbar punctures are examined, CSF is centrifuged and AFB smears are performed on the pellicle, or an experienced reviewer examines several high-powered fields.

Empiric antituberculous therapy see Principles of Management should be initiated as emteritis as clinical, laboratory, or imaging findings suggest tuberculous meningitis. Delay in initiation of therapy has been directly associated with adverse outcomes. Antituberculous therapy is recommended for at least nine to 12 months. Abdominal tuberculosis may involve the gastrointestinal tract, peritoneum, mesenteric lymph nodes, or genito-urinary tract. Tuberculous enteritis can result from swallowing of infected sputum, ingestion of contaminated food, hematogenous spread, and direct extension from adjacent organs.

Symptoms include abdominal pain, diarrhea, weight loss, and fever. Melena, rectal bleeding, and abdominal tenderness also can be present.