Tuberculosis chest x ray

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mashal Awais, M.D.[2];Sophia Saad, Associate Editor - WikiDoc [3] Alejandro Lemor, M.D. [4]

Tuberculosis chest x-ray

Overview

The chest radiograph (CXR) is the first-line imaging study in suspected pulmonary tuberculosis and the primary imaging tool for TB screening and triage. It is sensitive but poorly specific in HIV-negative populations, and substantially less sensitive in people with HIV. In screening of HIV-negative adults and adults of unknown HIV status, pooled sensitivity for any CXR abnormality is 94.7% (95% CI 92.2–96.4; very low-certainty evidence) with specificity 89.1% (95% CI 85.6–91.8; low certainty); restricting to abnormalities suggestive of TB yields sensitivity 84.8% (95% CI 76.7–90.4; low certainty) and specificity 95.6% (95% CI 92.6–97.4; high certainty).[1] CXR cannot establish or exclude a diagnosis of TB; bacteriologic confirmation is mandatory. This performance does not transfer to people with HIV. In an individual participant data meta-analysis of 22 studies among ambulatory people living with HIV, chest radiography had lower sensitivity than the WHO four-symptom screen in studies directly comparing both tests, making it unsuitable as a standalone screening test in this population. Among outpatients receiving antiretroviral therapy, the best-performing strategy for maximizing sensitivity was parallel use of the four-symptom screen with any chest radiograph abnormality, which detects more cases than symptom screening alone but at the cost of specificity.[2][3] Inter-reader agreement is a major limitation. A systematic review of 13 studies of CXR scoring systems for adult pulmonary TB found median sensitivity 96% (IQR 93–98) but median specificity 46% (IQR 35–50), with upper lobe infiltrates (pooled diagnostic OR 3.57; 95% CI 2.38–5.37) and cavities (diagnostic OR range 1.97–25.66) significantly associated with TB; none of the included studies reported intra- or inter-reader reproducibility. Scoring systems are useful for ruling out TB in hospital settings but their low specificity precludes ruling it in.[4] Combining radiography with symptom screening in parallel maximizes sensitivity. Adding cough of two or more weeks to either any CXR abnormality or CXR abnormalities suggestive of TB yielded a summary sensitivity of 99.2% (95% CI 96.8–99.8) and specificity of 84.9% (95% CI 81.2–88.1) across 15 studies.[1] Programmatic specificity may be considerably lower than pooled estimates: in a state-wide Indian prevalence survey of 130,932 individuals, abnormal CXR had a sensitivity of 86.4% (95% CI 77.9–92.5) but a specificity of only 42.1% (95% CI 41.3–42.8).[5] Principal clinical functions are triage and screening, triggering airborne isolation and sputum collection, excluding TB disease before treating TB infection, and informing treatment duration through the presence of cavitation.[6][7]

Technique and indications

An erect posteroanterior (PA) radiograph is the initial study. The ACR–SPR–STR practice parameter defines routine chest radiography as PA plus left lateral projections in full inspiration, with a single frontal view appropriate in selected circumstances such as pregnancy; for TB specifically, a lateral view adds little to detection of TB-related findings in adults.[6][8] ATS/CDC/IDSA specify that adults and children aged ≥5 years receive a single PA radiograph, whereas children younger than 5 years should receive both PA and lateral radiographs.[9]

Indications include symptoms suggestive of TB; a positive TST or IGRA prior to treating TB infection; contact investigation; pre-immunosuppression and pre-transplant evaluation; immigration and refugee medical examination; and systematic screening in high-prevalence populations.[10] The yield of chest radiography in asymptomatic high-risk patients ranges from 1% to 7%, and it is not clear how many of these cases would have been suspected on the basis of clinical symptoms alone; radiography may be of low yield in patients with new evidence of exposure who have no clinical symptoms.[6] In contact investigation, ATS/CDC/IDSA direct that a chest radiograph be obtained regardless of tuberculin skin test result in three groups: persons with symptoms of TB, persons who are immunosuppressed or otherwise at risk of progression from infection to disease, and all children younger than 5 years. Contacts with a skin test reaction ≥5 mm and no prior positive result should receive a chest radiograph and medical evaluation for TB disease.[9] Adding radiography to symptom-based contact screening increases yield: among 5,553 household contacts in Chennai, symptom screening followed by Xpert detected 20 cases, whereas symptoms plus CXR followed by Xpert detected 35 — a 75% increase — with CXR alone accounting for 40.5% of screen-positives.[11]

In immunocompromised hosts, particularly those with low CD4 counts, CT should be considered when the radiograph is normal or equivocal.[6] Portable anteroposterior radiography should be reserved for patients who cannot be transported for standard erect imaging. The AP projection magnifies the cardiac silhouette, and poor inspiratory effort crowds basilar bronchovascular markings and widens the mediastinum, which can mimic airspace disease; portable films therefore warrant conservative interpretation and, where TB remains suspected, repeat erect PA imaging or CT.[12]

Radiographic patterns

Primary tuberculosis

The classic triad is lymphadenopathy, parenchymal consolidation, and pleural effusion; it predominates in young children and severely immunocompromised patients.[7][6]

Lymphadenopathy (hilar and paratracheal) is the radiologic hallmark in children, present in 92% of 191 children with primary TB, and is more prevalent in children aged 0–3 years.[13]

Consolidation may involve any lobe, frequently the middle or lower lobes or the anterior segment of an upper lobe. In a classic series, consolidation occurred in 50%, atelectasis in 18%, effusion in 24%, and intrathoracic adenopathy in 35% of primary cases, with a normal radiograph in 15%.[14]

Pleural effusion is typically unilateral.[15] Radiography may also reveal ancillary findings of TB such as pleural effusion or spondylitis, but a tuberculous effusion cannot be distinguished radiographically from other exudative effusions; pleural fluid sampling, with pleural biopsy where indicated, is required.[6]

Post-primary (reactivation) tuberculosis

There is a predilection for the apical and posterior segments of the upper lobes and the superior segment of the lower lobes (91% of cases in the Woodring series), though lesions may occur anywhere. Cavitation is the hallmark, present in approximately 45–50%, typically thick-walled with irregular margins; bronchogenic spread was present in 21%. Additional findings include patchy, ill-defined consolidation; marked fibrotic response (29%); pleural effusion (18%), empyema (4%), pleural fibrosis (41%); upper-lobe mass-like lesions (7%); pneumothorax and intrathoracic adenopathy each rare (~5%).[14][15] Much of the quantitative pattern data above derives from case series predating routine HIV co-infection and digital radiography, and should be interpreted as descriptive rather than as contemporary operating characteristics.

Miliary tuberculosis

Innumerable discrete 1–2 mm nodules of uniform size and distribution throughout both lungs reflect hematogenous dissemination. Miliary disease is more common in immunocompromised patients and is often accompanied by multiorgan involvement. It was seen in 6% of primary cases radiographically.[14][7]

Modifiers of radiographic appearance

HIV and CD4 count

The radiographic distinction between primary and reactivation disease is unreliable; immune status appears to be a stronger determinant of radiographic pattern than the timing of infection, and the preferred descriptive term is simply "active TB."[6][16]

  • CD4 >200 cells/mm³: appearance resembles TB in people without HIV — upper-lobe infiltrates with or without cavitation.[17][3]
  • CD4 <200 cells/mm³: infiltrates show no upper-lobe predilection, cavitation is uncommon, and lower-zone noncavitating nodular opacities or consolidation with hilar/mediastinal adenopathy predominate.[17][3]

A normal chest radiograph occurs in 8–29% of patients with culture-positive pulmonary TB and HIV; thoracic CT may show reticulonodular infiltrates despite a normal radiograph.[3][17]

In a prospective cohort of 268 co-infected patients, CD4 <200 cells/µL was associated with less cavitation (32% vs 68%; P=.008) and less consolidation (47% vs 63%; P=.002), and more miliary pattern (64% vs 36%; P=.04).[18]

Children

In children with presumptive intrathoracic TB, CXR features with >90% specificity for bacteriologically confirmed TB and at least moderate inter-reader agreement were enlargement of perihilar (aOR 6.6; 95% CI 3.80–11.72) and/or paratracheal lymph nodes (aOR 5.14; 95% CI 2.25–12.58), bronchial deviation/compression (aOR 6.22; 95% CI 2.70–15.69), cavities (aOR 7.45; 95% CI 3.38–17.45), and pleural effusion (aOR 2.27; 95% CI 1.04–4.78). Alveolar opacification was not associated with confirmed TB (aOR 1.16; 95% CI 0.76–1.77), reflecting overlap with bacterial pneumonia.[19] At the screening level in children who are close TB contacts, CXR read as "any abnormality" had a sensitivity of 87% and specificity of 99% against a composite reference standard; both estimates are likely overestimated owing to incorporation bias, since the radiograph contributes to the reference standard. Chest radiography (any abnormality) appears to be the most accurate screening test for pulmonary TB in children, but performance is influenced by radiograph quality and inter-reader variability, and CXR has limited accuracy for detecting mediastinal lymphadenopathy compared with CT.[20] WHO limits systematic screening in children to close contacts of persons with pulmonary TB and children living with HIV, and in 2022 conditionally recommended two treatment decision algorithms — one for settings with and one without access to chest radiography.[20][21]

An abnormal radiograph carries prognostic as well as diagnostic weight in exposed children. Among 4,468 TB-exposed children screened by tuberculin skin test, symptom assessment, and chest radiography, asymptomatic children with abnormal radiographs were 25.1-fold more likely to have coprevalent TB (95% CI 1.02–613.76) and 26.7-fold more likely to be diagnosed with incident TB over 1 year of follow-up (95% CI 10.44–68.30) than asymptomatic children with normal films. Among 29 symptom-negative, CXR-abnormal contacts, incident TB occurred in 20% (3/15) of isoniazid preventive therapy recipients versus 57% (8/14) of non-recipients (82% efficacy). Radiographic abnormalities not conventionally regarded as suggestive of TB may indicate incipient or subclinical disease, for which preventive treatment is generally adequate.[22]

Chest radiography in pregnancy

Chest radiography should not be withheld in pregnancy when TB is suspected. The ACR–SPR practice parameter states that verification of pregnancy status is not required before chest radiography, since the beam does not directly expose the gravid uterus except potentially in the third trimester, when dose to the fetus remains very low and the fetus is less radiosensitive than earlier in gestation; performing a frontal view only is cited as an example of dose optimization. The ACR–SPR parameter recommends against protective pelvic shielding when the pelvis is outside the field of view, as shielding may increase internal scatter and thereby fetal dose. Guidance is not uniform: the 2026 HIV opportunistic infections guidelines continue to recommend chest radiography "with abdominal shielding" in pregnant patients with HIV. ACOG notes that fetal anomalies, growth restriction, and pregnancy loss have not been reported below 50 mGy, well above the dose from diagnostic chest radiography.[23][24][17]

The normal or nondiagnostic radiograph

A normal radiograph does not end the evaluation when clinical suspicion persists. Chest CT is appropriate when TB is suspected and radiography is nonrevealing or nondiagnostic.[6] In people with HIV who have symptoms of TB and a normal chest radiograph, sputum AFB smear, nucleic acid amplification testing, and AFB culture should still be performed, as should testing in those without pulmonary symptoms but with evidence of TB elsewhere.[17] In a retrospective analysis from two London trusts, 8% of patients diagnosed with pulmonary TB and 32% of those with intrathoracic lymph node TB had normal chest radiographs in the 6 weeks preceding diagnosis; additional cases were identified by CT and by respiratory sampling, supporting both investigations even when the radiograph is normal.[25]

Subclinical (asymptomatic) tuberculosis

Chest radiography is the principal tool for detecting tuberculosis in people who screen negative for symptoms. Across publicly available prevalence surveys since 1990, between 36.1% and 79.7% (median 50.4%) of prevalent bacteriologically confirmed TB was subclinical, and chest radiography detected 89% (range 73%–98%) of bacteriologically confirmed disease.[26]

The radiographic phenotype of subclinical disease is subtle. In a 16-year Canadian cohort of 1,656 patients with pulmonary TB, 347 (21%) had subclinical disease; these patients were more often smear-negative (88.2% vs 43.5%) with longer time to culture positivity (median 18 vs 12 days), and parenchymal disease was absent or minimal on chest radiography in 86.4%. More advanced radiographic disease was associated with shorter time to culture positivity.[27]

Radiography substantially under-detects key features relative to CT in this group: among 296 subclinical patients, cavitation was 4.77 times (95% CI 1.95–11.66), endobronchial spread 19.36 times (95% CI 8.05–46.52), and moderate or far-advanced parenchymal disease 3.23 times (95% CI 1.66–6.30) more commonly identified on CT than on CXR.[28]

Conversely, a radiograph suggestive of TB carries prognostic weight even when sputum is negative: in a meta-analysis of 24 studies comprising 139,212 participants across 34 pre-chemotherapy-era longitudinal cohorts, individuals with a chest x-ray suggestive of tuberculosis but negative sputum bacteriology progressed to bacteriologically confirmed disease at an approximately 10% annualised rate over the subsequent 3 years.[29]

Active versus inactive disease

A single radiograph cannot distinguish active from inactive disease. Sequelae of prior TB appear as fibronodular opacities in the apical and upper zones; radiographic stability over 6 months is a conventional, though not formally validated, marker of inactivity.[7]

Any patient with radiographic findings in either the "active" or "inactive" category who has symptoms or a positive AFB smear must be managed as potentially having TB disease.[30]

In patients with a positive IGRA/TST, negative cultures, low clinical suspicion for active disease, and an abnormal but unchanged radiograph after 2 months (ATS/CDC class 4), treatment for TB infection is indicated — these patients have case rates 2.5–19 times higher than infected persons with normal radiographs and are high-priority candidates for preventive therapy.[31]

Radiographic findings that influence treatment

Cavitation on the initial chest radiograph is a risk factor for relapse. In patients treated with the standard 6-month regimen, the combination of baseline cavitation and a positive culture at completion of 2 months of therapy is associated with a relapse rate of approximately 20%, versus 2% when neither is present.[31] This framework was derived for and applies to the standard rifampin-based 6-month regimen.

For patients with both features, ATS/CDC/IDSA expert opinion is to extend the continuation phase of isoniazid and rifampin by 3 months (7-month continuation phase; 9 months total).[31]

With only one of the two features, additional considerations favoring prolongation include >10% below ideal body weight, active smoking, diabetes, HIV or other immunosuppression, and extensive disease on chest radiograph.

The 4-month rifapentine–moxifloxacin (HPMZ) regimen, recommended by CDC and conditionally recommended by the 2025 ATS/CDC/ERS/IDSA guideline (conditional recommendation, moderate certainty of evidence) for people aged ≥12 years with drug-susceptible pulmonary TB, was validated in a population in which the majority of participants had cavitation on chest radiography (1,703 of 2,343 microbiologically eligible participants in Study 31/A5349), and the 17-week regimen is not formally extended on the basis of baseline cavitation alone.[32][33][34] A recurrence-risk stratification framework equivalent to that used for standard therapy has not been established for HPMZ. Noncavitary status on the baseline radiograph contributes to eligibility for a 4-month regimen in smear-negative, culture-negative disease, but cavitation is not itself an exclusion criterion for HPMZ. Non-radiographic eligibility criteria (age, weight, CD4 count, QT interval, drug interactions, and resistance) are addressed in the medical therapy microchapter.[33]

ATS/CDC/IDSA recommend against once-weekly continuation-phase therapy with isoniazid 900 mg plus rifapentine 600 mg (strong recommendation; high certainty in the evidence). In uncommon situations where more-than-once-weekly directly observed therapy is difficult to achieve, it may be considered only in HIV-uninfected persons without cavitation on chest radiography. In TBTC Study 22, cavitation on chest radiograph was independently associated with failure or relapse.[31] Suboptimal rifapentine penetration into the cavity wall has been proposed as a contributing mechanism.[35]

Upper-lobe or superior-segment fibrocavitary disease, or lobar pneumonia with hilar/mediastinal adenopathy, in an appropriate clinical setting is sufficient to warrant respiratory isolation pending sputum results.[6][36] The chest radiograph informs initiation of airborne isolation but is not a criterion for its discontinuation; see primary prevention for infection-control details.[37]

Follow-up radiography during treatment

In culture-positive pulmonary TB, a repeat radiograph at 2 months may be useful but is not essential; response is monitored bacteriologically.[31]

In culture-negative patients treated presumptively, a chest radiograph is recommended at 2–3 months and at completion of therapy to document response, since radiographic improvement supports the presumptive diagnosis (expert opinion).[31]

An end-of-treatment radiograph is often obtained as a baseline for future comparison, but is not essential. Routine systematic radiographic follow-up after treatment completion is generally not necessary.[31]

Post-tuberculosis radiographic sequelae

Residual radiographic abnormality after treatment completion is common and should not by itself prompt re-treatment. On chest radiography after treatment, reported prevalences are cavitation 8.3%–83.7%, bronchiectasis 4.3%–11.2%, and fibrosis 25.0%–70.4%, with wide between-study variability; CT identifies a broader range of residual abnormality, including nodules (25.0%–55.8%) and emphysema (15.0%–45.0%), and detects bronchiectasis far more often than CXR (35%–86% vs 4.3%–11.2%).[38] Approximately half of those treated for pulmonary TB have abnormal spirometry at or after treatment completion, and roughly a quarter are symptomatic; most individuals show some recovery in imaging and lung function over the year after treatment, so an abnormal end-of-treatment film should be interpreted against this expected trajectory rather than as evidence of failure.[39]

Computer-aided detection (CAD)

WHO screening guidelines recommend CAD software for CXR interpretation in TB screening in individuals aged ≥15 years as a conditional recommendation based on low-certainty evidence, with performance similar to human readers but variable across contexts. CAD has not been validated for TB diagnosis in children, and its accuracy for identifying non-TB abnormalities remains to be established.[40] This sits within a broader framework recommending untargeted screening where background prevalence exceeds 500 per 100,000 and targeted screening of at-risk groups where prevalence exceeds 100 per 100,000.[41]

In an individual patient data meta-analysis of 3727 participants, at a pooled sensitivity fixed at 90%, pooled specificities were CAD4TB v6 56.9%, Lunit 54.1%, and qXR v2 60.5%. Sensitivity was lower in people with HIV (CAD4TB −13.4%; qXR −13.4%) and in smear-negative TB (−12.3% to −17.2%). Threshold scores must be locally derived and stratified by HIV and smear status; a single global threshold is not appropriate.[42]

Against a composite microbiological reference standard using 774 radiographs from the South African National TB Prevalence Survey, radiologist sensitivity ranged from 67.1% (95% CI 61.0–72.8; India) to 78.7% (95% CI 73.2–83.5; United Kingdom) and specificity from 75.8% (Nigeria) to 84.3% (United States). The best-performing CAD software outperformed all radiologist groups except Indian radiologists at matched specificity. Radiologist accuracy was significantly affected by patient HIV status, prior TB, and age, whereas reader experience, TB reading volume, and country of practice were not.[43]

In a prospective 5-country cohort of 1392 adults with cough ≥2 weeks (22% with confirmed TB), CAD4TB v7 achieved the highest specificity at 90% sensitivity (70.3%), outperforming Xpert Host Response (65.1%) and CRP (49.7%); two-test algorithms further increased accuracy.[44]

Whether sequencing CAD with a second screening test improves yield appears to depend on the screening population. In symptomatic adults presenting to primary care, two-test algorithms increased specificity at fixed sensitivity; in community-based screening of a largely asymptomatic population, CAD alone performed better. In a paired screen-positive community trial of 20,023 adults in Lesotho and South Africa, CAD4TBv7 alone identified 69 of 73 tuberculosis cases versus 60 of 73 for CAD4TBv7 followed by CRP (difference −12.3%; 95% CI −23.0 to −1.6), failing the −10% non-inferiority margin.[45]

In household contacts of rifampicin-resistant TB, >30% of participants scoring above recommended CAD thresholds with negative routine sputum were subsequently diagnosed with TB by enhanced sputum investigation or during follow-up, indicating that a "false positive" CAD result may represent early true disease.[46]

CDC classification for immigration and refugee medical examination

The CDC chest radiograph classification sorts findings by their probability of representing TB and drives sputum testing requirements. Any finding in the "suggestive of active TB" category mandates sputum examination.[30]

CDC chest radiograph findings suggestive of active TB (sputum examination required)
Finding Description
Infiltrate or consolidation Parenchymal opacity, dense or patchy, with irregular, ill-defined, or hazy borders
Any cavitary lesion Parenchymal lucency, thick- or thin-walled, with or without surrounding consolidation, nodular or fibrotic density, or calcification
Nodule with poorly defined margins Rounded parenchymal density with indistinct margins, indicating coexisting airspace consolidation
Pleural effusion Substantial pleural fluid; to be distinguished from costophrenic angle blunting (except in children, in whom even minor blunting is considered suggestive of active TB)
Hilar or mediastinal lymphadenopathy Nodal enlargement in one or both hila or the mediastinum, with or without consolidation or atelectasis
Linear, interstitial disease (children only) Prominence of linear/septal interstitial markings
Other Any other finding indicating active TB, including a miliary pattern (1–2 mm nodules)
CDC chest radiograph findings suggestive of inactive TB
Finding Description
Discrete fibrotic scar or linear opacity Reticular densities with distinct edges without intervening airspace haziness; termed fibrocalcific if calcified
Discrete noncalcified nodule(s) One or more rounded densities with distinct borders and no surrounding airspace opacification
Fibrotic scar with volume loss or retraction Linear densities with upper lobe volume loss, usually with ipsilateral hilar elevation and thoracic asymmetry
Nodule(s) with volume loss or retraction Discrete nodular densities with upper lobe volume loss
Other Other evidence of prior TB, e.g., upper lobe bronchiectasis

Findings not requiring TB follow-up include pleural thickening and apical capping, diaphragmatic tenting, costophrenic angle blunting in adults, and solitary calcified nodules, granulomas, or calcified lymph nodes. The former Class B3 designation was removed from the classification scheme because such calcified lesions have not been associated with active TB.[30] Non-TB findings requiring follow-up after resettlement are classified separately for post-arrival evaluation.

Radiographic sequelae and complications of tuberculosis

Thoracic sequelae and complications on chest radiography
Complication Radiographic findings
Cicatrization / fibrotic sequelae Upper lobe volume loss and atelectasis, compensatory lower lobe hyperinflation, hilar retraction, mediastinal shift, parenchymal bands, fibrotic cavities and nodules, traction bronchiectasis
Residual thin-walled cavity May occur in active or inactive disease; may regress with therapy; residual air-filled cysts may persist and be mistaken for an emphysematous bulla or pneumatocele
Aspergilloma Intracavitary mass with a surrounding crescent of air; mobile with positional change; may calcify
Broncholithiasis Calcified material within the airway lumen originating from a calcified node, with obstruction, atelectasis, expiratory air trapping, mucoid impaction, and interval change in position of the calcification (CXR findings are nonspecific; CT is confirmatory)
Fibrosing mediastinitis Mediastinal widening, hilar or mediastinal mass, calcification, pulmonary infiltrates, atelectasis (CXR findings are nonspecific; CT is confirmatory)

Adapted from imaging reviews.[7]

Spinal involvement (Pott disease) is better characterized on MRI; see the dedicated imaging microchapters.

Differential diagnosis on chest radiography

Radiographic findings overlap substantially with nontuberculous pulmonary infection, which is the principal reason for the low specificity of CXR. Nontuberculous mycobacterial disease can closely mimic active TB, and laboratory confirmation is required to distinguish them. Other mimics include bacterial pneumonia and lung abscess, endemic fungal infection, chronic pulmonary aspergillosis, sarcoidosis, granulomatosis with polyangiitis, and lung cancer.[6][7]

Clinical recommendations

  1. Obtain an erect PA chest radiograph as the initial imaging study in any patient with suspected pulmonary TB. Adults and children ≥5 years receive a single PA film; children younger than 5 years should receive both PA and lateral radiographs.[6][9]
  2. Never diagnose or exclude TB on radiography alone. Any suggestive finding mandates sputum collection for smear, molecular testing, and culture.[6][30]
  3. Initiate airborne isolation on the basis of a compatible radiograph plus clinical suspicion, without waiting for microbiology.[6][36]
  4. Do not rely on a normal radiograph to exclude TB in advanced HIV (CD4 <200) or other severe immunosuppression; proceed to sputum testing and consider CT.[3][17]
  5. When the radiograph is normal or nondiagnostic and suspicion persists, proceed to sputum testing regardless and consider chest CT.[6][25][17]
  6. Obtain a chest radiograph in every person with a positive TST/IGRA before treating TB infection; screening tests alone cannot differentiate TB infection from TB disease, and imaging with selective sputum sampling is the step used to exclude disease before offering preventive treatment.[10][47]
  7. Document the presence or absence of cavitation on the baseline radiograph; it influences continuation-phase decisions for the standard 6-month regimen and eligibility considerations for once-weekly rifapentine or shortened regimens.[31][33]
  8. In culture-negative presumptively treated patients, obtain follow-up radiographs at 2–3 months and at treatment completion; in culture-positive patients, follow response bacteriologically.[31]
  9. Where CAD is deployed, derive operating thresholds locally and stratify by HIV and smear status; use CAD as a triage test followed by confirmatory molecular testing (not validated in children).[42][40]

References

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