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Summary Table

Category	High-Yield Detail
Risk Factors	HIV (18x risk), diabetes mellitus, smoking (2-4x risk), malnutrition (BMI <18.5), chronic kidney disease, immunosuppressive therapy, household/close contact with active TB case, incarceration, healthcare workers, elderly (age ≥60), alcohol use disorder
Etiology	Mycobacterium tuberculosis complex (obligate aerobe, acid-fast bacillus); transmitted via respiratory droplets; thrives in the oxygen-rich apical segments of the upper lobes
Patient Presentation	Chronic cough ≥2 weeks OR any cough with constitutional symptoms: unintentional weight loss, intermittent low-grade fever, night sweats. In HIV-positive individuals, any single symptom (cough, fever, weight loss, night sweats) qualifies as a TB suspect
Classic Physical Exam	Often unremarkable early on; may reveal cachexia, post-tussive crackles over the upper lobes, dullness to percussion with effusion, or cervical lymphadenopathy (extrapulmonary). In advanced disease: amphoric breath sounds over cavities
Key Diagnostic Results	Rapid molecular test (Xpert MTB/RIF Ultra) positive for M. tuberculosis with rifampicin sensitivity. Sputum AFB smear for monitoring. CXR: upper-lobe infiltrates, cavitation, miliary pattern, unilateral pleural effusion. Culture on LJ/MGIT is the gold standard
Management	Standard regimen: 2HRZE/4HR (6 months total). Intensive phase: isoniazid + rifampicin + pyrazinamide + ethambutol daily for 2 months. Continuation phase: isoniazid + rifampicin daily for 4 months. Vitamin B6 supplementation throughout
Keywords	"Night sweats," "weight loss," "chronic cough," "apical infiltrate," "cavitary lesion," "acid-fast bacilli," "Ghon focus," "caseating granuloma," "hemoptysis," "immigrant from endemic area"

1. Pathophysiology

Tuberculosis begins when a susceptible host inhales aerosolized droplet nuclei containing Mycobacterium tuberculosis. These particles, measuring 1 to 5 micrometers, are small enough to bypass the mucociliary apparatus and reach the terminal alveoli, where they are engulfed by alveolar macrophages. However, M. tuberculosis has evolved a critical survival mechanism: its mycolic acid-rich cell wall resists phagolysosome fusion, allowing the organism to replicate intracellularly within the macrophage. This is the reason why TB cannot be easily cleared by the innate immune system alone.

Over 2 to 8 weeks, the host mounts a cell-mediated (Type IV) immune response driven by CD4+ T-helper cells and macrophages. Activated macrophages surround the infected cells and form a granuloma, the histopathological hallmark of TB. The center of this granuloma undergoes caseating necrosis (cheese-like, pale yellow material), a finding that distinguishes TB granulomas from those of sarcoidosis (non-caseating). Within this granuloma, multi-nucleated Langhans giant cells and epithelioid cells are characteristic findings on histopathology.

In immunocompetent hosts, this immune containment results in latent TB infection (LTBI), where the bacilli remain dormant. Approximately 5 to 10% of individuals with LTBI will progress to active disease in their lifetime, and the majority of those who do will reactivate within the first 2 years. This probability jumps dramatically in immunocompromised patients: HIV-positive individuals have an annual risk of 5 to 15% of reactivation, compared to 5 to 10% over a lifetime in healthy individuals.

Reactivation TB preferentially occurs in the apical and posterior segments of the upper lobes and the superior segments of the lower lobes. The reason is aerobic: these zones have the highest ventilation-to-perfusion ratio, providing the oxygen-rich environment that M. tuberculosis requires. This anatomic predilection is why classic CXR findings localize to the upper lung zones, and why lower-lobe TB should prompt you to consider HIV or other immunosuppression on an exam vignette.

When the immune system fails to contain the infection, cavitation occurs. The liquefied caseous center drains into an airway, creating a cavity. This cavity provides an aerobic, nutrient-rich niche where bacilli multiply to enormous numbers (up to $10^{7}$ to $10^{9}$), making the patient highly infectious. This is also why large cavities are associated with slower sputum conversion and higher risk of treatment failure.

In the context of TB-HIV coinfection, the depleted CD4 count impairs granuloma formation. Consequently, HIV-positive patients present atypically: lower-lobe disease, miliary patterns, extrapulmonary TB, adenopathy without cavitation, and sometimes a normal CXR altogether. The lower the CD4 count, the more atypical the presentation. This is a frequently tested concept.

2. Classification and Clinical Manifestation

Axis	Subtypes	Key Details
Anatomical location	TB Paru (Pulmonary)	Non-severe: single lobe, no cavity, paucibacillary
		Extensive/severe: bilateral disease, cavitation, widespread parenchymal destruction
	TB Ekstra Paru (Extrapulmonary)	Lymph node, pleural, meningeal, pericardial, osteoarticular, peritoneal, genitourinary, miliary
Treatment history	New case	Never treated or <1 month of prior OAT
	Relapse	New episode after prior "cured" or "treatment completed"
	Previously treated	Prior treatment with outcome of "failed" or "defaulted"
Bacteriological status	Bacteriologically confirmed	Positive on rapid molecular test, culture, or microscopy; HIV+ patients with positive LF-LAM also qualify
Bacteriological status	Clinically diagnosed	Negative bacteriology but diagnosed by physician based on clinical/radiological grounds and decision to treat
Drug susceptibility	Drug-Sensitive (DS-TB)	Sensitive to both rifampicin and isoniazid
	Isoniazid-Resistant (Hr-TB)	Resistant to isoniazid, sensitive to rifampicin
	Rifampicin-Resistant (RR-TB)	Resistant to rifampicin (may or may not be isoniazid-resistant)
	MDR-TB	Resistant to at least both rifampicin and isoniazid
	Pre-XDR-TB	MDR/RR + resistance to at least one fluoroquinolone
	XDR-TB	Pre-XDR + resistance to at least one Group A agent (bedaquiline or linezolid)
HIV status	HIV-positive, HIV-negative, Unknown	All TB patients must be tested for HIV

Extrapulmonary TB by severity:

Severity	Forms
Non-severe extrapulmonary	TB lymphadenitis (peripheral or mediastinal without compression)
Severe extrapulmonary	TB meningitis, miliary TB, osteoarticular TB, pericardial TB

3. Diagnostic Workup

Test	Role	Turnaround	Key Details
Xpert MTB/RIF Ultra (LC-aNAAT)	Best initial test for diagnosis AND rifampicin resistance detection	Same day (2 hours)	Sensitivity 90.4%, specificity 94.9% on sputum (adults). Simultaneously detects Mtb + rifampicin resistance. Do NOT use for treatment monitoring
Sputum AFB Smear (Microscopy)	Monitoring tool during treatment	Same day	Used at end of month 2, 1 month before end of treatment (1-AP), and at end of treatment (AP). Low sensitivity for initial diagnosis; cannot distinguish Mtb from NTM
Culture (LJ/MGIT)	Gold standard / most accurate test	2 to 8 weeks	LJ (solid) or MGIT (liquid). Requires 10-100 viable bacilli/mL. Used for confirmation, DST, and discordant results
Drug Susceptibility Testing (DST)	Phenotypic confirmation	Weeks (after culture growth)	Determines resistance to individual drugs. Done at reference labs with BSL 2+ capacity
Chest X-ray	Supportive / screening	Same day	High sensitivity for screening; low specificity. Cannot confirm active vs. inactive TB alone. CAD-read CXR is for screening only, not diagnosis
LF-LAM (Urine)	Point-of-care for HIV+ patients	15 to 25 min	Only recommended for ODHIV (people living with HIV). A positive result counts as bacteriological confirmation
Histopathology	Supportive (extrapulmonary)	Days	Caseating granuloma with Langhans giant cells. Used when microbiological specimens are difficult to obtain
TST / IGRA / TBST	Detects latent TB infection	48-72h (TST) / Same day (IGRA)	Cannot distinguish latent from active disease. Used for LTBI screening, not for diagnosing active TB

Step 1: Identify the suspect. Any adult presenting with cough lasting ≥2 weeks, or any cough accompanied by weight loss, intermittent fever, or night sweats, should be classified as a TB suspect. For HIV-positive individuals, any single symptom (cough, fever, weight loss, or night sweats) is sufficient.

Step 2: Obtain sputum specimens. Collect two sputum samples (Spot-Spot, Spot-Morning, or Morning-Spot). The second spot specimen must be taken at least one hour after the first. Quality standard: volume 1-4 mL, mucopurulent.

Step 3: Rapid Molecular Testing (Best Initial Test). The preferred initial diagnostic test is the Xpert MTB/RIF Ultra, a nucleic acid amplification test (NAAT) that simultaneously detects M. tuberculosis DNA and rifampicin resistance mutations in the rpoB gene within approximately 2 hours. Only one quality specimen is needed for this test. If Xpert is unavailable, alternative molecular tests include Truenat MTB-RIF Dx or BD MAX MDR-TB.

Step 4: Interpret results.

If the test detects Mtb and rifampicin is sensitive, initiate DS-TB treatment. For patients with a history of prior TB treatment, order additional isoniazid resistance testing (e.g., Xpert MTB/XDR).

If the test detects Mtb and rifampicin is resistant, close the DS-TB case and transfer to the DR-TB treatment pathway.

If Mtb is not detected, consider CXR and/or a trial of broad-spectrum antibiotics. The clinician may diagnose TB clinically if the clinical picture is strongly suggestive.

Step 5: Radiographic findings (supportive, not confirmatory).

Findings supporting active TB: upper-lobe infiltrates or nodules (apical-posterior segments), cavitation, miliary pattern, unilateral pleural effusion. Findings more consistent with inactive TB: fibrosis, calcification, pleural thickening. Note that CAD-interpreted CXR may be used for screening but cannot serve as a basis for diagnosis.

Critical distinction: A previously "cured" patient who relapses within <6 months of treatment completion must NOT be tested initially with molecular tests (residual DNA may cause false positives). Instead, sputum AFB smear is done first. Only if the smear is positive should molecular testing with resistance detection follow.

Step 6: Culture (Gold Standard). Culture on Lowenstein-Jensen (solid) or MGIT (liquid) media is the most accurate test. It is reserved for confirmation, drug susceptibility testing, and discordant results. This test is not routinely ordered for every patient in primary care settings due to turnaround time and infrastructure requirements.

4. Management and Treatment

Component	Regimen	Duration	Key Notes
Standard regimen (6-month)	2HRZE / 4HR	Intensive: 2 months, Continuation: 4 months	All doses given daily. Fixed-dose combination (FDC) preferred. 1 week = 7 days, 1 month = 28 days
Short regimen (4-month)	2HPMZ / 2HPM	Intensive: 2 months, Continuation: 2 months	Age ≥12, weight >40 kg, pulmonary TB only. Not for pregnancy, breastfeeding, severe extrapulmonary TB
Severe extrapulmonary TB	Same initial regimen	Extended to 9-12 months	TB meningitis, osteoarticular TB, spinal TB, CNS TB
Vitamin B6 supplement	25 mg/day	Throughout treatment	Prevents isoniazid-induced peripheral neuropathy. Increase to 50-100 mg/day if neuropathy develops

Dosing by Body Weight

Drug	Dose per kg	<30 kg	30-34 kg	35-49 kg	50-64 kg	65-79 kg
FDC-HRZE (intensive)	Per table	2 tab	3 tab	4 tab	4 tab	5 tab
FDC-HR (continuation)	Per table	2 tab	3 tab	4 tab	4 tab	5 tab
Isoniazid (H)	4-6 mg/kg	150 mg	300 mg	300 mg	300 mg	375 mg
Rifampicin (R)	8-12 mg/kg	300 mg	450 mg	600 mg	600 mg	750 mg
Pyrazinamide (Z)	20-30 mg/kg	800 mg	1200 mg	1600 mg	1600 mg	2000 mg
Ethambutol (E)	15-25 mg/kg	600 mg	800 mg	1200 mg	1200 mg	1600 mg

Before starting treatment: Confirm HIV status (mandatory for all TB patients). Screen for diabetes, hepatitis, renal function, and nutritional status. Measure weight and height. Identify household contacts. Assign a treatment supporter (PMO).

Intensive phase (months 1-2): Give HRZE daily. OAT should be taken on an empty stomach (1 hour before or 2 hours after meals) for optimal rifampicin absorption. After 2 weeks of regular therapy, infectiousness drops substantially. Sputum AFB smear is checked at the end of month 2. If the month-2 smear is still positive (non-conversion), evaluate for poor adherence, incorrect dosing, comorbidities, or drug resistance. Order molecular testing for rifampicin resistance at this point, not earlier.

If month-2 smear is still positive: Do NOT extend the intensive phase (no more "extension/sisipan"). Continue the regimen and recheck BTA monthly. If BTA remains positive, the patient can be declared treatment failure at the earliest at the end of month 5 (1-AP).

Continuation phase (months 3-6): Give HR daily. Sputum AFB is checked at 1 month before end of treatment (1-AP) and at end of treatment (AP).

Treatment outcome determination: "Cured" requires documented negative BTA at end of treatment. "Treatment completed" is assigned when the full course is finished but BTA results are missing. "Failed" is declared if BTA is positive at month 5 or later. If a BTA turns positive after a prior negative result (reversal), repeat BTA within 7 days before declaring failure.

Molecular testing must NOT be used for treatment monitoring. Only sputum AFB microscopy is permitted for follow-up.

TB-HIV Coinfection Management

Principle	Detail
Treatment sequence	Start OAT first, then ARV within 2 weeks (regardless of CD4 count), then cotrimoxazole prophylaxis (PPK)
Exception: TB meningitis	Delay ARV initiation by approximately 2 weeks after OAT to reduce IRIS risk
Duration	Same as non-HIV: 6 months (2HRZE/4HR)
Preferred ARV	TLD (tenofovir + lamivudine + dolutegravir) or TLE (tenofovir + lamivudine + efavirenz)
TLD with rifampicin	Add an extra DTG 50 mg tablet taken 12 hours after the main TLD dose (because rifampicin lowers dolutegravir levels). After OAT completion, return to once-daily TLD
TLE with rifampicin	No dose adjustment needed
Contraindicated ARV	Nevirapine-containing regimens must NOT be used concurrently with rifampicin
Cotrimoxazole prophylaxis	Given to all TB-HIV patients to prevent opportunistic infections, once daily, throughout and beyond TB treatment
Screening	LF-LAM urine test can be used for TB diagnosis in ODHIV at facilities with access to the test

TB with Diabetes Mellitus

Standard 6-month regimen is used. DM increases risk of treatment failure, relapse, and death. Rifampicin induces CYP enzymes that reduce the effectiveness of sulfonylureas, so tighter glucose monitoring or a switch to insulin is recommended. Supplement vitamin B6 at 20 mg/day (isoniazid worsens diabetic neuropathy). Ethambutol requires cautious use due to additive risk of optic neuropathy.

TB with Chronic Kidney Disease

The standard regimen 2HRZE/4HR is used, but dose adjustments are needed for severe CKD (CC <30 mL/min):

$$CC\ (mL/min) = \frac{Weight\ (kg) \times (140 - Age)}{72 \times Serum\ Creatinine\ (mg/dL)}$$

For females, multiply by 0.85. Isoniazid and rifampicin need no adjustment (biliary excretion). Pyrazinamide and ethambutol require dose spacing: 25-35 mg/kg and 15-25 mg/kg respectively, given 3 times per week after dialysis.

TB in Pregnancy

Standard 6-month regimen (2HRZE/4HR) is safe. Add vitamin B6 throughout. Check baseline liver function. The 4-month regimen (HPMZ) is contraindicated in pregnancy and breastfeeding. Chest X-ray can be performed with abdominal shielding. Breastfeeding should continue; no need to separate mother and infant after 2 weeks of treatment. If TB active is excluded in the infant, give TPT with 6H followed by BCG vaccination.

5. Drug-Induced Liver Injury (DILI) and Side Effect Monitoring

Side Effects

Drug	Side Effect	Clinical Features	Management
Isoniazid (H)	Peripheral neuropathy	Numbness, tingling, pain in hands/feet	Continue OAT; give vitamin B6 50-100 mg/day. Refer to neurology if grade 3-4
Isoniazid, Pyrazinamide, Rifampicin	Hepatotoxicity (DILI)	Abdominal pain, nausea/vomiting, jaundice, dark urine, pale stool, fatigue	Stop ALL OAT if SGOT/SGPT >3x ULN with symptoms OR >5x ULN with or without symptoms OR total bilirubin ≥2 mg/dL. Hospitalize as needed. Monitor LFTs every 3-5 days
Ethambutol (E)	Optic neuritis	Blurred vision, impaired color vision	Stop ethambutol permanently. Refer to ophthalmology
Pyrazinamide (Z)	Hyperuricemia / Gout	Elevated uric acid, joint pain	Give analgesics/NSAIDs. If severe and persistent, stop pyrazinamide
Pyrazinamide (Z)	GI upset	Nausea, vomiting, anorexia	Symptomatic (antiemetics, take with food). If severe, stop pyrazinamide
Rifampicin (R)	Thrombocytopenia (purpura)	Low platelets, gum bleeding, petechiae	Stop rifampicin immediately and permanently. Do NOT rechallenge
Rifampicin (R)	Orange discoloration	Urine, sweat, tears turn orange	Benign. Educate patient
All OAT	Hypersensitivity (rash)	Urticaria, maculopapular rash, blistering	Mild: antihistamine, continue. Moderate: topical/oral steroids. Severe (SJS/TEN/anaphylaxis): stop ALL OAT immediately, emergency management

DILI Management Protocol

The three hepatotoxic first-line drugs in order of greatest risk are pyrazinamide > isoniazid > rifampicin. Ethambutol is not hepatotoxic and is considered safe.

When to stop OAT:

SGOT/SGPT >5x upper limit of normal (with or without symptoms): stop all OAT, hospitalize.

SGOT/SGPT >3x ULN with symptoms (nausea, vomiting, jaundice): stop all OAT, hospitalize.

SGOT/SGPT >3-5x ULN without symptoms: stop OAT, outpatient monitoring with SGOT/SGPT every 3-5 days.

Total bilirubin ≥2 mg/dL: stop all OAT, hospitalize.

Rechallenge protocol (done at referral hospital only):

Begin rechallenge only when ALT falls to ≤2x ULN, bilirubin normalizes, and symptoms resolve. Reintroduce drugs one at a time, every 2-3 days, starting with the least suspected drug and ending with the most suspected. The recommended order is: ethambutol first, then rifampicin, then isoniazid, then pyrazinamide (because PZA is most hepatotoxic). Check LFTs before each new drug addition. If hepatotoxicity recurs, the last drug added is identified as the culprit and permanently discontinued. Full rechallenge should be completed within a maximum of 21 days.

If pyrazinamide cannot be reintroduced: Extend the continuation phase by 3 months (total treatment: 9 months).

If recurrent hepatotoxicity occurs despite rechallenge: Switch to a non-hepatotoxic regimen using ethambutol, levofloxacin, and/or streptomycin. Plan for a minimum total treatment duration of 9 months with regular liver function monitoring.

Rechallenge is absolutely contraindicated in SJS, TEN, and anaphylaxis. In these cases, desensitization may be considered under strict inpatient monitoring only for essential drugs like rifampicin, and only when alternative regimens cannot meet the minimum of 2 bactericidal agents.

TB with Pre-existing Liver Disease

Managed by Child-Turcotte-Pugh (CTP) score:

CTP Score	Allowed OAT	Notes
CTP ≤7 (mild-moderate)	Rifampicin, Isoniazid, Ethambutol	Avoid pyrazinamide. Extend treatment to 8-9 months total
CTP 8-10 (moderate-severe)	Limit to ONE hepatotoxic drug (rifampicin preferred over isoniazid)	Close monitoring required
CTP ≥11 (severe)	Avoid ALL hepatotoxic drugs	Use ethambutol + fluoroquinolone-based regimen

Monitoring Schedule

Timepoint	Assessment
Baseline (month 0)	Weight, height, BMI, HIV test, blood glucose, liver function (SGOT/SGPT), renal function (creatinine), visual acuity (baseline for ethambutol), CXR
Every 2 weeks (intensive phase)	Clinical visit, weight, adherence assessment, side effect screening
End of month 2	Sputum AFB smear. If positive: evaluate for resistance and adherence
Monthly (continuation phase)	Clinical visit, weight, adherence, side effect screening
1 month before end of treatment (1-AP)	Sputum AFB smear
End of treatment (AP)	Sputum AFB smear. Determine final treatment outcome
As indicated	SGOT/SGPT (weekly in hepatotoxicity), blood glucose (DM), creatinine (CKD), visual acuity

TB Preventive Therapy (TPT) Overview

Regimen	Drugs	Duration	Frequency	Eligible Populations
6H	Isoniazid	6 months	Daily	All ages, including pregnant women. Safest and most established
3HP	Isoniazid + Rifapentine	3 months	Weekly	Age ≥2. Contraindicated in pregnancy. Note interaction with hormonal contraceptives
3HR	Isoniazid + Rifampicin	3 months	Daily	All ages. Alternative when 3HP is unavailable
4R	Rifampicin	4 months	Daily	All ages. Used when isoniazid is not tolerated
1HP	Isoniazid + Rifapentine	1 month	Daily	Age ≥13. Shortest regimen. Newer; requires good patient education

Priority recipients: household contacts of index cases, people living with HIV, immunocompromised individuals. All TPT recipients must have active TB excluded first. Vitamin B6 10-25 mg/day is mandatory with any isoniazid-containing TPT regimen.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Community-Acquired Pneumonia	Cough, fever, infiltrates on CXR	Acute onset (days, not weeks). Responds to standard antibiotics within 48-72 hours. TB has chronic, insidious onset with weight loss and night sweats
Lung Cancer	Chronic cough, weight loss, upper-lobe mass, hemoptysis	TB shows cavitation with air-fluid levels; cancer shows a spiculated, solid mass without air bronchograms. Biopsy shows malignant cells, not granulomas
Sarcoidosis	Bilateral hilar lymphadenopathy, granulomas on biopsy	Non-caseating granulomas (no central necrosis). Elevated ACE, hypercalcemia. Young Black women. AFB smear and culture are negative
Lung Abscess	Cavitary lesion with air-fluid level, fever, cough	Usually polymicrobial, foul-smelling sputum, dependent segments (aspiration history). TB cavities are typically upper-lobe and thin-walled
Non-Tuberculous Mycobacteria (NTM/MOTT)	AFB smear positive, similar CXR findings	Differentiated by molecular testing (Xpert detects M. tuberculosis complex only). NTM commonly affects patients with structural lung disease (bronchiectasis)
Fungal Infection (Histoplasmosis, Aspergilloma)	Upper-lobe cavitary lesion, granulomas	Travel/exposure history (Ohio/Mississippi River Valley for histoplasma). Aspergilloma shows a "fungus ball" (crescent sign) within a pre-existing cavity
Pneumocystis Pneumonia (PCP)	HIV+ patient with respiratory symptoms, bilateral infiltrates	PCP shows bilateral, diffuse, ground-glass opacities (not upper-lobe). LDH elevated. Diagnosed by silver stain of induced sputum or BAL
Silicosis	Upper-lobe fibrosis, "eggshell" calcification of hilar nodes	Occupational history (mining, sandblasting). Silicosis itself increases TB risk, so both may coexist

6. Traps and High-Yield Pearls

The single most common trap on TB questions is confusing the screening/initial test with the monitoring test and the confirmatory test. Students must remember that Xpert MTB/RIF Ultra is the best initial diagnostic test but must NEVER be used for treatment monitoring (residual DNA causes false positives). Sputum AFB microscopy is the monitoring test, done at months 2, 5 (1-AP), and 6 (AP). Culture remains the gold standard for confirmation and resistance profiling.

A second frequent error involves TB-HIV. When the vignette describes an HIV-positive patient with lower-lobe infiltrates, no cavitation, and lymphadenopathy, students often dismiss TB in favor of pneumonia or lymphoma. The lesson: in advanced HIV, TB does not look like "classic TB." Any single symptom (even just a fever) in an ODHIV qualifies that person as a TB suspect, and LF-LAM urine testing is a valid point-of-care diagnostic tool in this group.

The hepatotoxicity rechallenge sequence is another testing target. Remember to reintroduce drugs from least to most hepatotoxic: E first, then R, then H, then Z. If a student starts the rechallenge with isoniazid or pyrazinamide (the most hepatotoxic agents), that is the wrong answer. Also, if rifampicin causes thrombocytopenic purpura, it is permanently discontinued and never rechallenged.

For TB in pregnancy, the trap is stopping ethambutol out of unwarranted fear. All four first-line drugs (HRZE) are considered safe in pregnancy. Streptomycin, however, is contraindicated (ototoxicity to the fetus). The 4-month regimen (HPMZ) is also contraindicated in pregnancy and lactation.

Finally, do not confuse LTBI testing (TST/IGRA) with active TB diagnosis. TST and IGRA cannot distinguish latent from active disease. A positive TST in a patient with symptoms does not confirm active TB. The diagnosis still requires bacteriological confirmation. Conversely, a negative TST in an HIV-positive patient with a low CD4 count does not rule out TB (anergy).

The core competency being tested across TB questions is this: can you correctly sequence the diagnostic workup (molecular test before culture, never the reverse), identify the right monitoring tool (AFB, not Xpert), and manage drug toxicity using a stepwise rechallenge protocol? Mastering this sequence is what separates a correct from an incorrect answer on exam day.

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