IM27.1-18 | Tuberculosis — Graded Quiz

Correct. This is new (previously untreated) smear-positive pulmonary TB with DS-TB confirmed by CBNAAT (RIF sensitive). NTEP regimen: 2HRZE + 4HRE daily, weight-band FDC. Ethambutol is maintained throughout (not dropped in continuation phase). Thrice-weekly dosing is the obsolete RNTCP regimen. BPaL is reserved for pre-XDR/XDR-TB.

DS-TB = 2HRZE + 4HRE daily (total 6 months). Never drop ethambutol to HR in continuation phase under current NTEP. Thrice-weekly DOTS is obsolete. Weight-band FDC tablets — never prescribe individual drugs separately for routine DS-TB.

NTEP DS-TB regimen is 2HRZE + 4HRE — daily FDC, ethambutol included in both phases. The RNTCP thrice-weekly regimen is abolished. The continuation phase is HRE (not HR), because dropping ethambutol was an older modification. BPaL is for DR-TB.

Correct. NACO Treat-All policy: ATT is started first; ART is initiated within 2–8 weeks (within 2 weeks if CD4 <50 cells/mm3) to avoid severe Immune Reconstitution Inflammatory Syndrome (IRIS) while not deferring ART unnecessarily. Rifampicin induces CYP3A4/CYP2B6, reducing efavirenz levels — efavirenz dose may need to be increased to 800 mg in patients >60 kg, or dolutegravir-based ART may be preferred. Rifabutin is not routinely used in India's public sector.

HIV-TB: ATT first → ART within 2–8 weeks (or 2 weeks if CD4 <50); total ATT 6 months standard. Rifampicin-EFV interaction = CYP induction → consider dolutegravir-based ART (preferred under NACO) or increase EFV to 800 mg. Monitor for IRIS after ART initiation.

Deferring ART for 6 months is dangerous — it raises mortality. ART starts within 2–8 weeks of ATT initiation (2 weeks if CD4 <50). Rifampicin-efavirenz interaction requires dose adjustment or switching to dolutegravir. Rifabutin is a resource-limited option not standardly used in NTEP.

Correct. A 1+ AFB smear indicates 1–9 AFB per 100 oil immersion fields (Ziehl-Neelsen scale). Under NTEP 2020, CBNAAT (Xpert MTB/RIF) must be performed on all smear-positive specimens — not just retreatment cases. This confirms MTB species (since other mycobacteria can give AFB-positive smears) and simultaneously identifies rifampicin resistance. Starting ATT on smear positivity alone without CBNAAT is a departure from current NTEP protocol.

NTEP diagnostic hierarchy: CBNAAT first for all presumptive TB. If smear-positive and CBNAAT pending, do NOT start ATT until RIF sensitivity is confirmed. 1+ = 1–9 AFB/100 fields; 2+ = 10–99 AFB/100 fields; 3+ = ≥1 AFB/field. Grading guides infectiousness assessment.

Under NTEP, CBNAAT is mandatory on ALL sputum specimens — not just retreatment. A smear-positive result alone is insufficient to start treatment without CBNAAT confirmation of both MTB species and RIF sensitivity. This prevents missing RR-TB and treating non-tuberculous mycobacteria with ATT.

Correct. Lymph node TB is classified as extrapulmonary TB. Under NTEP, most forms of extrapulmonary TB (lymph node, pleural, abdominal, pericardial, genitourinary) are treated with the standard 6-month regimen: 2HRZE + 4HRE. The 12-month regimen (2HRZE + 10HRE) is reserved for CNS TB (meningitis, tuberculoma) and bone/joint TB. CBNAAT on the aspirate confirming MTB + RIF sensitive removes the need to wait for culture before starting ATT.

Extrapulmonary TB regimen rule: 6 months (2HRZE + 4HRE) for lymph node, pleural, pericardial, abdominal, genitourinary TB; 12 months (2HRZE + 10HRE) for CNS and bone/joint TB only. Classify as extrapulmonary — not pulmonary — when chest X-ray is normal.

NOT all extrapulmonary TB requires 12 months — only CNS TB and bone/joint TB. Lymph node TB = 6 months standard (2HRZE + 4HRE). Caseating granulomas on histology plus CBNAAT-confirmed MTB is diagnostic — deferring treatment awaiting culture is inappropriate.

Correct. This presentation is consistent with drug-induced liver injury (DILI) — the criteria (jaundice + ALT >5x ULN OR >3x ULN with symptoms) mandate stopping ALL ATT immediately. Isoniazid, rifampicin, and pyrazinamide are all potentially hepatotoxic; stopping pyrazinamide alone is insufficient. After LFT normalisation, drugs are reintroduced sequentially: rifampicin first, then isoniazid, then pyrazinamide (or pyrazinamide may be omitted if not tolerated). A non-hepatotoxic bridging regimen (streptomycin + ethambutol + fluoroquinolone) may be used during the washout period for severe TB.

ATT DILI thresholds for stopping ALL ATT: ALT >5x ULN (asymptomatic) OR ALT >3x ULN with symptoms or jaundice. All three hepatotoxic drugs (INH, RIF, PZA) stopped together. Sequential reintroduction order: RIF → INH → PZA. Bridging with S + E + FQ if ATT cannot be withheld.

All three hepatotoxic drugs (INH, RIF, PZA) must be stopped when ATT-DILI is suspected with jaundice and ALT >5x ULN. Stopping pyrazinamide alone or continuing with hepatoprotective agents is insufficient and dangerous. Sequential reintroduction after LFT normalisation is the standard approach.

Correct. India accounts for approximately 26% of the global TB burden (2.8 million new cases annually as of recent estimates). The epidemiological determinants are multifactorial: high population density and overcrowding facilitate airborne transmission; undernutrition impairs cellular immunity; high rates of undiagnosed or late-diagnosed TB sustain the infectious pool; HIV co-infection (though relatively lower in prevalence than sub-Saharan Africa) multiplicatively increases risk; poverty limits healthcare access. India does not have a more virulent strain, and BCG coverage is actually high.

India = 26% of global TB burden (highest absolute count). Key epidemiological drivers: poverty, overcrowding, undernutrition (TB and malnutrition co-epidemic), high prevalence of latent TB infection (40% estimated), delayed/missed diagnosis sustaining the infectious pool. Goal: TB elimination by 2025 (incidence <1/million).

India's TB burden is not driven by a more virulent strain or low BCG coverage (BCG coverage is ~90%+ in India). Climate is not the primary driver. The convergence of social determinants — overcrowding, undernutrition, poverty, delayed diagnosis — combined with a massive susceptible population sustains transmission.

Correct. Under NTEP (aligned with WHO definitions), 'Cured' is the outcome when a bacteriologically confirmed TB patient completes treatment AND has a negative bacteriological result (smear or culture) at the end of treatment AND on at least one previous occasion. 'Treatment completed' applies when the patient completes treatment but does NOT have a negative bacteriological result at the end of treatment (e.g., clinically confirmed TB without bacteriology, or bacteriology not performed). 'Treatment success' is the combined outcome of cured + treatment completed. This patient is specifically 'Cured'.

NTEP TB outcomes: Cured = bacteriologically confirmed case + negative smear/culture at end of treatment + on at least one prior occasion. Treatment completed = clinical case or bacteriology not done at end. Treatment failed = smear/culture positive at month 5 or later. Defaulter (lost to follow-up) = interrupted treatment ≥2 consecutive months.

Under NTEP, 'Cured' requires bacteriological confirmation at treatment end (smear or culture negative) in a bacteriologically confirmed case. 'Treatment completed' is used when bacteriology was not done at end of treatment. This patient has bacteriological negativity confirmed — the correct outcome is 'Cured', not merely 'Treatment completed'.

Correct. Smear positivity at month 5 or later defines treatment failure. The NTEP approach to treatment failure is: (1) collect sputum for CBNAAT to confirm RIF resistance; (2) perform line probe assay (LPA) for full first-line DST; (3) notify as presumptive DR-TB on Ni-kshay; (4) refer to DR-TB centre. The RNTCP Category II regimen (SHRZE) is abolished under NTEP since it was creating streptomycin-resistant outcomes without addressing the underlying resistance. Empirical fluoroquinolone addition without DST is inappropriate.

Treatment failure (smear/culture positive at month 5 or later) → CBNAAT for RIF resistance + LPA for full DST + Ni-kshay notification as presumptive DR-TB + DR-TB centre referral. Category II regimen (SHRZE) is abolished under NTEP. Never add a single drug to a failing regimen.

Treatment failure at month 5 requires CBNAAT for RIF resistance and full DST — not empirical drug addition or the obsolete Category II regimen. The NTEP has eliminated Category II; all treatment failures are evaluated as presumptive DR-TB pending DST results.

Correct. M. tuberculosis is a chromosomally resistant organism — it does NOT acquire resistance via transferable plasmids. Isoniazid is a prodrug that requires activation by katG (catalase-peroxidase). The most common mechanism of INH resistance is mutation in katG (particularly Ser315Thr) that reduces drug activation. Mutations in the inhA promoter region (the INH target, enoyl-ACP reductase) also confer resistance, typically at lower levels. Efflux pumps play a minor role in clinical resistance. Beta-lactamase does not inactivate INH.

DR-TB molecular mechanisms: INH resistance = katG (prevents activation) + inhA promoter; RIF resistance = rpoB; PZA resistance = pncA; EMB resistance = embB; FQ resistance = gyrA/gyrB. All chromosomal — no horizontal transfer. LPA (line probe assay) detects katG + inhA + rpoB mutations directly from sputum.

M. tuberculosis does NOT use plasmid-mediated resistance. INH resistance = chromosomal mutation in katG (prevents drug activation) or inhA promoter (alters target). Efflux pumps are a minor mechanism. RIF resistance = rpoB mutations. PZA resistance = pncA mutations. PZA resistance is the key driver of XDR-TB complexity.

Correct. Active TB in pregnancy is an emergency — deferring ATT is more dangerous than treating. The standard regimen (2HRZE + 4HRE) is used in pregnancy. Streptomycin (an aminoglycoside) is the only first-line ATT drug absolutely contraindicated in pregnancy due to fetal ototoxicity (VIII nerve damage). Pyridoxine (vitamin B6) supplementation is co-administered with isoniazid to reduce peripheral neuropathy risk, which is heightened in pregnancy. Rifampicin, isoniazid, pyrazinamide, and ethambutol are all used in pregnancy.

TB in pregnancy: treat immediately — the risk of untreated TB far exceeds drug risk. Use standard 2HRZE + 4HRE. Contraindicated: streptomycin (fetal VIII nerve damage). Add pyridoxine with INH. All four first-line drugs are WHO-approved for use in pregnancy. Screen for gestational diabetes (DM-TB-pregnancy triple burden).

Deferring ATT in pregnancy risks maternal and fetal mortality from untreated TB. Standard 2HRZE + 4HRE is used in pregnancy. The only absolute contraindication is streptomycin (fetal ototoxicity). Pyridoxine supplementation with INH is essential. Pyrazinamide is safe in pregnancy.

Correct. Disseminated BCG disease (BCGosis) is a rare but life-threatening complication of BCG vaccination occurring almost exclusively in severely immunodeficient infants (severe combined immunodeficiency, DiGeorge syndrome, CGD, or HIV-exposed unimmunised infants with primary immunodeficiency). BCG is a live attenuated vaccine — in immunocompetent hosts, it causes only local reactions (injection site papule → pustule → scar) or, rarely, regional lymphadenopathy. Miliary pattern + hepatosplenomegaly + BCG vaccination history = BCGosis until proven otherwise. Management: ATT (HRZ, not cycloserine unless fully drug-resistant) and evaluation for primary immunodeficiency.

BCG complications (ascending severity): local ulcer (common), BCG-itis/local abscess (uncommon — treat with INH), regional lymphadenopathy (uncommon — usually self-limiting), BCGosis (rare — disseminated, implies severe immunodeficiency, treat with ATT). Never give BCG to known immunodeficient individuals or HIV-exposed infants with symptoms.

BCGosis (disseminated BCG disease) is a rare complication of BCG vaccination occurring in immunocompromised infants. It is not a normal response. BCG-itis causes local abscess at the injection site — not miliary dissemination. This clinical picture requires immediate evaluation for primary immunodeficiency and ATT.

Correct. The wife has latent TB infection (positive Mantoux, active TB excluded) as a household contact of a smear-positive index case. She is eligible for isoniazid preventive therapy (IPT: INH 300 mg/day for 6 months). However, INH prophylaxis in pregnancy carries a risk of INH-induced hepatotoxicity in the perinatal period. The standard recommendation is to defer IPT until after delivery and the immediate postpartum period, then administer INH 300 mg/day for 6 months with pyridoxine supplementation. Full ATT (2HRZE + 4HRE) is only for active disease.

Pregnant contact with positive Mantoux and no active TB: defer IPT until postpartum (perinatal INH hepatotoxicity concern). After delivery: INH 300 mg/day + pyridoxine for 6 months. Rule of thumb: treat latent TB contacts with IPT, but time initiation to minimise maternal risk.

This is latent TB — full ATT is not indicated. The correct approach is IPT (INH 300 mg/day × 6 months), but deferred until after delivery due to perinatal hepatotoxicity risk of INH. A positive Mantoux of 14 mm in a household contact is significant and cannot be dismissed as BCG effect alone.