1
Q
What is Tuberculosis (TB)?
A
A common and deadly infectious disease caused by Mycobacterium tuberculosis. It most commonly affects the lungs (pulmonary TB) but can affect any organ system (extrapulmonary TB).
2
Q
Why is M. tuberculosis considered ‘one of the most successful pathogens affecting mankind’?
A
Because it has infected up to 2 billion people worldwide, mostly in sub-Saharan Africa and Asia. It has co-evolved with humans for millennia and has sophisticated immune evasion mechanisms.
3
Q
Who discovered the tuberculosis bacillus and when?
A
Robert Koch first described M. tuberculosis on March 14, 1882. This discovery later earned him the Nobel Prize in 1905.
4
Q
What is the global burden of TB in 2023?
A
An estimated 10.8 million people developed TB globally in 2023 – a continued increase following the COVID-19 pandemic disruption.
5
Q
How many people died from TB in 2023?
A
Approximately 1.25 million deaths (including 161,000 among people with HIV). TB remains the second leading infectious killer after COVID-19.
6
Q
What is Nigeria’s position in the global TB burden?
A
Nigeria remains among the top countries for TB burden globally, accounting for a significant portion of the African region’s cases. Continuous efforts are needed to close the case-detection gap.
7
Q
What was the incidence of TB in Nigeria between 1990 and 2005 and why did it increase?
A
Incidence doubled from 149 to 343 per 100,000. The HIV epidemic was the most important factor causing this upsurge – HIV impairs cellular immunocompetence, increasing susceptibility to TB.
8
Q
What is the End TB Strategy?
A
A WHO strategy launched in 2014 with targets for 2035: 95% reduction in TB deaths (from 2015 baseline) and 90% reduction in TB incidence. Also aims to eliminate catastrophic costs for affected families.
9
Q
What percentage of the world’s population is infected with M. tuberculosis?
A
One-third of the world’s population (approximately 2 billion people) is infected with TB – but most have latent TB infection, not active disease.
10
Q
How many people are co-infected with HIV and TB?
A
Estimated 1.32 million people are co-infected with HIV and TB. About 79% of these are in Africa and 11% in South-East Asia.
11
Q
What is the classification of M. tuberculosis?
A
Kingdom: Bacteria. Family: Mycobacteriaceae. Genus: Mycobacterium. Species: M. tuberculosis.
12
Q
How long can M. tuberculosis survive in a dry state?
A
It can survive in a dry state for weeks – which contributes to its transmission via airborne droplet nuclei that can remain suspended in air.
13
Q
What is the generation time of M. tuberculosis compared to E. coli?
A
M. tuberculosis divides every 15-20 hours (very slow). E. coli divides every 20 minutes (60 times faster). This slow growth explains why TB cultures take weeks.
14
Q
What oxygen requirement does M. tuberculosis have and why?
A
It is an aerobic bacillus that survives best at a partial pressure of oxygen (PaO₂) of 140 mmHg. This explains its predilection for the upper lobes of the lungs, which have higher oxygen tension.
15
Q
What are the physical characteristics of M. tuberculosis?
A
A slender rod-shaped bacillus, 2-4 μm long and 0.2-0.5 μm wide. It has a waxy coat that is acid-fast (AFB – Acid-Fast Bacillus).
16
Q
What organisms make up the M. tuberculosis complex?
A
Three closely related organisms: 1) M. tuberculosis (primary human pathogen), 2) M. bovis (bovine TB – can infect humans via unpasteurized dairy), 3) M. africanum (causes TB in West Africa).
17
Q
How is TB transmitted?
A
By droplet nuclei (1-5 microns in diameter) expelled when a person with infectious pulmonary TB coughs, sneezes, speaks, or sings. Close contacts are at highest risk.
18
Q
Can a person with latent TB infection transmit the disease?
A
No. Transmission occurs only from persons with active, infectious TB disease (usually pulmonary TB). Latent TB infection is not contagious.
19
Q
What are the agent factors that affect TB transmission?
A
1) Virulence of the strain, 2) Concentration of infectious droplet nuclei in the air.
20
Q
What environmental factors affect TB transmission?
A
1) Degree of ventilation (poor ventilation increases risk), 2) Duration of exposure (prolonged contact increases risk), 3) Darkness (UV light kills TB – darkness may preserve viability).
21
Q
What host factors in the index patient increase TB transmission?
A
1) Disease in the lungs (especially cavitary), 2) Presence of cough or other forceful expiratory acts, 3) Presence of acid-fast bacilli in sputum (smear-positive), 4) Presence of cavities on chest radiograph, 5) Failure to cover mouth/nose when coughing/sneezing.
22
Q
List the risk factors for progression from latent TB infection to active TB disease.
A
HIV infection (strongest risk factor – 5-15% annual risk vs 5-10% lifetime in immunocompetent), Malnutrition, Recent infection (<2 years), CXR findings suggestive of previous TB, Diabetes mellitus, Silicosis/other lung fibrosis, Prolonged corticosteroid/immunosuppressive therapy, Cancer of head/neck, Hematologic/reticuloendothelial diseases, End-stage renal disease, Intestinal bypass/gastrectomy, Chronic malabsorption syndromes, Low body weight (>10% below ideal), Toxic factors (alcohol, smoking).
23
Q
What is ‘herd immunity’ in the context of TB?
A
Population-level immunity that occurs when a sufficient proportion of the population is immune to TB (either through infection or vaccination with BCG), reducing the overall transmission in the community.
24
Q
What is the difference between TB infection and TB disease?
A
TB infection (latent): Tubercle bacilli are present in small numbers in a dormant state; no symptoms; not contagious. TB disease (active): Bacilli multiply and overcome the immune system; produces signs and symptoms; usually contagious (pulmonary).
25
Is drug-resistant TB transmitted the same way as drug-susceptible TB?
Yes. Drug-resistant TB (MDR-TB, XDR-TB) is transmitted via the same airborne droplet nuclei route as drug-susceptible TB. This is why infection control is critical in high-burden settings.
26
What happens when M. tuberculosis is inhaled?
Inhaled M. tuberculosis reaches the alveoli where it initiates a non-specific inflammatory response. The bacilli are ingested by macrophages and taken to regional lymph nodes.
27
What determines whether the infection is contained or spreads?
The bacilli are either contained in the regional lymph nodes OR spread via lymphatics or bloodstream to other organs (miliary dissemination).
28
When does specific cell-mediated immunity develop after TB infection?
2-8 weeks after infection. This is the typical time for tuberculin skin test (TST) conversion and corresponds to the development of adaptive immunity.
29
What is a granuloma in TB?
An organized collection of activated macrophages (epithelioid cells) and lymphocytes that forms around M. tuberculosis to wall off the organism. It is the characteristic pathological lesion of TB.
30
Can M. tuberculosis persist in a quiescent state?
Yes. M. tuberculosis can persist intracellularly in a quiescent (dormant) state within macrophages, retaining the ability to reactivate at a later date. This is known as latent TB infection (LTBI).
31
What percentage of immunocompetent adults infected with M. tuberculosis eventually develop active disease?
Approximately 10% of immunocompetent adults infected with M. tuberculosis eventually develop active disease at some point in their lifetime.
32
How is the 10% risk of reactivation distributed over time?
Half of this risk (5%) is concentrated in the first two years after infection. The other half (5%) is distributed over the remaining lifespan.
33
What is progressive primary TB?
A rare form of TB that occurs when primary infection progresses directly to active disease without a latent phase. Most common in infants, young children, and severely immunocompromised individuals (including advanced HIV).
34
What is post-primary TB (reactivation TB)?
TB that occurs as a reactivation of latent infection, sometimes years or decades after the primary infection. This is the most common form of TB in adults.
35
Can patients be re-infected with TB after successful treatment?
Yes. Patients (particularly HIV-infected individuals) can be re-infected with a new strain of M. tuberculosis after successful treatment of TB. This is called exogenous reinfection.
36
List the common sites of TB disease.
1) Lungs (pulmonary TB – most common), 2) Pleura (pleural TB), 3) Central nervous system (TB meningitis), 4) Lymphatic system (TB adenitis), 5) Genitourinary systems, 6) Bones and joints (including Pott's disease), 7) Disseminated (miliary TB).
37
What are the typical symptoms of pulmonary TB?
Productive cough >3 weeks (most common), weight loss, hemoptysis, breathlessness, fever (usually low-grade, evening), night sweats, malaise, chest pain.
38
What are the typical signs of pulmonary TB on examination?
Signs may be non-specific or normal. Possible findings: chest deformity, crackles (post-tussive), signs of pleural effusion (stony dullness, decreased breath sounds), signs of consolidation, signs of weight loss/underlying immunosuppression, signs of fibrosis, signs of lung cavitations.
39
What is the appearance of pleural fluid in pleural TB?
Straw-colored effusion (yellow, clear). It is an exudate (fluid protein >50% of serum protein concentration). The fluid shows increased lymphocytes. It is seldom AFB-positive.
40
How is pleural TB diagnosed?
Physical exam and CXR suggest effusion. Diagnostic aspiration confirms exudative lymphocytic effusion. Culture of pleural biopsy is very sensitive. Histology of pleural biopsy shows granuloma.
41
Which lymph nodes are most commonly affected by TB adenitis?
Cervical lymph nodes are most commonly affected (scrofula). Can also involve axillary, inguinal, and abdominal nodes.
42
What is the clinical evolution of TB lymphadenitis?
Nodes become rubbery and non-tender initially. Later they become matted and fluctuant (soft). May spontaneously discharge through skin, forming chronic sinuses with scarring.
43
How is TB adenitis diagnosed?
Fine Needle Aspiration Biopsy (FNAB) and lymph node biopsy (excisional biopsy). Culture and histology (granuloma, caseation) confirm diagnosis.
44
What is Pott's disease?
Spinal TB (tuberculous spondylitis). Commonly affects the thoracic and lumbar spine. Vertebral collapse produces an angular deformity called a gibbus (angular kyphosis).
45
What is a paravertebral 'cold' abscess in Pott's disease?
An abscess that forms adjacent to the affected vertebrae, often tracking along the psoas muscle (psoas abscess). Called 'cold' because it lacks the classic signs of inflammation (rubor, calor) – it is not hot or red.
46
Besides the spine, which other bones and joints are commonly affected by TB?
Hip and knee joints are commonly affected. Other sites: sacroiliac joints, wrist, ankle, and shoulder.
47
What is miliary TB?
An aggressive, hematogenously disseminated form of TB. More common in infants, young children, and immunosuppressed individuals (especially HIV). Named for the 'millet seed' appearance of tiny nodular opacities on CXR.
48
What are the clinical features of miliary TB?
Progressive history of fever, malaise, and weight loss. Non-specific signs including hepatomegaly, mild splenomegaly, tachypnea, and wasting. History of contact with a TB patient is an important clue.
49
What is the CXR finding in miliary TB?
Diffuse, tiny nodular opacities (1-3 mm) – described as 'miliary shadows' or 'millet seed' appearance. May be subtle initially.
50
What is a choroidal tubercle?
A tuberculous granuloma in the choroid of the eye. Seen on fundoscopy as a yellowish-white nodule. Highly suggestive of miliary TB or TB meningitis.
51
What is the clinical presentation of TB meningitis?
Progressive febrile illness with headache, vomiting, irritability, decreased consciousness, and ultimately coma. The pace of illness is SLOWER than acute bacterial meningitis (subacute to chronic).
52
What neurological findings are common in TB meningitis?
Cranial nerve palsies (CN III, IV, VI, and VIII – oculomotor, trochlear, abducens, vestibulocochlear). Seizures and focal neurological deficits. Neck stiffness is variable (may be absent, especially in HIV).
53
How is TB meningitis diagnosed?
CSF examination is key. Findings: lymphocytic pleocytosis, elevated protein (often very high >100 mg/dL), low glucose. Brain imaging (CT/MRI) may show basilar meningeal enhancement, hydrocephalus, or tuberculomas.
54
What are the clinical features of abdominal TB?
Fever, abdominal pain, weight loss, diarrhea, or partial bowel obstruction. Can occur at any GI site but most commonly the terminal ileum (similar to Crohn's disease). Peritoneal TB presents with ascites.
55
How is abdominal TB diagnosed?
Culture and histology of biopsy taken at laparoscopy, colonoscopy, or surgery. Abdominal CT scan is useful to identify lymphadenopathy, bowel wall thickening, and ascites.
56
What is pericardial TB?
TB infection of the pericardium. More common in patients with HIV infection. Can present as pericardial effusion, tamponade, or constrictive pericarditis (late complication).
57
What is the CXR finding in pericardial TB?
Globular (enlarged, water-bottle shaped) heart shadow due to large pericardial effusion. May be normal in early disease.
58
What are the clinical features of cardiac tamponade from TB pericarditis?
Elevated JVP (jugular venous pressure), pulsus paradoxus (>10 mmHg drop in systolic BP during inspiration), hypotension, and muffled heart sounds (Beck's triad).
59
How is pericardial TB diagnosed?
Echocardiography confirms effusion and may show fibrinous strands. ECG may show low voltage and electrical alternans. Pericardiocentesis yields fluid for AFB smear, culture, and PCR. Pericardial biopsy may show granuloma.
60
What are the clinical features of renal TB?
Dysuria (painful urination), hematuria (blood in urine), flank pain or mass. Often part of genitourinary TB.
61
What is the classic urinalysis finding in renal TB?
Sterile pyuria – pus cells (white blood cells) in urine with negative routine bacterial culture. This should always raise suspicion for renal TB.
62
How is genitourinary TB diagnosed?
Urine TB culture (requires 3 consecutive early morning urine samples). Imaging: CT urography may show papillary necrosis, strictures, or autonephrectomy. Biopsy if needed.
63
What is TB epididymo-orchitis?
TB infection of the epididymis and testis. Presents as a painless or mildly tender scrotal mass that may be mistaken for tumor. Can cause infertility.
64
What are the cutaneous manifestations of TB?
Lupus vulgaris (chronic, progressive form – apple-jelly nodules), Scrofuloderma (neck sinuses from underlying lymphadenitis), Tuberculosis verrucosa cutis (warty lesions – 'prosector's wart'), Tuberculous gumma (subcutaneous abscess), Tuberculids (hypersensitivity reactions), Erythema nodosum (painful red nodules on shins – associated with primary TB).
65
What is TB adrenalitis (Addison's disease from TB)?
Result of disseminated TB affecting the adrenal glands. Leads to primary adrenal insufficiency (Addison's disease). TB was the most common cause of Addison's disease historically.
66
What are the clinical features of TB adrenalitis?
Weakness, apathy, anorexia, weight loss, abdominal pain, oligomenorrhea (women). Signs: hypotension, hyperpigmentation (bronze skin – due to elevated ACTH), vitiligo (autoimmune association). May present with adrenal crisis (hypotension, dehydration, shock).
67
What laboratory findings are seen in TB adrenalitis?
Hyperkalemia (high K⁺), hyponatremia (low Na⁺), uremia, acidosis, hypercalcemia, eosinophilia, and SIADH (syndrome of inappropriate antidiuretic hormone).
68
What are the key components of TB evaluation?
1) Medical history (symptoms, TB exposure, risk factors), 2) Physical examination, 3) Mantoux tuberculin skin test (TST) or IGRA, 4) Chest X-ray/other imaging, 5) Bacteriologic or histologic examination (smear, culture, molecular testing).
69
What are the two definitive ways to diagnose TB?
1) Isolation (culture) of M. tuberculosis from a clinical specimen (gold standard), OR 2) Demonstration of AFB in a clinical specimen with high index of suspicion (smear microscopy – presumptive diagnosis).
70
What is GeneXpert MTB/RIF?
A cartridge-based, automated Nucleic Acid Amplification Test (NAAT) that uses real-time PCR to detect M. tuberculosis DNA. Dual functionality: detects MTB complex AND simultaneously detects mutations in the rpoB gene (rifampicin resistance – a proxy for MDR-TB).
71
What are the advantages of GeneXpert over traditional methods?
Speed: Results in under 2 hours (vs weeks for culture). Simplicity: Minimal hands-on time; can be used near point-of-care. Sensitivity: Significantly more accurate than smear microscopy (especially in HIV and smear-negative patients).
72
What is the 'gold standard' sample for GeneXpert in pulmonary TB?
Sputum – either raw expectorated sputum or induced sputum. Minimum volume 1-4 mL.
73
What samples are used for extrapulmonary TB diagnosis by GeneXpert?
1) Gastric aspirate/lavage (children), 2) Lymph node FNA or tissue biopsy, 3) Cerebrospinal fluid (CSF) – for suspected TB meningitis (high priority), 4) Stool (WHO-recommended for children who cannot produce sputum), 5) Pleural, peritoneal, or synovial fluids (sensitivity varies).
74
What is the lateral flow urine LAM (LF-LAM) test?
A rapid point-of-care test that detects lipoarabinomannan (LAM), a mycobacterial cell wall antigen, in urine. Used for patients with advanced HIV or those who are seriously ill and cannot produce sputum.
75
What is Computer-Aided Detection (CAD) for TB?
AI software that assists in interpreting chest X-rays for TB screening. Can improve diagnostic accuracy and efficiency, especially in resource-limited settings with a shortage of radiologists.
76
What are the two main staining methods for AFB microscopy?
1) Ziehl-Neelsen stain (ZN) – most commonly used in developing countries. 2) Auramine-Rhodamine fluorescence stain – more sensitive but requires fluorescence microscope.
77
What is the sensitivity of Ziehl-Neelsen staining?
50-60%. Requires about 5,000–10,000 tubercle bacilli per milliliter of specimen to detect AFB. Smear-negative TB is common, especially in HIV co-infection.
78
How many specimens are recommended for AFB smear microscopy?
2 specimens are typically collected – usually spot morning and early morning specimens.
79
What is the Ziehl-Neelsen staining procedure?
1) Cover smear with carbol fuchsin (red dye), 2) Heat to steam for 5 minutes, 3) Wash with water, 4) Cover with 3% acid alcohol for 2 minutes (decolorization – removes dye from non-acid-fast organisms), 5) Wash, 6) Cover with malachite green (counterstain – 4 minutes). AFB appear red against a green background.
80
How is the Mantoux tuberculin skin test performed?
Inject 0.1 ml of 5 TU (tuberculin units) PPD (purified protein derivative) intradermally on the volar forearm. This produces a wheal 6-10 mm in diameter. Read reaction 48-72 hours after injection.
81
How is the Mantoux test read?
Measure only the induration (palpable firm swelling), NOT erythema (redness). Record reaction in millimeters transversely across the forearm.
82
What are the chest X-ray findings in pulmonary TB?
Cavitary lesions (typically upper lobe – APICAL and POSTERIOR segments), Infiltrates (upper lobe predilection), Fibrosis and volume loss (chronic disease), Hilar/mediastinal lymphadenopathy (more common in children and HIV), Pleural effusion, Miliary pattern (diffuse tiny nodules).
83
What is the gold standard for definitive TB diagnosis?
Culture – recovery of M. tuberculosis on culture medium. More sensitive than microscopy, detecting 10-100 viable organisms per ml (vs 5,000-10,000 for smear).
84
Can culture distinguish between members of the M. tuberculosis complex?
No – culture alone cannot distinguish among M. tuberculosis, M. bovis, and M. africanum. Additional testing (biochemical or molecular) is required.
85
What are the three main groups of culture media for TB?
1) Egg-based: Lowenstein-Jensen medium (LJ) – most common in developing countries. 2) Agar-based: Middlebrook 7H10/7H11 medium. 3) Liquid medium: BACTEC, Kirchner – automated, faster.
86
What is the optimal temperature for M. tuberculosis growth?
35-37°C (body temperature). M. tuberculosis does not grow at room temperature.
87
How long does M. tuberculosis take to grow on Lowenstein-Jensen medium?
Produces cream-colored, rough, dry colonies after incubating for 2-6 weeks. This is why TB culture is slow – the organism's generation time is 15-20 hours.
88
What are the components of Lowenstein-Jensen medium?
Malachite green (inhibits contaminating bacteria), Egg (provides protein), Mineral salts, Glycerol (for human-type M. tuberculosis) or pyruvate (for M. bovis).
89
What is the BACTEC liquid culture system?
An automated liquid culture technique developed by Becton Dickinson. Specimen is inoculated into a BACTEC liquid medium containing C14-labeled palmitic acid. As M. tuberculosis metabolizes the fatty acid, it releases radioactive C14, which is detected by the instrument.
90
How long does BACTEC take to yield results?
Positive sputum: 5-7 days. Negative samples: up to 42 days. Drug susceptibility testing (DST): 8-12 days from culture.
91
What are the newer tests for TB diagnosis?
1) LED Microscopy (Light Emitting Diode – more sensitive than conventional fluorescence), 2) MODS (Microscopic Observation for Detection and Susceptibility), 3) LAMP (Loop-Mediated Isothermal Amplification), 4) T-spot TB test (ELISPOT-based IGRA), 5) MycoDot antibody test, 6) DNA fingerprinting, 7) QuantiFERON-TB Gold (IGRA).
92
What is QuantiFERON-TB Gold?
An interferon-gamma release assay (IGRA) that measures T-cell response to M. tuberculosis-specific antigens (ESAT-6 and CFP-10). Advantages over TST: No false positives from BCG vaccination, single patient visit (no return for reading), not affected by prior BCG.
93
What are the case definitions in TB?
NEW CASE (N): Patient never treated for TB or took <4 weeks of treatment. RELAPSE (R): Previously treated, declared cured but now has positive smear/culture. TREATMENT FAILURE: Smear/culture positive at month 5 or later during treatment. RETURN AFTER DEFAULT (RAD): Previously treated for ≥4 weeks, returned after 2+ months interruption. TRANSFER IN (TI): Transferred from another treatment unit.
94
What is the standard first-line anti-TB drug regimen for drug-susceptible TB?
The intensive phase (2 months): RHZE – Rifampicin (R), Isoniazid (H), Pyrazinamide (Z), Ethambutol (E). The continuation phase (4 months): RH – Rifampicin and Isoniazid. Total duration: 6 months.
95
What is Directly Observed Therapy (DOTS)?
A health care worker (or trained observer) watches the patient swallow each dose of medication. DOTS is recommended for all TB patients and reduces relapse and acquired drug resistance.
96
Is DOTS only for pulmonary TB?
No. DOTS should be used for ALL TB patients (pulmonary and extrapulmonary) to promote adherence and prevent drug resistance.
97
How long should extrapulmonary TB be treated?
Most forms (lymph node, pleural, pericardial, abdominal, genitourinary): same 6-month regimen as pulmonary TB. Bone/joint TB, miliary TB, and TB meningitis: treat for 12 months.
98
What is MDR-TB?
Multi-Drug Resistant Tuberculosis: TB whose isolates are resistant in vitro to at least INH (isoniazid) and rifampicin (the two most powerful first-line drugs).
99
What is the BPaLM regimen for MDR-TB?
A shorter, all-oral regimen for MDR-TB: Bedaquiline + Pretomanid + Linezolid + Moxifloxacin. Replaces older injectable-based regimens (which were toxic and less effective).
100
What is TB Preventive Treatment (TPT)?
Treatment given to high-risk individuals with latent TB infection to prevent progression to active disease. High-risk groups: household contacts of infectious TB patients, people living with HIV (PLWHIV), and other immunocompromised individuals.
101
What is the most important factor causing the upsurge in TB incidence in sub-Saharan Africa?
The HIV epidemic. HIV impairs cellular immunocompetence, increasing susceptibility to TB. People with HIV have a 5-15% annual risk of developing active TB (vs 5-10% lifetime risk in immunocompetent).
102
What is the association between diabetes and TB?
Diabetes mellitus increases the risk of progressing from latent TB to active disease (2-3 fold increased risk). Diabetic patients with TB have worse treatment outcomes (higher mortality, higher relapse) and are more likely to have smear-positive disease.
103
What is the association between smoking and TB?
Smoking increases the risk of: 1) Acquiring TB infection, 2) Progressing from latent to active disease, 3) Developing cavitary disease, 4) Poor treatment outcomes (including relapse and death).
104
What is the role of vitamin D in TB?
Vitamin D deficiency is associated with increased susceptibility to TB and worse treatment outcomes. Vitamin D enhances macrophage killing of M. tuberculosis. Supplementation may improve outcomes but not yet standard of care.
105
What is paradoxical reaction in TB treatment?
Worsening of existing TB lesions or appearance of new lesions during appropriate TB therapy. Caused by immune reconstitution (especially in HIV patients starting ART). Common in TB meningitis, lymphadenitis, and pericarditis. May require corticosteroids.
106
What is immune reconstitution inflammatory syndrome (IRIS) in TB/HIV co-infection?
Exaggerated inflammatory response to TB antigens after starting ART in HIV/TB co-infected patients. Presents with worsening TB symptoms, fever, lymphadenopathy, or CNS manifestations. Management: continue TB treatment and ART, add corticosteroids for severe cases.
107
What is the public health importance of contact tracing in TB?
To identify individuals with latent TB infection (who need preventive treatment) and early cases of active TB. Household contacts of smear-positive TB patients have a 30-50% risk of being infected and 2-5% risk of developing active disease in the first 2 years.
108
How long is a patient with pulmonary TB considered infectious?
Usually 2-4 weeks after starting effective anti-TB therapy, provided there is clinical improvement and adherence to treatment. Smear conversion (negative sputum smear) is the best indicator of reduced infectiousness.
109
What infection control measures should be taken for suspected TB patients in healthcare facilities?
1) Respiratory hygiene: Cover mouth when coughing, 2) Triage: Separate from immunocompromised patients, 3) Ventilation: Natural (open windows) or mechanical (negative pressure), 4) Personal protective equipment: N95 respirators (not surgical masks) for staff, 5) Ultraviolet germicidal irradiation (UVGI) in high-risk areas.
110
What is the BCG vaccine and what does it protect against?
Bacille Calmette-Guérin – a live attenuated vaccine derived from M. bovis. Given intradermally at birth in TB-endemic countries. Protects against severe forms of TB in children (TB meningitis and miliary TB) but has variable efficacy against pulmonary TB in adults.
111
What is the WHO recommendation for BCG vaccination in HIV-exposed infants?
BCG is contraindicated in infants with known HIV infection (risk of disseminated BCG disease). HIV-exposed infants should have HIV testing before BCG if possible, or delay BCG until HIV excluded.
112
What are the adverse effects of anti-TB drugs?
Rifampicin: orange-red body fluids (harmless), hepatotoxicity, drug interactions (P450 inducer). Isoniazid: peripheral neuropathy (prevent with pyridoxine/vitamin B6), hepatotoxicity. Pyrazinamide: hepatotoxicity, hyperuricemia (arthralgia – joint pain). Ethambutol: optic neuritis (dose-dependent, causes red-green color blindness).
113
What is the management of a patient with TB who develops jaundice?
Stop all hepatotoxic drugs (especially isoniazid, rifampicin, pyrazinamide). Monitor LFTs. After LFTs improve, reintroduce drugs one by one. Refer to specialist for management. MDR-TB drugs (bedaquiline, linezolid) are alternatives if severe hepatotoxicity.
114
What is the management of TB in pregnancy?
First-line drugs (rifampicin, isoniazid, ethambutol) are safe. Pyrazinamide is also considered safe. Streptomycin (aminoglycoside) is CONTRAINDICATED (ototoxic to fetus). Treatment should NOT be delayed. Breastfeeding is safe on TB treatment.
115
What is the management of TB in patients with renal impairment?
Ethambutol requires dose reduction (excreted renally). Pyrazinamide dose reduction (but often avoided in severe renal impairment). Rifampicin and isoniazid – no dose adjustment (hepatically metabolized). Avoid streptomycin and other aminoglycosides (nephrotoxic and ototoxic).
116
What is the follow-up schedule for TB patients on treatment?
Monthly follow-up during treatment: clinical assessment (symptoms, weight), medication adherence check, adverse effects monitoring. Sputum smear/culture at months 2, 5, and at end of treatment. Chest X-ray at end of treatment (baseline for future comparison).
117
What is the definition of TB treatment failure?
Smear or culture positive at month 5 or later during treatment, despite adherence. Requires evaluation for drug resistance and change to MDR-TB regimen.
118
What is the cure rate for drug-susceptible TB with standard 6-month DOTS?
Approximately 85-95% in well-functioning programs. Poor outcomes are due to: default (loss to follow-up), treatment failure (usually due to drug resistance), and death (especially in HIV co-infection).
119
What is the WHO End TB target for catastrophic costs?
Zero TB-affected households facing catastrophic costs (costs >20% of annual household income) by 2035. TB often pushes families into poverty due to direct medical costs and lost income.
120
What is the role of digital technologies in TB control?
1) Video Directly Observed Therapy (vDOT) – remote adherence monitoring via smartphone. 2) Electronic pillboxes with adherence sensors. 3) Mobile phone reminders for appointments. 4) Electronic TB registers for surveillance.
121
What is the impact of COVID-19 on TB control?
The COVID-19 pandemic reversed years of progress in TB control. Globally, TB case notifications dropped by 18% in 2020 (from 7.1M to 5.8M), but TB deaths increased for the first time in over a decade due to reduced diagnosis and treatment.
122
What is the relationship between silicosis and TB?
Silicosis (occupational lung disease from silica dust exposure) is one of the strongest risk factors for TB. Silicosis impairs macrophage function. The risk of active TB in silicosis patients is 2-30 times higher than general population.
123
What is the definition of XDR-TB?
Extensively Drug-Resistant Tuberculosis: MDR-TB plus resistance to any fluoroquinolone (e.g., levofloxacin, moxifloxacin) AND to at least one of the second-line injectable drugs (amikacin, kanamycin, capreomycin) – though injectables are being phased out, newer definitions include resistance to bedaquiline or linezolid.
124
What is the treatment duration for MDR-TB with the BPaLM regimen?
6 months (for most patients) – significantly shorter than older MDR-TB regimens which lasted 9-24 months. BPaLM is all-oral, injectable-free.
125
What is the role of linezolid in MDR-TB treatment?
Linezolid is a key component of the BPaLM regimen. It has potent anti-TB activity but adverse effects include myelosuppression (anemia, thrombocytopenia, neutropenia) and peripheral/optic neuropathy (dose and duration dependent).
126
What is bedaquiline?
A new anti-TB drug (diarylquinoline) that inhibits mycobacterial ATP synthase. It is a key component of MDR-TB regimens (including BPaLM). Adverse effects include QT prolongation (monitor ECG) and hepatotoxicity.
127
What is pretomanid?
A newer nitroimidazole drug that inhibits mycobacterial cell wall synthesis. It is part of the BPaLM regimen for MDR-TB and has activity against both replicating and dormant bacteria.
128
What is the role of surgery in TB treatment?
Indications: 1) MDR/XDR-TB with localized disease not responding to medical therapy, 2) Massive hemoptysis (may require lobectomy or pneumonectomy), 3) Destroyed lung with recurrent infections, 4) Spinal TB with cord compression or severe deformity, 5) Pericardial constriction (pericardiectomy).
129
What is the prognosis of TB meningitis?
Mortality is 20-30% even with treatment. Poor prognostic factors: very young or old age, advanced HIV, coma at presentation (GCS <8), stage 3 disease (comatose), cranial nerve palsies, hydrocephalus, delays in diagnosis and treatment. Survivors often have neurological sequelae (cognitive impairment, motor deficits, hearing loss).
130
What is the difference between TB and non-tuberculous mycobacteria (NTM)?
NTM are environmental mycobacteria that do not cause TB and are not transmitted person-to-person. They cause opportunistic infections (lung disease, lymphadenitis, skin/soft tissue). NTM are often resistant to standard anti-TB drugs (especially isoniazid and pyrazinamide).
131
How do you differentiate TB from NTM infection?
Clinical context (NTM often in older adults with underlying lung disease – COPD, bronchiectasis, cystic fibrosis). Imaging (NTM – often upper lobe cavitary or nodular bronchiectasis). Microbiology: NTM are not detected by TB-specific molecular tests (GeneXpert). Culture and species identification required.
132
What is the 'TB-related stigma' and why is it important?
Fear, shame, and discrimination associated with TB diagnosis. Stigma leads to: delayed healthcare seeking, non-disclosure to family (increasing transmission), poor adherence to treatment, and social isolation. TB programs must address stigma through community education and patient support.
Internal Medicine
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