Pulmonary tuberculosis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Mycobacterium tuberculosis is transmitted through airborne particles, most efficiently from untreated pulmonary or laryngeal disease with bacilli in respiratory secretions. Individual infectivity depends on cough, disease site, smear burden, treatment response and environment; it cannot safely be reduced to a fixed number of treatment days.

Diagnosis and management are inseparable from public health. Respiratory sampling, rapid resistance testing, isolation, notification, contact investigation and support for adherence should proceed in parallel. Treatment is prolonged and toxic enough that a named specialist TB team, not an isolated prescription, owns the regimen and response.

Key points

Think of pulmonary TB with cough lasting weeks, weight loss, fever, night sweats, haemoptysis or unexplained upper-lobe/cavitary change, especially after exposure or residence in a high-incidence setting.
Older, immunocompromised and pregnant patients may have atypical or disseminated disease; ask about HIV risk, immunosuppressants, housing, detention, homelessness and prior TB treatment.
Place potentially infectious pulmonary or laryngeal TB in the locally approved airborne-isolation pathway and involve infection prevention and the specialist TB service immediately.
Send multiple respiratory specimens for acid-fast microscopy, mycobacterial culture and molecular testing; culture remains essential for species identification and full susceptibility.
A nucleic-acid result can accelerate diagnosis and rifampicin-resistance assessment but does not replace culture, and a negative smear does not exclude infectious TB.
Standard drug-susceptible pulmonary TB is usually treated with rifampicin, isoniazid, pyrazinamide and ethambutol for 2 months followed by rifampicin and isoniazid for 4 months, under a specialist weight-banded regimen.
Check liver risk, vision, neuropathy risk, renal function, pregnancy and interactions before treatment; rifampicin substantially reduces exposure to many medicines including hormonal contraception and anticoagulants.
Suspected or confirmed active TB is notifiable under applicable UK legislation; identify the nation-specific route, do not wait for culture, and coordinate contact tracing.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Airborne Mycobacterium tuberculosis

Infectious aerosols from a person with pulmonary or laryngeal disease transmit bacilli, especially during prolonged close indoor contact.

Reactivation risk

HIV, immune-suppressing medicines, transplantation, undernutrition, diabetes, renal failure and ageing weaken containment of previously acquired latent infection.

Recent exposure and social factors

Household contact, high-incidence settings, overcrowding, homelessness and barriers to healthcare increase acquisition, delayed diagnosis and onward transmission.

Drug-resistant organisms

Prior incomplete therapy, exposure to resistant disease and transmission in high-resistance settings increase the chance that standard medicines will be ineffective.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Alveolar infection
Inhaled bacilli reach alveoli and survive within macrophages by resisting intracellular killing, with effects that increase as the pathological process progresses.
2
Granuloma formation
Cell-mediated immunity walls organisms within granulomas, producing latent infection when replication is controlled but not eradicated.
3
Loss of containment
Inadequate or waning immunity allows bacillary proliferation, caseous necrosis and tissue destruction, and the downstream physiological effect determines clinical severity.
4
Cavitation and airway spread
Necrotic lesions erode into bronchi, creating cavities with high organism burden that promote cough and infectious aerosol generation.
5
Haematogenous dissemination
Bacilli may enter blood and seed meninges, bone, kidneys and other organs, particularly in profound immune suppression.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Typical pulmonary diseaseRed flag

Persistent cough, sputum or haemoptysis with weight loss, anorexia, fever and night sweats; radiology may show upper-lobe infiltrates, cavitation, nodules or lymphadenopathy.

Smear-positive infectious diseaseRed flag

Acid-fast bacilli in a respiratory sample plus compatible illness indicates potentially infectious mycobacterial disease; maintain airborne precautions while rapid testing distinguishes TB from NTM.

Immunocompromised presentationRed flag

HIV, transplantation, anti-TNF therapy or other immunosuppression can produce lower-zone, non-cavitary, lymph-node, miliary or extrapulmonary disease with low smear burden.

Drug resistance riskRed flag

Previous incomplete treatment, contact with resistant TB, treatment abroad or origin in a high-resistance setting requires rapid molecular resistance assessment and expert regimen design.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Chest radiographFirst step
Why
Identify pulmonary patterns and guide respiratory sampling while assessing severity.
Interpretation and limitations
Upper-lobe cavitation supports contagious pulmonary disease but is not specific; normal radiography is less reassuring in immunocompromise, and CT may reveal miliary, nodal or occult disease.
02
Respiratory mycobacterial samples
Why
Confirm organism, assess smear burden and obtain culture susceptibility.
Interpretation and limitations
Send multiple sputum samples, including an early-morning specimen where feasible; induced sputum or bronchoscopy may be needed. Label suspected TB so the laboratory applies safe processing.
03
Rapid molecular TB and resistance testing
Why
Accelerate identification of M. tuberculosis complex and important resistance.
Interpretation and limitations
A positive result can guide early treatment; a negative result does not exclude paucibacillary disease. Rifampicin resistance triggers urgent expert MDR/RR-TB assessment.
04
Baseline treatment-safety assessment
Why
Identify toxicity and dose modifiers before multidrug treatment.
Interpretation and limitations
Check FBC, renal and liver profile, visual acuity/colour vision, pregnancy, hepatitis risk and a complete interaction list; offer HIV testing because it changes urgency and treatment coordination.
05
Public-health exposure assessment
Why
Define infectious period, vulnerable contacts and barriers to adherence.
Interpretation and limitations
Document household, workplace, education, healthcare and congregate-setting contacts with the TB/health-protection team; clinical staff should not attempt an uncoordinated contact screen.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Lung cancer

Weight loss, haemoptysis, cavitation and nodes overlap; microbiology and adequate tissue are often needed because cancer and tuberculosis can coexist.

Non-tuberculous mycobacterial disease

Species identification distinguishes environmental NTM, which has different transmission, diagnostic and treatment implications, and corroborating objective findings prevent an incorrect diagnostic label.

Chronic pulmonary aspergillosis

Progressive cavities and fungal balls in damaged lung may follow prior tuberculosis; fungal markers and cultures identify superimposed disease.

Bacterial lung abscess

Aspiration risk, acute sepsis and polymicrobial infection favour abscess, while chronic epidemiology and acid-fast results favour tuberculosis.

Sarcoidosis

Non-caseating granulomatous disease and symmetrical hilar nodes can resemble tuberculosis; directed microbiology is important before immune suppression because treatment could worsen unrecognised infection.

Additional chapter-specific clues

Alternative cavitary disease

NTM, lung abscess, fungal disease, squamous lung cancer, vasculitis and septic emboli can mimic pulmonary TB; microbiological confirmation prevents inappropriate months of therapy.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Suspected infectious TBIsolate, sample and notifyFirst stepCompatible pulmonary illness with epidemiological or radiological concern.

1Use local airborne precautions and appropriate room/respirator arrangements, minimise avoidable transfers and inform infection prevention and the TB team.
2Obtain respiratory samples for smear, culture and molecular testing, plus baseline bloods and HIV testing, without delaying treatment in a severely ill person.
3Notify suspected active TB through the current jurisdictional route and share exposure details with the health-protection team; do not wait for culture confirmation.

02Drug susceptibleStart specialist standard therapyActive pulmonary TB is confirmed or sufficiently likely and resistance risk is addressed.

1Use a specialist-prescribed daily weight-banded four-drug intensive phase—rifampicin, isoniazid, pyrazinamide and ethambutol—normally for 2 months.
2When susceptibility and response support it, continue rifampicin and isoniazid for a further 4 months; longer courses apply to selected sites or complications.
3Provide adherence support, interpreters, side-effect education and directly observed or video-supported treatment when a person-centred risk assessment indicates it.

03Resistance or intoleranceDo not improvise a regimenMolecular resistance, previous treatment, severe toxicity or poor response.

1Contact a specialist MDR-TB service immediately and avoid adding a single drug to a failing regimen.
2AlternativeRepeat culture and susceptibility, verify adherence and absorption, and assess interactions or an alternative diagnosis.
3Continue jurisdiction-specific isolation and public-health management based on infectivity and effective treatment, not a simplistic time cutoff.

04Follow-upProve response and protect completionA specialist tuberculosis treatment regimen has started.

1Review symptoms, weight, adherence, toxicity and respiratory culture at specialist-defined intervals; confirm conversion where initially culture positive.
2Act urgently on jaundice, vomiting, visual change, neuropathy, rash or major interaction and modify only with the TB team.
3At completion, document regimen, susceptibility, microbiological response and recurrence advice; coordinate ongoing contact and latent-infection care.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Provides multidrug treatment that prevents selection of resistance while rapidly reducing viable drug-susceptible pulmonary TB.

Rifampicin, isoniazid, pyrazinamide and ethambutol

Give once daily using the current specialist weight-banded BNF/NICE regimen for the usual 2-month intensive phase; fixed-dose combinations may be used when suitable.

Check baseline and symptomatic liver tests, renal function and vision. Rifampicin is a potent inducer with major contraceptive, anticoagulant, antiretroviral, transplant and many other interactions.

Completes eradication of drug-susceptible pulmonary TB after the initial four-drug phase.

Rifampicin plus isoniazid continuation

Use the current daily weight-banded specialist regimen for a usual further 4 months after the intensive phase when susceptibility and disease site support six total months.

Do not reduce treatment without susceptibility and response review. Hepatotoxicity and rifampicin interactions continue; missed treatment may require a revised completion plan.

Reduces isoniazid-associated peripheral neuropathy risk in pregnancy, malnutrition, diabetes, alcohol dependence, HIV, renal disease and other susceptible groups.

Pyridoxine

A common preventive regimen is 10 mg once daily with isoniazid for people at increased neuropathy risk; use higher specialist treatment doses if neuropathy develops.

Pyridoxine does not remove the need to assess new neuropathy or review isoniazid. Confirm current BNF dose for the indication and patient.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Respiratory failure

Extensive bilateral disease, airway destruction or acute respiratory distress can cause severe gas-exchange impairment, creating an additional need for recognition and targeted treatment.

Massive haemoptysis

Cavities erode bronchial vessels or develop pulmonary-artery pseudoaneurysms, producing life-threatening bleeding, and potentially prolonging treatment and functional recovery.

Disseminated tuberculosis

Bloodstream spread causes meningitis, miliary disease, bone, renal or other organ involvement with high morbidity, with severity determined by its extent and the patient's underlying reserve.

Post-tuberculous lung disease

Healing leaves fibrosis, volume loss, bronchiectasis and cavities that cause chronic breathlessness, infection and fungal colonisation.

Transmission and resistance

Delayed isolation or incomplete effective treatment exposes contacts and can select or propagate drug-resistant disease, with severity determined by its extent and the patient's underlying reserve.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review symptoms, weight and adherence regularly because weight changes can alter dose bands and missed doses can compromise completion.
Check liver tests promptly for nausea, vomiting, abdominal pain, jaundice or unexplained malaise; use the TB service's thresholds for stopping hepatotoxic drugs.
Ask about visual acuity and colour change during ethambutol; stop and obtain urgent ophthalmic/TB advice for suspected optic toxicity.
Repeat respiratory cultures through the specialist pathway until conversion is demonstrated where relevant; persistent positivity requires adherence, resistance and absorption review.
Update the health-protection team on infectivity, contact tracing and treatment outcome while respecting the legal framework of the relevant UK nation.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Smear is not species

Acid-fast bacilli may represent M. tuberculosis or NTM. Rapid molecular testing and culture are essential before assuming either diagnosis.

Negative smear is not no transmission

Smear-negative pulmonary TB can still be infectious, particularly with cough and cavitation; infection-control decisions require the whole assessment.

Rifampicin changes other prescriptions

Enzyme induction can cause contraceptive failure or loss of anticoagulant, antiretroviral, anticonvulsant and transplant-drug effect; a formal interaction review is mandatory.

Pregnancy is not a reason to ignore TB

Active disease threatens parent and fetus. Regimen selection, pyridoxine and monitoring require prompt specialist obstetric/TB coordination.

Isolation ends by assessment

Effective regimen, susceptibility, clinical response, smear burden and contact vulnerability matter; a universal 'two-week rule' is unsafe.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for culture before notifying a clinically suspected active TB case.
02
Assuming an acid-fast smear proves M. tuberculosis rather than NTM.
03
Starting rifampicin without reviewing contraception, anticoagulation and other major interactions.
04
Stopping airborne precautions solely because an arbitrary number of treatment days has passed.
05
Adding one antibiotic to a suspected failing or resistant TB regimen.