Tuberculosis

Definition

Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis, a slow-growing bacterium spread in tiny airborne droplets when a person with infectious pulmonary TB coughs, sings or sneezes. It usually settles in the lungs (pulmonary TB) but can affect almost any organ (extra-pulmonary TB). The disease exists in two quite different states — latent TB infection, where the bacteria are present but dormant and the person is well and not infectious, and active TB disease, where the bacteria multiply and cause illness.

Pathophysiology

Inhaled bacteria reach the small airways and are engulfed by lung macrophages. Rather than being destroyed, M. tuberculosis survives inside them, provoking a cell-mediated immune response that walls the infection off inside a granuloma. In most people this containment holds indefinitely — latent infection, with a normal chest X-ray and a lifelong reactivation risk of roughly 5–10%, considerably higher with immunosuppression.

When containment fails, either soon after infection or decades later, the granuloma breaks down. Caseous necrosis liquefies its centre, the lesion erodes into an airway, and the cavity that results discharges enormous numbers of bacteria into the sputum — which is what makes pulmonary TB infectious. Because the upper lobes are the best ventilated and most oxygen-rich part of the lung, this classically happens there, producing the upper-zone shadowing and cavitation seen on imaging. Progressive inflammation and tissue destruction leave permanent scarring, distorted airways and lost lung volume even after the infection is cured.

Co-morbidities

Risk of progression and severity is increased by human immunodeficiency virus (HIV) infection, diabetes, immunosuppressive and biologic therapy, chronic kidney or liver disease, malnutrition, smoking, alcohol and silica exposure. Two co-morbidity relationships matter particularly for cardiorespiratory practice. Silicosis raises TB risk substantially, so any worker with silica exposure and a persistent cough warrants TB testing. And after cure, post-TB lung disease — scarring, bronchiectasis or fixed airflow obstruction — is now recognised as a chronic respiratory condition in its own right, affecting a large proportion of survivors.

Prevalence

Australia has one of the lowest TB rates in the world, at around five to six notified cases per 100,000 people each year. Most occur in people born in higher-incidence regions, with higher risk also in some Aboriginal and Torres Strait Islander communities and in the Torres Strait–Papua New Guinea treaty area. Globally the picture is very different: TB remains among the leading infectious causes of death worldwide, and drug-resistant disease is a substantial and growing share of it.

Causes and risk factors

• Exposure — prolonged close contact with someone with infectious pulmonary TB, particularly in crowded or poorly ventilated spaces. Household contacts are at highest risk.
• Country of birth or travel — birth, residence or extended travel in a high-incidence region.
• Immunosuppression — HIV infection (the single strongest risk factor for progression), transplant, chemotherapy, tumour necrosis factor (TNF) inhibitors and long-term corticosteroids.
• Diabetes mellitus — roughly triples the risk of active disease.
• Silica exposure — silicosis and even silica exposure without established silicosis increase TB risk markedly, a well-established occupational association.¹
• Smoking, alcohol dependence and malnutrition.
• Age — very young children and older adults are more likely to progress to active disease.

Symptoms

Latent versus active TB

Latent TB has no symptoms at all. A person with latent infection feels entirely well, has a normal chest X-ray and cannot pass TB to anyone. This distinction is the source of most of the confusion and anxiety patients bring to a consultation, and is worth stating plainly.

Typical features of active pulmonary TB

• A persistent cough lasting more than two to three weeks, usually productive of sputum.
• Coughing up blood or blood-stained sputum (haemoptysis).
• Fevers and drenching night sweats.
• Unintended weight loss and loss of appetite.
• Fatigue and a general sense of being unwell, often developing over weeks to months rather than days.
• Breathlessness or pleuritic chest pain where the pleura or larger airways are involved.

Extra-pulmonary presentations

Around one in five cases in Australia is extra-pulmonary, and the presentation follows the organ involved: a painless swollen neck lymph node, back pain and deformity in spinal TB, headache and confusion in TB meningitis, abdominal pain and ascites, sterile pyuria in renal TB, or a monoarthritis. These forms are generally not infectious, which is an important reassurance.

When to seek assessment

A cough lasting more than three weeks, or unexplained fevers, night sweats or weight loss, should be assessed — particularly after time in a high-incidence country or known contact with someone with TB. That warrants a prompt appointment and a chest X-ray rather than same-day care.

Diagnosis

Why diagnosis matters

Prompt diagnosis allows effective treatment, prevents onward transmission through isolation and contact tracing, and identifies drug resistance early — all critical to cure and to public-health control. TB is a notifiable disease in Australia: confirmed and suspected cases are reported to the public health unit, which coordinates contact tracing and screening.²

How is it diagnosed?

No single test is sufficient. Diagnosis combines clinical suspicion, imaging, microbiology and tests of immune response, and the sequence depends on whether latent infection or active disease is in question. Anyone with suspected infectious pulmonary TB is managed with airborne precautions from the outset, before results return.

Radiology

The chest X-ray is the workhorse. Active pulmonary TB classically shows upper-lobe or apical infiltrates, often with cavitation; in primary or paediatric disease, hilar and mediastinal lymphadenopathy with lower-zone consolidation is more typical. Miliary TB produces a fine diffuse nodular pattern throughout both lungs. CT is more sensitive for early or subtle disease, for tree-in-bud change indicating endobronchial spread, and for defining the bronchiectasis, cavitation and fibrosis of established post-TB lung disease.

Microbiology

Three sputum specimens are collected, ideally early morning, for smear microscopy, nucleic acid amplification and culture. Smear-positive patients are the most infectious. Where sputum cannot be produced, induced sputum, bronchoscopic sampling or gastric aspirate in children may be used — each aerosol-generating and requiring appropriate precautions. Culture remains essential because it enables full drug-susceptibility testing.

Tests of infection: TST and IGRA

These detect the immune response and therefore identify infection, latent or active, without distinguishing between them. They are used chiefly to diagnose latent TB in contacts and in people about to start immunosuppression. Both can be falsely negative in advanced disease, severe immunosuppression and young children.

Lung function

Spirometry has no role in diagnosing active TB, but is central afterwards. Post-TB lung disease commonly produces obstructive, restrictive or mixed defects with reduced gas transfer, and baseline spirometry at treatment completion gives a reference point for the years of respiratory follow-up that many survivors need.

Investigations for related conditions

Testing for HIV is routine in all cases, along with blood glucose or glycated haemoglobin, and baseline liver and kidney function — the latter because the drug regimen is hepatotoxic. Vision and colour vision are checked before ethambutol. Contacts are screened for latent and active TB by the public health unit.

Management

Management and goals

The goals are to cure the individual, prevent transmission to others, prevent the emergence of drug resistance, and limit permanent lung damage. Treatment is coordinated through specialist TB or respiratory services together with the public health unit, and is provided free of charge in Australia regardless of visa or Medicare status — a point worth making explicitly to patients who fear cost.

Treatment options

Active drug-sensitive TB is treated with combination antibiotics over six months (see Medications below). Latent TB is treated preventively in those at higher risk of reactivation — contacts, children, people with HIV, and those about to begin immunosuppression — which substantially reduces the chance of ever developing active disease. Drug-resistant disease requires longer, specialised regimens.

Isolation and infection control

People with infectious pulmonary TB are isolated with airborne precautions — a negative-pressure room where available, and fit-tested particulate respirators for staff — until they are no longer considered contagious, usually after about two weeks of effective treatment with clinical improvement and falling smear positivity. Aerosol-generating procedures, which include several physiotherapy techniques, carry particular risk and must follow local infection-control policy.³

Adherence and directly observed therapy

Completing every dose is the single most important determinant of cure, and the reason directly observed therapy (DOT) is widely used. Six months of daily tablets while feeling well after the first few weeks is genuinely difficult, and the consequences of stopping early — relapse and acquired resistance — are severe. Practical support, reminders, treatment supporters and video-observed therapy all improve completion.

Identifying deterioration

Worsening cough, fever or weight loss after an initial response, new or increasing haemoptysis, or failure to improve by two months of treatment should prompt urgent review for drug resistance, poor adherence or an alternative diagnosis. New jaundice, dark urine, nausea or right upper abdominal pain suggests drug-induced hepatitis and requires immediate assessment.

Action plan

Every person on TB treatment should know which symptoms mean stop and call — jaundice, persistent vomiting, visual change, rash or fever — who to contact after hours, when they may return to work or study, and the date of their next review. Written information in the person's preferred language, with an interpreter for consultations, is standard rather than optional.

Medications

Medications for tuberculosis

Active drug-sensitive TB is treated over six months: a two-month intensive phase of four drugs — rifampicin, isoniazid, pyrazinamide and ethambutol — followed by a four-month continuation phase of rifampicin and isoniazid. Pyridoxine (vitamin B6) is given alongside isoniazid to prevent peripheral neuropathy. Shorter four-month regimens containing rifapentine and moxifloxacin have been shown non-inferior to the standard six-month course in drug-susceptible pulmonary TB and are entering guidelines internationally.⁴

Order and combination of medications

TB is never treated with a single drug. Multiple agents are used together from the start precisely because monotherapy selects for resistance within weeks. Fixed-dose combination tablets reduce pill burden and make inadvertent monotherapy less likely. The intensive phase eliminates the rapidly dividing bacterial population; the continuation phase eliminates the slowly dividing persisters that cause relapse — which is why the later months, when the person feels well, cannot be dropped.

Drug-resistant tuberculosis

Multidrug-resistant (MDR) and extensively drug-resistant (XDR) TB require longer regimens built around newer agents, managed exclusively by expert services. All-oral six-month regimens have substantially improved on the older injectable-containing courses: a bedaquiline, pretomanid, moxifloxacin and linezolid regimen was superior to standard care in rifampicin-resistant disease,⁵ and linezolid dose and duration can be reduced to limit toxicity while preserving efficacy.⁶

Side effects to watch for

Hepatotoxicity is the most important, and liver function is monitored. Rifampicin turns urine, tears and sweat orange — harmless, but alarming if unexpected, and it stains soft contact lenses. It also induces liver enzymes and interacts with many drugs, including hormonal contraception, warfarin and antiretrovirals. Ethambutol can cause optic neuritis, so any change in vision or colour perception must be reported immediately. Isoniazid causes peripheral neuropathy, and pyrazinamide raises uric acid and may provoke gout.

Multi-system manifestations

Pleura

Tuberculous pleuritis presents with pleuritic pain, fever and a lymphocyte-rich exudative pleural effusion, and may resolve leaving pleural thickening or, uncommonly, a fibrothorax that restricts chest wall movement.

Lymph nodes

The commonest extra-pulmonary site. Cervical lymphadenitis produces painless, firm, often matted nodes that may soften and discharge. Nodes can paradoxically enlarge during effective treatment, which is a recognised immune response rather than treatment failure.

Spine and bone

Spinal TB (Pott disease) causes insidious back pain, vertebral collapse and kyphotic deformity, with risk of cord compression and paraparesis — a neurological emergency. It has direct physiotherapy implications for posture, bracing, mobility and rehabilitation after surgical stabilisation.

Central nervous system

TB meningitis is the most lethal form, presenting subacutely with headache, fever, vomiting, confusion and cranial nerve palsies. Survivors are frequently left with lasting neurological deficit requiring prolonged rehabilitation.

Abdomen and genitourinary tract

Abdominal TB causes pain, ascites and bowel obstruction; renal TB may be silent for years and present with sterile pyuria or haematuria, and can cause infertility through genital tract involvement.

Post-TB lung disease

The most relevant long-term manifestation for cardiorespiratory practice. Cure of the infection does not restore the lung: survivors are left with combinations of fibrosis, cavitation, bronchiectasis, airflow obstruction, reduced gas transfer and, in some, pulmonary hypertension. Clinical standards now exist for the assessment, management and rehabilitation of this population.⁷ Functional consequences are substantial — measurably reduced exercise capacity and quality of life persisting well after microbiological cure, and worse after drug-resistant disease.⁸

Living with tuberculosis

Treatment as a long haul

Six months is a long time to take tablets, and most people feel better within weeks. Anticipating the mid-course dip in motivation, and normalising it, does more for adherence than repeating warnings.

Nutrition

Weight loss and poor appetite are near-universal at diagnosis, and undernutrition both worsens outcomes and slows recovery. Regular small energy- and protein-dense meals, with dietetic input where weight loss has been marked, support both cure and rehabilitation.

Sleep and fatigue

Night sweats, cough and anxiety disrupt sleep early on, and fatigue outlasts the infection by months. Graded activity rather than complete rest is the better approach once treatment is established and precautions allow.

Work, study and travel

Return to work or study is guided by the treating team and public health unit, and for infectious pulmonary TB usually follows about two weeks of effective treatment with clinical improvement. Air travel is generally deferred until non-infectious.

Family and contacts

Household and close contacts are screened for latent and active TB. Explaining that screening protects the family, and that latent infection is neither illness nor contagion, prevents much distress.²

Stigma and mental health

TB still carries significant stigma, particularly in some migrant communities, and fear of disclosure can delay presentation and undermine treatment. Confidentiality, interpreters and a matter-of-fact tone matter clinically, not just socially. Anxiety and low mood are common and should be asked about.

Prognosis

Drug-sensitive TB is curable, with cure rates above 85–90% when treatment is completed in full, and most people recover well. Outcomes are worse with delayed diagnosis, drug resistance, HIV co-infection, extensive cavitation and significant co-morbidity. Cure is not always the end of the story: a substantial minority are left with post-TB lung disease and persistent functional limitation, and this group warrants long-term respiratory follow-up and rehabilitation rather than discharge.

Role of the physiotherapist

Physiotherapy does not treat the infection, and during the infectious phase the priority is safety: recognising that several core techniques — sputum induction, airway clearance, nebulised therapy and exercise testing — are aerosol-generating, and delivering them only with appropriate airborne precautions and local infection-control approval, or deferring them until the person is non-infectious.

Once treatment is established, the role expands considerably. Where the airways are involved or secretions are retained, airway clearance and the active cycle of breathing technique help sputum clearance and reduce the work of breathing. As people recover, cardiorespiratory rehabilitation and graded exercise rebuild the fitness and muscle mass lost to a long febrile illness — pulmonary rehabilitation improves exercise capacity and quality of life in people with TB pulmonary sequelae.⁹ Post-TB bronchiectasis is managed on the same principles as bronchiectasis from any cause, with regular airway clearance and exercise as the mainstays.^10,11 Breathing retraining addresses the dysfunctional breathing pattern and breathlessness-related anxiety that frequently persist, and spinal or neurological TB brings the physiotherapist into a primary rehabilitation role.

Part 1 · References

1. Ehrlich R, Akugizibwe P, Siegfried N, Rees D. The association between silica exposure, silicosis and tuberculosis: a systematic review and meta-analysis. BMC Public Health 2021;21(1):953.
2. Communicable Diseases Network Australia. Tuberculosis: CDNA national guidelines for public health units. Canberra: Australian Government Department of Health and Aged Care; 2024.
3. World Health Organization. WHO guidelines on tuberculosis infection prevention and control: 2019 update. Geneva: WHO; 2019.
4. Dorman SE, Nahid P, Kurbatova EV, et al. Four-month rifapentine regimens with or without moxifloxacin for tuberculosis. N Engl J Med 2021;384(18):1705–1718.
5. Nyang'wa BT, Berry C, Kazounis E, et al. A 24-week, all-oral regimen for rifampin-resistant tuberculosis (TB-PRACTECAL). N Engl J Med 2022;387(25):2331–2343.
6. Conradie F, Bagdasaryan TR, Borisov S, et al. Bedaquiline–pretomanid–linezolid regimens for drug-resistant tuberculosis (ZeNix). N Engl J Med 2022;387(9):810–823.
7. Migliori GB, Marx FM, Ambrosino N, et al. Clinical standards for the assessment, management and rehabilitation of post-TB lung disease. Int J Tuberc Lung Dis 2021;25(10):797–813.
8. Muñoz-Torrico M, Cid-Juárez S, Góchicoa-Rangel L, et al. Functional impact of sequelae in drug-susceptible and multidrug-resistant tuberculosis. Int J Tuberc Lung Dis 2020;24(7):700–705.
9. Visca D, Zampogna E, Sotgiu G, et al. Pulmonary rehabilitation is effective in patients with tuberculosis pulmonary sequelae. Eur Respir J 2019;53(3):1802184.
10. Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for bronchiectasis in adults. Thorax 2019;74(Suppl 1):1–69.
11. Muñoz G, de Gracia J, Buxó M, Alvarez A, Vendrell M. Long-term benefits of airway clearance in bronchiectasis: a randomised placebo-controlled trial. Eur Respir J 2018;51(1):1701926.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.