Tuberculosis (TB) is an infectious disease caused mainly by <i>Mycobacterium tuberculosis</i>, a slow-growing bacterium that most often infects the lungs but can damage almost any organ. It spreads through the air when people with active pulmonary disease cough, sneeze, or speak, and it is among the oldest human diseases with physical evidence from ancient remains. Despite being preventable and largely curable with antibiotics, it remains one of the most lethal infectious diseases in the world. Its causes are biological, but its distribution follows poverty, malnutrition, crowding, and unequal access to health care, which is why it is treated as a problem of public health and social determinants as much as of medicine.
This entry covers the organism and how infection becomes latent or active, the host immune response that produces TB's characteristic tissue damage, and the clinical forms of the disease. It then reviews the global burden and its drivers, the methods of diagnosis, and the treatment of both drug-susceptible and drug-resistant disease, including the shorter regimens recommended in recent years. Prevention through vaccination, preventive therapy, and infection control is discussed alongside special populations such as children, pregnant women, and people living with HIV. The entry closes with the historical discovery of the pathogen, the cultural history of the disease, the governance and funding of global TB control, the economic and human-rights dimensions, zoonotic TB in animals, and the open research questions that remain.
Causative organism and biology
Taxonomy and the acid-fast property
Tuberculosis is caused mainly by Mycobacterium tuberculosis, one member of the bacterial M. tuberculosis complex (MTBC). The MTBC is divided into nine lineages based on whole genome single nucleotide polymorphisms. The name acid-fast describes a staining property. When stained with alternative dyes, the cell wall resists decolorization with acid alcohol, which gives these bacteria the name "acid-fast." The Ziehl–Neelsen stain exploits this property and is used in microbiology and cytopathology to identify acid-fast bacteria under microscopy, particularly members of the Mycobacterium genus. Because the stain works on the cell envelope rather than on any single protein, it gives a quick, low-cost indication of mycobacteria, though it cannot distinguish M. tuberculosis from other mycobacteria by itself.
The waxy cell envelope
The envelope is unusual for a bacterium. It consists of a thick, lipid-rich outer layer composed primarily of mycolic acids. This lipid layer lies on top of a layer of peptidoglycan and the polysaccharide arabinogalactan, which are anchored to the inner membrane common to all bacteria. The lipid layer has practical consequences for survival. Acid-fast organisms are highly resistant to disinfectants and dry conditions. It also protects the bacterium inside host cells. Mycobacteria with mycolic acid in their cell wall are resistant to phagocytic destruction. Disrupting the envelope has direct effects. In one study, chemically inhibiting the enzymes that modify mycolic acids led to a loss of acid fastness and increased membrane permeability. The same biology explains why isoniazid, a first-line drug, works: it inhibits the synthesis of mycolic acids, and M. tuberculosis grown in the presence of isoniazid loses its acid-fastness.
Slow growth, dormancy, and persistence
M. tuberculosis divides slowly. Under typical culture conditions its doubling time is 18–24 hours, and in one minimal-medium study it grew with acetate as the sole carbon source at a doubling time of about 21 hours, similar to rich media (18 to 20 hours). Under nutrient limitation the rate falls further. In one chemostat experiment, doubling times of 69 hours and 23 hours corresponded to the two growth rates tested.
Slow division is linked to a dormant subpopulation. Nutrient limitation and low oxygen tension inside the granuloma are thought to trigger a metabolic downshift in subpopulations of bacteria. Regulators such as DosR and PhoP control entry into a nonreplicative state under hypoxia and acid stress, while RelA mediates starvation-induced nonreplication. Dormancy has a pharmacological cost: the metabolic downshift is accompanied by increased antibiotic tolerance. Most TB drugs act on processes needed for growth, so they fail to eradicate nonreplicating bacilli, which could explain the prolonged treatment time required to cure disease. Drug-tolerant "persister" cells are one observed form of this tolerance. In culture, persisters were a few during lag and early exponential phases, but made up to 1% in late exponential and stationary phases. Clinically, the bacteria can remain dormant for years without showing clinical symptoms. Studies of short regimens suggest that persisters also contribute to relapse: attempts to shorten therapy for drug-susceptible TB to less than 6 months in phase III trials resulted in high rates of treatment failure and relapse, often attributed to the capacity of drug-tolerant persister bacilli to survive antibiotic exposure.
Genetic lineages
The MTBC contains lineages whose geographic distribution, transmissibility, and disease phenotype differ. M. tuberculosis lineages show variability in geographic distribution, transmissibility, and disease phenotype. Lineages 1–4 are the most widely distributed, and different parts of the world are dominated by different lineages. Lineage 1 is concentrated in a few high-burden countries: more than 80% of the global Lineage 1 burden was in India, the Philippines, Indonesia, and Bangladesh. In sub-Saharan Africa, Lineage L4 dominates, and drug resistance was found in 80% of countries.
Lineages also differ in drug-resistance patterns. In one global whole-genome analysis, multidrug resistance rates by lineage were 3% for lineage 1, 48% for lineage 2, 4% for lineage 3, and 23% for lineage 4. Lineage 2 (the Beijing family) has been especially studied in this respect. Research on it describes the impact of compensatory mutations on the development of high transmissibility and virulence, which suggests that resistance and fitness can evolve together in some strains. Because these associations come from sequencing studies of varying size and setting, they describe patterns observed in particular populations rather than fixed properties of each lineage.
Transmission, latent infection, and progression to disease
Airborne transmission
Tuberculosis spreads through the air rather than by touching contaminated surfaces. TB is transmitted from an infected person to a susceptible person in airborne particles, called droplet nuclei. These particles are released when people with pulmonary or laryngeal disease cough, sneeze, speak, or sing. Their size is what matters: droplet nuclei are the residuals of droplets that, when suspended in air, subsequently dry and produce particles ranging in size from 1–5 μm. Because they are so light, the tiny bacteria can be carried by air currents throughout a room or building. Only particles in the 1–5 μm range reach the terminal airspaces of the lung, and each is understood to contain only a few bacteria. Larger droplets settle quickly or are caught in the mucus of the upper airway.
Whether a given contact becomes infected depends mainly on dose and duration. The likelihood of transmission depends on the number of infectious droplet nuclei per volume of air (infectious particle density) and the length of time that the uninfected individual spends breathing that air. Confined rooms with recirculated air and little ultraviolet light allow viable bacilli to accumulate, and MTB germs survive in droplet nuclei unless exposed to UV light, sunlight. Proximity matters mainly because it increases the concentration a person inhales.
The infectiousness of the source case is equally important. Patients with high loads of the bacteria in their expelled sputum are more likely to transmit the infection than those with low numbers of bacteria. Bacterial load alone is not decisive: the physical and chemical properties of sputum, and/or cough characteristics or behavior may determine whether they produce a large or small number of droplet nuclei. Before treatment begins, sputum smear positivity can be used to estimate infectiousness. Effective treatment is the most powerful way to reduce it.
Infection without disease
Latent tuberculosis infection describes a person who carries <i>M. tuberculosis</i> without signs of illness. People with LTBI do not have signs and symptoms of TB disease, and they cannot spread M. tuberculosis to others. Without treatment, about 5–10% of infected people will develop TB disease over their lifetimes. One-half of this risk occurs within the first two years after infection. The risk is uneven: the risk is particularly high among children under the age of 5 years and among people with compromised immunity. The WHO notes a 5–15% lifetime risk of falling ill with TB, so published figures vary with the population and method used.
Reactivation
Latent infection does not always remain quiescent. While latency may last for decades following infection, most patients who progress to active TB disease do so within the first 2 years following exposure. Reactivation happens when the host's control of the bacteria weakens. Host factors that increase the risk of progression to active TB disease include immunosuppression and advancing age. Persons with compromised immune systems, such as people living with HIV, malnutrition or diabetes, or people who use tobacco, have a much higher risk of falling ill. HIV is the strongest of these triggers: the risk of progression from LTBI to TB disease is 7% to 10% each year for those with both LTBI and untreated HIV infection. Socioeconomic hardship and therapy with immune modulatory agents such as tumour necrosis factor inhibitors are also associated with progression.
Why most infections never cause symptoms, and what this means for transmission
Because most infected people never become ill, the infected population is very large and long-lived. Its size is hard to measure directly: the global prevalence of LTBI is unknown due to difficulties in diagnosis. Still, the overall estimate is considerable, with the WHO estimating that 1.8 billion people, close to one quarter of the world's population, are infected with Mycobacterium tuberculosis.
This structure shapes the disease's reservoir. Latent carriers are not themselves contagious, so transmission is driven by people with active disease. However, active disease can go unrecognized for some time, since when a person develops active TB disease, the symptoms may be mild for many months. During that period an untreated person may keep expelling bacteria. Meanwhile, the latent pool acts as a slow, persistent source of future cases, because each reactivation can produce a new infectious case years or decades after the original infection. Interrupting transmission therefore requires finding active cases quickly, while controlling the disease over the long term also depends on identifying and treating latent infection.
Immune response and pathology
Alveolar infection and the early innate response
When bacilli reach the lower airways, alveolar macrophages are the first cells in the lung to be infected after aerosol transmission. Mouse studies suggest that this early response is less inflammatory than earlier in vitro work implied. Infected alveolar macrophages up-regulate a cell-protective antioxidant transcriptional signature, and they generate a less robust inflammatory response than the uninfected cells around them. The bacteria therefore exploit these cells as a replicative shelter. In animal models, recruitment of innate cells such as neutrophils and monocytes to the lung and T cell priming in the draining mediastinal lymph nodes does not occur until 11-14 days following infection, by which time the bacteria have replicated nearly 1,000-fold in the lung. The bacterial niche later shifts: the dominant infected cellular niche shifts from alveolar to monocyte-derived macrophages (MDM) once T-cell immunity begins.
Granulomas: containment and tissue damage
The granuloma is the organized lesion that the host builds around infected cells. Early on, macrophage infection drives a localized inflammatory response recruiting mononuclear cells that contribute to host defense but may also provide new uninfected cells for mycobacterial growth. The inflammatory cells that die then form the caseous center of the granuloma, and with the arrival of lymphocytes, the granuloma acquires a more organized structure. Specific T lymphocytes, together with CD8+, NK and γδ T cells, infiltrate the lesion once adaptive immunity is established when adaptive immunity is initiated with the infiltration of specific T lymphocytes and also CD8+, NK and γδT cells.
The same structure is a double-edged one. It confines bacteria, yet its necrotic core can be a place where the mycobacteria can survive and may grow. Containment is not always permanent. Often the granulomas will undergo fibrosis or calcification and the infection is contained and becomes latent. Estimates of how often this containment fails vary; one preprint puts the share of latently infected people whose granuloma eventually fails at about 5-10%.
Caseous necrosis and cavitation
Caseous necrosis is named for its texture: the centre of the granuloma may exhibit caseous necrosis and have a cheese-like appearance. It is regarded as the pathophysiological hallmark of tuberculosis, and the region of caseous necrosis is lipid rich. The conventional account holds that macrophage death drives necrosis, which then destroys tissue. A competing view proposes that collagen destruction may be a critical initial event, causing caseous necrosis as opposed to resulting from it.
Cavity formation is most closely associated with liquefaction of the necrotic core. Once liquefied, the centre may liquefy, producing an environment in which the bacteria can grow extracellularly. A cavity can then arise when the liquefied contents are released into the bronchial tree where they can then be expelled externally and the infection transmitted to others. In post-primary disease, the lipid-rich necrosis has been linked to obstruction of small airways, in which caseation follows the development of an obstructive, lipid pneumonia in primarily small, apical pulmonary lobules, which results from the interaction of 6, 6'trehalose di-mycolate (cord factor) on the surface of Mycobacterium tuberculosis with surfactant. Tissue-degrading enzymes also contribute, since the degradation of fibrous tissue at the periphery of secondary granuloma by MMP-1 and MMP-9 has been implicated, and an excessive immune response is considered another factor.
T cells, cytokines, and how immune dysfunction shifts the outcome
Control of the infection depends heavily on CD4 T cells and interferon-gamma (IFN-γ). Human genetic studies point the same way: humans with genetic deficiencies in IFN-γ signaling or IL-12, a cytokine required for Th1 cell differentiation, succumb to lethal infections by environmental mycobacteria as well as the attenuated Mycobacterium bovis strain BCG. Loss of CD4 T cells in HIV infection also increases the risk of reactivation of latent infection. In mice, CD8 T cells protect only when they can make IFN-γ, since IFN-gamma production was essential for CD8 cell mediation of protective immunity against M. tuberculosis. IFN-γ activates macrophages in part by helping them deliver the bacterium to an acidic lysosome.
The picture is not fully settled. One mouse study identified Th1 CD4 T cells specific for the Mtb antigen ESAT-6 restrict in vivo Mtb growth, while this inhibition is independent of IFNγ or TNF, pointing to an alternative pathway. A more recent mouse study reported that control of lung Mtb burden is in fact dependent on T cell-derived IFNγ, and mice selectively deficient in T cell-derived IFNγ develop exacerbated disease. IFN-γ may also act on the bacterium itself: recombinant and T-cell derived IFN-γ rapidly induced a dose-dependent increase in the oxygen consumption rate (OCR) of Mtb, consistent with increased bacterial respiration.
Outcome depends on the balance between these responses and host state. One model holds that a stable granuloma harboring dormant Mtb becomes destabilized due to "immunosuppression," leading to liquefaction of the central caseous necrosis and subsequent multiplication of Mtb. In this view, the same lesion that held the infection in check can become the site of progression when host immunity weakens.
Clinical presentation and extrapulmonary forms
Pulmonary tuberculosis
Pulmonary disease is the most common form of the illness, and its onset is usually slow. Symptoms of active TB disease in the lungs usually begin gradually and worsen over a few weeks. The cough is the most frequent complaint. It may at first bring up only a little yellow or green sputum, often on waking, and becomes more productive as the disease advances. Clinicians grow more suspicious when a cough lasts beyond two to three weeks and is accompanied by fever, night sweats, weight loss, or enlarged lymph nodes, particularly in someone with known exposure or who lives in or has travelled to an endemic area.
Systemic symptoms are common but not specific. Low-grade fever is frequent though not universal, and drenching night sweats are a classic feature that does not by itself indicate TB. Fever tends to peak in the late afternoon. Chest pain and breathlessness can arise from inflamed pleura, lung tissue damage, or a collapsed lung. Coughing up blood is uncommon and usually reflects cavitary disease in which granulomatous damage erodes into bronchial blood vessels. Because these features overlap with pneumonia, lung cancer, and chronic obstructive disease, misdiagnosis is possible. One reported case of endobronchial TB, for example, was first treated as pneumonia after a pulmonary embolism had been considered. In children the picture is often vaguer: most have few symptoms apart from a characteristic brassy cough, although low-grade fever and poor growth can occur.
Extrapulmonary disease
Spread through the bloodstream and lymphatic vessels can seed the bacillus into other organs. Up to a quarter of tuberculosis cases involve sites outside the lungs. The most frequent locations are the lymph nodes, the pleura, and the bones and joints.
Lymph node involvement is the most common extrapulmonary form. It usually presents as painless enlargement of one or more nodes, most often in the posterior or anterior cervical chain or the supraclavicular fossa. Diagnosis depends on finding mycobacteria in aspirates or biopsy material. In the pleura, the disease typically causes pleuritic chest pain, a dry cough, and breathlessness, with a usually one-sided effusion that is small to moderate in size. Osteoarticular disease is also notable. Bone and joint involvement may account for up to 35 percent of extrapulmonary cases, and the spine is most often affected, which produces the condition known as Pott disease. Abdominal and urogenital forms can be harder to detect; the kidney and urinary tract are among the sites most frequently affected in the genitourinary category.
Clinicians distinguish less severe localized forms, such as nodal, bone, and joint disease, from severe forms that include meningitis, abdominal involvement, miliary tuberculosis, pericarditis, extensive pleural effusion, spinal involvement, and genitourinary involvement.
Tuberculous meningitis and other central nervous system involvement
Central nervous system tuberculosis includes tuberculous meningitis, which is the most common presentation, along with intracranial tuberculomas and spinal arachnoiditis. The mechanism is intense inflammation that follows the rupture of a small subependymal focus into the subarachnoid space, where the cerebrospinal fluid circulates. Early symptoms are nonspecific and laboratory tests have limited sensitivity, which makes diagnosis difficult.
The outcomes are severe. A 2020 meta-analysis of adult cases reported a pooled six-month mortality of 24%, and mortality was far higher among HIV-positive adults (57%) than among HIV-negative adults (16%). Physical disability was reported in 32 percent of adult survivors. In children, a meta-analysis of childhood cases estimated a mortality risk of about 19% and a risk of neurological disability of 54% among survivors. Prognosis is worse with delayed diagnosis and treatment, higher disease-severity grades, and drug resistance. Hydrocephalus and cerebral infarcts are also linked to poor outcomes, and adjunctive dexamethasone has been shown to reduce mortality, although its effect on long-term survival is less clear.
Miliary and disseminated disease
Miliary tuberculosis is the most serious form of disseminated disease. It arises when bacteria enter the bloodstream in large numbers and settle across many organs at once. The liver, spleen, and adrenal glands are commonly affected in the miliary form. Disseminated disease often involves both pulmonary and extrapulmonary sites.
The clinical picture is generally one of systemic severity: high fever, marked weight loss, breathlessness that may reflect low blood oxygen, enlargement of the liver and spleen, and involvement of several organ systems. Imaging typically shows numerous small nodules scattered through the lungs, which gives the disease its name from the resemblance to millet seeds. Concurrent meningitis or adrenal involvement is a sign of especially advanced illness, and such patients usually require urgent evaluation and hospital-level care.
Epidemiology and global burden
The WHO's Global Tuberculosis Report 2025, which summarises data for 2024, puts incident cases at 10.7 million, with a 95% uncertainty interval of 9.9–11.5 million. Those cases translate into an incidence of 131 per 100,000 people per year, with a 95% interval of 122–141. WHO also estimated 1.23 million deaths that year, and about 150,000 of them occurred among people living with HIV 2-9,5-15. The 2024 total was only slightly below the 10.8 million estimated for 2023 3-12, but the decline ended three consecutive years of increases linked to pandemic-era service disruption 23-5.
Burden is unevenly distributed across WHO regions. The South-East Asia Region carried 34% of new cases in 2024, the Western Pacific 27%, and the African Region 25% 4-10. South-East Asia's incidence was 201 per 100,000, and its rate had fallen 16% since 2015, compared with a global decline of 12% 20-2,20-6. In the Americas the trend is less uniform. A regional analysis of South America, drawing on 2024 report data, found that most countries there recorded significant rises in incidence and that the region's 2025 milestone had become virtually unattainable 21-7,21-8,21-9. Peru, for example, reported an incidence of 173 per 100,000 in 2023, matching the average for WHO's high-burden countries 17-2.
Concentration in a small group of countries remains marked. Around 87% of new cases occur in the 30 high-burden countries 4-2, and the largest contributors are India, Indonesia, the Philippines, China, Pakistan, Nigeria, the Democratic Republic of the Congo, and Bangladesh 23-4. India alone accounts for roughly one in four cases worldwide 3-14. The composition of the leading group has shifted over successive reports. In the 2024 report, India (26%), Indonesia (10%), China (6.8%), the Philippines (6.8%) and Pakistan (6.3%) together accounted for 56% of the global burden 15-2. The 2025 report's leading group extends that list to include Nigeria, the Democratic Republic of the Congo and Bangladesh, all of which now sit among the eight countries that together account for about two-thirds of cases 23-4.
Long-term progress has been real but slow relative to targets. WHO estimates that global efforts have saved 83 million lives since 2000 5-11. Between 2015 and 2024, incidence fell by 12% and deaths by 29% 7-9. The SDG-linked End TB Strategy set milestones for 2025 of a 50% reduction in incidence and a 75% reduction in deaths, compared with 2015 21-3, and a target of an 80% reduction in incidence by 2030 2-11. Progress also varies sharply between countries. By 2024, 101 countries had reduced incidence by at least 20%, and 30 had achieved a reduction of at least 50% 25-5,25-6, while 37 countries still showed rising incidence 25-8.
The COVID-19 pandemic disrupted this trajectory. Global incidence fell by only about 1% between 2023 and 2024, and it remained above its 2020 level 23-2,23-6. Early in the pandemic, the number of newly reported cases dropped steeply, which WHO attributed to disrupted diagnosis and care 28-6. Notifications have since recovered: about 8.3 million people were diagnosed and treated in 2024, roughly 78% of estimated incident cases 23-3, up from about 8.2 million in 2023 15-1. Detection nonetheless remains incomplete. Prevalence surveys continue to find substantial numbers of bacteriologically confirmed cases with no symptoms, which points to ongoing transmission that routine case finding misses 23-3.
Risk factors and social determinants
Infection with Mycobacterium tuberculosis is necessary but not sufficient for disease. Most infected people never develop symptoms, and whether infection progresses depends largely on host immunity, which can be weakened by biological conditions, and on the social environment, which determines exposure and access to care.
Biological risk factors
HIV carries the largest individual risk of the factors listed by WHO. People living with HIV are 12 times more likely to fall ill with TB disease than people without HIV. In WHO's 2021 risk-factor estimates, the pooled relative risk for HIV was about 16, compared with about 3.2 for undernutrition, 3.3 for alcohol use disorders, 1.6 for smoking and 1.5 for diabetes. The two epidemics feed each other: TB is the leading cause of death among people with HIV. In 2024, about 150 000 people died of HIV-associated TB.
Population-level impact tells a different story, because common conditions affect far more people than HIV does. Globally in 2023, an estimated 0.96 million incident cases of TB were attributable to undernutrition, 0.75 million to alcohol use disorders, 0.70 million to smoking, 0.61 million to HIV infection and 0.38 million to diabetes. Undernutrition is therefore the largest contributor overall, although its estimate depends on the relative risk chosen. Recent attributable-fraction calculations have used a higher relative risk of 4.49, which comes from a single study that a WHO-commissioned review judged to be indirect evidence. Undernourished patients may also have more extensive lung involvement and cavitation, and they face higher risks of treatment failure, relapse and death.
Diabetes raises risk substantially. Diabetic individuals face a threefold increased risk of developing TB disease, with higher bacterial loads, delayed sputum culture conversion, increased mortality, higher relapse, and elevated drug resistance even during first TB episodes. The contribution of diabetes is also strongly setting-dependent: in an earlier analysis from India, a substantial proportion of incident tuberculosis was attributable to diabetes, at 14.8% of pulmonary tuberculosis and 20.2% of smear-positive tuberculosis. Smoking and harmful alcohol use act through similar immune and tissue pathways. Alcohol use has been estimated to be responsible for around 10% of TB cases worldwide. Across the 30 high-burden countries, undernutrition, alcohol use disorders and smoking are leading TB determinants in most countries, although HIV infection is the top contributor in several African countries, especially in southern and east Africa.
Structural drivers of transmission and disease
Poverty is the broadest determinant. The WHO describes it as a powerful determinant of tuberculosis. Its effect operates mainly through conditions that favour transmission: crowded and poorly ventilated living and working environments, often associated with poverty, are direct risk factors for tuberculosis transmission. Poverty also raises exposure to other risk factors, because it is associated with poor general health knowledge and a lack of empowerment to act on health knowledge, which increases exposure to HIV, smoking and alcohol abuse. Historically, declines in incidence in western Europe and North America followed economic change: the numbers of people developing TB and dying from the disease started to decline around the turn of the 20th century, as incomes grew, levels of poverty fell, and housing and nutrition improved.
Food insecurity and poor living and working conditions also matter for progression and treatment, not only for infection. Food insecurity and inadequate living and working conditions increase the risk of TB infection, disease progression and challenges in managing treatment, including its medical, financial and social demands. Occupational exposure can add a further biological burden: silicosis, for example, is one of the comorbidities that increase susceptibility to disease after infection. Indoor air pollution from solid fuels, which is concentrated in poorer households, is commonly cited as a further structural factor, although the evidence on its size is less settled.
Migration, incarceration and high-density settings
Transmission risk rises with the concentration of infectious aerosols and with the length of exposure, which explains why dense indoor settings are so important. Prisons often combine these features. Many prisons combine high occupancy density, prolonged indoor exposure, inadequate ventilation, and delays in separating or treating infectious individuals. Burden in prisons is therefore high relative to the general population. In high-burden countries, the prevalence and incidence of tuberculosis and the incidence of M tuberculosis infection were much higher among incarcerated individuals than in the general population. Among incarcerated people, the tuberculosis prevalence of 8,210 cases per 100,000 prisoners in those living with HIV is more than three times higher than in incarcerated people living without HIV. Prisons can also affect the surrounding community. Modelling work suggests that a substantial fraction of community TB cases in high-burden settings may be attributable, directly or indirectly, to transmission associated with incarceration.
Migration works through a different mechanism, mainly reactivation of old infection. The reasons for the TB burden in the migrant population are likely to be the reactivation of remotely-acquired latent tuberculosis infection following migration from low- or intermediate-income high TB burden settings to high-income, low TB burden countries. A substantial proportion of new TB cases in high-income countries arise among individuals who have migrated from another country. Migrants, prisoners and people in crowded housing are thus groups in which structural conditions and biological risk factors overlap, which is why the WHO links protection of these groups to poverty reduction, better housing and improved conditions in prisons and other congregate settings.
Diagnosis and screening
Sputum examination is the oldest routine method for diagnosing TB. Acid-fast staining, most often the Ziehl–Neelsen technique, makes mycobacteria visible under a light microscope, and the approach dates to the late nineteenth century. Smear examination offers speed and low cost, rarely yields false positives, and tends to catch the most infectious patients, yet it misses many cases in people co-infected with HIV. A slide typically needs a substantial bacterial load before it reads positive: under optimal conditions the threshold of detection is between 10^4 and 10^5 bacilli per ml, and field conditions often lower the yield further. Staining also cannot tell M. tuberculosis apart from other acid-fast organisms, so a positive slide needs confirmation.
Sensitivity varies widely between studies. In one Tanzanian cohort, the overall sensitivity of sputum microscopy was 61.8%, but sensitivity varied from 22.6% in specimens with fewer than 20 colony forming units per specimen to 94.2% in patients with more than 100 CFU per specimen plus confluent growth. Smear results come back negative in a considerable share of HIV-negative adults with lung disease, with published ranges spanning 20–60%. Children are a particular difficulty. Sputum smear microscopy and culture may be limited in young children and in children with HIV, because these children often have paucibacillary disease, which yields sputum with a low bacterial load. Because young children often cannot expectorate, clinicians may turn to induced sputum, gastric lavage or bronchoscopy to improve test sensitivity.
Culture remains the reference standard against which other methods are judged. Solid media such as Lowenstein–Jensen medium require incubation for several weeks before a culture is reported as negative, whereas liquid broth systems usually detect growth sooner, often within one to two weeks. Identification of the isolate and drug-susceptibility testing (DST) for agents such as rifampicin and isoniazid add further time, but they are needed to guide treatment, particularly where resistance is suspected.
Molecular tests have shortened this interval considerably. The Xpert MTB/RIF is a cartridge-based nucleic acid amplification test that detects MTB complex DNA and putative rifampin resistance mutations in a conserved 81 base-pair region of the rpoB gene. Within the PCR-based family of assays, the platform was first recommended in 2010, when the World Health Organization endorsed the test for people with HIV-associated TB or presumptive multidrug-resistant TB, and the recommendation was later extended to adults in general. Xpert Ultra has replaced Xpert MTB/RIF in many settings, and WHO recommends Truenat tuberculosis technology as well. Sensitivity still falls short in paucibacillary disease and in HIV, and false-positive and false-negative results can lead to incorrect treatment of patients, including overuse of second-line anti-TB drugs. A follow-on assay, Xpert MTB/XDR, is used to detect isoniazid (sensitivity 94.2%) and fluoroquinolone (sensitivity 93.2%) resistance in patients with bacteriologically confirmed pulmonary TB.
Global data show the gradual shift toward rapid testing. In 2024, 8.3 million people were newly diagnosed with TB, a small increase from 8.2 million in 2023 and about 78% of the estimated number of incident cases. Of these, 54% were initially tested with a rapid test, up from 48% in 2023.
Chest radiography is the usual imaging step. Upper-lobe infiltrates, cavities and nodules raise suspicion, but none of these findings is specific, so an image cannot confirm disease alone. Computer-aided detection (CAD) software assigns abnormality scores to digital radiographs and is used to screen and triage adults; WHO's 2025 report highlights AI-driven screening among its newly recommended tools. Within the AI field, these systems rely on computer vision trained on labelled images, and their accuracy must be validated in each population before routine use.
Tests for infection rather than disease are different again. The tuberculin skin test injects purified protein derivative under the skin and reads the local induration after roughly 48 to 72 hours. In people with HIV, ≥5 mm of induration after TST placement is considered a positive test, yet even with this lower cutoff, sensitivity remains poor. Interferon-gamma release assays (IGRAs) instead measure interferon-gamma released by T cells in a blood sample after stimulation with TB-specific antigens, and they are not affected by most prior BCG vaccination. Neither test separates latent infection from active disease: a positive result indicates exposure to the bacterium, while a negative result does not exclude infection in people with weakened immunity.
Treatment of drug-susceptible tuberculosis
The standard six-month regimen
Drug-susceptible TB is treated with several drugs at once, so that a bacterium carrying a mutation for resistance to one agent is still killed by the others. The conventional regimen uses isoniazid, rifampicin, pyrazinamide and ethambutol. The WHO guidelines of 2010 and 2017 centred on a six-month course built from these four first-line medicines. In the usual schedule, all four drugs are given for the first two months (the intensive phase), and isoniazid and rifampicin alone continue for the next four months (the continuation phase). The long course reflects the slow growth of Mycobacterium tuberculosis and the bacterial subpopulation that tolerates drugs for a time.
Shorter four-month regimens
The main test of a shorter course came from a phase 3 trial, TBTC Study 31/ACTG A5349, which compared several four-month regimens with the six-month standard. The regimen combining rifapentine and moxifloxacin was found to be non-inferior to the control regimen, whereas the rifapentine regimen that kept ethambutol did not meet the non-inferiority criteria. The safety profile of the rifapentine-moxifloxacin arm was similar to the standard treatment. The current CDC schedule consists of eight weeks of daily rifapentine, moxifloxacin, isoniazid and pyrazinamide, followed by nine weeks of rifapentine, isoniazid and moxifloxacin, for 119 doses in total, and is recommended for people aged 12 and older who weigh at least 40 kg and whose disease is not known or suspected to be drug-resistant. A pharmacokinetic analysis of the trial found that low rifapentine exposure is the strongest driver of tuberculosis-related unfavorable outcomes, which suggests that drug levels, not only the regimen itself, shape results. WHO now recommends, conditionally, that people aged 12 or older with drug-susceptible pulmonary TB may receive this four-month regimen, based on moderate-certainty evidence. For children, a four-month regimen of 2HRZ(E)/2HR is recommended for children and adolescents aged 3 months to 16 years with non-severe TB, without suspicion or evidence of MDR/RR-TB.
Directly observed therapy and adherence
Incomplete treatment is one of the main routes to drug resistance. Non-adherence is the leading contributor to the selection of drug-resistant strains of Mycobacterium tuberculosis and to subsequent treatment failure. Directly observed therapy (DOT) is the main countermeasure. It means that a healthcare worker watches the patient swallow each dose of the prescribed drugs. Under the CDC schedule, at least 5 of 7 weekly doses should be administered under direct observation. Adherence strategies also include patient-centred models. In Tanzania, for example, new TB patients may choose between home-based treatment supervised by a treatment supporter of their own choice and facility-based treatment observed by a medical professional. Timing matters as well: a shortened regimen must be completed within a fixed window, and if this target is not met, the patient should be considered to have interrupted therapy.
Adverse reactions and hepatotoxicity monitoring
Isoniazid and, to a lesser degree, other first-line drugs can injure the liver, and monitoring is designed around this risk. A review of antituberculosis hepatotoxicity sets the threshold for stopping isoniazid at alanine aminotransferase at least three times the upper limit of normal when jaundice or hepatitis symptoms are reported, or at least five times the upper limit in the absence of symptoms. Face-to-face monthly assessments and patient education about adverse drug events are considered essential, and a rapid rise in enzyme levels may call for more frequent checks. Pregnant women are at higher risk of isoniazid-induced liver injury and should have monthly ALT monitoring. Hepatotoxicity also affects whether people finish treatment. In a cohort of healthcare workers taking nine months of isoniazid for latent infection, those who discontinued had more hepatotoxicity than those who completed treatment (44.2% vs. 11.3%). Because the drugs are given to people who feel well, a treatment-related reaction is a common reason for stopping, so early identification and management of side effects supports completion.
Interactions with antiretroviral therapy
Rifampicin is a strong enzyme inducer, and its interaction with antiretroviral drugs is the main complication of treating TB in people with HIV. When the six-month regimen is used, these interactions may lower concentrations of antiretroviral drugs. The clearest example is dolutegravir, a first-line ART drug. Rifampicin induces UGT1A1 and cytochrome P450 3A4, increasing dolutegravir metabolism and reducing its plasma concentrations. The usual adjustment is to give dolutegravir 50 mg twice daily, and to keep this for two weeks after the last dose of rifampicin. In the RADIANT-TB trial, the higher dose was effective and well tolerated in people with HIV and tuberculosis. Efavirenz, by contrast, has no major drug–drug interaction with rifampicin, which is one reason the choice of ART depends partly on the TB regimen. Interactions also vary by drug: with tenofovir alafenamide, for instance, rifampicin lowers plasma levels of the drug, yet the active tenofovir metabolite still reaches levels that may be adequate for HIV treatment.
Drug-resistant tuberculosis
Definitions and drivers
Resistance is classified by which first-line drugs an isolate survives. Rifampicin-resistant TB is defined as TB caused by an isolate that shows resistance to rifampicin, but is susceptible to isoniazid. MDR-TB is defined as TB caused by an isolate that shows resistance to at least isoniazid and rifampicin. Because almost all M. tuberculosis strains resistant to rifampicin are also resistant to isoniazid, most rifampicin-resistant disease is MDR. Newer molecular assays have made rifampicin mono-resistance more visible, and many regions report a growing burden of rifampicin mono-resistant TB. Further categories exist: pre-extensively drug-resistant TB is defined as TB caused by an isolate that shows resistance to isoniazid, rifampicin, and either fluoroquinolones or injectable agents.
At the molecular level, resistance is associated with random mutations that alter the structure or quantity of intracellular drug targets. In isoniazid resistance, mutations in its activator, KatG, are the main mechanism, whereas mutations in the inhA gene represent the second most common mechanism. Together, mutations in these two genes are responsible for approximately 75% of the cases seen clinically.
The main driver at the population level is treatment failure. Inadequate treatment can result in drug-resistant MTB among these patients (acquired resistance), and those resistant strains can be transmitted to other individuals (primary resistance). Inadequately treated patients become chronic carriers and spread drug-resistant TB to their families and communities.
Older regimens and their limits
Before the newer regimens, MDR-TB treatment was long. It was administered either a shorter (9 months) or individualized treatment regimen (18 months). The drugs were costly and hard on patients: multidrug-resistant TB is difficult to treat; treatment requires drugs that are expensive, toxic, and less effective. Injectable agents were central to the most severe categories, since extensively drug-resistant TB was defined partly by resistance to amikacin, capreomycin, or kanamycin. The duration and side-effect burden also weakened adherence, with long treatment duration with various adverse events affects patient compliance.
The six-month all-oral BPaLM regimen
The 2022 WHO update added a six-month regimen of bedaquiline, pretomanid, linezolid and moxifloxacin for MDR/RR-TB, including pre-XDR-TB, alongside a nine-month all-oral option in patients with multidrug-resistant or rifampicin resistant TB (MDR/RR-TB) and those with additional resistance to fluoroquinolones (pre-XDR-TB). The evidence came from trials: 6 months of oral bedaquiline, pretomanid, linezolid, and moxifloxacin (BPaLM) treatment cured 89% of people with RR-TB, irrespective of their fluoroquinolone-resistance status, while ZeNix reported favorable outcomes in 91% of participants with XDR, pre-XDR, or RR-TB. In the Nix-TB trial, the long-term administration of linezolid was likely the causative agent resulting in bone marrow myelosuppression, peripheral neuropathy, optic neuritis, and anemia at the higher linezolid dose. ZeNix tested a 600 mg dose, and in its 600 mg arm 91% cured and 24% experiencing at least one adverse event. For people with fluoroquinolone resistance or intolerance, health care providers can use a six-month treatment regimen (BPaL) of bedaquiline (B), pretomanid (P), and linezolid (L).
The 2025 guideline update and implementation
On 15 April 2025, WHO released its consolidated Module 4 on treatment and care, which introduced significant improvements in treatment options for people with multidrug-resistant or rifampicin-resistant tuberculosis. It added a novel, all-oral, 6-month regimen – BDLLfxC – for the treatment of MDR/RR-TB, with or without additional resistance to fluoroquinolones (pre-XDR-TB). The modified nine-month options apply where fluoroquinolone resistance has been excluded. The new regimen rests on the BEAT-Tuberculosis and endTB trials. The chapter retains BPaLM, so programmes now choose among several six-month options.
Scaling these regimens is constrained by testing. Because the choice between BPaLM and BPaL depends on fluoroquinolone status, the regimen selected depends on drug-susceptibility results. Universal DST is not always available, but rapid DST for key medicines, including rifampicin, isoniazid and the fluoroquinolones, is available and is expanding at an accelerated pace. Linezolid toxicity also requires clinical monitoring, given the haematological and neurological effects noted above. WHO has framed drug-resistant TB as a major driver of the global antimicrobial resistance crisis and poses a serious threat to global health security.
Prevention: vaccines, preventive therapy, and infection control
BCG (bacillus Calmette–Guérin) is the only licensed tuberculosis vaccine and is given to infants in many national immunization programmes. Its protection against adult lung disease is uneven. Randomized trials ranged from a rate ratio of 0.22 in the UK Medical Research Council trial to 1.05 in the Chingleput trial in South India, which found no clinically important benefit Protection against pulmonary tuberculosis in adults is variable, ranging from substantial protection in the UK MRC trial {rate ratio 0.22 [95% confidence interval (CI) 0.16 to 0.31]}, to absence of clinically important benefit, as in the large Chingleput trial. A 1994 pooled analysis estimated an average risk reduction of about half BCG vaccine significantly reduces the risk of TB by 50%. Efficacy against pulmonary disease appears to be greater at latitudes farther from the equator protection against pulmonary tuberculosis in adults is variable and greater away from the equator. Prior exposure matters too: efficacy is higher in people without earlier <i>M. tuberculosis</i> infection or sensitization to environmental mycobacteria, which means new vaccine trials must account for infection that may blunt their effects Absence of prior M. tuberculosis infection or sensitization with environmental mycobacteria is associated with higher efficacy of BCG against pulmonary tuberculosis and possibly against miliary and meningeal tuberculosis. Evaluations of new tuberculosis vaccines should account for the possibility that prior infection may mask or block their effects.
Protection also appears to decline over time. Reviewed studies generally support protection for about ten years, while only a handful of studies measured measurable effect at fifteen years or more BCG vaccination protects against pulmonary and extrapulmonary tuberculosis for up to 10 years. Most studies either did not follow up participants for long enough or had very few cases after 15 years. This should not be taken to indicate an absence of effect: five studies (one trial and four observational studies) provided evidence of measurable protection at least 15 years after vaccination. Interpretations differ; one review of the long-term data argues that efficacy remains high for 15–20 years and is substantial for as long as 50 years The efficacy of BCG against pulmonary TB remains high for at least 15–20 years and is substantial for as long as 50 years. Revaccination has been studied as well, but it is not a reliable route to preventing infection BCG vaccination does not guarantee protection against TB infection.
Tuberculosis preventive treatment (TPT) is given to people with latent infection and, in some settings, to contacts of drug-resistant cases. Rifamycin-containing regimens are preferred because rifamycins act on bacteria that are not dividing, which isoniazid acts on less effectively Each regimen includes a rifamycin (more active than isoniazid against M. tuberculosis in a non-replicating state because it acts independently of cell division). The WHO regimens are 1HP · One month of rifapentine plus isoniazid daily; 3HP · Three months of rifapentine plus isoniazid weekly; 3HR · Three months of daily rifampicin plus isoniazid; 4R · Four months of daily rifampicin monotherapy; 6H · Six months of daily isoniazid monotherapy; 9H · Nine months of daily isoniazid monotherapy. The WHO lists 9H, 3HP and 3HR as first-line options, with 1HP and 4R as alternatives The WHO recommends 9H, 3HP, or 3HR as first-line options and 1HP and 4R as alternative regimens.. Trial evidence is one reason for the shift away from long isoniazid courses: a multicentre trial of 6,859 people found daily rifampicin for four months non-inferior to nine months of isoniazid, with better completion and safety a multicentre clinical trial among 6859 subjects showed that 4-months of daily rifampicin (4R) was non-inferior to 9-months of daily isoniazid (9H) for the prevention of active TB. A network meta-analysis of individual patient data comparing 3HP with 4R found higher completion with 3HP, but also more adverse events, and no difference in the incidence of TB disease 3HP provided an increase in treatment completion over 4R, but was associated with a higher risk of adverse events.
Choice of regimen also depends on HIV treatment. Rifampicin- and rifapentine-based regimens require caution in people taking antiretroviral therapy because of drug–drug interactions Regimens containing rifampicin and rifapentine should be prescribed with caution to PLHIV who are on ART because of potential drug-drug interactions. These regimens should not be administered to people receiving protease inhibitors or nevirapine.. For contacts of multidrug-resistant cases, WHO guidance uses a levofloxacin-based course of about six months, which is a separate regimen from those above. Uptake has grown: in 2023, 77 countries reported using the 3-month weekly regimen of rifapentine and isoniazid (3HP) and 20 reported using the 1-month daily regimen of rifapentine and isoniazid (1HP).
Interrupting transmission depends on finding people who are sick before they infect others. Contact investigation evaluates household and close contacts of a confirmed case through symptom review, infection testing, and, where indicated, preventive treatment or prompt evaluation for disease. Case finding and screening target groups at higher risk of disease, such as people living with HIV, people in prisons, and people with diabetes, using symptom screening and rapid tests.
Infection control in health facilities relies on rapid identification and separation of people with presumptive TB, usually through triage, masks for coughing patients, and isolation in well-ventilated rooms. Measures include natural or mechanical ventilation, ultraviolet germicidal irradiation where ventilation is poor, and respirators for staff in high-risk areas. Household transmission is reduced by ventilation, early treatment of the index case, and separating infectious members where possible. Congregate settings such as prisons and shelters need ventilation, early screening on entry, and access to treatment, because crowding and poor airflow amplify exposure.
Several candidate vaccines are in development. The leading candidate, M72/AS01E, is a fusion-protein vaccine with a GSK adjuvant. In a phase 2b trial it provided protection against active pulmonary disease in people with latent infection; in infected adults, the vaccine provided 54.0% protection against active pulmonary tuberculosis disease, without evident safety concerns. The confidence interval around the efficacy estimate was wide, and the phase 3 design was built to confirm it. Its efficacy trial is assessing the efficacy of the M72/AS01E TB vaccine candidate in preventing the progression from latent TB infection to active pulmonary TB in adolescents and adults. Because disease is relatively rare in the study population, the trial is event-driven: simulations projected a 90% probability of accruing 110 events within 3.5 to 4 years and 185 within 5.5 to 6 years. The trial reportedly reached full enrollment, with about 20,000 participants the Phase 3 clinical trial of the M72/AS01E tuberculosis (TB) vaccine candidate has reached full enrollment eleven months ahead of schedule– with approximately 20,000 participants enrolled.
Special populations: children, pregnancy, and HIV
Children
Children aged less than 15 years account for 11% (about 1.2 million) of the estimated TB patients in 2021. Household transmission is the main route for the youngest children, and a household contact is often the source of infection in children under 5 years of age. Risk is concentrated in this group: up to 70% of children living with an adult who has infectious TB become infected, and more than 20% of them develop active disease, usually within 12 months. The risk of progression is highest under the age of five, and children under 5 years are at higher risk of developing disseminated forms of TB.
Diagnosis is difficult because children often have few bacilli and rarely produce sputum. In one Karachi series of child household contacts, only about a third of pulmonary cases were smear-positive (smear positivity rate in pulmonary cases was 32.6%). Children are considered infectious mainly when they have smear-positive pulmonary TB or cavitary disease on chest radiography, not uncommon in older children and adolescents. For this reason, WHO-aligned guidance calls for evaluating all children aged 0–4 years who have been in close contact with a case, whether or not they have symptoms, and symptomatic older children in the same situation (All children aged 0–4 years (regardless of symptoms) and children aged 5 years and above who are symptomatic, who have been in close contact with a TB case, must be evaluated for TB.). Tuberculin testing can be used for screening, but contact management can proceed without it. Preventive therapy has a large effect: a meta-analysis found that timely preventive treatment could reduce the risk of developing TB disease by 85% among those identified with TB infection, yet only 32% of child household contacts (aged <5 years) received TPT in 2021 globally. Child-specific dosing and formulations, such as weight-band dosing and dispersible tablets, are needed for treatment itself.
Pregnancy and the postpartum period
Pregnancy and the weeks after delivery raise TB risk. WHO reports incidence rate ratios of 1.4 and 1.9 for pregnant and postpartum women compared with non-pregnant women. WHO recommends that all pregnant and postpartum women in high TB burden countries and all pregnant and post-partum women living with HIV should be screened for TB at every visit to a healthcare facility using a four-symptom checklist. Standard drug-susceptible treatment is considered safe in pregnancy, with first-line drugs—isoniazid, rifampin, ethambutol, and pyrazinamide—generally acceptable in pregnancy. Clinicians monitor the liver, give vitamin B6 with isoniazid, and consider vitamin K with rifampicin, while aminoglycosides are, in principle, contraindicated due to oto-/nephrotoxicity. The six-month regimen remains the WHO standard for drug-susceptible disease in pregnancy. Drug-resistant TB is harder to manage: amikacin is the only injectable regarded as contraindicated, and pretomanid may have reproductive toxicity and should be avoided until additional data are available.
Untreated maternal disease harms the newborn as well. Maternal TB more than doubles the risk of perinatal HIV transmission and significantly increases mortality for all children in the household. Infants infected with TB perinatally have a very high risk of death. For pregnant women living with HIV but without active disease, WHO recommends preventive therapy regardless of stage of pregnancy. This improves pregnancy outcomes for both mothers and their infants. Guidance on the timing of preventive therapy has been cautious because of safety concerns, but current evidence does not support systematic deferral of IPT until the postpartum period.
HIV co-infection and antiretroviral therapy
WHO recommends that children and adolescents living with HIV should be systematically screened for TB disease at each visit to a health facility. Treating both infections at once is complicated: concomitant administration of antiretroviral and antituberculous therapies poses significant challenges, including cumulative drug toxicities, drug-drug interactions, high pill burden, and the immune reconstitution inflammatory syndrome (IRIS). The best time to start antiretroviral therapy is still uncertain (the optimal timing of ART in patients with active tuberculosis is still unknown). In one randomized trial in Mozambique, therapy began 4 to 6 weeks after starting tuberculosis treatment.
TB-IRIS is an excessive immune response against Mycobacterium tuberculosis that may occur in either HIV-infected or uninfected patients, during or after completion of anti-TB therapy. Estimates of frequency vary by study. One review reported that up to 54% of patients develop hyperinflammatory reactions known as immune reconstitution inflammatory syndrome (IRIS) within the first month of ART initiation, while the Mozambique trial recorded tuberculosis-IRIS within 12 weeks of starting antiretroviral therapy in 9.2% of patients. Recognized risk factors include a low baseline CD4+ T-cell count (<50–100 cells per mm^3) before ART, a short interval between starting TB treatment and ART, and dissemination to extrapulmonary sites. In the Mozambique cohort, TB-IRIS was independently associated with 48-week mortality (aOR 2.72 95%CI 1.14-6.54).
Diabetes, other comorbidities, and occupational groups
Diabetes is one of the most significant non-HIV comorbidities. It is generally estimated to raise TB risk about threefold, and it can complicate treatment through drug levels, longer treatment, and worse outcomes, so glycaemic control is part of TB care. Health workers and others in congregate or poorly ventilated settings, such as clinics and wards, face higher occupational exposure. Infection-control measures, including ventilation, early identification of symptomatic staff, and periodic screening, are the usual response. Care for people with multiple comorbidities therefore combines TB treatment, HIV management, and attention to these background conditions.
Discovery and historical development of knowledge
Tuberculosis is among the oldest diseases that can be traced in human remains. Spinal collapse of the kind later named Pott's disease, after the English surgeon Sir Percivall Pott (1714-1788), has been recognized in Egyptian mummies, and one researcher linked skeletal changes in a mummy to a large abscess of the psoas muscle. Ancient DNA has since provided direct evidence. In 1997, a study of a mummy from Thebes-West reported molecular examination of mycobacterial DNA as a way to identify the disease in ancient material. Later spoligotyping of Egyptian samples found that some strains were ancestral to modern lineages and others resembled M. africanum, and no evidence of M. bovis was found in any historical samples. Identifying the disease in archaeological material is nonetheless difficult. Skeletal involvement occurs in only a fraction of pulmonary cases, so the incidence of TB in ancient human remains is extremely underestimated. Ancient DNA results have also been contested on technical grounds, and in one study only two cases of the individuals tested yielded evidence of the bacterium.
On March 24, 1882, Robert Koch announced to the Berlin Physiological Society that he had isolated the tubercle bacillus, which he suspected was the cause of all forms of tuberculosis. The organism was hard to grow. Koch eventually found that he could grow colonies on coagulated blood serum at 37–38 °C, and that these colonies appeared only in the second week of incubation. He also needed new staining methods, because the bacilli resisted conventional dyes. To establish causation, Koch used animal inoculation. He injected tissue from human cases into 217 animals, and their infected tissue showed the same bacillus. His criteria, now known as Koch's postulates, drew on the earlier work of Jacob Henle, Koch's teacher at the University of Göttingen, but the 1882 tuberculosis paper was the first major attempt to apply them to a specific microorganism and disease. Koch received the Nobel Prize in 1905 for this discovery.
The next decades brought both a diagnostic test and a vaccine candidate, and neither worked as first hoped. Koch's tuberculin, a protein extract of killed bacilli, failed to protect against disease. Koch himself believed that the reaction it produced provided diagnostic evidence of acute tuberculosis, and this use became the basis of the tuberculin skin test. The BCG vaccine, developed from an attenuated bovine strain by Albert Calmette and Camille Guérin and first given to humans in 1921, followed a different path, one that is covered in the section on prevention. Throughout this period, physicians still disputed how far tuberculosis was contagious and how far it reflected inherited predisposition, and the question of its causes remained ongoing among medical professionals. The disease was a major cause of death among young adults in Europe and North America, and tuberculosis was the most important cause of death of young adults in Europe and North America.
The first effective antibiotic against the bacterium came from a soil-microbe screening program. In 1943, Waksman and his students isolated streptomycin from the soil bacterium Streptomyces griseus, and laboratory work showed activity against M. tuberculosis. Clinical trials at the Mayo Clinic followed. In the 1948 trial run by the Medical Research Council in Britain, recovery of patients with miliary or meningitic tuberculosis was seen clearly, and patients often recovered from pulmonary tuberculosis, even from very advanced disease. Resistance appeared quickly. Mycobacterium tuberculosis tends to develop streptomycin-resistance, which led to the use of drug combinations. The credit for the discovery was contested: Albert Schatz, who did the isolation work, sued over royalties and recognition, and the 1952 Nobel Prize went to Waksman alone. Streptomycin, together with later drugs, sharply reduced deaths in high-income countries, although the long-term decline in mortality there had begun before antibiotics were introduced.
Culture, literature, and social history
Consumption as a romantic image
In nineteenth-century Europe, tuberculosis, known as consumption or phthisis, became closely tied to Romanticism. Its visible wasting was read as a sign of sensitivity rather than suffering. The large number of Romantic writers, painters and composers who had TB helped create a myth that the disease drove artistic genius. The idea drew on ancient medical language: Romanticists and Classicists treated the belief as consistent with spes phthisica, a euphoria mixed with depression that was thought to produce greater creativity. Keats's illness came to exemplify this notion in later decades (physical wasting was thought to lead to a euphoric flowering of the passionate and creative aspects of the soul). Lord Byron's remarks helped popularize tuberculosis as an artist's disease.
The myth persisted even though the disease was devastating. At its peak, tuberculosis caused about a quarter of deaths in Europe, yet the idealized consumptive death remained a mainstay of popular culture and even of medical texts. The romantic image also acquired a gendered character. In the mid-nineteenth century, tuberculosis became increasingly associated with women, and popular culture shifted from the sensitive male writer to the fragile upper- or middle-class Victorian woman.
Literature and opera
Consumption appeared repeatedly in fiction and drama. Dickens's Dombey and Son (1848) and Gaskell's North and South (1854) both include female consumptives and waifish women. Dumas fils's novel and play about a Parisian courtesan, La dame aux camélias, was the basis for Verdi's La traviata. Opera was especially important in fixing the image: the pallor, wasting, and burning eyes that marked the disease were treated as emblems of haunted feminine beauty and fevered passion. Other operas and novels of the period, such as Puccini's <i>La bohème</i> and Hugo's <i>Les Misérables</i>, deal with the crisis that tuberculosis caused. Charlotte Brontë, watching her sister Anne die of the disease, called consumption a "flattering malady."
As bacteriology spread, the image changed. As science advanced, the portrayal of the disease moved from something romantic and mysterious to a condition caused by a bacillus that could be defeated.
Sanatoria and the rest cure
The sanatorium movement grew from the belief that rest, fresh air, and good food could restore health. A sanatorium was founded in 1791 at Margate, England, by the Quaker physician John Cockley Lettsom, for patients with scrofula. After reading in 1882 about the Prussian physician Hermann Brehmer's rest cure in cold mountain air, Edward Livingston Trudeau founded the Adirondack Cottage Sanitarium in 1885. Throughout much of the 1800s, patients sought "the cure" in sanatoriums, where rest and a healthful climate were thought to change the course of the disease.
Sanatoria were also instruments of social control. Their design rested on the belief that foul air caused tuberculosis, and this foul-air theory kept shaping treatment in the twentieth century even after Robert Koch identified the bacterium in 1882. Sanatoria were placed in rural areas to expose patients to sunlight and fresh air and to separate them from the general population. Daily life was tightly structured: doctors set meals, sleep, mandatory exercise, and rest periods. Some surgical approaches were added, and artificial pneumothorax became a standard therapy in the first half of the twentieth century. The arrival of drugs ended this model. Streptomycin initially cured many patients, but many relapsed, and by the 1950s, widespread vaccination and mass-produced drugs had made spatial segregation of patients unnecessary.
Stigma and its persistence
The romantic glamour of the nineteenth century has given way to a stigma that is largely the opposite. Contemporary research links stigma to poorer care. Stigma delays diagnosis, contributes to misdiagnosis and underreporting, because people fear social exclusion and prejudice. Stigma stems from misconceptions about contagion, from the association between the disease and poverty, and from visible symptoms. In one cohort of newly diagnosed patients in Gauteng, South Africa, those with low internalized and enacted stigma were more than 2.6 times as likely to have favorable treatment outcomes. Self-stigma has also been linked to weaker adherence, and perceived stigma was associated with longer delays before first seeking care. Patients may conceal their diagnosis, delay seeking care, or stop treatment, which contributes to ongoing transmission.
Urbanization, industrialization, and public health
The disease's social history is closely tied to the growth of industrial cities. One historical account describes tuberculosis as born of the urban squalor of the Industrial Revolution. By the middle of the nineteenth century, TB accounted for a quarter of all deaths in Europe. Crowded tenements, poorly ventilated workplaces, and polluted water created conditions in which transmission flourished. Because the prevailing miasma theory held that bad air spread disease, sanitary reformers focused on ventilation, drainage, clean water, and housing. Edwin Chadwick's 1842 report on the sanitary condition of Britain's working population and the Public Health Act of 1848 were landmarks in this effort. Historians still debate how much of the later decline in mortality came from sanitation, better nutrition and living standards, or medical intervention.
Global health governance, programs, and funding
The main global framework for tuberculosis policy is the WHO End TB Strategy. WHO Member States adopted it in 2014, alongside the UN Sustainable Development Goals, and it sets milestones for 2020 and 2025, objectives for 2030, and an end-of-epidemic goal for 2035. The 2025 milestones include a 50% reduction in incidence and a 75% reduction in deaths compared with 2015, and zero households facing catastrophic costs. The WHO's 2025 report, which covers data for 2024, shows the world far from these targets. Incidence fell by about 12% between 2015 and 2024, and deaths fell by 29%. Over 100 countries reached at least a 20% fall in incidence, and 65 reached a 35% fall in deaths, but the global totals remain well short of the milestones. The 2030 target is an 80% reduction in incidence, which the 2024 data are far from meeting.
The second UN High-Level Meeting on tuberculosis took place at UN Headquarters on 22 September 2023, following the first in 2018. Its political declaration, which the UN General Assembly later adopted, is the most detailed set of time-bound TB commitments to date. Member States pledged to provide treatment to up to 45 million people between 2023 and 2027, including up to 4.5 million children and 1.5 million people with drug-resistant TB. They also committed to preventive treatment for up to 45 million people, including 30 million household contacts and 15 million people living with HIV. The declaration set a target of mobilizing US$22 billion a year for TB by 2027, rising to US$35 billion by 2030, and of raising research and innovation spending to US$5 billion a year by 2027, from about US$1 billion. It also called for at least one new vaccine to be licensed, and for universal access to rapid diagnostic tests and to social benefit packages for people with TB. Critics noted that the declaration lacked a robust accountability mechanism for monitoring, and the financing wording was a compromise between competing positions.
National TB programmes deliver most diagnosis and treatment, and their capacity largely determines whether global targets are met. India alone accounts for roughly one in four TB cases worldwide, and it carried about 32% of the world's new multidrug-resistant or rifampicin-resistant cases in 2024. International donors and multilateral mechanisms supplement domestic budgets in many low- and middle-income countries. The Global Fund to Fight AIDS, Tuberculosis and Malaria is the largest multilateral source of TB financing, and the Stop TB Partnership's Global Drug Facility pools demand for medicines and procures them to lower prices for national programmes. Global TB funding has stagnated since 2020. In 2024, about US$5.9 billion was available for prevention, diagnosis, and treatment, roughly a quarter of the 2027 target. Baseline figures differ between sources depending on the year and definition used.
Recent cuts in international donor support pose a direct threat to this system. The WHO has warned that the gains made in recent years could be undone if funding continues to shrink. Donor money often pays for sputum and molecular tests, drug procurement and supply chains, and surveillance and laboratory networks, so reductions can affect each of these functions at once. The 2024 gains show what is at stake: the share of new cases diagnosed with a WHO-recommended rapid test rose from 48% in 2023 to 54% in 2024, and about 8.3 million people were newly diagnosed and started treatment, equivalent to about 78% of the estimated cases that year. Because the 2025 report's data end in 2024, the effects of cuts that began later are not yet reflected in the global series, and their impact on testing, drug stocks, and case reporting will become measurable only in subsequent reporting cycles.
Economics, stigma, and human rights
Costs to patients and households
Tuberculosis imposes financial burdens that extend well beyond clinic fees. About 50% of people treated for TB and their households face total costs, covering direct medical spending, direct non-medical spending and indirect losses such as lost income, that are catastrophic, meaning above 20% of annual household income, according to WHO's 2025 global report. A separate review of 2025-report analyses puts the share of affected households facing catastrophic costs at 47% globally, so the exact figure depends on the source and method used. Indirect costs are often the decisive element. A systematic review across income settings found that hospitalization and loss of income were the largest drivers of cost, and that costs were consistently higher amongst persons with drug resistant TB and among people found through passive case finding.
Free care and hidden costs
Free diagnosis and drugs in national programmes do not remove financial exposure. Even where charges are waived, the reviewed studies document significant catastrophic costs for patients. The hidden expenses include travel to clinics, arrangements for childcare during repeated visits, and income lost during illness, which together can push a family past the catastrophic threshold even where TB care is free. Financial pressure also delays care-seeking: economic hardship intensifies health inequalities and hinders timely treatment. Treatment completion is affected too, since the cost of staying in treatment for months can become unaffordable for households that depend on daily earnings. Reducing these costs requires faster progress towards universal health coverage and better social protection, as well as active case finding and social protection measures that the systematic review recommends to mitigate the burden of out-of-pocket expenditures.
Human rights and the rights of vulnerable groups
The right to health, set out in Article 25 of the Universal Declaration of Human Rights, is the usual reference point for rights-based TB policy as an acknowledged human right. Migrants illustrate the practical gap. Irregular migrants face particular challenges such as fear of deportation, which can postpone diagnosis and treatment. Detention and removal also disrupt care: legal analyses argue that detention and/or deportation undermines TB control by contributing to interruption or discontinuation of TB treatment or prophylaxis. Treatment broken off through removal can select for resistant strains, with consequences for origin, transit and destination countries alike and increased chances of spreading TB.
Prisons form another high-risk setting. Prisons are known to have extremely high tuberculosis prevalence, including multidrug-resistant and extensively drug-resistant forms, together with poor treatment outcomes. Georgia's national programme responded with a rights-based approach that sought to promote prisoners' rights, access to health information, development of useful skills among the prison population, and facilitation of return into the general community. For people with drug-resistant disease, critics of coercion argue that the supposed trade-off between public health and individual rights is largely a false one, and that rights-respecting, community-based treatment is often neglected by governments that prefer detention-based responses.
Economic analyses of TB control
Economic analyses generally find that TB spending yields high returns. A cost-benefit study of the Global Plan to End Tuberculosis for 2023–2030 gave a central benefit–cost ratio of 46, meaning every US$ 1 invested in TB yields US$ 46 in benefits. Alternative assumptions produced ratios in the range of 28 to 84. The estimate counts only deaths averted as benefits, so averted illness is left out In this cost-benefit analysis, only averted deaths are incorporated as benefits. Including direct and indirect costs, the cost per averted death is slightly over US$ 2,000.
Macroeconomic and full-income studies arrive at larger aggregate figures. In a study of 120 countries, the 1.4 million deaths due to all forms of tuberculosis in 2018 resulted in $580.1 billion in full-income losses. For diagnostics, a South African evaluation estimated a return of about 20 for TB testing alone, for TB 20.3, measured as economic value relative to investment. Modelling for India attributes most projected GDP gains to averted labour force mortality rather than to healthcare savings, which underlines that the economic case rests largely on keeping working-age people alive and productive.
Zoonotic and animal tuberculosis
Animal tuberculosis is caused mainly by *Mycobacterium bovis*, a close relative of the human pathogen within the Mycobacterium tuberculosis complex. The bacterium infects a wide range of hosts. It can infect domestic livestock, wildlife, and humans, so it may be an important and underappreciated human health burden in countries with infected livestock and wildlife reservoirs. Cattle are the most important animal reservoir. In cattle, the organism leaves the body in breath droplets, saliva, milk, urine, feces, and other secretions, so close contact and shared environments drive spread. Transmission between herds depends heavily on the setting. Where prevalence is low and control is strong, with frequent testing, removal of infected animals, abattoir surveillance, and restrictions on cattle movement, transmission between herds may be relatively low. By contrast, where livestock is traded without restrictions in developing countries, transmission between herds is common.
Humans acquire zoonotic infection mainly by drinking unpasteurized milk and eating dairy products made from it, and secondarily by breathing aerosols near infected cattle, carcasses, and organs in slaughterhouses. A 2022 study of dairy farms in Ethiopia illustrates the exposure pattern: 61% of the farm workers who had TB symptoms did not know about bovine TB or its zoonotic potential, and over two-thirds of them drank raw milk. Before milk pasteurization and cattle control programmes, approximately 25-30% of all tuberculosis cases were thought to be caused by M. bovis. Current estimates are far lower. Zoonotic TB due to M. bovis is approximately 1.4% of the global human TB burden, equivalent to over 140,000 new cases annually, with the highest proportions reported in Africa and parts of South-East Asia, and these figures are probably underestimates. Only 26 countries reported zoonotic TB cases in 2023, totaling just 371 notifications, which reflects serious under-diagnosis, especially in Africa and Asia.
Clinically, zoonotic TB is often hard to recognise. It often affects sites other than the lungs, but in many cases is clinically indistinguishable from TB caused by M. tuberculosis. Because M. bovis is naturally resistant to pyrazinamide, one of the four first-line drugs, standard regimens are less effective against it, and diagnostic delay adds to the problem.
The zoonotic picture is not limited to M. bovis. Other members of the complex, including M. caprae, M. microti, M. pinnipedii, and M. canetti, can cause human disease in addition to infecting animals. WOAH's international standards recognise that any member of the complex can be transmitted from animals to people. The flow can also run in the other direction. Three probable cases of human-to-cattle MTBC transmission have occurred in the United States since 2013. Researchers have also shown that M. tuberculosis can indeed infect and cause disease in cattle, challenging the long-standing belief of its strict host specificity.
Control increasingly relies on a One Health framework, which links human medicine, veterinary care, and environmental health. In 2017, the WHO, FAO, the World Organization for Animal Health (OIE), and The Union launched a comprehensive roadmap for zoonotic TB in people and bovine TB in animals. A multicountry assessment of that roadmap found gaps. Among 33 countries, 15 reported having One Health coordination, but none had a joint surveillance mechanism between the animal and human sectors for zoonotic TB. Human and animal cases are also typically diagnosed, managed, and reported independently, which limits the picture available to public health authorities.
Animal control has traditionally relied on test-and-removal. The main screening test of herds is a tuberculin-based skin test, and animals that test positive are slaughtered. Ireland shows both the gains and the limits of this approach. Cattle incidence fell from 17% in 1954 to 0.5% in 1965, but progress towards eradication has stalled in recent years, in part due to the presence of infected wildlife such as badgers. Badger culling was added in the early 2000s, and as badgers are protected animals under Wildlife Acts, this practice is now progressively being replaced by badger vaccination. In England, a badger control policy begun in 2013 was associated with a 56% reduction in herd incidence rate up to the fourth year of interventions, and from 2017 areas with badger control were required to add interferon-gamma testing to skin testing. The United Kingdom has since announced plans to accelerate research on cattle vaccines, test more cattle, and end the controversial culling of wild badgers.
Diagnosis in animals and humans also differs. Cattle are screened mainly with skin tests and interferon-gamma assays, while human suspects are assessed with sputum and clinical evaluation. Distinguishing species needs specialised methods; a recent review lists region-of-difference typing, line probe assays, next-generation sequencing, and CRISPR-based tools as options for zoonotic TB. The economic burden falls heavily on livestock industries. In Ireland, the wildlife control aspect of the eradication programme cost €7.7 million in 2023, up 20% on 2022. Farmers in the UK have also raised concerns that vaccinating wildlife is expensive and burdensome, which shows how cost shapes policy choices across both sectors.
Research frontiers and unresolved questions
Most people who acquire <i>Mycobacterium tuberculosis</i> never develop disease, so a test that separated the minority who will progress from the majority who will not would let preventive treatment go to the people who need it. No such test is in routine use. Researchers have reported a 16-gene blood signature that predicts progression to active TB within a year with a 66% predictive value. A separate four-gene signature was able to predict the progression of the disease up to 2 years before onset and has been validated in multiple cohorts across Africa. Work on household contacts has combined plasma proteins into panels; one such panel of GM-CSF, CXCL10 and IL-1Ra showed high accuracy in predicting progression to active tuberculosis disease. The obstacle is that the markers must still be reproduced in independent populations, and existing tests perform poorly on this question: in one modelling exercise, the NNT is 85 for current interferon-γ release assays, meaning that roughly 85 people would need preventive treatment to avert one case. A related gap is the lack of reliable correlates of protection. A recent infant vaccination study identified enhanced expression of T-cell activation markers as a correlate of risk, and T-cell responses to TB latency antigens, including heparin-binding haemagglutinin and DosR-regulon-encoded antigens have also been correlated with protection. Without a validated correlate, vaccine developers cannot easily use immune readouts to shorten the path to licensure, a point that links to the vaccine trial pipeline discussed elsewhere.
Host-directed therapies (HDTs) take a different approach: rather than killing bacteria directly, they aim to moderate the host inflammation that damages lung tissue, while standard antibiotic drugs still do the killing. The motivation is clinical. Current regimens can leave patients with lasting lung injury, and HDTs are being tested as adjuncts that might protect lung function and shorten treatment. A phase 2 randomised trial in South Africa tested four oral agents, CC-11050, everolimus, auranofin and ergocalciferol, added to standard therapy in patients with pulmonary disease. Two of the 4 arms (CC-11050 and everolimus) showed superior recovery of lung function at day 180 compared to control; none showed accelerated eradication of MTB infection. The safety profile was not uniformly benign, and the investigators reported serious adverse events in the trial, including a life-threatening thrombocytopenia in one auranofin recipient. Evidence for other candidates is mixed. Trials of adjunctive atorvastatin was associated with early reductions in sputum mycobacterial load, whereas a Phase IIB RCT evaluating rosuvastatin failed to show significant effect on sputum culture conversion, and vitamin D trials have also yield conflicting results. A network meta-analysis of twenty-eight RCTs (4,260 patients) has ranked candidates by effect on sputum conversion, but the authors also noted that heterogeneity was moderate, which limits firm conclusions. Efforts to shorten and detoxify the regimen are also pursued through new drug candidates, but these face the same demand for well-powered randomised trials and careful evidence appraisal. A specific caution comes from the HARVEST trial, which found no survival benefit from high-dose rifampicin in tuberculous meningitis and reported no survival benefit and higher risk of adverse outcomes, a reminder that dose intensification is not automatically beneficial.
Whole-genome sequencing (WGS) of the genome is now a central research and surveillance tool. Its appeal is that genetics is faster, potentially more accurate than phenotypic drug susceptibility testing (pDST), more comprehensive than molecular tests and also yields epidemiological insights. Its accuracy depends on a catalogue that links variants to resistance. The WHO catalogue is an expert-graded framework for interpreting variants associated with drug resistance, and WGS can also distinguish relapse from reinfection in patients with recurrent tuberculosis. Performance varies by drug. For bedaquiline, the second edition of the WHO catalogue was built from 14,135 clinical samples, and its 19 associated variants gave a reported sensitivity of 49.4%, a specificity of 98.7% and a positive predictive value (PPV) of 75.2%. The low sensitivity reflects conservative statistical rules that miss some true resistance, which is a practical problem for clinicians choosing regimens. Catalogue building is also slow. One group has described the expert-driven process as an irreproducible process and developed an automated alternative, which is a methodological direction still being tested. Across drugs, WGS has been effective in detecting resistance to RFP and INH, enabling the identification of multi-drug resistant TB patients, while results for other agents require further optimization and improvement. Surveillance and tracing remain the strongest uses, but routine clinical deployment will depend on mutation catalogues that are both comprehensive and regularly updated.
Artificial intelligence applied to chest imaging is one of the most visible research frontiers. Computer-aided detection (CAD) software that reads chest radiographs and flags abnormalities is already used in some screening programmes, and deep learning models based on computer vision have been developed to classify images, estimate disease severity and, in some studies, predict other diagnostic features. Their promise lies in speed and in relieving shortages of experienced readers. Their validation, however, is demanding. Models trained on one hospital's images can perform poorly on equipment, patient populations or disease prevalence that differ from the training data, and prior TB, which leaves scarring, is a common source of false positives. Reference standards also matter: performance measured against radiologist opinion is not the same as performance measured against bacteriological confirmation. Sensitivity and specificity must be chosen at an operating threshold, and the balance between missed cases and unnecessary testing differs in screening and in triage. Routine use therefore requires prospective, multi-site evaluation in the populations where the tool will be used, including people with HIV and children, along with assessment of cost and of whether patient outcomes actually improve. Similar requirements apply to AI applied to digital microscopy and to molecular data, where artificial intelligence tools and deep learning methods remain largely at the research stage.
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