TB killed poets, kings, and everyday workers long before we knew the germ behind it. It still kills more people each year than any other single infectious disease in adults, even after antibiotics. This story isn’t just old hospitals and sepia photos. It explains why a 19th‑century “wasting” illness became a curable disease-and why drug resistance and missed diagnoses keep it alive today. Expect a clear timeline, the pivotal discoveries, what actually worked (and what didn’t), and a quick toolkit to make sense of today’s tests, vaccines, and treatments.

What you likely want to do after clicking this: 1) get a fast, accurate overview; 2) follow a clean timeline; 3) learn which breakthroughs changed the game; 4) understand today’s diagnostics, vaccines, and resistance; 5) walk away with a cheat‑sheet you’ll actually use.

TL;DR: The fast version

  • For centuries TB was “consumption,” blamed on bad air and weak lungs; autopsies showed tell‑tale tubercles, but no one knew the cause.
  • Between 1865 and 1882, Villemin proved transmissibility and Koch identified Mycobacterium tuberculosis, flipping the story to germ theory.
  • Sanatoria, rest, and surgery dominated until antibiotics: streptomycin (1943), PAS, and isoniazid (1952) made cure realistic when used in combination.
  • BCG vaccine (1921) protects infants from severe TB; it’s inconsistent against adult lung TB. New vaccine candidates are in late trials.
  • Today we use rapid molecular tests (GeneXpert), shorter regimens for drug‑susceptible TB, and new drugs for resistant TB-yet TB still caused ~1.3 million deaths in 2022 (WHO).

From “consumption” to germ theory: the long road to naming the enemy

Ancient skeletons and Egyptian mummies show spinal deformities from TB more than 3,000 years ago. Hippocrates described phthisis-wasting with cough and blood-so common it shaped the language of illness. By the 18th and 19th centuries, “consumption” was everywhere in crowded cities. Poets romanticised the pale look. Doctors saw tiny nodules (tubercles) at autopsy but argued over cause-inheritance, climate, or moral failings.

The first real crack came from controlled observation. In 1865, Jean‑Antoine Villemin inoculated rabbits with material from human TB and produced disease. That experiment hinted contagion, not constitution. Then, on 24 March 1882, Robert Koch stained and visualised the tubercle bacillus, cultured it, and outlined what became Koch’s postulates. In one stroke, TB moved from a misty idea to a microbe you could see. Public health caught up: prevent crowding, ventilate, trace contacts, isolate the sick. The germ had a name, and names change behaviour.

Still, naming the culprit didn’t give us a cure. TB spreads by air in tiny droplets. It thrives in poverty-overcrowded housing, malnutrition, and weak health systems. The science said “microbe,” but the solution also needed food, space, and time.

Sanatoria, surgery, and the antibiotic revolution

Sanatoria, surgery, and the antibiotic revolution

Before drugs, the best doctors could offer was time and clean air. Sanatoria appeared across Europe, the US, and Australia: regimented rest, high‑calorie diets, sunlight, and strict routines. It sounds quaint now, but sanatoria slowed transmission by separating infectious patients from crowded homes and workplaces. Some improved because their immune systems finally got a chance.

When rest failed, surgeons tried to collapse the diseased lung. Artificial pneumothorax, thoracoplasty (removing ribs), and plombage (inserting inert material) aimed to let cavities “rest.” Brutal by today’s standards, sometimes effective, and often a measure of how desperate the fight was.

Prevention took a bold step with BCG. In 1921, Calmette and Guérin tested a live attenuated vaccine derived from Mycobacterium bovis. BCG became a global mainstay and still prevents severe TB in infants (like meningitis), but it varies widely against adult pulmonary TB. That inconsistency reflects local strains, prior mycobacterial exposure, and host differences-one reason new vaccines are such a big deal.

The antibiotic age changed everything. In 1943, Selman Waksman’s lab isolated streptomycin. The 1948 UK Medical Research Council trial, one of the earliest randomised controlled trials, proved it worked-but resistance emerged fast when used alone. The lesson became a rule of life in TB: never treat with a single active drug. Para‑aminosalicylic acid (PAS) helped, and then isoniazid arrived in 1952, potent and orally simple. Combining drugs knocked the bacilli at different stages and cut resistance risk. By the 1960s-70s, rifampicin and pyrazinamide enabled the six‑month, short‑course therapy we still recognise.

Public health adopted DOTS (Directly Observed Treatment, Short‑course) in the 1990s-standardised regimens, drug supply, tracking, and supervision endorsed by WHO. When DOTS was implemented well, cures soared. But where systems were weak and supply chains shaky, inconsistent treatment bred resistant strains.

By the late 1980s and 1990s, multidrug‑resistant TB (MDR‑TB) took hold-resistant to at least isoniazid and rifampicin. Extensively drug‑resistant TB (XDR‑TB) followed, resistant to fluoroquinolones and key injectables. Treatment stretched to 18-24 months with toxic drugs. Outcomes worsened. The pendulum had swung: we had drugs, but we’d taught the bug some new tricks.

Modern TB: diagnostics, vaccines, and drug resistance in 2025

Diagnostics grew up. For decades, smear microscopy was the backbone-cheap and fast, but it missed many cases and couldn’t see resistance. Culture remains the gold standard for sensitivity and drug susceptibility, but it’s slow, often taking weeks on Löwenstein-Jensen media.

Then came rapid molecular tools. GeneXpert MTB/RIF (2010) and Xpert Ultra detect TB DNA and rifampicin resistance in under two hours. Line probe assays map resistance mutations for multiple drugs. In high‑resource labs, whole‑genome sequencing can read a strain’s resistance profile and track outbreaks. For latent TB infection, tuberculin skin tests and IGRAs (like QuantiFERON and T‑SPOT) measure immune memory-useful for screening, not for diagnosing active disease.

Treatment has also moved. Drug‑susceptible TB traditionally took six months: two months of rifampicin, isoniazid, pyrazinamide, and ethambutol, then four months of rifampicin and isoniazid. Large trials published in 2021 showed a four‑month regimen with rifapentine and moxifloxacin can be non‑inferior in many patients-shorter is better for adherence when feasible.

MDR‑TB, once a treatment marathon, is finally getting shorter and safer. New drugs-bedaquiline (2012 approval), delamanid (2014), and pretomanid (2019)-made all‑oral, injection‑free regimens possible. WHO guidance from 2022 supports six‑month BPaLM regimens (bedaquiline, pretomanid, linezolid, moxifloxacin) for many MDR cases; variants like BPaL are used when quinolones don’t work. Toxicity still needs careful handling (linezolid neuropathy, QT prolongation), but cure rates are improving.

Vaccines are the looming frontier. BCG remains on duty for infants in most high‑burden countries. A candidate called M72/AS01E showed about 50% efficacy against pulmonary TB in infected adults in a phase 2b trial, spurring big phase 3 programmes. Several whole‑cell and subunit candidates are also in late stages. If one works in adults, the historical arc of TB could finally bend toward elimination.

The global picture keeps us honest. According to the WHO Global Tuberculosis Report 2023, about 10.6 million people fell ill with TB in 2022 and around 1.3 million died. COVID‑19 reversed years of progress by disrupting clinics and supply chains; many countries are still catching up on missed diagnoses. TB/HIV co‑infection remains dangerous without integrated testing and antiretroviral therapy.

Context matters by country. In Australia, TB incidence sits low (around 5-6 per 100,000), with cases concentrated among people born overseas and, disproportionately, among Aboriginal and Torres Strait Islander peoples. BCG isn’t in the routine childhood schedule; it’s targeted for high‑risk infants and specific jobs. That’s why someone in Adelaide might never meet a TB patient-until a hospital rotation, a community cluster, or a travel‑related case brings the history lesson to life. These patterns match reports from the Australian Institute of Health and Welfare and state health departments in recent years.

Three practical rules that stand the test of time:

  • Think TB if cough lasts more than two weeks-especially with weight loss, night sweats, fever, or blood in sputum. Test, don’t guess.
  • Never add a single drug to a failing regimen. Resistance loves half‑measures.
  • Treat the person and the conditions-nutrition, housing, and support matter as much as pills for finishing therapy.
Cheat‑sheets, examples, and what to do next

Cheat‑sheets, examples, and what to do next

Quick visual timeline you can recall on a walk:

  1. Ancient era: TB in mummies and bones; Hippocrates’ phthisis.
  2. 1865: Villemin proves transmissibility in animals.
  3. 1882: Koch identifies the tubercle bacillus, sets postulates.
  4. 1921: BCG vaccine begins.
  5. 1930s-40s: Sanatoria and collapse therapy.
  6. 1943-52: Streptomycin, PAS, isoniazid; combination therapy era.
  7. 1960s-70s: Rifampicin, short‑course therapy.
  8. 1990s: DOTS scale‑up; MDR and XDR emerge.
  9. 2010s: GeneXpert, bedaquiline, delamanid.
  10. 2019-2024: Pretomanid; shorter MDR regimens; 4‑month DS‑TB options; vaccine candidates in late trials.

Suspicion checklist (what should trigger testing):

  • Cough >2 weeks, fever, night sweats, weight loss, chest pain, haemoptysis.
  • Close contact with someone diagnosed with TB.
  • HIV infection, diabetes, malnutrition, or immunosuppression.
  • Recent travel or migration from high‑burden regions.
  • Abnormal chest X‑ray with upper lobe cavitation or persistent infiltrates.

Diagnostic flow (simple, practical):

  1. Symptoms or X‑ray suggest TB? Collect sputum-ideally two samples, one early morning.
  2. Order a rapid molecular test (e.g., Xpert) first; add smear and culture where available.
  3. If Xpert detects rifampicin resistance, escalate to MDR pathway and send for extended susceptibility testing.
  4. For close contacts without symptoms, screen with TST or IGRA and chest X‑ray to rule out active disease; offer preventive treatment if eligible.

Therapy heuristics you can trust:

  • Directly observed or digitally supported therapy beats “see you in six months.”
  • Manage side effects early-nausea, neuropathy, vision changes-to prevent drop‑outs.
  • Document every dose. What gets measured gets done.

Examples make it stick:

  • A 22‑year‑old student returns from a four‑month internship in India with a cough and night sweats. Xpert confirms TB, no rifampicin resistance. She completes a four‑ or six‑month short‑course regimen with support from campus health. Contacts from her lab are screened; a roommate with latent infection takes a three‑month preventive regimen.
  • A 48‑year‑old chef in a crowded share‑house misses doses and returns with persistent symptoms. Culture shows MDR‑TB. He’s shifted to a six‑month all‑oral BPaLM regimen, with weekly ECGs for QT checks and side‑effect monitoring. A social worker sorts transport vouchers and time‑off paperwork; adherence rebounds.
  • A newborn in a remote community where TB is present receives targeted BCG at birth to prevent severe childhood TB. The clinic runs contact tracing after a family member’s diagnosis; several adults start preventive therapy after IGRA conversion.

Mini‑FAQ

  • Why was it called “consumption”? Because people wasted away-literally consumed by coughing illness-long before microscopes showed the bacillus.
  • Is TB still a big threat? Yes. WHO counted roughly 10.6 million illnesses and 1.3 million deaths in 2022. It’s curable, but many go undiagnosed or undertreated.
  • Can I get TB twice? Yes. Prior infection or even prior disease doesn’t guarantee protection, especially with heavy exposure.
  • What’s the difference between latent and active TB? Latent means the immune system holds the bacteria in check-no symptoms, not contagious, positive TST/IGRA. Active TB means the bacteria are multiplying-symptoms and contagiousness until treated.
  • Does BCG work? It strongly protects infants from severe TB like meningitis. Its protection against adult lung TB is mixed. New vaccines aim to fix that.
  • How fast do you stop being contagious after starting treatment? Many drug‑susceptible cases become much less infectious within two weeks of effective therapy, but it varies. Public health teams guide isolation based on tests and symptoms.
  • What are MDR and XDR again? MDR resists isoniazid and rifampicin. XDR adds resistance to fluoroquinolones and key second‑line drugs. Both need specialised regimens.

Next steps tailored to you

  • Student or history buff: Save the timeline above. If you need a primary source, look for Koch’s 1882 lecture, the 1948 MRC streptomycin trial report, and the WHO Global Tuberculosis Reports (latest 2023). They’re the spine of this story.
  • Clinician or trainee: Build a habit-order Xpert on first suspicion, collect good sputum, and check HIV, diabetes, and smoking status. If rifampicin resistance shows, call your TB program immediately.
  • Public health or policy: Invest in rapid testing, consistent drug supply, and patient support (food, transport, SMS reminders). That trio outperforms posters and slogans.
  • Traveler or migrant: If you’ve had close exposure or long stays in high‑burden settings and develop a persistent cough, get tested. If a clinic offers screening for contacts, take it.

Where the field is heading

  • Vaccines: Phase 3 trials of adult‑protective vaccines could be the biggest shift since rifampicin. Watch M72/AS01E and other candidates over the next few years.
  • Diagnostics: Portable molecular tests and AI‑assisted chest X‑rays are expanding screening in clinics with limited staff.
  • Treatment: Shorter, safer regimens for both drug‑susceptible and resistant TB are edging closer to standard care, with careful monitoring for side effects.

Credible anchors for the claims here: WHO Global Tuberculosis Report 2023; CDC TB basics and treatment guidelines; the 1948 MRC streptomycin trial; regulatory approvals of bedaquiline (2012), delamanid (2014), and pretomanid (2019); and major trials on four‑month regimens published in 2021. These sources shaped policy and practice. They’re also how this tuberculosis history moved from myth to measurable progress.