# Tuberculosis

> CIE A-Level Biology · 9700
> Source: https://www.owlsprep.com/study/cie-9700-u10-tuberculosis/

This sub-topic covers the cause, transmission, pathophysiology, and control of tuberculosis (TB), a leading bacterial infectious disease of major global public health concern. You will distinguish latent from active TB and explain drivers of antibiotic resistant TB.

**Prerequisites:** [Classification of pathogens](https://www.owlsprep.com/study/cie-9700-u10-infectious-disease/); [Antibiotic action and resistance](https://www.owlsprep.com/study/cie-9700-u6-microorganisms-defence/)

## Learning objectives

- Describe the cause, transmission and pathogenesis of tuberculosis
- Distinguish between latent and active tuberculosis infection
- Explain the emergence and spread of drug-resistant tuberculosis
- Outline control and prevention strategies for TB

## Causative Agent and Transmission

**Tuberculosis (TB)** — A chronic airborne infectious disease caused by mycobacterial species, most commonly *Mycobacterium tuberculosis*.

*Notation:* TB

*Example:* TB most frequently affects the lungs (pulmonary TB) but can spread to other organs (extrapulmonary TB).

*Mycobacterium tuberculosis* has a unique waxy cell wall rich in mycolic acid, which makes it resistant to desiccation, disinfectants and the host immune system. It is transmitted via droplet infection: when an individual with active pulmonary TB coughs, sneezes or speaks, they release tiny respiratory droplets containing the bacteria that can be inhaled by others.

- Close prolonged contact with an individual with active TB
- Weakened immune system (e.g. HIV co-infection, immunosuppressant drugs)
- Overcrowded living conditions (e.g. prisons, homeless shelters)
- Poor access to healthcare and antibiotic treatment

**Worked example:** Explain why *Mycobacterium tuberculosis* is able to survive inside host macrophages after inhalation.

1. First, recall the key structural adaptation of *M. tuberculosis* that protects it from host defences.
2. The bacterium has a thick, waxy cell wall made of mycolic acid.
3. This cell wall prevents lysosomes in host macrophages from fusing with the phagosome containing the bacterium, so the bacterium avoids being broken down by digestive enzymes.
4. The waxy cell wall also makes the bacterium resistant to many antibiotics and host immune chemicals, allowing it to persist long-term in the host.

> **Exam tip:** Always link the waxy mycolic acid cell wall to its function in TB questions — this is a common exam mark point.

## Pathogenesis: Latent vs Active TB

**Latent Tuberculosis Infection (LTBI)** — A state of asymptomatic TB infection where bacteria are contained within immune cell aggregates called tubercles by the host immune system. Bacteria are not replicating actively and cannot be transmitted.

*Example:* Around 1/4 of the global population is estimated to have latent TB.

After inhalation, bacteria are taken up by alveolar macrophages in the lungs. Most bacteria are killed, but some survive and replicate slowly inside macrophages. The host immune system forms a granuloma (tubercle) that walls off the bacteria, stopping them from spreading: this is latent TB. If the immune system becomes weakened, tubercles can break down, bacteria start replicating rapidly and cause symptomatic active TB, which is transmissible.

| Feature | Latent TB | Active TB |
| --- | --- | --- |
| Symptoms | None | Persistent cough, weight loss, fever, night sweats |
| Transmissibility | Non-transmissible | Transmissible via respiratory droplets |
| Chest X-ray | No visible lung damage | Visible lesions/scarring in lungs |
| Treatment | Preventative therapy to stop progression | Long-course combination antibiotic therapy |

**Worked example:** Why does HIV co-infection greatly increase the risk of developing active TB from latent TB?

1. HIV infects and destroys CD4+ helper T cells, which coordinate the immune response against *M. tuberculosis*.
2. A reduced number of functional T cells weakens the immune system's ability to contain bacteria within tubercles.
3. The granuloma structure that walls off bacteria can no longer be maintained.
4. Bacteria are released, start replicating actively, and cause symptomatic active TB.

## Multi-Drug Resistant TB (MDR-TB)

**Multi-drug Resistant Tuberculosis (MDR-TB)** — A strain of TB that is resistant to at least the two most powerful first-line anti-TB antibiotics: isoniazid and rifampicin.

*Example:* MDR-TB requires longer treatment with more expensive, toxic second-line drugs and has a much lower cure rate.

MDR-TB arises primarily through incorrect or incomplete use of antibiotics. When patients do not complete their full course of TB treatment, not all bacteria are killed, and the remaining resistant bacteria survive and multiply, passing on their resistance genes. Extensively drug-resistant TB (XDR-TB) is an even more severe form resistant to most second-line drugs.

**Worked example:** Explain how incomplete antibiotic treatment leads to the evolution of MDR-TB.

1. Within a TB bacterial population, natural genetic variation creates some bacteria with random mutations that confer antibiotic resistance.
2. Incomplete treatment kills all non-resistant bacteria but leaves resistant bacteria alive, as treatment was stopped too early.
3. Resistant bacteria replicate without competition from non-resistant strains and pass resistance alleles to offspring.
4. Over multiple cycles of incomplete treatment, resistance to multiple antibiotics accumulates, producing MDR-TB.

> **Exam tip:** Remember TB requires 6–9 months of combination therapy, far longer than most bacterial infections — this is a common exam question point.

## Control and Prevention of TB

Global TB control focuses on three core strategies: early identification and treatment, vaccination, and reducing transmission in high-risk populations.

- **Directly Observed Therapy Short-course (DOTS):** Healthcare workers observe patients taking their full antibiotic course to ensure completion and reduce resistance development.
- **BCG vaccination:** Given to infants and children in high TB prevalence regions to protect against severe childhood TB.
- **Contact tracing:** Close contacts of TB cases are tested for latent/active TB to stop further spread.
- **HIV co-infection management:** Antiretroviral treatment for HIV improves immune function and reduces progression to active TB.

**Worked example:** Explain why BCG vaccination is rarely given to adults in low TB prevalence countries like the UK.

1. BCG is very effective for protecting children from severe disseminated TB, but has variable, often low effectiveness in adults, and protection wanes over time.
2. In low prevalence countries, most adults have very low risk of TB exposure, so vaccine benefits do not outweigh small risks of adverse effects.
3. Public health resources are instead focused on early detection and treatment of rare cases rather than mass adult vaccination.

## Common pitfalls

- **Wrong:** Stating TB is caused by a virus rather than a bacterium.
  - Why it fails: TB is often confused with viral respiratory infections like influenza.
  - Correct: TB is a bacterial infection caused by *Mycobacterium tuberculosis*.
- **Wrong:** Claiming that latent TB is transmissible to other people.
  - Why it fails: Students frequently mix up the transmissibility of latent and active TB.
  - Correct: Only active pulmonary TB is transmissible via droplets; latent TB is asymptomatic and not contagious.
- **Wrong:** Stating BCG vaccine provides lifelong full protection against all forms of TB for all age groups.
  - Why it fails: Students often over-generalise BCG effectiveness, a common exam trap.
  - Correct: BCG protects children from severe TB but has limited effectiveness against adult pulmonary TB, and protection wanes over time.
- **Wrong:** Claiming antibiotic resistance in TB arises because the patient becomes resistant to the drug.
  - Why it fails: Students confuse resistance of the bacterium with patient tolerance of drug side effects.
  - Correct: Antibiotic resistance is a property of the bacterial population, evolved via natural selection for resistant mutations.

## Cheatsheet

| Key Feature | Core Fact |
| --- | --- |
| Causative agent | *Mycobacterium tuberculosis* (acid-fast bacterium) |
| Transmission route | Airborne respiratory droplet infection |
| Key structural adaptation | Waxy mycolic acid cell wall → resists immune attack |
| Latent TB | Asymptomatic, non-transmissible, contained in tubercles |
| Active TB | Symptomatic, transmissible, active bacterial replication |
| MDR-TB definition | Resistant to first-line drugs isoniazid + rifampicin |
| Main control strategy | DOTS (directly observed treatment) + BCG |
| Top risk for active TB | HIV co-infection / weakened immune system |

## What's next

Tuberculosis is a key example of a persistent bacterial infectious disease that illustrates core concepts in immunology, evolution of antibiotic resistance, and global public health. Understanding TB also provides a foundation for learning about other airborne infectious diseases, and how pathogen structure relates to pathogenicity, treatment, and control. After mastering the key facts and concepts for TB, you can extend your knowledge to other major bacterial and viral pathogens covered in this unit, and explore how public health strategies are designed to limit the spread of communicable diseases. You can also dive deeper into the evolutionary mechanisms of antibiotic resistance, which is one of the most pressing global public health challenges of the 21st century.

- [HIV and AIDS](https://www.owlsprep.com/study/cie-9700-u10-hiv-aids/)
- [Malaria](https://www.owlsprep.com/study/cie-9700-u10-malaria/)
- [Antibiotics and Antibiotic Resistance](https://www.owlsprep.com/study/cie-9700-u10-antibiotics-and-antibiotic-resistance/)

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