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Apr 24
Tuberculosis (TB) is caused by the bacterium Mycobacterium tuberculosis. When a person inhales droplets containing the bacteria, the bacteria can enter the lungs and infect the alveolar macrophages, which are immune cells that normally help to fight off infections.
Once inside the macrophages, the bacteria can multiply and spread to other parts of the body through the bloodstream or lymphatic system. The immune system responds by sending more immune cells to the site of infection, leading to the formation of granulomas, which are small, organized collections of immune cells that surround and contain the bacteria.
In some cases, the immune response is able to control the infection and the bacteria become dormant, leading to latent TB infection. However, in other cases, the bacteria continue to multiply and cause active TB disease. This can lead to the destruction of lung tissue and the formation of cavities, which can allow the bacteria to spread to other parts of the body.
If left untreated, TB can cause severe damage to the lungs, as well as other organs such as the brain, kidneys, and bones. It can also be fatal if not properly managed. Treatment typically involves a combination of antibiotics taken over a period of several months to effectively kill the bacteria and prevent the development of drug-resistant strains.
Once inside the macrophages, the bacteria can multiply and spread to other parts of the body through the bloodstream or lymphatic system. The immune system responds by sending more immune cells to the site of infection, leading to the formation of granulomas, which are small, organized collections of immune cells that surround and contain the bacteria.
In some cases, the immune response is able to control the infection and the bacteria become dormant, leading to latent TB infection. However, in other cases, the bacteria continue to multiply and cause active TB disease. This can lead to the destruction of lung tissue and the formation of cavities, which can allow the bacteria to spread to other parts of the body.
If left untreated, TB can cause severe damage to the lungs, as well as other organs such as the brain, kidneys, and bones. It can also be fatal if not properly managed. Treatment typically involves a combination of antibiotics taken over a period of several months to effectively kill the bacteria and prevent the development of drug-resistant strains.
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Google Gemini AI
Apr 24
Pathophysiology of Tuberculosis (TB)
1. Inhalation and Transmission:
- Mycobacterium tuberculosis (MTB), the causative agent, is inhaled into the lungs as aerosolized droplets from infected individuals.
- It typically infects the lower lobes due to better ventilation and less phagocytic activity.
2. Intra-alveolar Phase:
- Within the alveoli, MTB is phagocytized by alveolar macrophages.
- However, some MTB can escape phagocytosis and replicate inside macrophages.
3. Primary Complex Formation:
- The infected macrophages spread to regional lymph nodes, forming a primary complex (Ghon focus and hilar lymphadenopathy).
4. Latency:
- In most cases (90%), the immune response controls the infection, and MTB enters a latent state within macrophages.
- Latency is maintained by the host immune response, particularly cell-mediated immunity (CMI).
5. Reactivation:
- In some individuals (10%), MTB reactivates from latency due to a weakened immune system (e.g., HIV, immunosuppressive drugs).
- Reactivation usually occurs from the primary complex or other latent foci in the lungs.
6. Post-Primary TB:
- Reactivated MTB spreads rapidly through the airways, causing extensive lung inflammation.
- It can lead to caseating granulomas, tissue necrosis, and cavitation.
- The cavitary lesions generate sputum, which contains large numbers of MTB and is infectious.
7. Extrapulmonary TB:
- TB can also spread hematogenously to other organs, such as the lymph nodes, kidneys, bones, brain, and peritoneum.
- Extrapulmonary TB accounts for about 20% of all TB cases.
8. Immune Response:
- The immune response against TB involves both innate and adaptive immunity:
- Innate immunity: Phagocytosis by macrophages, release of inflammatory mediators
- Adaptive immunity: T-cell activation, production of cytokines (e.g., IFN-γ), formation of granulomas
- Granulomas are organized immune structures that contain infected macrophages, lymphocytes, and fibroblasts. They help to localize and contain the infection.
9. Clinical Manifestations:
- Pulmonary TB: Cough, expectoration of sputum, fever, night sweats, weight loss
- Extrapulmonary TB: Depends on the affected organ (e.g., lymphadenopathy, meningitis, bone pain)
1. Inhalation and Transmission:
- Mycobacterium tuberculosis (MTB), the causative agent, is inhaled into the lungs as aerosolized droplets from infected individuals.
- It typically infects the lower lobes due to better ventilation and less phagocytic activity.
2. Intra-alveolar Phase:
- Within the alveoli, MTB is phagocytized by alveolar macrophages.
- However, some MTB can escape phagocytosis and replicate inside macrophages.
3. Primary Complex Formation:
- The infected macrophages spread to regional lymph nodes, forming a primary complex (Ghon focus and hilar lymphadenopathy).
4. Latency:
- In most cases (90%), the immune response controls the infection, and MTB enters a latent state within macrophages.
- Latency is maintained by the host immune response, particularly cell-mediated immunity (CMI).
5. Reactivation:
- In some individuals (10%), MTB reactivates from latency due to a weakened immune system (e.g., HIV, immunosuppressive drugs).
- Reactivation usually occurs from the primary complex or other latent foci in the lungs.
6. Post-Primary TB:
- Reactivated MTB spreads rapidly through the airways, causing extensive lung inflammation.
- It can lead to caseating granulomas, tissue necrosis, and cavitation.
- The cavitary lesions generate sputum, which contains large numbers of MTB and is infectious.
7. Extrapulmonary TB:
- TB can also spread hematogenously to other organs, such as the lymph nodes, kidneys, bones, brain, and peritoneum.
- Extrapulmonary TB accounts for about 20% of all TB cases.
8. Immune Response:
- The immune response against TB involves both innate and adaptive immunity:
- Innate immunity: Phagocytosis by macrophages, release of inflammatory mediators
- Adaptive immunity: T-cell activation, production of cytokines (e.g., IFN-γ), formation of granulomas
- Granulomas are organized immune structures that contain infected macrophages, lymphocytes, and fibroblasts. They help to localize and contain the infection.
9. Clinical Manifestations:
- Pulmonary TB: Cough, expectoration of sputum, fever, night sweats, weight loss
- Extrapulmonary TB: Depends on the affected organ (e.g., lymphadenopathy, meningitis, bone pain)
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