LUNG INFECTION 1 Flashcards
Introduction of pulmonary tuberculosis
•One of the most important contagious disease in the world.
• Caused by a mycobacterium. Most commonly mycobacterium
tuberculosis.
Also mycobacterium bovis (rare). Only common with unpasteurised
milk)
• Acquired by inhalation.
• The mycobacterium is resistant to drying thus can survive in the
atmosphere for weeks.
Susceptibility factors to TB include:
- age (children, elderly due to depressed immunity)
- immunity: People who are immuno-compromised have high susceptibility,
Diabetic, AIDS, malnutrition (Kwashiorkor in children), immunosuppressive
therapy (cancer treatment) - Silicosis of the lung increases the risk of TB.
- Immunisation: All new-borns get BGC vaccination. (Bacille-CalmetteGuerin). This is a vaccine with attenuated bacilli.
Host Response to TB
• Bacillus enters the lung.
• First response is neutrophils. Neutrophils are not capable of killing
the bacteria so they disappear.
• A few days later, macrophages influx. These ingest the bacteria but
also cannot kill them.
• Macrophages eventually die leaving the bacilli alive and well.
• Lymphocytes influx. Lymphocytes release lymphokines which attract
more macrophages.
• Lots of macrophages then enter the area
These macrophages then become larger and they change their
appearance to epithelioid histiocytes. Their function changes from
ingestion to secretion.
• The epithelioid histiocytes release substances which are more
efficient killers of these bacteria.
• This results in granuloma formation. Macrophages may fuse to form
Langhan’s giant cells.
• The central portion of the granuloma may undergo
necrosis. Typically caseation. Macroscopically this is visible as
white spots on the lung called tubercles
gross appearance of lung tubercle
– Lung tubercle
• Central area causative necrosis
Necrotiizing granulomatous inflammation central area of necrosis, surrounding epithelioid histocytes
Non-necrotiizing granuloma Coalescence of epithelioid histiocytes
No necrosis
Ziehl-Neelsen Stain is positive for acid-fast bacilli.
Primary TB
Primary TB
• Occurs when the individual is exposed for the first time to mycobacterium
tuberculosis.
• Most cases of TB in South Africa are post-primary cases which occurs when
immunised.
• Occurs mostly in children who haven’t been given BCG vaccination.
• The lesion in primary TB will occur at the site of the bacillus entry. (Invariably in
the lungs but can also occur in the GIT, tonsils, skin (rarely)
PRIMARY TB LESIONS
The lesion in primary TB will occur at the site of the bacillus entry. (Invariably in
the lungs but can also occur in the GIT, tonsils, skin (rarely)
This lesion is the Ghon focus
• In the lungs, there is a typical site. In the right lung it is the lower part of the
upper lobe and upper part of the middle lobe.
• In the left lung it is the lower part of the upper lobe or upper part of the
lower lobe. It is subpleural.
Lesion is usually small (between 1 and 2 cm). Appears white macroscopically
due to caseation necrosis and is surrounded by fibrous tissue.
• Early lymphatic spread occurs. This is rapid.
• Bacilli enter the hilar lymph nodes which become enlarged and caseous.
• Bacilli multiply rapidly within the lymph nodes.
• Ghon focus+ Hilar lymphadenopathy = Ghon Complex
Lesions are Ghon focus together with regional lymph node. This is termed the
primary complex/ ghon complex
• In most people, the Ghon focus heals spontaneously. A fibrous nodule is
left. Calcification (dystrophic) occurs leaving a hard fibrotic calcified nodule in
the subpleural area.
Lymph nodes also become hard and fibrotic.
• In most people, the immune system is adequate to allow the primary complex to
heal spontaneously.
• Although the Ghon focus may heal, there may still be viable bacilli which remain
dormant for long periods of time. (years) Whenever there is immune
suppression, the bacilli become active and cause disease
Gross and microscopic findings( primary lesions)
- Caseative granulomas / necrotizing granulomatous inflammation
- Concentric arrangement
- Caseative necrosis centrally
- Surrounded by epithelioid histiocytes
- Peripheral cuff of lymphocytes
- Multinucleated giant cells are present in the granulomas
- Langhans type
- Foreign body-type
- Necrosis has characteristic appearance
- Grossly –cream-white, semisolid and resemble cottage cheese (‘caseation’)
- Microscopically- eosinophilic, bland and structureless with karyorrhectic debris
- Surviving bacilli often seen at the periphery of the lesion
chest x ray
- Ghon focus+ Hilar lymphadenopathy
* = Ghon Complex
Ghon focus+ Hilar
lymphadenopathy =
Ghon Complex
Caseative granulomas
- Concentric arrangement
- Caseative necrosis centrally
- Surrounded by epithelioid histiocytes
- Peripheral cuff of lymphocytes
HE stain of a Necrotizing Granuloma
microscopically
• Necrotizing granulomatous inflammation • characterized by the central area of casous necrosis • Surrounding collection of epithelioid histiocytes and giant cells
H&E stain of a granuloma
microscopically
• Non-necrotizing granulomatous inflammation • characterized by the collection of epithelioid histiocytes and Langhans giant cells • Surrounding peripheral chronic inflammation comprising lymphocytes
Zehl-Neelsen Stain
it is positive for acid-fast bacilli.
Acid-fast bacilli are bright red after staining. Methylene Blue stains the background blue. Bacilli are rod-shaped and are straight or slightly curved
This is not Gram stain
Complications of Primary TB
• Immunosuppression: If a person has an inadequate immune system, the bacilli
will spread. (AIDS, Diabetics, immunosuppressive therapy, malnutrition,
Kwashiorkor, renal failure, lymphomas, leukaemia)
• Large dose of bacteria.
• If the Ghon focus doesn’t heal, it may rupture into the pleural cavity to cause a
TB pleurisy with associated effusion.
Lymph nodes may be enlarged and obstruct a bronchus. This results in
segmental collapse of the lung. The lymph node may rupture into the bronchus
and spread along the bronchus into the bronchioles then into the surrounding
lung tissue resulting in TB broncho-pneumonia.
• Lymph nodes may also rupture into the pericardial space causing TB
pericarditis.
• Lymph nodes may rupture into the pulmonary artery or its branches. This will
go to the rest of the lung.
Lymph node can rupture into pulmonary vein to cause systemic dissemination
resulting in miliary TB.
• Rupture of lymph nodes in the abdomen can cause a TB peritonitis.
• The enlarged caseous mesenteric lymph nodes are termed tabes mesenterica.
• Bacilli may spread via the thoracic duct to the systemic circulation resulting in
miliary TB.
TB meningitis is fatal in almost all cases if untreated.
• If the bacilli are swallowed, intestinal TB can result causing ulcers especially in
the terminal ileum.
TB meningitis, TB broncho-pneumonia and miliary TB are the major causes of
death from primary TB.
post primary TB
Referred to by different names:
• Post-primary TB / Reactivation TB / Secondary
TB
Reactivation frequently occurs in the setting of decreased
immunity
This occurs in individuals who have previously been exposed to TB.
• This is the commonest type of TB thus the most important.
• Patients thus infected are responsible for infecting others.
• Pathogenesis is different to Primary TB since there is strong cell
mediated response to TB due to activated T lymphocytes.
Lesions associated with post-primary TB are hypersensitivity related.
• It can occur either due to reactivation or reinfection. Reactivation is more
common. (due to malnutrition, AIDS, corticosteroid therapy, malignancies–
same as before)
• Found mainly in the upper lobes of the lungs especially the posterior
segment. The reason being a good ventilation with a relatively poor blood
supply which favours the bacilli.
Lesions in the lung show areas of caseation in the upper lobes / apical region.
• The areas of necrosis enlarge slowly over a period of weeks or months. It
eventually join to form a confluent mass which is surrounded by fibrosis.
• The patient starts to cough up the necrotic tissue to leave a cavity in the lung.
