L13 Tuberculosis Flashcards
Bacterium responsible for most TB cases
Mycobacterium tuberculosis
How is TB transmitted and is it acute or chronic
water droplets inhaled into alveoli
chronic
What factors will influence the outcome of TB
number and type of organism immune response (malnutrition, age, immunosuppression etc) administration of appropriate antibiotics
What two things does the pattern of disease depend upon
primary: first exposure to bacteria
OR
secondary: previously exposed individual
5 basic stages to primary TB
- exposure to MTB
- alveolar macrophage endocytosis
- T lymphocyte hypersensitivity
- cell-mediated immune response
- granuloma formation
What happens with macrophages trying to phagocytose bacteria?
can’t degrade
MTB has special wall lipids which prevents a phagosome from forming
no phagosome = no antigen processing
bacilli replicate slowly within macrophages every 16-24 hrs
some macrophages to lymph nodes then blood stream
bacteria continue to proliferate in alveoli (primary site) and lymph nodes = Ghon complex
What is a Ghon complex
alveoli and lymph node involvement
What is a Ghon focus
only alveoli
How does T lymphocyte hypersensitivity occur
some bacteria degraded
present antigen to T lymphocytes (approx. 3 weeks) for T-helper cell response
hypersensitivity reaction activated
What happens with the cell-mediated immune response
Th1 cells produce interferon gamma
IFN gamma activates macrophages to become epithelioid macrophages
now MTB can be destroyed if good enough
What cytokine prompts macrophages to become epithelioid macrophages
interferon gamma
Steps in formation of granuloma
T helper cells form granuloma with caseous necrosis
epithelioid macrophages come together to form giant cells
TNF secreted and more monocytes recruited
What are the 5 layers of a granuloma
caseous necrosis epithelioid macrophages giant cells lymphocytes fibroblasts
What does the course of the disease depend upon
whether patient is sensitized to organism
What are latent TB lesions
MTB adapt by changing metabolism
- slow down active replication
- increase cell wall thickness
- “dormant” state that can be reactivated
What do 10% of primary TB patients usually develop
progressive primary TB = dissemination disease (military TB, small spots of infection which can spread to other organs)
Type of lesion in primary TB
peripheral
Type of lesion in secondary TB
apical
How can secondary TB develop
reactivation
reinfection
HAS TO BE AFTER HAVING PRIMARY
How can secondary TB be characterized
apical lesions in apex of lungs in area with higher oxygen content
little lymph node involvement
T- cell mediated response is familiar = tissue necrosis and cavitation (ie nuclear bombing site of infection)
What is secondary TB treated with
prolonged antibiotics
What are the symptoms of secondary TB
malaise, anorexia, weight loss, fever purulent sputum (green) erosion of cavities into airways blood in sputum (haemoptysis) pleuritic pain
What will the best case of secondary TB result in
calcification of apical lesions
What is the worst case scenario with secondary TB
lesion erodes blood vessels, bronchi, pleura
