Resp Session 7 Flashcards
What causes TB?
7 closely linked but genetically distinct species of which M.tuberculosis, M.bovis and M.africanum are the most relevant
What is the definition of a clinical case of TB?
Infectious individual who is producing infectious droplets
Is M.tuberculosis fast or slow growing?
Slow-generation time is 15-20 hrs
How is M.tuberculosis spread?
Infected droplets
How easily is M.tuberculosis transmitted?
Infectious dose is 1-10 bacilli but needs prolonged exposure
What virulence factors do M.tuberculosis possess?
Complex waxes and glycolipids in cell wall
Long-chain mycolic acid in wall
Structural rigidity
Able to survive in lower airway macrophages
Acid and alcohol fast
Doesn’t dry in environment
How does an individual exposed to TB not become infected?
Not prolonged enough exposure
Insufficient infecting dose
Mucosal barriers
How does an individual exposed to TB clear the infection?
95% of infections will self cure due to effective immune response
How does an individual exposed to TB contain the infection?
Mounts T-lymphocyte response to intracellular infection in local lymph nodes to form Gohn’s focus and draining lymph nodes
Describe the epidemiology of TB.
1/3 of the world’s population infected with the majority in Africa, Asia and Latin America. In UK leaks of case reports in non-UK born young adults and elderly
How does an individual exposed to TB develop latent infection?
Mycobacteria remain in lung focus and multiply but do not cause damage due to immune control by cell-mediated immune response
How does an individual exposed to TB develop active/primary TB?
Immune destruction of the lungs by response to causative agent –> S/S and visible X-ray changes
How does primary TB usually present?
Usually pulmonary but can be extra-pulmonary in miliary or disseminated TB seen in the larynx, brain, kidney, bone
How does latent TB develop into post primary TB?
Exogenous reinfection/reactivation leads to immune destruction of lungs
Why must all suspected and confirmed cases of TB have an HIV test?
Risk of post primary TB increases with immunocompromise
How is active TB identified?
Blood test usually +ve
CXR abnormal
Smears and cultures +ve
Cough, fever, weight loss
Are pts with primary TB infectious?
Yes
How do the tubercle bacilli differ in active and latent TB?
Active and multiplying in active
Inactive and contained in latent
How does latent TB present?
IFN-alpha results +ve due to immune response
CXR normal
Smears and sputum -ve
No S/S
Are pts with latent TB infectious?
No
Where are caseating granulomas found in TB?
Anywhere there is infection e.g. Lung parenchyma, mediastinal lymph nodes, hilar lymph nodes, liver
When do cavities form in the pathogenesis of caseating granulomas?
When responding cells successfully remove the caseous dead cell material
What are the responding cells present in a caseating granuloma?
Lymphocytes
Epithelioid cells
Langhans cells
How is TB controlled in the community?
Treat index cases –> notify PHE –> contact tracing –> identify primary and secondary cases
Vaccinate and prevent transmission
Which pts fit into the index of suspicion for TB?
Non-UK born HIV Immunocompromise Homeless IV drug users Close, prolonged contacts
What Hx leads to a suspicion of TB?
Ethnicity Recent arrival/travel Contact with TB BCG vaccination Specific clinical features: fever, weightloss, malaise
What S/S are seen in pts with TB?
General chronic inflammation symptoms + Cough Haemoptysis SoB \+/- CXR abnormalities and pleural involvement
What does SoB in a pt with TB indicate?
Pleural effusion
What investigations can be performed in assessment of suspected TB?
CXR Microscopy Culture Speciation Tuberculin skin test Interferon-gamma-releasing assays
How does the CXR of a pt with TB appear?
Ill defined, patchy consolidation with cavitation
Healing –> fibrosis