TB:
Clinical features
Primary TB – endemic, usually in childhood in those countries, good immune response so damage is limited and it is in the midzone of the lungs with hilar node involvement. Ghon focus – calcification of the hilar lymph nodes. Clinical disease is rare at the time of primary infection, especially in childhood and adolescence.
Post-primary TB – when people clinically present, 80% used to be pulmonary but nowadays 50% is elsewhere than in the lungs. Usually due to reactivation of the Ghon focus but it can be reinfection with another strain of TB. The main symptoms are cough, weight loss, malaise, fever, night sweats and a third of patients get haemoptysis. O/E not much but CXR shows abnormal apices (if normal then don’t have pulmonary TB) and infiltration and cavitation which heals with fibrotic change.
The main complications are severe haemoptysis and bronchopleural fistulae and TB empyema and aspergilloma.
Extra-pulmonary TB – everywhere can get TB. Pleural TB get after you’ve had it in lungs, gives cough and pleuritic pain. Lymph node TB is after primary infection and after reactivation, 70% is in cervical lymph nodes. Painless discrete nodes which enlarge in size and are matted, then eventually break down and discharge from skin. Bone and joint TB is normally in spine (Pott’s disease). Paravertebral abscesses, can get cord compression. TB meningitis, risk of permanent neurological damage with insidious onset. A focus ruptures into the CSF from blood-borne spread. Pericardial TB spreads from lungs or mediastinal lymph nodes. Three distinct clinical syndromes:
Acute pericarditis plus or minus effusion.
Chronic pericardial effusion.
A chronic constrictive pericarditis – pericardium calcifies and shrinks.
Miliary TB – disseminated disease everywhere in people with chronic underlying disease or immunosuppression. BCG protects against this more than the others. Insidious symptoms usually affecting lungs, liver and CNS. Lots of little seeds all over lungs. 50% get choroidal tubercles. Classic CXR shows loads of 1-2mm nodules.
Diagnose TB:
Pulmonary dx is a Ziel-Nielssen/oramine stain for AFB.
Culture a sputum sample on a special media, takes 8 weeks to get the results back.
Open TB is where you can see the AFB in the sputum.
Extra-pulmonary, culture everything you can and histology will show a caseating granuloma and traditionally you do the Mantoux skin test which showed if you had been infected in the past but it’s unhelpful because a third of the world have had primary TB and it’s positive if you’ve had BCG. Nowadays use the ELISPOT test.
In CSF meningitis you will get lymphocytes low sugar and very high protein, higher than in normal bacterial and in normal bacterial you will get more neutrophils.
The best test of the whole lot is to do a PCR to diagnose it and to do sensitivity testing.
Drug treatment:
Most TB you can do a short course of chemotherapy (six-months). You start with all four drugs then switch down to three or two after the first few weeks when you have the resistance back.
Isoniazid for full six months. Most important side-effects are hepatotoxicity, neuropathy (prevent with vitamin B6) and a granulocytosis.
Rifampicin also for six months. Classically raises metabolism as an enzyme inducer so cannot take OCP but can take POP. Loads of drug interactions and is hepatotoxic and gives you orange wee.
Pyrazinamide is for first two months. Hepatotoxicity and arthralgia.
Ethambutol is also for the first two months and can...