Tuberculosis Flashcards
(27 cards)
What is the leading single infectious killer in adults world-wide (excluding HIV)
Tuberculosis
How many people got TB in 2019?
10 mil
Why are mycobacteria hard to grow, diagnose & treat?
Mycobacteria are slow growing and have a lipid rich wall making them difficult to treat with antibiotics. They are hard to culture and therefore, hard to diagnose.
What 8 countries accounted for 2/3rds of the total new cases of TB
India Indonesia China Philippines Pakistan Nigeria Bangladesh South Africa
What is the relationship and effect of TB and HIV concurrent illness?
- HIV makes people more likely to get TB
- TB makes those with HIV more likely to die
- TB is still curable in HIV
- TB makes HIV progress more rapidly
- HIV patients have a higher mortality with TB
- HIV makes TB more difficult to diagnose
- HIV drugs and TB drugs interact
how is TB transmitted?
Spread in aerosols from infected individuals lung to another or via spitting or sneezing on plates or hands
what do we mean by smear positive and smear negative in TB? what effect does this have on transmissibility?
If we can’t see the bacteria in the sputum, we say they are smear negative, if we can see the bacteria in sputum, we say they are smear positive.
Smear positive = 27/50% of household contacts become infected (more infectious)
Smear negative = <5% household contacts become infected (less infectious)
how is bovine tb spread?
through cows and unpasteurised milk drinking. more common in butchers or abattoir workers.
why are mycobacteria good at surviving intracellularly?
they have a waxy outer coat so they can survive in phagolysosomes.
pathology of TB
- Bacilli are taken in lymphatics to hilar lymph nodes and the adaptive immune response is activated
- Macrophages and lymphocytes seal in, contain and kill majority of infecting bacilli in a granuloma to stop further replication of the bacteria or make the bacteria go into a dormant stage = latent TB
- Primary infection is contained but cell mediated immune response persists
- Latent TB = no clinical disease, may be tiny granulomata that become calcified, detectable CMI to TB on tuberculin skin test
- If immune response is not strong, the granuloma does not work to suffocate the mycobacteria
- As granuloma grows it develops into a cavity (more likely in apex of lung as there is more air and less blood supply and immune cells which is favourable for the bacteria)
- The cavity is full of TB bacilli which are expelled when the patient coughs
- Bacilli + macrophages coalesce to form a granuloma this is called the primary (ghon) focus
When there is a primary (goon) focus + mediastinal lymph nodes enlarged what is this called?
Ghon complex
Presentation of TB (systemic features)
weight loss night sweats low grade fever anorexia malaise
Presentation of TB (pulmonary features)
Chronic cough >3 weeks
Chest pain
breathlessness
haemoptysis
Presentation of TB (extra-pulmonary features)
lymph node tb, miliary tb
Bone pain, swelling of joint or Potts disease
Abdominal TB - ascites, abdominal nodes, ileal malabsorption
GU TB: epididymitis, frequency, urgency, haematuria
CNS TB: meningitis, CN palsy, tuberculoma
natural course of tb infection?
- At some point there is a primary infection which can develop into primary disease (5% cases) (either specific organ which is usually the lung or all over the body)
- This can lead to dormant TB and at some point it can re-activate and the patients can develop disease (post-primary disease)
- Post primary disease usually occurs wherever the dormant TB were hiding (usually lung)
- Those who have had TB can become re-infected even after being treated and lead to disease again and some die from TB
What percentage of people have been identified to have latent TB?
25%
Diagnosing active TB?
Microbiology, microscopy, PCR, culture Sputum Urine CSF Pleural fluid Biopsy specimens of lymph nodes, peritoneum, bone brain etc.
Other non-specific
- prolonged inflammatory. response, normochromic normocytic anaemia, thrombocytosis, raised eSR or CRP, low albumin, hypercalcaemia, sterile pyruria.
diagnosing latent tb?
Not possible to find dormant bacteria so we use TB skin test where we inject a protein derived from organism into the dermis and it stimulates a reaction if the person has been exposed (doesn’t distinguish between BCG used in vaccine)
Interferon gamma release assays - antigens specific to M tuberculosis which does distinguish between BCG and TB.
What is the standard UK treatment for TB?
Rifampicin - 6m
Isoniazid - 6m
Pyrazinamide - first 2m
Ethambutol - first 2m
what is DOTS?
directly observed treatment short-course. It is the TB strategy from WHO to have successful treatment of TB. It involves 5 main things, one of which is giving medication in a supervised fashion.
What is a common side effect for TB drugs?
hepatitis
why is the course of antibiotics so long for TB and why are so many drugs used?
Most bacteria are killed within weeks but a group of mycobacteria are dormant and can re-activate so using a combination of drugs means most can be effectively killed.
In the UK, what percentage of patients are thought to have isoniazid resistance and MDR to TB drugs?
7% isoniazid
1% MDR
Why is drug resistant TB worse?
DR TB is more difficult to treat, more side effects from IV/IM injections required, >20m treatment and increased relapse rate
XDR TB is now present in many countries and is very difficult to treat with a very high mortality.
