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Mycobacteria and TB: mycobacterium TB facts

- 2-4 μ by 0.2-0.5 μ

- Obligate aerobe: well-aerated upper lobes

- Facultative intracellular parasite: usually macrophages - because it's made up of a lot of lipids so can grow inside the macrophages without being killed

- Slow generation time
15-20 h

M.bovis from cattle


Mycobacteria and TB: Where does TB most commonly affect?

Lungs - pulmonary TB but can also affect the lymph nodes, bones, joints and kidneys and it can cause meningitis


Mycobacteria and TB: How does TB spread and who is more likely to affect?

TB is most commonly spread in droplets being coughed or sneezed into the air

Frequent or close prolonged contact with an infected person is necessary

People with already weakened immune system


Mycobacteria and TB: Who are the at risk groups of TB?

HIV infection

Steroids, chemotherapy, transplants, elderly

Unhealthy, over-crowded conditions

Stay in high-rate country- S.E. Asia, sub-Saharan Africa, parts E.Europe

Those exposed to TB in youth

Children of parents from high-rate countries

Prisoners, drug addicts, alcoholics



Mycobacteria and TB: Where and how does primary TB start?

Droplet nuclei inhaled

Taken up by alveolar
macrophages – not
activated (lipids)

Droplet nuclei (c.5 μ) reach the alveoli where the infection begins

Granuloma in lung = Ghon focus
Enlarged lymph nodes + GF = Primary Complex
---> mild flu like symptoms


Mycobacteria and TB: how does secondary TB occur?

Reactivation of dormant mycobacteria when something happens to the T cells: impaired immune function

Reinfection in a person previously sensitised to mycobacterial antigens

- occurs months, years or decades after primary infection
- reactivation most commonly occurs at apex of lungs - highly oxygenated


Mycobacteria and TB: What is the mechanism of secondary TB?

- Caseous centres of tubercles liquefy
- Organisms grow very rapidly in this
- Large Ag load
- bronchi walls become necrotic and rupture
- cavity formation
- organisms spill into airways and spread to other areas of lung: highly infectious
- Primary lesions heal
- Ghon complex, Simon foci


Mycobacteria and TB: What is milliary TB?

rapid dissemination of th organism


Mycobacteria and TB: How do you classify a TB infection (not lung disease) LEARN

Organism present
Tuberculin skin test positive
Chest X-ray normal
Sputum smears negative
Sputum culture negative
No symptoms
Not infectious
Not defined as a case of TB

Only 3-4% of those infected develop active disease upon initial infection, 5-10% within one year


Mycobacteria and TB: How do you classify a TB lung disease? LEARN

Organism present
Tuberculin skin test positive
Lesion on chest X-ray
Sputum smear positive
Sputum culture positive
Defined as a case of TB


Mycobacteria and TB: What are the most common symptoms?

Cytokines (TNF, IL-3, GM-CSF) 
Persistent cough, +/- sputum
Weight loss
Swollen glands (usually in the neck)
Night sweats
Sense of tiredness and being unwell
Coughing up blood

can't really diagnose from symptoms


Mycobacteria and TB: What is the standard recommended regimen?

Isoniazid, rifampicin, pyrazinamide and ethambutol
for two months followed by isoniazid and rifampicin for four months

Trying to treat without the organism becoming resistant to the antibiotic, that's why there is a standard regime


Mycobacteria and TB: Why is there a standard recommended regimen?

Prevent spread of MDR-TB
standardized drug regimens
directly observed treatment (DOT)
good supply of high quality drugs
isolation of infectious patients - negative pressure isolation room


Mycobacteria and TB: What role does vitamin D play in TB?

Vitamin D has role in activating macrophages to destroy mycobacteria

Often a vitamin D deficiency in ethnic populations in UK


Mycobacteria and TB: What is the timeline of treatment of TB?

Non-infectious after c. 2 weeks

Begin to feel better after 2-4 weeks

Treatment must continue for 6 months + - must prevent resistance developing

Longer treatment for TB meningitis or if TB is resistant


Mycobacteria and TB: What are the fatality rates?

Untreated TB - 40 to 60%

Treated TB
- 5 to 50%
- depending on nutrition; quality and availability of medical care; HIV status


Mycobacteria and TB: What is the BCG vaccine and how does it affect the skin test?

Protection restricted to childhood tuberculosis which is rarely infectious
No impact on HIV-related TB
Does not prevent infection – only disease
Invalidates tuberculin skin test
Therefore – targeted vaccination; effective for about 15 y


Mycobacteria and TB: what is the link between TB and HIV?

HIV / AIDS and TB are overlapping epidemics – “the unholy alliance”
- Worldwide 30-80% of AIDS patients get TB

HIV increases risk of acquiring TB
Destroys immune system

TB makes HIV worse
Increases replication rate of HIV

TB treatment slows down HIV and keeps patients alive to get HIV drugs


Mycobacteria and TB: What are the obstacles to TB control?

Lack of financial resources- half of all cases in China, Indonesia, India, Pakistan and Bangladesh

Social instability - e.g. Russia

HIV epidemic
- HIV/AIDS doubles the TB death rate
- 30 to 70% of TB cases in Africa are HIV positive
- reinfection in South Africa

Drug resistance



Mycobacteria and TB: What do skin tests do?

Heaf, Tine, Mantoux
- ascertains infection rather than disease
- may be negative in severe TB or concomitant HIV, malnutrition, steroids
- may be positive with BCG or after exposure to environmental mycobacteria


Mycobacteria and TB: What are T- SPOT TB & QuantiFeron gold?

Blood tests to replace tuberculin tests

Detect reactive T cells - specific for mycobacterium TB, not for BCG

Specific for Mtb



Mycobacteria and TB: How is microscopy used to look at TB sputum?

Ziehl-Neelsen stain: Needs > 10,000 organism/ml at 100X lens

or flourescent
Rhodamine-Auramine is more sensitive

One-third of pulmonary TB (two-thirds extra-pulmonary) undiagnosed by microscopy


Mycobacteria and TB: How do you culture TB sputum?

Homogenise (Sputasol - breaks it down)

Decontaminate (4% NaOH Petroff) - kills all bacteria but the mycobacterium

Concentrate (centrifugation)

(Middlebrook’s medium)

Löwenstein-Jensen medium

4-6 weeks for visible colonies

(Liquid media; Kirchner’s)


Mycobacteria and TB: how does automatic culturing work?

MGIT 960
- Fluorescent reaction quenched by O2
- Growth of mycobacteria lifts quenching and tubes fluoresce
- 10 days

another test - MPT64 - antigen ONLY given off by TB so this test is done afterwards


Mycobacteria and TB: Look at nucleic acid detection tests again -

MTB complex - rifampicin resistance genes


Mycobacteria and TB: how is typing carried out?


- Variable Number of Tandem Repeats
- Mycobacterial Interspersed Repetitive Units

- e.g. VNTR 84455 MIRU 244428223533
17 digit profile given - fingerprint of that organism so can track the infection


Respiratory viruses and atypical pathogens: Why are some viruses restricted to infecting certain areas?

expression of different types of cell expressed receptors.


Respiratory viruses and atypical pathogens: What are the types of infection? and the two types of invaders?

Surface: - local spread
- short incubation
e.g. common cold, Candida

Systemic: - spreads from mucosal site of entry to other site in the body
- returns to surface for final shedding stage
- longer incubation: weeks
- e.g. measles, mumps, rubella

Professional invaders:- infect healthy respiratory tract

Secondary invaders: - infect compromised tract


Respiratory viruses and atypical pathogens: What is Rhinitis and sinusitis?

The common cold

Caused by various viruses
Transmission by aerosol
Self-limiting (surface infections) and not systemic in healthy people
Identification usually not necessary unless clinical symptoms worsen- Involvement of LRT.
Molecular methods most common for ID, epidemiololgical info only

no vaccines - viruses change regularly and many of them cause the same symptoms


Respiratory viruses and atypical pathogens: How do viruses cause the classic cold symptoms?

Virus adheres to ciliated epithelium and avoids flushing out

Then enters cells and replicates inside cells, this cell damage leads to release of the clear runny nose fluid.

And leads to activation of host defenses release of cell debris and transient damage to ciliated epithelium.

Then there is an immune response that might be accompanied by overgrowth of normal flora and finally recovery and regeneration of ciliated epithelium.