Respiratory tract infections: TB Flashcards

1
Q

TB and HIV

A

HIV infection has caused much of recent increase in TB in developing countries

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2
Q

TB in humans is caused by

A

mycobacterium TB

M. bovis known to have caused TB in cattle (M. tuberculosis is human-adapted farm)

many harmless species of mycobacteria in environment

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3
Q

M. kansasii and M. abscessus:

A

uncommon cause of respiratory infection esp those with compromised lung function (eg. CF)

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4
Q

M. avium-intracellulare

A

causes disseminated disease in AIDS patients (only in immune compromised)

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5
Q

M. marinum

A

uncommon cause of skin infections (‘fish-tank granuloma’)

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6
Q

M. chelonei

A

rapid growing ‘environmental’ species: may contaminate bronchoscopes!(water, can cause confusion in diagnosis when they grow bacteria in lab)

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7
Q

M. leprae

A

cause of Leprosy (cannot be grown in vitro)- only survives inside cells

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8
Q

Tuberculoid leprosy

A

common
strong cellular IR
few bacilli in lesions
depigmented anaesthetic lesions

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9
Q

Lepromatous leprosy

A

uncommon
weak cellular IR
many bacilli lesions
thick granulomatous lesions

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10
Q

M. tuberculosis

A
  • Obligate aerobes - grow in tissues with a high O2 content (i.e. the lungs).
  • Facultative intracellular pathogens - usually infecting mononuclear phagocytes (e.g. macrophages).
  • Slow-growing - slow signs and symptoms
  • Hydrophobic - high lipid content in the cell wall. Less permeable to usual bacterial stains (e.g. Gram stain).
  • Known as “acid-fast bacilli” because, once stained, the cells resist decolourisation.
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11
Q

pathophysiology of M. tuberculosis

A
  • Active TB is spread by airborne droplet nuclei
  • Nuclei can remain airborne after coughing for several hours.
  • Droplets are inhaled, lodge in alveoli and the organism is taken up by alveolar macrophages.
  • Slow replication and spread (via lymphatic system) to hilar lymph nodes.
  • In most individuals – cell-mediated immunity (CMI) develops 2-8 weeks after infection (associated with the development of a positive tuberculin skin test).
  • Activated T lymphocytes and macrophages form granulomas that limit further replication and spread.
  • Bacterial cells remain (sometimes viable) in centre of necrotic ‘caseating’ granulomas.
  • Most individuals are asymptomatic (latent infection) and never develop active disease (unless a subsequent defect in CMI occurs).
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12
Q

are extra-pulmonary contagious?

A

No

it is more common in HIV+

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13
Q

Tuberculous ‘caseous’ granuloma

A

Langhan’s giant cell
epithelioid cells
central necrosis
surrounded by lymphocytes

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14
Q

Clinical features of TB: non specific B symptoms

A

fever
weight loss
night sweats

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15
Q

clinical features of TB: respiratory symptoms

A

cough
SoB
haemoptysis
chest pain

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16
Q

chest radiograph

A

upper zone cavitating lesions most common

17
Q

most serious form of TB

A

CNS disease:
TB meningitis
space-occupying lesions (tuberculomas)
cerebral tuberculoma

18
Q

other sites of infection: skin/ soft tissue infection

A
commonest type of non-pulmonary disease 
cervical lymphadenitis (firm, discrete, painless lymph nodes) 
diffuse swelling in neck as doesnt cause inflammation
19
Q

other sites of infection

A

bones and joints (Pott’s disease- TB in spine)

disseminated disease
many organs involved simultaneously
- primary progressive disease or reactivation of latent infection
- miliary pattern on CXR

20
Q

other sites of infections: genitourinary tract

A
prostatitis 
orchitis 
renal lesions 
may cause infertility in women 
sterile pyuria (WBC in urine but no growth)
21
Q

Diagnosis

A
  • Early diagnosis improves survival and prevents spread of TB.
  • Category 3 pathogen (potential for laboratory-acquired infection).
  • Only handled in a designated containment level 3 (Category 3) laboratory.
  • Samples from patients suspected of having TB labelled accordingly.
  • All sputum samples handled in a Category 3 lab.
22
Q

samples

A
•	Sputum - decontamination required
•	Bronchoalveolar lavage (BAL)
•	Pus / Tissue 
•	Urine - 3 x24 hour collections
o	NB M. smegmatis may contaminate urine and cause confusion. 
•	Cerebrospinal fluid (CSF)
23
Q

Ziehl- Neelsan stain

A

• Remains crucial to TB diagnosis and control
• Rapid, cheap, simple, robust
• Moderate specificity & sensitivity
• Treated for active until know otherwise
(acid fast stays red as opposed to blue)

24
Q

Microscopy for TB

A
  • Auramine staining (UV microscopy) - sensitive but not highly specific
  • ZN stain may be used to confirm auramine positive samples
25
Q

Culture of Mycobacterium tuberculosis

A

Slow (2-8 weeks)
• Requires specialised media: Löwenstein-Jensen slopes in ‘shatter-proof’ glass containers
• Culture performed in a Category 3 facility
• Grow to see whether they are resistant stains

cauliflower or verrucose colonies

26
Q

‘Rapid’ culture of M. tuberculosis

A
  • 1-2 weeks
  • Liquid media e.g. Kirchner’s liquid medium
  • Automated system – Mycobacteria Growth Indicator Tube (MGIT)
27
Q

Antibiotic sensitivity tests

A

to detect resistance
especially in multi drug resistant TB= resistant to rifampicin and isoniazid- longer courses
(MDR-TB)

must treat with multiple agents

28
Q

extensively drug resistant TB (XDR-TB) definition

A

tuberculosis that is resistant to rifampicin and isoniazid AND to any member of the quinolone family and at least one second-line anti-TB agents: kanamycin, capreomycin, or amikacin

other countries where treatment isnt monitored- cannot afford resistance

29
Q

Genomic tests for Mycobacteria

A
  • Polymerase chain reaction (PCR)
  • DNA probes - allows speciation
  • Rapid detection of Rifampicin resistance
  • Increasing use of whole-genome sequencing (WGS) for species identification and typing
30
Q

Treatment of pulmonary TB

A

– Initial phase: 2 months of 4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol)
– Continuation phase: 4 months of rifampicin and isoniazid
– If resistance is suspected, 5 drugs may be used initially. For confirmed resistant strains, longer courses are required with second line agents.

31
Q

Prevention of tuberculosis

A

• Early diagnosis and treatment:
– ‘Open’ (ZN stain positive) pulmonary disease usually rendered non-infectious after 2 weeks of effective therapy.
– Contact tracing and detection of latent infection:
• Tuberculin skin test
• Chest radiography
• In vitro Interferon-gamma release tests (T SPOT-TB or QuantiFERON-TB Gold)
– Contacts treated if evidence of infection.
– TB is a formally notifiable disease (HPE co-ordinates contact tracing and investigation of outbreaks in the community).

32
Q

Vaccination

A
  • Bacillus Calmette-Guerin (BCG)
  • Live attenuated M. bovis strain.
  • Main role is protecting children against severe disease (meningitis & miliary disease) doesn’t prevent pulmonary TB asia ad Africa shows no effect