Tuberculosis Flashcards

(45 cards)

1
Q

epidemiology of TB - worldwide

A

incidence rate worldwide is falling 2%/yr
number 1 killer of comunicable disease (> HIV and malaria combined)
2/3 of all cases in 8 countries: India, China, Indonesia, Philippenes, Pakistan, Nigeria, Bangladesh, South Africa
30 high TB burden countries account for 87% of all the world’s cases
~2bln people infected worldwide

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2
Q

epidemiology of TB - national

A

major problem in London - immigration from high incidence areas
39% of TB cases in UK are in London
2/3 cases born abroad
clusters in cities

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3
Q

vulnerable groups in the UK

A

those from high prevalence countries
70% are non-UK born, most aged 15-44
HIV +ve, immunosuppressed
elderly, neonates, diabetics

homeless, alcoholics, IDUs, mental health problems, prison - 1/10 of all cases

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4
Q

mycobacteria

A

numerous species, ubiquitous in soil, water

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5
Q

which species of mycobacteria cause human disease

A

Tuberculosis (M. TUBERCULOSIS, M. africanum, M. bovis (bovine TB, BCG strain)

non-tuberculosis mycobacteria, NTM infections/atypical mycobacteria

Leprosy (M. leprae)

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6
Q

why does TB take a long time to treat

A

non-motile bacillus, very slow growing

disease is slow, treatment is long

cultures take a long time to grow to recieve results back

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7
Q

is TB aerobic or anaerobic

A

aerobic - predilection for apices of lungs where there is a higher oxygen conc

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8
Q

describe the cell wall of mycobacteria

A

uniquely has a very thick fatty cell wall - have to treat with many antibiotics for a long period of time
resistant to acids, alkalis and detergents
resistent to neutrophil and macrophage destruction
acid and alcohol fast bacilli - Ziehl Nielson stain

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9
Q

are all AAFBs TB

A

NO

can’t differentiate mycobacteria from TB on initial stain

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10
Q

how is TB spread

A

airbone - pulm and laryngeal TB
someone with TB bacteria in their lungs coughs/sneezes/yells
TB bacteria attached to aerosol droplets which remain suspended in air for many hours esp w/ poor air circulation
someone else breathe in the bacteria
usually requires prolonged closed contact

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11
Q

what is TB NOT spread by

A
shaking hands
sharing food
touching surfaces
sharing toothbrushes
kissing
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12
Q

what are outdoors mycobacteria eliminated by

A

UV radiation

dilution

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13
Q

what is the exeption to the spread of TB

A

M. bovis

can be spread by the consumption of unpasteurised infected cow milk

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14
Q

why do HIV patients respond worse to TB

A

Their T cell response is impacted

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15
Q

what does the T cell immune response cause

A

tissue destruciton

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16
Q

immunopathology of TB

A

activated macrophages –> epithelioid cells –> Langhan’s giant cells

accumulation of macrophages, epithelioid and Langhan’s cells –> Granuloma

central caseating necrosis which may later calcify

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17
Q

is the Th1 cell mediated response good or bad

A

eliminated/reduces number of invading mycobacteria

tissue destruction is a consequence of activation of macrophages

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18
Q

what affects the outcome of TB infection

A

infection - virulence, number

susceptibility - genetics, nutrition, age, immunosuppression

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19
Q

primary TB infection

A

no preceding exposure or immunity
mycobacteria spread via lymphatics to draining hilar lymph nodes
usually no symptoms
can be fever, malaise, erythema nodosum, rarely chest signs

associated with development of immunity to tuberculoprotein

20
Q

what happens in the majority of 1y TB infections

A

> 85%
initial lesion and local lymph node (1y complex)
heals w/ or w/o scar
may calcify (Ghon focus and complex)

21
Q

what are the 3 different outcomes of 1y TB infections

A

progressive disease
contained latent
cleared cured

22
Q

tuberculous bronchopneumonia

A

small number of 1y infections (1%) progress
1y focus continues to enlarge - cavitation
enlarged hilar lymph compress bronchi, lobar collapse
enlarged lymph node discharges into bronchus
poor prognosis

23
Q

miliary TB

A

occurs in 1-3% of 1y TB infections
hematogenous spread of bacteria to multiple organs
fine mottling on X ray, widespread small granulomata
CNS TB in 10-30%

24
Q

post-1y disease

A

most common outcome
only in humans
typically 1-5yrs after exposure
2 main theories:
1. TB bacteria enter dormant stage with low/no replication over prolonged time period
2. balanced state of replication and destruction by immune mechanisms

25
clinical presentation of TB
cough - present with pulmonary TB fever sweats (mainly night) weight loss all 3 symptoms
26
what % of patients have extra-pulmonary TB
50
27
in what % of patients are CRP and ESR normal
CRP - 15% | ESR - 21%
28
in what % of pts are symptoms absent
fever - 37% sweats - 39% weight loss - 38% all 3 absent in 25%
29
appearance of pulmonary TB on CXR
classical: apices, soft 'fluffy/nodular' upper zone, cavitation in 10-30% lymphadenopathy rare normal CXR in 13% of definitive pulm TB (22% in HIV)
30
when to consider CT
``` normal CXR but clinical suspicion miliary TB cavitation and other differential lymphadenopathy, alternative diagnosis targets for BAL ```
31
appearance of 1y TB on CXR
mediastinal lymphadenopathy (mainly unilateral, 15% bilateral) pleural effusion miliary (hematogenous spread, 1-3%) pnuemonic lesion w/ enlarged hilar nodes - consider 1y TB (no swollen lymph nodes in pneumonia)
32
how to sample the bacteria
sputum: 3 samples, 8-24hrs gap, at least 1 early morning sample induced sputum if they can't cough bronchoscopy with BAL endobronchial US with biopsy lumbar puncture (CNS TB) urine (urogenital TB) aspirate/biopsy from tissue (lymph node, bone, joint, brain, abscess) mantous/IGRA are NOT routinely used in diagnosing active TB
33
what are the 4 drugs used to treat TB
isoniazid (H) pyrazinamide (Z) rifampicin (R) ethambutol (E)
34
rules of TB treatment
multiple drug therapy is essential - single agent treatment leads to drug resistant organisms within 14 days therapy must continue for at least 6 months legal requirement to notify all cases test for HIV, hep B and C (risk of hepatotoxicity)
35
standard TB treatment
2 mths R/H/Z/E + 4 R/H | 6 mths duration minimum
36
other drugs used in TB treatment
pyridoxine (vit b6) with isoniazid to reduce risk of neuropathy steroids (CNS, miliar, pericardial) vit D substitute?
37
when is TB treatment >6mths
7-9mths - monoresistance 12 mths - CNS TB, h monoresistance extensive disease 9-12-18-20 mths - MDR RR TB treatment in the brain/drug resistance takes longer
38
how long does it take to kill the MTB
90% MTB dead in 2 days when using isoniazid | 99% MTB dead in 14days when also using rifampicin
39
side effects of rifampicin
orange urine/tears/lenses - indicates tablet is being absorbed induces liver enzymes, prednisolone, anticonvulsants all hormonal contraceptive methods ineffective hepatititis rash
40
side effects of isoniazid
hepatitis peripheral neuropathy - pyridoxine B6 to prevent this rash
41
side effects of pyrazinamide
hepatitis gout rash
42
side effects of ethambutol
optic neuropathy | rash
43
BCG vaccination
given selectively to risk groups neonates or unvaccinated children under 5, whose parent/grandparents were born in a country with an annual incidence of TB of 40/100 000 or greater unimmunised contacts of cases unimmunised high risk employees
44
latent TB screening
screen: contacts of people with active pulmonary/laryngeal TB who are <65 (hepatotoxitity increases with age), new entrants from high endemic areas, pre-biologics (TNF-alpha inhibitors), outbreaks asymptomatic with normal CXR and norma examination AND +ve mantous/IGRA test
45
treatment of LTBI
``` always rule out actie TB rifampicin and isoniaid for 3 mths OR isoniazid only for 6mths OR rifampicin only for 6mths OR rifapentine and isoniazide once weekly for 12 weeks (underserved population) ```