tuberculosis Flashcards

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1
Q

what is the epidemiology of TB

A

Commonest cause of infectious disease related mortality worldwide
WHO ¼ of global population have latent TB infection
Global incidence is falling
8% HIV positive
1.5 million deaths per year
Increasing drug-resistance

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2
Q

what is the epidemiology of TB in the UK

A

TB now declining rapidly in UK
Example of major multiagency intervention
Less than 500 new cases
People born outside UK account for 72% of cases

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3
Q

what is the pathogenesis of TB

A

Airborne droplet spread
Inhaled – deposited in airspaces
Macrophages ingest bacilli – replicate within endosomes
Transported to regional lymph node
Killed
Multiply – primary TB
Dormant – asymptomatic (LTBI if exposed to host immune system)
Proliferate after period of latency – reactivation of disease

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4
Q

Natural history of TB infection

A

Exposure - elimination/inability to control (transmission)/immune control - latent TB elimination/lifelong containment/reactivation to active TB
Approx 50% develop active disease within 5 years of exposure
Risk of developing active TB 10-15% over lifetime in immunocompromised
HIV+ risk 10% per annum

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5
Q

what is TB

A

Aerobic bacillus
Divides every 16-20 hours (slow)
Cell wall but lacks phospholipid outer membrane
Does not strain with gram stain (weakly positive)
Retains stains after treatment with acid (acid fast bacillus)

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6
Q

what is the pathology of TB

A

Granulomatous inflammation
Rim of lymphocytes
Fibroblasts
Central infected macrophages (giant cells)
Central necrosis – caseation
Secretion of cytokines (IFNy). – activate macrophages to kill bacteria
AFBs in granulomas

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7
Q

What are transmission risks of TB

A

Close contacts of infectious cases (smear +)
Contact with high risk groups:
High incidence country
Frequent travel to high incidence areas
Immune deficiency – HIV, steroids, chemo and biologics, nutritional deficiency (vit D), diabetes and end stage renal failure

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8
Q

What lifestyle factors influence TB contraction

A

Drug/alcohol missuse
Homelessness/hostels/overcrowding
Prison inmates
Genetic susceptibility (twin studies of gene polymorphisms)

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9
Q

how does primary TB progress

A

1-5% cases, bacilli overcome immune system soon after initial infection

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10
Q

how does latent TB progress

A

majority (immune memory of exposure to TB), 2-23% cases – reactivation disease, risk of reactivation increases with immunosuppression (HIV + risk 10% per year and HIV risk 1%)

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11
Q

how is active TB diagnosed

A

Principles – identify the infected area, isolate the organism, obtain information regarding susceptibility to antibacterials

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12
Q

how is latent TB diagnosed

A

Principles – identify immune response to TB proteins or TB specific antigens

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13
Q

what is the tuberculin TB test

A

mantoux
Requires
Circulating memory T lymphocytes
Ability to mount a delayed hypersensitivity reaction
Cross reactive with other mycobacterial antigens so non-specific
Maybe falsely negative in severely ill or immunosuppressed individuals

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14
Q

what are interferon gamma release assays

A

ELISPOT/ELISA enzyme linked immunological assay of release of interferon-gamma in whole blood following stimulation by specific tuberculosis antigen
More specific than Mantoux
Correlates better with degree of exposure than Mantoux
Does not differentiate between latent infection and disease
T-spot TB or quantiferon gold

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15
Q

what is pulmonary TB

A

Majority (55%) of cases

Infection risk, cavitatory diease – more infectious

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16
Q

What are the clinical features of pulmonary TB

A
Cough
Haemoptysis
Chest pain 
Weight loss
Fever
Night sweats
Diagnosis 
Chest imaging
Sputum/BAL
17
Q

how is pulmonary TB seen on X-ray

A

Upper lobe consolidation, can be bilateral too
Hilar lymph node changes (Hilar lymphadenopathy)
TB pleural effusion

18
Q

what are other types of TB

A
Extra pulmonary disease 
More common in non-UK born Asian origin
Reactivation
Sites
Lymph nodes, CNS, none (pott’s disease of the spine), genitourinary system, GI tract and disseminated/military
19
Q

what is TB lymphadenitis

A

Often get worse on treatment – paradoxical reaction
Can form sinus tracts with chronic discharge
Cold abscess formation

20
Q

what are symptoms of disseminated/miliary TB

A

Fevers, sweats, weight loss and malaise very common
Respiratory symptoms in majority
GI or CNS symptoms in 20%
Abdo pain, diarrhoea, abnormal LFTs, hepatomegaly in 50%, headache or confusion, altered mental state in 20%

21
Q

What are other forms of TB

A

Skeletal TB
Around 15-30% of all extrapulmonary cases
Genitourinary TB
Kidney/bladder/pelvic involvement, pus in urine but repeatedly negative standard cultures (sterile pyuria)
TB enteritis
Ileo-caecal commonest weight loss, diarrhoea, blood in stools
TB of the eye
Any part of eye, probably more common than we think
Pericardial TB
CNS TB
TB meningitis, TB arachnoiditis, Tuberculoma, spinal cord compression – extension of discitis

22
Q

What is the epidemiology of extra pulmonary forms of TB

A

1% all TB cases
6%. Extrapulmonary TB in immunocompetent host
More common in HIV coinfected
Mortality 15-40% despite effective Rx (CDC)

23
Q

How is TB controlled

A

Government global policy
Consider the diagnosis
Early diagnosis and treatment (even if negative cultures/smear)
Optimal treatment and adherence (DOT/VOT/section)
Contact tracing
Prevention – BCG
Latent treatment programs, prevent TB becoming active

24
Q

how is TB treated

A

Standard treatment for TB is minimum 6 months
2 months (initial phase) – standard quadruple therapy (isoniazid, rifampicin, pyrazinamide and ethambutol)
4 months (continuation phase) of I and R, standard dual therapy
TB treatment taken all together on empty stomach 1 hour before breakfast, compliance essential for cure
(CNS- 12 month treatment)
Latent: 3 months R or 6 months I

25
Q

what are the main treatment side effects

A

P: hepatoxicity, joint pain and N&V
R: hepatoxicity, reddish colour to urine
I: hepatoxicity, fever, peripheral neuropathy and optic neuritis
E: peripheral neuropathy, optic neuropathy and gout
All: nausea and skin rashes