Tuberculosis Flashcards
Vulnerable groups for TB?
High prevalence countries
Incidence among non-UK born individuals 19 times higher than those born in the UK (2023 TB Annual Report for Scotland)
HIV positive, Immunosuppressed
Elderly, Neonates*, Diabetics
Homeless, Alcoholics, IDU’s, those with mental health problems and those in prisons – approximately 1 in 10 of all cases
Epidemiology?
TB incidence over time is falling, 2% per year. But, recent rise
TB is still a disease of the poor / social risk factors
TB is the number 1 killer of communicable diseases
TB kills more than HIV and Malaria together
TB is not evenly distributed, globally or nationally
2/3 of all TB cases (prevalence) in 8 countries
An estimated 2 billion people are infected worldwide
What class of bacteria cause TB?
Mycobacteria
(M. tuberculosis, M.africanum, M. bovis (“bovine TB”, BCG strain)
Non-tuberculous mycobacteria, NTM-infections / ‘Atypical mycobacteria
Leprosy (M.leprae)
What does alcohol and acid fast bacilli indicate?
That there is mycobacteria but doesn’t indicate specificity
How does TB spread?
airborne
Someone with TB bacteria in their lungs coughs (sneezes, yells, sings)
TB bacteria attached to aerosol droplets which can remain suspended in air for many hours, especially if there is poor air circulation
Someone else breath these bacteria in
Usually requires prolonged close contact (min 8 hours)
Outdoors mycobacteria eliminated by UV radiation and dilution
Exception to transmission by M. Bovis?
Exception to rule of how TB is spread is Mycobacterium bovis, which can be spread by consumption of unpasteurized infected cows’ milk (very uncommon in the U.K.)
Pathology and Immune response?
TB in alveoli macrophages
Th1 cells from lymph nodes activate macrophages
once activated macrophages turn to epithelial cells and get Langerhans giant cells or giant multi nucleated cells
Accumulation of macrophages, epithelioid & Langhan’s cells
- GRANULOMA (to wall of infection)
Granuloma develops central caseating necrosis - dead tissue falling off and may later calcify
Why is Th1 cell mediated immunological response a two edged sword?
Eliminates / Reduces number of invading mycobacteria
Tissue destruction is a consequence of activation of macrophages
Describe primary infection of TB?
feel unwell , fever but no respiratory symptoms
some systemic symptoms but only short
in vast majority- immune system clears it
calcified nodule in the lung
What can happen after primary infection?
people can clear it
contain it
small have progressive disease and high mortality
Describe tuberculous bronchopneumonia?
Primary focus continues to enlarge - cavitation
(aggressive type of pneumonia)
Enlarged hilar lymph compress bronchi, lobar collapse
Enlarged lymph node discharges into bronchus
Poor prognosis
Describe miliary TB?
Miliary TB (looked like millet seeds on autopsy) develops, with hematogenous spread of bacteria to multiple organs
Fine mottling on X-ray, widespread small granulomata
CNS TB in 10-30%
What is most common type of TB?
post primary disease - takes 1-5 years to typically present
Timeline of TB conditions?
primary complex- 85% of people get
progressive primary disease- 1% of people get
miliary, meningeal , pleural TB- 6-12 months to develop
post primary disease -1-5 years
pulmonary, skeletal -30-40% develop
genitourinary, cutaneous TB- 10-15 but maybe 30-40% will develop
Clinical presentations of TB?
cough
fever
sweats (mainly at night)
weight loss
Test results from TB testing?
CRP (C- reactive protein) normal in 15% , ESR (Erythrocyte sedimentation rate)normal in 21%
Diagnosing post primary TBm(reactivated)?
affects upper part of lungs and cavitation in 10-30%
Lymphadenopathy rare
Normal CXR in 13% of definitive pulm. TB (22% in HIV)
When would you consider CT?
Normal CXR but clinical suspicion
Miliary TB
Cavitation & other differential
Lymphadenopathy, alternative diagnosis
targets for BAL
Diagnosing active pulmonary TB?
CXR
Mediastinal lymphadenopathy (mainly unilateral, 15% bilateral)
Pleural effusion
Miliary (hematogenous spread, 1-3%)
Pneumonic lesion w enlarged hilar nodes –
consider primary TB
How is bug obtained from the body?
FOR LUNG:
Sputum; 3 samples, 8-24hrs gap, at least 1 early morning sample
Induced sputum
Bronchoscopy with BAL
Endobronchial ultrasound (EBUS) with biopsy
FOR BRAIN:
Lumbar puncture in CNS TB / biopsy
Urine in urogenital TB
Aspirate/biopsy from tissue ( lymph-node, bone, joint, brain, abscess …)
Mantoux or IGRA are NOT routinely used in diagnosing active TB- instead in latent
Rules for treatment of tuberculosis?
Multiple drug therapy is essential
Single agent treatment leads to drug resistant organisms within 14 days
Therapy must continue for at least 6 months
TB therapy is a job for committed specialists only
Legal requirement to notify all cases
Test for HIV, Hepatitis B and C
standard treatment of tuberculosis?
start with four drugs over two months and then continue with two of those drugs for remaining four months
2 R/H/Z/E + 4 R/H
Isoniazid (H)
Pyrazinamide (Z)
Rifampicin (R)
Ethambutol (E)
Pyridoxine (Vitamin B6) with isoniazid to reduce risk of neuropathy
Steroids (CNS, Milliary TB, Pericardial)
Vitamin-D substitution
Side effects?
Rifampicin- Orange ‘Irn Bru’ urine/tears/lenses
Induces liver enzymes, prednisolone, anticonvulsants
All hormonal contraceptive methods ineffective
Hepatitis
Isoniazid Hepatitis
Peripheral neuropathy (pyridoxine B6)
Pyrazinamid-Hepatitis
Gout
Ethambutol- Optic neuropathy (check visual acuity)
All four drugs can cause rash
Who is screened?
look for contacts of active cases
infectiveness of cases
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