Epidemiology, Clinical Presentation and Management

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Tuberculosis

EPIDEMIOLOGY, CLINICAL PRESENTATION AND MANAGEMENT

 Tuberculosis is largely due to Mycobacterium tuberculosis.

 TB is present worldwide with an extremely high


prevalence in Asia/Africa.

 60-80% of children below 14years are infected.

 Tuberculosis is spread predominately by droplet


infection.
• The prevalence of tuberculosis increases with poor
social conditions, inadequate nutrition and
overcrowding.

• TB is leading cause of death from a single infectious


disease.

• This is the result of:


1. Inadequate programme for disease control
2. Multiple drug resistance
3. Co-infection with HIV
4. A rapid rise in world’s population of young adults – the age
group with more mortality from TB.
PATHOLOGY
• The first infection with M. tuberculosis is known as
primary tuberculosis.

• It is usually sub-pleural often in the mid to upper


zones.

• Within an hour of reaching the lung, tubercle bacilli


reach the draining lymph at the hilum of the lung
and a few escape into the bloodstream.
• The initial reaction comprises exudation and
infiltration with neutrophil granulocytes.
• These interact with T-lymphocytes, with
development of cellular immunity.

• This CI can be demonstrated 3-8 weeks after initial


infection by a positive reaction in the skin to an
intradermal injection of protein from tubercle bacilli.

• Granulomatous lesions consist of central area of


necrotic material of chessy nature, called caseation;
surrounded by epithaloid cells and Langhan’s giant
cells with multiple nuclei, both cells being derived
from the macrophage.
• Lymphocytes are present and there is varying degree
of fibrosis.

• Subsequently, the caseated areas heal completely and


may become calcified.

• 20% of these calcified primary lesion contain tubercle


bacilli in dormancy but capable of activation with
depressed host defence system.

• Reactivation leads to typical post-primary PTB with


cavitations usually in apex or upper zone of the lungs.
CLINICAL FEATURES
• In majority it is symptomless

• Occasionally there may be vague illness sometimes


associated with cough and wheeze.

• A small transient pleural effusion or erythema


nodosum may occur occasionally.

• Enlargement of lymph nodes compressing the bronchi


can give rise to collapse of segments or lobes of the
lungs.
• Apart from cough and monophonic wheeze,
the individual remains remarkably well and
the collapse disappears as the primary
complex heals.

• Occasionally persistent collapse can give rise


to subsequent bronchiectasis.
MILIARY TB
• Result of acute diffuse dissemination of tubercle
bacilli via bloodstream.

• Fatal without treatment

• Vague illness, loss of weight and fever

• Usually no abnormal physical signs in early stage

• Eventually liver and spleen enlarge


• Choroidal tubercle are seen in the eyes

• CXR may be entirely normal until miliary shadows are 1-


2mm in diameter.

• Mantoux test may be positive or in severe disease may be


negative.

• Biopsy & culture of liver and bone marrow may be


necessary

• A trial of anti TB may be necessary in patients presenting


with PUO.
ADULT POST-PRIMARY TB
• Gradual onset of symptoms over week/month redness,
malaise, anorexia & loss of weight together with fever &
cough.

• Drenching night sweats.

• Sputum may be mucoid, purulent or blood stained.

• Pleural effusion or pneumonia may be presenting feature.


CXR
Abnormal CXR may be present without symptoms. Reverse
is extremely rare CXR or nodular shadows in upper zones,
loss of lung volume fibrosis  cavitation, calcification may
be present.

DIAGNOSIS
• Imaging – CXR, CT Scan
• Staining – Ziehl-Nielsen (ZN) stain for acid and alcohol fast
bacilli
• Culture – Sputum is cultured on Dover’s or Lowenstein –
Jensen medium for 4-8weeks. Sensitivity takes a further 3-
4 weeks.
Fibre-optic bronchoscopy. Useful if no sputum is produced. This
replaced gastric washings in adults.
TREATMENT
DOT
Six months regimen: two months of intensive phase and four months of
continuation phase.
Daily Rifampicin 600mg
Daily Isoniazid 300mg
Daily Pyrazinamide 1.5g
Daily Ethambutol 800mg
Give pyridoxine to counter the side effect of Isoniazid effect (Peripheral
neuropathy)
Rifampicin is reduced to 450mg if patient is less than 55kg
Taken 30minutes before breakfast
Absorption of Rifampicin is influenced by food.
This is supplemented for the first two months b
Pyrazanamide at 1.5g (body wt < 55kg) or 2g daily if >55mg

Longer regimens
Bonee tuberculosis – 9months
Tuberculosis Meningitis – 12months

Unwanted effects of drug treatment


Rifampicin: Liver enzymes
Thrombocytopenia may occur
Stains dresses – sweat, urine, fears
Oral contraceptive – less effective
Isomazid
• Polyneuropathy to use pyridoxine
• Skin rash & fever
• Hepatitis – in less than 1% pyrazinamide
• Severe hapatic toxicity
• Gout may occur

Ethambutol
• Retrobulbar palsy/neuritis – colour blindness for green, reduction in visual
acuity central scotoma.
• Streptomycin.
• Irrevocable damage to vestibalar nerve

Prevention
• BCG Vaccination
• Contact tracing

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