Tuberculosis in Children

By Professor K. Osinusi

TUBERCULOSIS

An important infectious disease globally

About 30% of the world’s population are infected by

the organism that causes tuberculosis

8 to 10 million people develop the disease annually

About 3 million of them are in sub-Saharan Africa

CAUSES OF RESURGENCE IN INCIDENCE OF TB:

Worsening economic situations

Multidrug resistance

HIV pandemic

Decline of national tuberculosis control programmes

Large number of displaced persons living in poor conditions

as a result of conflicts and wars

EPIDEMIOLOGY (I)

Aetiological agent mycobacterium tuberculosis and mycobacterium bovis mycobacterium africanus

Characteristics of mycobacteria

It multiples slowly

It is resistant to many anti- microbial drugs

It remains viable in macrophages by subverting macrophages-killing

Its waxy coat together with its many components substances depress immune

responses against it.

EPIDEMIOLOGY (II)

Sources of Infections: Most important source is sputum of persons with open tuberculosisMode of Spread: Inhalation Ingestion Penetration of skin and mucous membranePredisposing Factors: Age Sex Malnutrition Intercurrent infection Overcrowding & poor living conditions

Pathophysiology

Tuberculosis is a chronic inflammatory disease i.e inflammation of prolonged duration in which active inflammation, tissue destruction and attempt at repair proceed simultaneously

The tubercle bacilli being of low toxicity evokes an immune response called delayed hypersensitivity reaction.

Granulomatous inflammation is a specific type of chronic inflammation which occurs in TB

A focal area of granulomatous inflammation is known as granuloma

In tuberculosis the granuloma is referred to as a tubercle which is classically characterized by the presence of central area of caseous neurosis.

PRIMARY INFECTIONS

Primary focus ) + ) Primary Complex

regional lymph nodes )Primary Focus- Size – varies from a few millimeter to 2 centimeter in diameter- Site – usually situated in the sub-pleural region- Symptoms & signs

May be symptomless May be associated with minor symptoms like malaise and anorexia May be associated with muco-cutaneous manifestations ie erythema

nodosum and phlycternular conjunctivitis

- Primary complex can heal or progress into active disease- Risk of primary infection developing into an active disease is about

15% in the first ten years after infection

Ways in which primary infection can progress to active disease

1. Primary focus can spread to contiguous part of the lungs giving rise to tuberculous pneumonia.

2. Primary focus and the regional lymph nodes may merge and give rise to an area of consolidation.

3. Extensive caseation and liquefaction can develop giving rise to cavity formation.4. The inflamed nodes may compress the neighbouring bronchi giving rise to atelectasis

or emphysema.5. Node may erode through the bronchial wall causing endobronchial tuberculosis.6. There may be discharge of the tubercle bacilli into the lumen leading to bronchogenic

dissemination to other areas of the lungs.7. Nodes may erode into the blood vessels giving rise to haematogenous spread to other

tissue.8. The affected nodes may develop fibrosis and encapsulation with viable tubercule

bacilli persisting within the node for many years and may be the source of reactivation tuberculosis.

Period between primary and the appearance of clinical evidence of various forms of TB

Pulmonary tuberculosis – within a few months of primary infection.

Miliary and meningeal tuberculosis – 2-6 months.

TB adenitis - 3-9 months.

Bones and joints – several years.

Renal and genital tuberculosis – may take over a decade.

Pulmonary lesions occurring as a result of reactivation of a dormant

tuberculosis focus previously established in the body takes a number of years

after primary infection.

PULMONARY TUBERCULOSIS

Commonest form of tuberculosis – occurring alone or in combination with other

forms in 70% of cases.

Pulmonary tuberculosis in children consists mainly of primary complex and direct

progression of its component.

Pathological findings include:

* Hilar enlargement which may lead to bronchial compression with resulting

hyperinflation or atelectasis.

* Consolidation – patchy or lobar with or without pneumothorax and pleural effusion.

* Cavitation.

Clinical Features

Early symptoms are usually vagueChronic coughFeverAnorexiaWeight lossFailure to gain weightHaemoptysis

Signs:- Dyspnoea- Tachypnoea- Localized wheezing- Decreased breath sounds- Crepitations- Bronchial breath sounds- Chest examination may reveal no abnormality- Clinical features of reactivation tb in older children are similar to those of the primary infection but

cough is usually productive and there may be chest pain.

DIAGNOSIS

History Detailed history of current illness Past medical history Family and social history History of contact

INVESTIGATIONS1. Tuberculin skin test2. Chest radiograph Hilar adenopathy Parenchymal lesions

- Patchy infiltrates- Consolidations- Atelectasis- Pleural effusion- Cavities

3. Bacteriological investigations- Sputum ) staining- Gastric washings ) and culture

4. ESR5. FBC

Differential Diagnosis

Pneumonia- Bacterial- Viral- Mycoplasma

Lung abscess Bronchiectasis Pulmonary fungal infections Pulmonary neoplasm

PLEURAL EFFUSION

TB pleural effusion occurs when:

- Sub pleural primary focus ruptures into the pleural cavity.- A caseous node ruptures into the pleural cavity.- During haematogenous spread.- As a result of allergic response to tuberculo-protein.

Clinical Features:Symptoms: Fever

Weight lossChest pain on deep inspiration

Signs: Dullness to percussionDiminished or absent breath sounds.

PLEURAL FLUID:

- Sero-Fibrinous, sometimes blood-stained

- Protein 2-4 g/dL

- High white cell count with predominance of lymphocytes

- Culture yields tubercle bacilli in less than 20%.

MILIARY TUBERCULOSIS

Most severe form of disseminated TB.

Clinical Manifestations:- Variable, depending on the load of organism, organs affected and immune status of the

child.- Onset of symptoms may be explosive or insiduous.Symptoms: Fever

AnorexiaWeight lossCoughWheezing

Signs: Generalised lymphadenopathy.Hepato-splenomegaly.Respiratory distresssigns of meningitis or peritonitis present in 20-40% of cases.Choroidal tubercles.

INVESTIGATIONS

Tuberculin skin testCXRCSF tapHistological examination of

Lymph nodeLiver biopsyMarrow biopsy

Diff. Diagnosis of miliary picture on CXR

- Sarcoidosis- Eosinophilic pneumonia- Pulmonary fungal infection- Chicken-pox pneumonia- Childhood histiocytosis syndrome

TUBERCULOSIS OF THE CNS

Comprises:- Tuberculous meningitis- Tuberculoma

Tuberculous meningitis- Occurs about 2-6 months after the primary infection

- Most common in children aged 6 months to 4 years

- Arises as a result of haematogenous spread of tubercule bacilli to the cerebral cortex and meninges.

Clinical Manifestation

Can be divided into 3 stagesStage I:

Non-specific symptoms like:FeverHeadacheweight lossIrritabilityDrowsiness

Stage II

- Lethargy- Nuchal rigidity- Seizures- Positive Kernig’s sign- Vomiting- Stigns of brainstem involvement- Cranial nerve palsies- + other focal neurological signs

Stage III

- Hemiplegia or paraplegia- Coma- Decrebrate rigidity- Opisthotonus- Fundoscopy may show papilloedema and choroidal

tubercles.

INVESTIGATIONS

1. Tuberculin skin test2. CXR3. Examination of CSF

CSF Picture:May be straw-coloured or may be clear and colourless- WBC 10-500cells/cmm with predominance of lymphocytes

Protein may be over 1GM/dl- Glucose – Low, less than 40mg/dl- Staining with ZN stain may yield Afb- Culture may be positive

PROGNOSIS

Depends on the stage of disease at commencement of therapy.Stage I - Prognosis goodStage III -Mortality is high and a high percentage of those who survive have complications like: - blindness

- deafness- paraplegia- mental retardation- speech disturbance- cranial nerve palsies- Hydrocephalus

TUBERCULOMA

- Presents as an intracranial space-occupying lesion- Usually infratentorial- May be single or multiple

CLINICAL MANIFESTATIONHeadacheFeverConvulsionLateralizing signsInvestigations- Tuberculin skin test- Skull X-ray- CXR- CT Scan of the brain shows discrete masses with surrounding oedema

Diagnosis is often made at surgical exploration for intracranial tumour.